New Frontiers in Dialysis

New Frontiers in Dialysis 88 ∏π‘µ ®√‘ ππ— ∑∏å «—™  √‘ ¿‘ “ ™â“ß»√‘ ‘°≈ÿ ™¬— ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°≈ÿ √ªŸ ∑’Ë 6 ·∫∫®”≈ÕߢÕß Fixed volume, single pool urea kinetic model ∑µË’ ¥— º≈¢Õߧ“à G, UF ·≈– Kr ∑”„Àâ §”π«≥À“§“à Ct ‰¥„â π√ªŸ  ¡°“√∑ßË’ “à ¬¢πÈ÷ ®“° ¡°“√„π√ªŸ ∑Ë’ 6 Ct = C0e- Kt/V Ct / C0= e- Kt/V Kt/V = - ln (Ct / C0) ‡¡ÕË◊ R = Ct / C0 Kt/V = - ln R ¥ß— ππ—È  “¡“√∂À“§“à Kt/V ®“° natural logarithm ¢Õߧ“à Õµ— √“ «à π postdialysis BUN µÕà predialysis BUN ª√– ∑‘ ∏¿‘ “æ¢Õß°“√∑” dialysis  “¡“√∂∫ßà ™‰È’ ¥¥â «â ¬§“à Kt/V ´ß÷Ë ‡ªπì §“à ∑‰Ë’ ¡¡à À’ π«à ¬ ‡¡ÕË◊ ¥®Ÿ “°§“à K §≥Ÿ ¥«â ¬ t ·≈–À“√¥«â ¬ V ®–‡ÀπÁ «“à ‡ªπì §“à fractional clearance ¢Õß solute ‡¡ÕË◊ ‡∑¬’ ∫°∫— distribution volume ¢Õß solute ππÈ— ®“°°“√∑πË’ ” UKM ¡“„™â ∑”„À‰â ¥µâ «— ·ª√ ”§≠— §Õ◊ §“à Kt/V ´ßË÷ π”¡“„™„â π°“√ ª√–‡¡π‘ §“à adequacy of hemodialysis ‡ªπì ¡“µ√∞“π„πª®í ®∫ÿ π— 5.1.2 Variable volume, single pool (VVSP) UKM ·∫∫®”≈Õßπ§È’ ≈“â ¬°∫— «∏‘ ’ FVSP UKM ·µ‡à ªπì ·∫∫®”≈Õß∑„Ë’ °≈‡â §¬’ ߧ«“¡‡ªπì ®√ß‘ ¡“°¢πÈ÷ ‚¥¬ °”Àπ¥„À§â “à V  “¡“√∂‡ª≈¬’Ë π·ª≈߉¥®â “°°“√¥ß÷ ultrafiltrate (UF) ÕÕ°¢≥–∑” HD ·≈–®–¡’ fluid retention ¢πÈ÷ „π™«à ß√–À«“à ß°“√∑” HD ¥ß— √ªŸ ∑Ë’ 7 ´ßË÷ ®–‰¥·â ∫∫®”≈Õß∑¡Ë’ §’ «“¡´∫— ´Õâ π¢πÈ÷ °«“à FVSP UKM

Optimum and Adequacy of Hemodialysis ∏𵑠®√‘ ππ— ∑å∏«—™ 89 √ªŸ ∑Ë’ 7 ·∫∫®”≈ÕߢÕß Variable volume, single pool urea kinetic model 5.1.3 Variable volume, double pool (VVDP) UKM „𧫓¡‡ªπì ®√ß‘ ·≈«â urea √«¡∑ßÈ— dialyzable low molecular weight molecules ÕπË◊ Ê ‡™πà Cr, uric, inorganic phosphate ‡°≈Õ◊ ·√µà “à ßÊ ®–°√–®“¬Õ¬„Ÿà π plasma ·≈– RBC water (Vb), interstitial (Vi) ·≈– intracellular (VI) water °“√‡§≈ÕË◊ π¬“â ¬√–À«“à ß compartment ‡À≈“à πÈ’ Õ“»¬— ¢∫«π°“√ diffusion ‚¥¬ rate ¢Õß°“√ transfer = mass transfer coefficient x concentration gradient between compartment æ∫«“à mass transfer coefficient ¢Õß “√ solute ¢π“¥‡≈°Á ®“° interstitial compartment ‡¢“â  àŸ plasma ¡§’ “à  ßŸ ¡“° ¥ß— ππÈ— concentration equilibrium √–À«“à ß Vb & Vi  “¡“√∂§¥‘ √«¡‡ªπì single extracellular compartment ‰¥â = VE ·∫∫®”≈Õß VVDP ®”≈Õß°“√‡§≈ÕË◊ π∑¢Ë’ Õß urea, Na, water √–À«“à ß HD ∑»‘ ∑“ß°“√‡§≈ÕË◊ π∑®Ë’ “° VI ‰ª àŸ VE ·≈–®“° VE ÕÕ°®“°√“à ß°“¬∂Õ◊ «“à ‡ªπì ∫«° ∑»‘ ∑“ßµ√ߢ“â ¡∂Õ◊ «“à ‡ªπì ≈∫ ·≈–¡¢’ Õâ °”Àπ¥ ¢Õß°“√‡§≈Õ◊Ë π∑¢’Ë Õß “√¥ß— °≈“à «§Õ◊ 1. rate of urea transfer √–À«“à ß VI & VE (JcU) = whole body cell urea mass transfer coefficient (KcU) x concentration gradient (CIU-CEU) 2. osmotically active solute  «à π„À≠¢à Õß VE §Õ◊ Na+ 3. osmotically active solute  «à π„À≠¢à Õß VI §Õ◊ osmotically active intracellular cation (IC+) ·≈–°“√‡§≈ÕË◊ π∑¢Ë’ Õß IC+ ®“° VI ‰ª àŸ VE ‡°¥‘ ¢πÈ÷ πÕâ ¬¡“° 4. ¥ß— ππÈ— rate of water flow √–À«“à ß VI & VE (Q0) ´ßË÷ ‡°¥‘ ®“°·√ߥπ— osmosis ®–‡∑“à °∫— whole body cell UF coefficient (Kcf) x concentration gradient ¢Õß urea (CEU-CIU) ·≈– cation √–À«“à ß VI & VE (CENa-CIC+) ·∫∫®”≈ÕߢÕß VVDP UKM ‡ªπì ·∫∫®”≈Õß∑„Ë’ °≈‡â §¬’ ß ¿“æ®√ß‘ ∑‡Ë’ °¥‘ ¢πÈ÷ „π√“à ß°“¬¡“°°«“à FVSP UKM ·≈– VVSP UKM ·µ à µŸ √∑§Ë’ ”π«≥¡§’ «“¡¬ßàÿ ¬“°¡“° ‰¡‡à À¡“–π”¡“„™ªâ Ø∫‘ µ— ‘ µÕâ ß„™°â “√ ·° â ¡°“√ differential ·≈–‡πÕ◊Ë ß®“°µ¥‘ §“à µ«— ·ª√∑ß—È À¡¥ 7 µ«— §Õ◊ G, VI, VE, VIU, CIU, CINa, CIC+ Õ¬“à ߉√ °µÁ “¡‡æÕË◊ „À â “¡“√∂·° â ¡°“√À“§”µÕ∫¢Õߧ“à µ“à ßÊ µÕâ ß„™„â ™§â “à §ß∑µË’ “à ßÊ ∑¡Ë’ º’ ‰Ÿâ ¥»â °÷ …“‰«â ·≈–«∏‘ ’

New Frontiers in Dialysis 90 ∏π‘µ ®√‘ π—π∑∏å «—™  ‘√¿‘ “ ™â“ß»√‘ ‘°ÿ≈™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°ÿ≈ °“√§≥µ‘ »“ µ√√å «à ¡°π— ‡æÕË◊ „À‰â ¥§â ”µÕ∫ ¥ß— √ªŸ ∑Ë’ 8 5.2 Empirical method ‡ªπì «∏‘ §’ ”π«≥‚¥¬·∑π§“à K, t, V ‚¥¬µ√ß °“√À“§“à in vivo dialyzer urea clearance 14-16 ‚¥¬‡®“–‡≈Õ◊ ¥®“° arterial ·≈– venous port À≈ß— ∑” HD 30 π“∑’ ·≈«â §”π«≥®“° µŸ √´ßË÷ ª√∫— º≈¢Õß water content ∑¡Ë’ „’ πæ≈“ ¡“·≈–‡¡¥Á ‡≈Õ◊ ¥·¥ß ‡∑“à °∫— 93% ·≈– 72% µ“¡≈”¥∫— ®–‰¥â QP = QB x [(1 - Hct) 0.93 + (Hct x 0.72)] = QB (0.93 - 0.21Hct) K = QP x (Ca - CV)/CA + Qf x CV/CA = QB (0.93 - 0.21Hct) x (Ca - CV)/CA + Qf x CV/CA ‚¥¬ QP = plasma flow rate QB = blood flow rate K = urea clearance in vivo ¢Õß dialyzer Ca = √–¥∫— BUN ®“° arterial port CV = √–¥∫— BUN ®“° venous port √ªŸ ∑’Ë 8 ·∫∫®”≈ÕߢÕß Variable volume, double pool urea kinetic model ·≈–«∏‘ °’ “√§≥µ‘ »“ µ√∑å µË’ Õâ ß„™â √«à ¡

Optimum and Adequacy of Hemodialysis ∏𵑠®‘√π—π∑å∏«™— 91  «à π§“à V À“‰¥Àâ ≈“¬«∏‘ ’ ‡™πà 1. V = 0.58 x BW (Kg) 2. §“à anthropometric urea distribution volume ®“°«∏‘ ’ Hume-Weyers sex-specific regression Male TBW = (0.194786 x height) + (0.296785 x weight) - 14.012934 Female TBW = (0.34454 x height) + (0.183809 x weight) - 35.270121 3. §“à anthropometric urea distribution volume ®“°«∏‘ ’ bioelectrical impedance (BEI) ∑„Ë’ ™â »°÷ …“ TBW „π§π‰¢‰â µ«“¬‡√ÕÈ◊ √ß— ´ßË÷ æ∫«“à ¡§’ «“¡∂°Ÿ µÕâ ß¡“°°«“à «∏‘ ¢’ Õß Hume-Weyers §”π«≥§“à V ®“° BEI-derived formula17 ‰¥®â “° TBW = -(0.07493713 x age) - (1.01767992 x male) + (0.12703384 x height) - (0.04012056 x weight) + (0.57894981 x diabetic) - (0.00067247 x weight 2) - (0.0348146 x age x male) + (0.11262857 x male x weight) + (0.00104135 x age x weight) + (0.00186104 x height x weight) ∂“â ‡ªπì º™âŸ “¬ À√Õ◊ ‡∫“À«“π „À·â ∑π§“à male À√Õ◊ diabetic ‡ªπì 1 5.3  µŸ √ Second generation of natural logarithm ¢Õß Daugirdas18 ‡ªπì «∏‘ ∑’ πË’ ¬‘ ¡„™„â πª®í ®∫ÿ π— ‡πÕË◊ ß®“° “¡“√∂§”π«≥‰¥ßâ “à ¬ ‚¥¬„™Àâ ≈°— °“√¢Õß VVSP UKM §Õ◊ ®“°§“à Kt/V = -ln R „π VVSP UKM π”¡“ª√∫— ª√ßÿ ‚¥¬ª√∫— º≈¢Õß urea generation rate ·≈–º≈¢Õß ultrafiltrate µÕà §“à R ®–‰¥ â ¡°“√ original formula19 §Õ◊ Kt/V = -Ln (R - 0.008 x t - UF/W) ´ß÷Ë  “¡“√∂§”π«≥§“à Kt/V ‰¥¥â „’ π™«à ß 0.7-1.3 ∂“â ¡“°°«“à 1.3 §“à Kt/V ®“°«∏‘ π’ ®’È – overestimate Daugirdas ®ß÷ ‰¥ªâ √∫— ª√ßÿ  µŸ √„À¡‡à æÕË◊ „À â “¡“√∂§”π«≥§“à Kt/V ‰¥¥â „’ π™«à ß∑°Ë’ «“â ߢπÈ÷ §Õ◊ 0.6-2.6 ¥ß—  ¡°“√∑„’Ë ™°â π— Õ¬∑àŸ «—Ë ‰ª„πª®í ®∫ÿ π— Kt/V = -Ln (R - 0.008 x t) + (4 - 3.5 x R) x UF/W R = Ct / C0 Ln = natural logarithm t = √–¬–‡«≈“∑” Hemodialysis (Àπ«à ¬ hour) Ct = postdialysis BUN C0 = predialysis BUN UF = ª√¡‘ “µ√ ultrafiltrate (Àπ«à ¬ Litre) W = postdialysis weight (Àπ«à ¬ Kilogram) 5.4 Direct dialysate quantitative (DDQ) method ‡ªπì «∏‘ °’ “√À“§“à Kt/V ‚¥¬¥°Ÿ “√¢®¥— urea ∑“ߥ“â π dialysate ‚¥¬‡°∫Á dialysate ∑ßÈ— À¡¥∑ºË’ “à π

New Frontiers in Dialysis 92 ∏π‘µ ®‘√ππ— ∑∏å «—™  √‘ ‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « π— µå  ÿ‡¡∏°ÿ≈ µ«— °√Õߢ≥–∑” HD ‡æÕË◊ À“§“à K ·≈– V ‚¥¬µ√ß ¡“§”π«≥µ“¡«∏‘ ¢’ Õß Milchesky20,21 ·≈–∂°Ÿ π”¡“ ª√∫— ª√ßÿ ‡æÕË◊ „À‡â ªπì double pool kinetics ·≈–·°‰â ¢º≈¢Õß ultrafiltration ‡ªπì «∏‘ ’ modified direct dialysate quantitative (mDDQ) 22 ∫“ß∑“à π°≈“à ««“à «∏‘ ’ mDDQ π“à ®–‡ªπì «∏‘ ∑’ ∂Ë’ °Ÿ µÕâ ß ‡πÕË◊ ß®“°‡ªπì °“√«¥— °“√¢®¥— ¬Ÿ ‡√¬’ ∑Õ’Ë Õ°®“°√“à ß°“¬®√ß‘ 6. Urea rebound ‡ªπì ª√“°Ø°“√≥ å ”§≠— ∑∑’Ë ”„À°â “√§”π«≥§“à Kt/V º¥‘ æ≈“¥ ‚¥¬ urea rebound ¡º’ ≈„À√â –¥∫— ¢Õß BUN „π‡≈Õ◊ ¥ ßŸ ¢πÈ÷ Õ¬“à ß√«¥‡√«Á ¿“¬À≈ß— ‡ √®Á  πÈ‘ HD ·¡«â “à urea ∑‡Ë’ °¥‘ ®“° urea generation À≈ß— ‡ √®Á  πÈ‘ HD ¡º’ ≈µÕà urea rebound ·µæà ∫«“à º≈¥ß— °≈“à «ππÈ— πÕâ ¬¡“° æ∫«“à urea rebound ·∫ßà ‡ªπì 3 phase23,24 ´ßË÷ ¡ ’ “‡Àµ·ÿ ≈–‡«≈“‡©æ“–‡®“–®ß √ªŸ ∑Ë’ 9 §Õ◊ 6.1 Access recirculation recirculation À¡“¬∂ß÷ °“√∑‡’Ë ≈Õ◊ ¥∑‰’Ë ¥¢â ®¥— ¢Õ߇ ¬’ ÕÕ°®“° dialyzer ·≈«â «π°≈∫— º“à π‡¢“â dialyzer Õ°’ §√ßÈ— °Õà π∑®Ë’ –‰À≈º“à π√∫— ¢Õ߇ ¬’  «à πÕπË◊ Ê ¢Õß√“à ß°“¬ ´ßË÷ ·∫ßà ‡ªπì 2 ™π¥‘ §Õ◊ access recirculation ·≈– cardiopulmonary recirculation access recirculation (AR)25 ‡°¥‘ ®“°§«“¡º¥‘ ª°µ¢‘ Õß vascular access ∑”„Àâ access flow ¡§’ “à µ”Ë °«“à blood flow rate ´ßË÷ µßÈ— ‚¥¬ blood pump ‡ªπì º≈„À‡â ≈Õ◊ ¥∑ºË’ “à π°“√øÕ°·≈«â ‰À≈®“° venous line ¢Õß vascular access °≈∫— ‡¢“â dialyzer ∑“ß arterial line ¢Õß vascular access Õ°’ access recirculation √ªŸ ∑’Ë 9 ª√“°Ø°“√≥å urea rebound ·∫ßà ‡ªπì 3 phase ´ßË÷ ¡ ’ “‡Àµ·ÿ ≈–‡«≈“‡©æ“–‡®“–®ß

Optimum and Adequacy of Hemodialysis ∏𵑠®‘√π—π∑∏å «™— 93 ®–∑”„À√â –¥∫— ¢Õß arterial line urea ≈¥≈ßÕ¬µŸà ≈Õ¥√–¬– dialysis ¥ß— ππÈ— ∑π— ∑∑’ ÀË’ ¬¥ÿ À√Õ◊ ™–≈Õ blood pump ‡≈◊Õ¥∑’ˇ§¬‰À≈¬âÕπ°≈—∫∑“ß access ‰¡à‡°‘¥¢÷Èπ √–¥—∫ urea „π‡≈◊Õ¥∑’Ë¥Ÿ¥®“° arterial line ®–‡æ‘Ë¡¢÷Èπ ∑π— ∑∑’ ‰Ë’ ≈‡à ≈Õ◊ ¥∑øË’ Õ°·≈«â ∑§Ë’ “â ßÕ¬„àŸ π dead space ¢Õß blood line ÕÕ°‰ª  “¡“√∂«¥— access recirculation ‚¥¬«∏‘ ’ slow flow method26 ≈¥ blood flow rate ‰ª∑Ë’ 120 ml/min π“π 10 «π‘ “∑’ 6.2 Cardiopulmonary recirculation Cardiopulmonary recirculation (CPR) ‡°¥‘ ¢π÷È ‡¡Õ◊Ë ‡≈Õ◊ ¥∑ø’Ë Õ°·≈«â ‰À≈°≈∫— ‡¢“â  ÀŸà «— „®‰ªªÕ¥·≈– °≈∫—  ÀàŸ «— „® ®“°ππÈ— ‰À≈°≈∫— ‡¢“â  Ÿà dialyzer Õ°’ §√ßÈ— ‚¥¬‰¡ºà “à π systemic capillary bed CPR ππÈ— ‡°¥‘ ¢πÈ÷ ‡©æ“–‡¡◊ËÕ„™â arteriovenous (A-V) access ‡∑à“π—Èπ ‚¥¬À≈—߇√‘Ë¡∑” dialysis ‡≈◊Õ¥∑’ËøÕ°·≈â«°≈—∫‡¢â“ Ÿà À—«„®·≈–ªÕ¥ ‚¥¬¡’‡≈◊Õ¥ à«πÀπ÷Ë߉À≈ºà“π°≈—∫‡¢â“ àŸ dialyzer ‚¥¬µ√ß‚¥¬ bypass ∑“ß A-V access ∑”„À√â –¥∫— urea „π‡≈Õ◊ ¥·¥ß≈¥≈ß ‡ªπì º≈„À‡â °¥‘ A-V gradient ¢Õß urea Õ¬µàŸ ≈Õ¥‡«≈“°“√∑” dialysis ·µ∑à π— ∑∑’ ÀË’ ¬¥ÿ °“√∑” dialysis ∑”„À‰â ¡¡à ‡’ ≈Õ◊ ¥ bypass ∑“ß A-V access ®ß÷ ‰¡¡à ’ CPR ‡°¥‘ ¢πÈ÷ A-V gradient ¢Õß urea ®–§Õà ¬Ê ≈¥≈ß ·≈–À“¬‰ª„π 1-2 π“∑’ ¥ß— ππ—È ‡æÕ◊Ë À≈°’ ‡≈¬’Ë ßº≈¢Õß CPR µÕâ ߇®“–‡≈Õ◊ ¥µ√«®√–¥∫— urea ∑‡Ë’ «≈“ 2 π“∑’ ‚¥¬„™â slow flow method ·µ∂à “â „™‡â ªπì venovenous (V-V) access ‡≈Õ◊ ¥∑ø’Ë Õ°·≈«â ®–‰À≈‰ªº ¡°∫— ‡≈Õ◊ ¥∑À’Ë ≈Õ¥‡≈Õ◊ ¥¥” ∑‰Ë’ À≈º“à π systemic capillary bed ¡“·≈«â ∑”„À‡â ªπì ‡≈Õ◊ ¥º ¡‰À≈°≈∫— ‡¢“â  ÀŸà «— „® (mixed venous blood) ‰¡¡à §’ «“¡·µ°µ“à ߢÕß√–¥∫— urea ®ß÷ ‰¡‡à °¥‘ CPR 6.3 Compartment effect12,24 ‡ªπì º≈®“°§«“¡‰¡ à ¡¥≈ÿ ¢Õß urea √–À«“à ߇≈Õ◊ ¥·≈–‡πÕ◊È ‡¬Õ◊Ë ¢≥–∑” HD ´ß÷Ë ‡°¥‘ ®“° 2  “‡Àµÿ §Õ◊ 6.3.1 Double pool effect ®“°¡°’ “√ delay urea removal ®“° intracellular compartment ‡¢“â  àŸ plasma ´ßË÷ ∂°Ÿ ®”°¥— ‚¥¬ whole body cell urea mass transfer coefficient (KcU) 6.3.2 Regional blood flow effect ®“°°“√∑‡Ë’ ≈Õ◊ ¥°√–®“¬‰ª‡≈¬È’ ßÕ«¬— «–µ“à ßÊ ‰¡‡à ∑“à °π— ¢≥– ∑” HD12 ‡πÕÈ◊ ‡¬ÕË◊ ´ßË÷ ¡‡’ ≈Õ◊ ¥‰ª‡≈¬È’ ßπÕâ ¬ ‡™πà °≈“â ¡‡πÕÈ◊ ·≈–°√–¥°Ÿ ®–¡°’ “√‡§≈ÕË◊ π¬“â ¬ urea ®“°‡πÕÈ◊ ‡¬ÕË◊ ‡¢“â  ‡àŸ ≈Õ◊ ¥πÕâ ¬ ∑”„À√â –¥∫— urea „π‡πÕÈ◊ ‡¬ÕË◊ ¥ß— °≈“à «®– ßŸ °«“à √–¥∫— urea „π mixed venous blood Õ¬Ÿà µ≈Õ¥‡«≈“ µ√ߢ“â ¡°∫— ‡πÕÈ◊ ‡¬ÕË◊ ∑¡Ë’ ‡’ ≈Õ◊ ¥‰ª‡≈¬’È ß¡“° ‡™πà À«— „® ªÕ¥  ¡Õß ®–¡°’ “√‡§≈ÕË◊ π¬“â ¬ urea ®“°‡πÕÈ◊ ‡¬ÕË◊ ‡¢“â  ‡Ÿà ≈Õ◊ ¥¡“° √–¥∫— urea „π‡πÕÈ◊ ‡¬ÕË◊ ¥ß— °≈“à «®ß÷ µ”Ë ‡¡ÕË◊ À¬¥ÿ ∑” HD urea ®“° «à π∑¡Ë’ ’ urea  ßŸ ®–§Õà ¬Ê ‡¢“â  °àŸ √–· ‡≈Õ◊ ¥ ®π°«“à ®–‰¥√â –¥∫— urea  ¡¥≈ÿ °∫— „π‡≈Õ◊ ¥ ´ßË÷ °π‘ ‡«≈“π“π 30-60 π“∑’ °“√‡®“–‡≈Õ◊ ¥µ√«®√–¥∫— ¢Õß urea „π‡≈Õ◊ ¥ ‚¥¬À≈°’ ‡≈¬Ë’ ߺ≈¢Õß urea rebound ®ß÷ §«√‡®“– ‡≈◊Õ¥∑’ˇ«≈“À≈—߇ √Á® ‘Èπ°“√øÕ°‡≈◊Õ¥‡ªìπ‡«≈“π“π 30-60 π“∑’ ∑”„À≥â§à“ equilibrated BUN ´÷Ëßπ” ‰ª„™§â ”π«≥À“§“à equilibrated Kt/V (eKt/V) ´ßË÷ π“à ®–‡ªπì §“à Kt/V ∑∂Ë’ °Ÿ µÕâ ß¡“°°«“à ‡πÕË◊ ß®“°‰¡¡à º’ ≈¢Õß urea rebound °“√«¥— ª√¡‘ “≥ urea rebound  “¡“√∂§¥‘ ‰¥®â “° rebound rate = (Ceq - Ct)/Ct x 100% º≈¢Õß

New Frontiers in Dialysis 94 ∏π‘µ ®‘√ππ— ∑∏å «™—  √‘ ¿‘ “ ™â“ß»√‘ ‘°ÿ≈™¬— ∏ππ— ¥“ µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ urea rebound „π·µ≈à –§π¡§’ “à ·µ°µ“à ß°π— ‰¥¡â “° ‚¥¬‡©≈¬Ë’ ¡§’ “à ª√–¡“≥ 17% ´ßË÷ Õ“®∑”„À§â “à eKt/V πÕâ ¬°«“à §“à spKt/V ‰¥ªâ √–¡“≥ 0.219 7 7. Rate equation 24,27-9 ‡ªπì «∏‘ À’ “§“à eKt/V ∑∂’Ë °Ÿ æ≤— π“¢π÷È ‡πÕ◊Ë ß®“°°“√√Õ‡®“–‡≈Õ◊ ¥∑‡’Ë «≈“À≈ß— ‡ √®Á  π‘È °“√øÕ°‡≈Õ◊ ¥ π“π 30-60 π“∑’ ‰¡ à –¥«°„π∑“ߪØ∫‘ µ— ‘ ‚¥¬„™Àâ ≈°— °“√∑«Ë’ “à urea disequilibrium πÕ°®“°®–‡°¥‘ ®“° °“√‡§≈ÕË◊ π¬“â ¬¢Õß urea √–À«“à ß intracellular ·≈– extracellular compartment ‰¡∑à π— °∫— °“√¢®¥— urea ÕÕ°®“°‡≈Õ◊ ¥∑“ß dialyzer ·≈«â ¬ß— ‡°¥‘ ®“°º≈¢Õß regional blood flow ´ßË÷ À¡“¬∂ß÷ ª√¡‘ “≥ blood flow ∑‰Ë’ ª‡≈¬È’ ßÕ«¬— «–µ“à ßÊ ¢≥–∑” HD ‰¡‡à ∑“à °π— visceral organs ®–‰¥√â ∫— ‡≈Õ◊ ¥‡ªπì  ¥—  «à π¢Õß cardiac output ¡“°°«“à  «à πÕπË◊ ‡™πà °≈“â ¡‡πÕÈ◊ °√–¥°Ÿ º«‘ Àπß— ∑”„À°â ≈“â ¡‡πÕ◊È ´ßË÷ ª√–°Õ∫¥«â ¬ 80% ¢Õß total body water ¡‡’ ≈Õ◊ ¥‰ª‡≈¬È’ ߇欒 ß 15-20% ¢Õß cardiac output ¥ß— ππÈ— À≈ß— ‡ √®Á  πÈ‘ HD °≈“â ¡‡πÕÈ◊ ®–¡√’ –¥∫— urea  ßŸ °«“à Õ«¬— «–ÕπË◊ ∑”„À‡â °¥‘ urea rebound Daugirdas ·≈– Schneditz ‰¥»â °÷ …“º≈¥ß— °≈“à « ‚¥¬∑”°“√ª√∫— §“à Kt/V ®“° VVSP UKM ‚¥¬ „™ â ¡°“√‡ πâ µ√ß (linear equation) æ∫«“à §«“¡™π— ¢Õß ¡°“√¡§’ «“¡ ¡— æπ— ∏°å ∫— rate ¢Õß dialysis (K/V) ∑”„À â “¡“√∂À“§“à eKt/V ‰¥¥â ß—  ¡°“√¢Õß Rate equation §Õ◊ ‡¡ÕË◊ „™â A-V access eKt/V = spKt/V - [0.6 x (spKt/V) / t] + 0.03 ‡¡ÕË◊ „™â V-V access eKt/V = spKt/V - [0.47 x (spKt/V) / t] + 0.02 ‚¥¬ spKt/V = single pool Kt/V ®–‡ÀπÁ «“à «∏‘ ’ Rate equation ‡ªπì °“√„™â spKt/V ‡æÕË◊ ª√–‡¡π‘ §“à eKt/V ·≈–‡ªπì «∏‘ ∑’ §Ë’ ”πß÷ ∂ß÷ º≈ ¢Õß urea rebound ‚¥¬‡©æ“–Õ¬“à ߬ßË‘ º≈¢Õß regional blood flow ∑”„Àπâ “à ®–‡ªπì «∏‘ ∑’ ∂Ë’ °Ÿ µÕâ ß°«“à «∏‘ Õ’ πË◊ Ê ∑ªË’ √–‡¡π‘ º≈¢Õß°“√¢®¥— urea ∑“ߥ“â π‡≈Õ◊ ¥¥«â ¬°π— ·≈–¬ß— ‡ªπì «∏‘ ∑’ ßË’ “à ¬„π°“√‡°∫Á µ«— Õ¬“à ß ¡ ’ ¡°“√ ‰¡´à ∫— ´Õâ π·≈–‡À¡“–„π∑“ߪØ∫‘ µ— ‡‘ ¡Õ◊Ë ‡ª√¬’ ∫‡∑¬’ ∫°∫— «∏‘ ’ urea kinetic model ´ß÷Ë ¡°’ “√§”π«≥∑¬’Ë ßÿà ¬“°°«“à 8. ¢Õâ ·π–𔇰¬Ë’ «°∫— «∏‘ °’ “√«¥— §«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥ 30,31 1. §«√«¥— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥∑º’Ë ªâŸ «É ¬§«√®–‰¥√â ∫— Õ¬“à ßπÕâ ¬‡¥Õ◊ π≈–§√ß—È 2. «∏‘ «’ ¥— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥§«√„™§â “à Kt/V ‚¥¬·π–π”°“√§”π«≥‚¥¬„™â formal urea kinetic model √Õß≈߉ª§Õ◊ Simplified multivariable equation ‡™πà  µŸ √ Second generation of natural logarithm ¢Õß Daugirdas √“¬≈–‡Õ¬’ ¥¥ß— · ¥ß„πµ“√“ß∑Ë’ 5 3. §“à Kt/V ∑‡Ë’ ≈Õ◊ °„™„â π¢Õâ ·π–𔇰¬Ë’ «°∫— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥ §Õ◊ spKt/V ·¡«â “à eKt/V ®–‡ªπì §“à ∑‰Ë’ ¡∂à °Ÿ º≈°√–∑∫®“° urea rebound ‡πÕË◊ ß®“°°“√§”π«≥§“à eKt/V ¬ß— µÕâ ߧ”π«≥§“à spKt/V °Õà π ·≈– KDOQI ‰¡ à π∫—  ππÿ „À∑â ”°“√øÕ°‡≈Õ◊ ¥ 3 §√ßÈ— µÕà  ª— ¥“Àå ‚¥¬„™‡â «≈“°“√øÕ°‡≈Õ◊ ¥πÕâ ¬°«“à 3 ™«Ë— ‚¡ß ´ßË÷ ®–∑”„À§â “à eKt/V µ“à ß®“°§“à spKt/V ¡“° ·≈–¬ß— ‰¡¡à À’ ≈°— ∞“π·π™à ¥— ∑·Ë’  ¥ß„À‡â ÀπÁ ∂ß÷ §«“¡

Optimum and Adequacy of Hemodialysis ∏π‘µ ®‘√ππ— ∑∏å «™— 95 µ“√“ß∑Ë’ 5 «∏‘ «’ ¥— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥∑Ë’ KDOQI ·π–π”„À„â ™â (‚¥¬‡√¬’ ßµ“¡≈”¥∫— ®“°¡“°‰ªπÕâ ¬) §¡âÿ §“à „π°“√∑®Ë’ –µÕâ ß„™§â “à eKt/V 9. ¢Õâ ·π–𔇰¬’Ë «°∫— ª√¡‘ “≥°“√øÕ°‡≈Õ◊ ¥30 9.1 ºªŸâ «É ¬∑√’Ë ∫— °“√øÕ°‡≈Õ◊ ¥ 3 §√ß—È µÕà  ª— ¥“Àå 1. ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë ∑ºË’ ªŸâ «É ¬§«√®–‰¥√â ∫— (Minimally adequate delivered dose)  ”À√∫— ºªŸâ «É ¬∑√Ë’ ∫— °“√øÕ°‡≈Õ◊ ¥ 3 §√ßÈ— µÕà  ª— ¥“Àå ·≈–¡§’ “à residual renal function < 2 ¡≈/π“∑/’ 1.73 µ√¡. §Õ◊ spKt/v = 1.2 µÕà §√ßÈ— (‰¡πà ∫— √«¡º≈°“√∑”ß“π¢Õ߉µ∑‡Ë’ À≈Õ◊ ) ( ”À√∫— °“√øÕ°‡≈Õ◊ ¥∑„Ë’ ™‡â «≈“ πÕâ ¬°«“à 5 ™«Ë— ‚¡ßµÕà §√ßÈ— Õ“®‡≈Õ◊ °„™§â “à URR ∑Ë’ 65%) 2. ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥‡ª“Ñ À¡“¬ (Target dose) ∑„Ë’ ™„â π°“√ ßË— °“√√°— …“ºªŸâ «É ¬∑√Ë’ ∫— °“√ øÕ°‡≈Õ◊ ¥ 3 §√ßÈ— µÕà  ª— ¥“Àå ·≈–¡§’ “à residual renal function < 2 ¡≈/π“∑/’ 1.73 µ√¡. §Õ◊ spKt/v = 1.4 µÕà §√ßÈ— (‰¡πà ∫— √«¡º≈°“√∑”ß“π¢Õ߉µ∑‡Ë’ À≈Õ◊ ) À√Õ◊ „™§â “à URR ∑Ë’ 70% 3. ºªâŸ «É ¬∑√Ë’ ∫— °“√øÕ°‡≈Õ◊ ¥ 3 §√ßÈ— µÕà  ª— ¥“Àå ·≈–¡§’ “à residual renal function > 2 ¡≈/π“∑/’ 1.73 µ√¡. Õ“®≈¥ª√‘¡“≥¢Õß°“√øÕ°‡≈◊Õ¥¢—ÈπµË”∑’˺⟪ɫ¬§«√®–‰¥â√—∫≈߉¥â ¥—ßµ“√“ß∑’Ë 6 ·≈–„Àâµ—Èß µ“√“ß∑Ë’ 6 ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë spKt/V µÕà §√ßÈ— (‰¡πà ∫— √«¡º≈°“√∑”ß“π¢Õ߉µ∑‡Ë’ À≈Õ◊ ) ∑ºË’ ªâŸ «É ¬§«√ ®–‰¥√â ∫— ‡æÕË◊ „À‰â ¥ªâ √¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë §Õ◊ spKt/v = 2.0 µÕà  ª— ¥“Àå

New Frontiers in Dialysis 96 ∏𵑠®√‘ ππ— ∑∏å «™—  ‘√‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™¬— ∏π—𥓠µ√–°“√«π™‘ « π— µå  ÿ‡¡∏°ÿ≈ ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥‡ª“Ñ À¡“¬„À â ߟ °«“à ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë Õ¬“à ßπÕâ ¬ 15% 9.2 ºªâŸ «É ¬∑√Ë’ ∫— °“√øÕ°‡≈Õ◊ ¥ 2 §√ßÈ— µÕà  ª— ¥“Àå 1. ºªâŸ «É ¬∑¡Ë’ §’ “à residual renal function < 2 ¡≈/π“∑/’ 1.73 µ√¡. ‰¡·à π–π”„Àøâ Õ°‡≈Õ◊ ¥ 2 §√ßÈ— µÕà  ª— ¥“Àå 2. ºªŸâ «É ¬∑øË’ Õ°‡≈Õ◊ ¥ 2 §√ßÈ— µÕà  ª— ¥“Àå µÕâ ß¡§’ “à residual renal function > 2 ¡≈/π“∑/’ 1.73 µ√¡. ·≈–§«√‰¥√â ∫— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë §Õ◊ spKt/v = 2.0 µÕà  ª— ¥“Àå 3. ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë ¢ÕߺªŸâ «É ¬∑øË’ Õ°‡≈Õ◊ ¥ 2 §√ßÈ— µÕà  ª— ¥“Àå ‡æÕË◊ „À‰â ¥ªâ √¡‘ “≥ ¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë spKt/v = 2.0 µÕà  ª— ¥“Àå §Õ◊ spKt/v = 2.0 µÕà §√ßÈ— ¥ß— µ“√“ß∑Ë’ 6 ·≈–„Àµâ ßÈ— ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥‡ª“Ñ À¡“¬„À â ߟ °«“à ª√¡‘ “≥¢Õß°“√øÕ°‡≈Õ◊ ¥¢πÈ— µ”Ë Õ¬“à ßπÕâ ¬ 15% 10.  √ªÿ §«“¡√‡âŸ °¬’Ë «°∫— §«“¡ ”§≠— ·≈–«∏‘ °’ “√ª√–‡¡π‘ §«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥¡§’ «“¡ ”§≠— Õ¬à“߬‘Ëß„π°“√¥·Ÿ ≈ºŸâªÉ«¬øÕ°‡≈◊Õ¥ §«“¡‡¢â“„®æ◊Èπ∞“π‡°’Ë¬«°—∫ urea kinetic model ®–™à«¬„À⇢Ⓞ® ∑’Ë¡“¢Õß«‘∏’°“√§”π«≥§à“ Kt/V «‘∏’°“√µà“ßÊ ∑’Ë„™â„π‡«™ªØ‘∫—µ‘ª√–®”«—π √«¡∑—Èß à߇ √‘¡„Àâ¡’°“√ æ—≤𓧑¥§âπ«‘∏’°“√„À¡àÊ ‡æ◊ËÕ„À≥⫑∏’°“√ª√–‡¡‘𧫓¡‡æ’¬ßæÕ¢Õß°“√øÕ°‡≈◊Õ¥∑’Ë∂Ÿ°µâÕß·≈–  –¥«°¬ßË‘ ¢πÈ÷ ∑ßÈ— π‡È’ æÕË◊ „Àºâ ªâŸ «É ¬¡§’ ≥ÿ ¿“晫’ µ‘ ∑¥Ë’ ·’ ≈– “¡“√∂¡Õ’ “¬¬ÿ π◊ ¬“«„°≈‡â §¬’ ߪ°µ¡‘ “°∑ Ë’ ¥ÿ ‡Õ° “√Õ“â ßÕß‘ 1. Chirananthavat T, Praditpornsilpa K. Current Status of Renal Replacement Therapy in Thailand. The 13th Annual Meeting of Japanese Society for Hemodiafiltration Proceeding 2007: 40. 2. Õ…ÿ ≥“ ≈«ÿ √’ –. °“√√°— …“‚√§‰µ«“¬‡√ÕÈ◊ √ß— √–¬– ¥ÿ ∑“â ¬‚¥¬«∏‘ ∑’ ¥·∑π‰µ„πª√–‡∑»‰∑¬. „π: Õ…ÿ ≥“ ≈«ÿ √’ –, æ√√≥∫ÿªº“ ™Ÿ«‘‡™’¬√, ∫√√≥“∏‘°“√. °“√√—°…“‚¥¬«‘∏’ Hemodialysis ·≈– CAPD. °√ÿ߇∑æ:  ”π—°æ‘¡æå °√ßÿ ‡∑懫™ “√ 2536: 147-54. 3. Levin NW. Adequacy of dialysis. Am J Kidney Dis 1994; 24: 308-15. 4. Linsay RM, Henderson LW. Adequacy of dialysis. Kidney Int 1988; 33 (Suppl 24): S 92-9. 5. Vanholder RC, Ringoir SM. Adequacy of dialysis: A critical analysis. Kidney Int 1992; 42: 540-58. 6. Vanholder R, Smet RD, Glorieux G, et al. Review on uremic toxins: Classification, Concentration and Interindividual variability. Kidney Int 2003; 63: 1934-43. 7. Blake P, Daugirdas JT. Quantification and prescription: General principles. In: Jacobs C, Kjellstrand CM, Koch KM, Winchester JF, eds. Replacement of renal function by dialysis. Netherlands: Kluwer Academic Publishers 1995. 619-56. 8. Owen WF JR, Lew NL, Liv Y, Lowrie EG, Lazarus JM: The urea reduction rate and serum albumin

Optimum and Adequacy of Hemodialysis ∏𵑠®√‘ ππ— ∑∏å «™— 97 concentration as predictors of mortality in patients undergoing hemodialysis. N Engl J Med 1993; 329: 1001-6. 9. Hakim RM. Assessing the adequacy of dialysis. Kidney Int 1990; 37: 822-32. 10. Laird NM, Berkey CS, Lowrie Eg. Modeling success or failure of dialysis therapy: the National Cooperative Dialysis Study. Kidney Int 1983; 28: S 101-6. 11. Gotch FA, Sargent JA. A mechanistic analysis of the NCDS. Kidney Int 1985; 28: 526-34. 12. Gotch FA. Kinetic modeling in hemodialysis. In: Nissenson AR, Fine RN, Gentile DE, eds. Clinical dialysis. London: Prentice-Hall International 1995. 156-188. 13. Sargent JA, Gotch FA. Principles and biophysics of dialysis. In: Jacobs C, Kjellstrand CM, Koch KM, Winchester JF, eds. Replacement of renal function by dialysis. Netherlands: Kluver Academic Publishers 1995. 156-88. 14. Bankhead MM, Toto RD, Star RA. Accuracy of urea removal estimated by kinetic models. Kidney Int 1995; 48: 785-93. 15. Lim VS, Flanigan MJ, Fangman J. Effect of hematocrit on solute removal during high efficiency hemodialysis. Kidney Int 1990; 37: 1557-62. 16. Leypoltdt JK, Cheung AK, Agodoa LY, Daugirdas JT, Greene T, Keshaviah PR, for the Hemodialysis (HEMO) study. Hemodialyzer mass transfer-area coefficients for urea increase at high dialysate flow rates. Kidney Int 1997; 51: 2013-7. 17. Chertow GM, Lowrie EG, Lew NL, Lazarus JM. Development of a population-specific regression equation to estimate total body water in hemodialysis patients. Kidney Int 1997;51: 1578-82. 18. Daugirdas JT. Second generation logarithm estimates of single-pool variable volume Kt/V: an analysis of error. J Am Soc Nephrol 1993; 4: 1205-13. 19. Daugirdas JT. The post:pre dialysis plasma urea nitrogen ratio to estimate Kt/V and NPCR: Mathematical modeling. Int J Artif Organs 1989; 12: 411-9. 20. Malchesky PS, Ellis P, Nosse C, Magnusson M, Lankhorst B, Nakamoto S. Direct quantification of dialysis. Dial Transpl 1982; 11: 42-4. 21. Barth RH. Direct calculation of Kt/V. Nephron 1988; 50: 191-5. 22. Depner TA, Keshavaih PR, Ebben JP, Emerson PF, Collins AJ, Jindal KK, Nissenson AR, Lazarus JM, Pu K. Multicenter clinical validation of an on-line monitor of dialysis adequacy. J Am Soc Nephro 1996; 7: 464-71. 23. Depner TA. Assessing adequacy of hemodialysis: Urea modeling. Kidney Int 1994; 45: 1522-35. 24. NKF-DOQI Clinical Practice Guidelines for Hemodialysis adequacy. Am J Kidney Dis 1997;30 (suppl 2): s22- s31. 25. Kopple JD, Jones MR, Keshaviah PR, Bergstrom J, Lindsay RM, Moran J, Nolph KD, Teehan BP. A proposed glossary for dialysis kinetics. Am J Kidney Dis 1995; 26: 963-81. 26. Sherman RA, Kapoian T. Recirculation, urea disequilibrium and dialysis efficiency: Peripheral arteriovenous versus central venovenous vascular access. Am J Kicney Dis 1997; 29: 497-89.

New Frontiers in Dialysis 98 ∏π‘µ ®‘√ππ— ∑å∏«—™  √‘ ‘¿“ ™â“ß»√‘ ‘°≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ÿ‡¡∏°ÿ≈ 27. Daugirdas JT, Schneditz D. Overestimation of hemodialysis dose depends of dialysis efficiency by regional blood flow but not by conventional two pool urea kinetic analysis. ASAIO J 1995; 41: M719-M724. 28. Daugirdas JT. Estimation of equilibrated Kt/V using the unequilibrated post dialysis BUN. Semin Dial 1995; 8: 283-4. 29. HEMO Study group, prepared by Daugirdas JT, depner TA, Gotch FA, Greene T, Keshaviah P, Lewin NW, Schulman G. Comparison of methods to predict equilibrated Kt/V in the HEMO pilot study. Kidney Int 1997; 52: 1395-1405. 30. NKF-K/DOQI clinical practice guidelines for hemodialysis adequacy 2006. Am J Kidney Dis 2006; 48, 1 (suppl 1): S1-90. 31. Chirananthavat T, Tungsanga K, Eiam-ong S. Accuracy of Using 30-Minute Post-Dialysis BUN to Determine Equilibrated Kt/V. J Med Assoc Thai 2006; 89(suppl2): S54-S64.

6 Update of Intravenous Iron and Anemia Management  √‘ ¿‘ “ ™“â ß»√‘ °‘ ≈ÿ ™¬— 1. ∫∑π” 2. º≈°√–∑∫®“°¿“«–´¥’ 3. °“√ª√–‡¡π‘ ¿“«–´¥’ 4. ·π«∑“ß°“√√°— …“¿“«–´¥’ 5. °“√√°— …“¿“«–´¥’ ¥«â ¬ erythropoiesis-stimulating agents (ESA) 6. °“√„À‡â À≈°Á 7. °“√„™¬â “À√Õ◊ «∏‘ √’ °— …“Õπ◊Ë √«à ¡°∫— °“√„Àâ ESA „πºªâŸ «É ¬∑∑Ë’ ” hemodialysis 8. °“√ª√–‡¡π‘ ºªâŸ «É ¬∑Ë’‰¡µà Õ∫ πÕßµÕà °“√√°— …“ 9. New erythropoiesis-stimulating agents 10.  √ªÿ

New Frontiers in Dialysis 100 ∏π‘µ ®√‘ ππ— ∑∏å «™—  ‘√‘¿“ ™“â ß»√‘ ‘°≈ÿ ™¬— ∏π—𥓠µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°ÿ≈ 1. ∫∑π” ¿“«–´¥’ ‡ªπì ª≠í À“À≈°— „πºªŸâ «É ¬‰µ‡ ÕË◊ ¡ (Chronic kidney disease; CKD) ‰¡«à “à  “‡Àµ¢ÿ Õ߉µ ‡ ÕË◊ ¡ππÈ— ®–‡°¥‘ ®“°Õ–‰√°µÁ “¡ §«“¡√πÿ ·√ߢÕß¿“«–´¥’ ®–·ª√ºπ— µ“¡§«“¡√πÿ ·√ߢÕßÀπ“â ∑‰Ë’ µ∑≈Ë’ ¥≈ß ºŸâªÉ«¬∑’Ë¡’Àπâ“∑’ˉµ≈¥≈ß¡“°¡—°®–¡’¿“«–´’¥√ÿπ·√ß¡“°°«à“ºŸâªÉ«¬∑’Ë¡’Àπâ“∑’ˉµ≈¥≈ßπâÕ¬°«à“ ·≈–®– æ∫Õ∫ÿ µ— °‘ “√≥¢å Õß¿“«–´¥’ ¡“°¢πÈ÷ µ“¡√–¬–§«“¡√πÿ ·√ߢÕß CKD 1 ºªŸâ «É ¬∑¡Ë’ ’ GFR πÕâ ¬°«“à 30 ml/min (CKD stage 4) ¡°— ®–¡√’ –¥∫— hemoglobin (Hb) πÕâ ¬°«“à 11 g/dl2 „πºªŸâ «É ¬‰µ‡ ÕË◊ ¡®“°‡∫“À«“π®–‡°¥‘ ¿“«–´¥’ ‰¥‡â √«Á °«“à ·≈–√πÿ ·√ß°«“à ºªŸâ «É ¬‰µ‡ Õ◊Ë ¡®“° “‡ÀµÕÿ π◊Ë 3, 4 √«¡∑ß—È æ∫Õ∫ÿ µ— °‘ “√≥¿å “«–´¥’ ‰¥¡â “°°«“à ‰µ‡ ◊ËÕ¡®“° “‡ÀµÿÕ◊Ëπ∑’Ë√–¥—∫ GFR ‡¥’¬«°—π5 ‚¥¬¿“«–´’¥„πºâŸªÉ«¬‰µ‡ ◊ËÕ¡¡’ “‡ÀµÿÀ≈—°®“°°“√¢“¥ erythropoietin ´ßË÷ ∂ß÷ ·¡«â “à erythropoietin ®– “¡“√∂∂°Ÿ  √“â ߢπÈ÷ ‰¥„â π‡πÕÈ◊ ‡¬ÕË◊ ¢Õß√“à ß°“¬À≈“¬µ”·Àπßà ·µà erythropoietin ∑®Ë’ ”‡ªπì µÕà °“√ √“â ߇¡¥Á ‡≈Õ◊ ¥·¥ß®– √“â ß®“° endothelial cell ∫√‡‘ «≥ renal tubule ¥—ßπ—Èπ‡¡◊ËÕ‰µ‡ ’¬ excretory function ®–∑”„Àâ¡’°“√ √â“ß erythropoietin ≈¥≈ߥ⫬ πÕ°®“°π’ȺŸâªÉ«¬ Õ“®¡¿’ “«–´¥’ ®“° “‡ÀµÕÿ π◊Ë Ê‡À¡Õ◊ π„πºªŸâ «É ¬∑‰’Ë ¡‰à ¥‡â ªπì ‚√§‰µ‡ Õ◊Ë ¡‡™πà ¿“«–¢“¥‡À≈°Á ,¿“«–¢“¥‚ø‡≈∑ (folate), ¿“«– malnutrition, ¿“«–‡ ¬’ ‡≈Õ◊ ¥ (blood loss), hemolysis ‡ªπì µπâ 2. º≈°√–∑∫®“°¿“«–´¥’ (Consequences of anemia) 1. º≈µÕà À«— „® ¿“«–‰µ‡ Õ◊Ë ¡‡ªπì ª®í ®¬— ‡ ¬’Ë ß ”§≠— µÕà °“√‡°¥‘ ‚√§À«— „®(independentriskfactor) ºâŸªÉ«¬∑’ˇªìπ‚√§À—«„®·≈–¡’¿“«–´’¥‡√◊ÈÕ√—ß∑’ˉ¡à‰¥â√—°…“Õ“®®–∑”„Àâ¡’º≈‡ ’¬µàÕÀ—«„®®π·°â‰¢‰¡à‰¥â ‡™àπ irreversible left ventricular hypertrophy, fibrosis6 ‚¥¬°≈‰°∑∑Ë’ ”„À‡â °¥‘ cardiovascular disease (CVD) ®“° ¿“«–´¥’ ‡ªπì º≈®“° tissue hypoxia (√ªŸ ∑Ë’ 1) ‰¥¡â °’ “√»°÷ …“æ∫«“à √–¥∫— Hb ∑≈Ë’ ¥≈ß∑°ÿ Ê 0.5 g/dl „π√–¬– predialysis ºªâŸ «É ¬®–¡§’ «“¡‡ ¬Ë’ ߥ“â π cardiovascular event ‡æ¡Ë‘ ¢πÈ÷ 32%7 ºªâŸ «É ¬∑¡Ë’ √’ –¥∫— Hb µ”Ë µÕπ‡√¡Ë‘ dialysis ®–¡Õ’ µ— √“°“√‡°¥‘ ¿“«–·∑√°´Õâ π¥“â πÀ«— „®·≈–‡ ¬’ ™«’ µ‘ „πª·ï √°¢Õß°“√∑” dialysis  ßŸ ·µ∂à “â „À°â “√√°— …“µß—È ·µ·à √°®–≈¥Õµ— √“°“√‡ ¬’ ™«’ µ‘ ‰¥6â -8 2. º≈µÕà ¿“«–‰µ‡ ÕË◊ ¡ (progression of CKD) ‡¡ÕË◊ ∑” multivariate analysis ¢Õâ ¡≈Ÿ °“√»°÷ …“ ®“° RENAAL10 æ∫«“à ¿“«–´¥’ ‡ªπì independent risk factor ∑∑Ë’ ”„ÀÀâ π“â ∑‰Ë’ µ≈¥≈ß ‚¥¬æ∫«“à ºªâŸ «É ¬∑¡Ë’ ’ √–¥∫— Hb πÕâ ¬°«“à 11.2 g/dl ®–¡§’ «“¡‡ ¬Ë’ ß∑ÀË’ π“â ∑‰Ë’ µ≈¥≈ß 60% ·µºà ªâŸ «É ¬∑√Ë’ –¥∫— Hb ¡“°°«“à 13.8 g/ dl ®–¡§’ «“¡‡ ¬’Ë ß∑À’Ë π“â ∑‰’Ë µ≈¥≈ß 20% °≈‰°∑¿’Ë “«–´¥’ ¡º’ ≈„ÀÀâ π“â ∑‰’Ë µ≈¥≈ß®“°∑”„À‡â °¥‘ hypoxic injury µàÕ tubule ‚¥¬∑—Ë«‰ª oxygen tension „π à«π medulla ®–µË”°«à“ cortex ¿“«–´’¥∑”„Àâ tubule ‚¥¬ ‡©æ“–„π «à π medulla ‡°¥‘ hypoxic injury ß“à ¬¢π÷È ¡°’ “√ª≈Õà ¬ reactive oxygen species ∑”„À‡â °¥‘ inflammation ·≈– scar ‡¡ÕË◊ ‡æ¡Ë‘ √–¥∫— Hb ®–‡æ¡Ë‘ ®”π«π red blood cell (rbc) ‡ªπì °“√‡æ¡Ë‘ oxygen ‰ª¬ß— tubule ≈¥ hypoxic injury, ≈¥ oxidative stress µÕà ‰µ ·≈–‡´≈µ“à ßÊ ¢Õß√“à ß°“¬¡’ erythropoietin receptor ‡¡ÕË◊ „Àâ erythropoietin ®–®∫— °∫— receptor ∑”„Àªâ ÕÑ ß°π— ‡´≈µ“¬ (apoptosis) (√ªŸ ∑Ë’ 2) ¡°’ “√»°÷ …“æ∫«“à ºªâŸ «É ¬ CKD ∑‰Ë’ ¥â erythropoietin ‡æÕË◊ √°— …“¿“«–´¥’ ®–¡Õ’ µ— √“°“√≈¥≈ߢÕßÀπ“â ∑‰’Ë µ™“â °«“à °≈¡àÿ ∑‰Ë’ ¡‰à ¥√â °— …“11 ·≈–¡’

Update of Intravenous Iron and Anemia Management  √‘ ‘¿“ ™“â ß»√‘ °‘ ÿ≈™¬— 101 √ªŸ ∑Ë’ 1 · ¥ß°≈‰°°“√‡°¥‘ ¿“«–·∑√°´Õâ π∑“ßÀ«— „®„π¿“«–´¥’ 9 °“√»°÷ …“„πºªâŸ «É ¬ nondiabetic CKD 88 √“¬ æ∫«“à ºªŸâ «É ¬∑‰Ë’ ¥√â ∫— erythropoietin ‡æÕË◊ √°— …“¿“«–´¥’ µßÈ— ·µà√–¬–·√°®–¡’Õ—µ√“°“√≈¥≈ߢÕß creatinine clearance ™â“°«à“ºŸâªÉ«¬∑’ˉ¥â√—∫ erythropoietin ‡æ◊ËÕ √°— …“¿“«–´¥’ „π√–¬–∑“â ¬12 3. º≈µÕà §≥ÿ ¿“晫’ µ‘ (Quality of life; QOL) ºªŸâ «É ¬∑´Ë’ ¥’ Õ“®®–¡Õ’ “°“√ÕÕà π‡æ≈¬’ ‡ÀπÕË◊ ¬ß“à ¬ µ–§√«‘ ª√– ∑‘ ∏¿‘ “æ°“√∑”ß“π≈¥≈ß ª«¥»√’ …– ¡ª’ ≠í À“°“√πÕπÀ≈∫— °“√‡√¬’ π√≈Ÿâ ¥≈ß ´¡÷ ‡»√“â 14 ¡’ °“√»°÷ …“æ∫«“à ∂“â ·°‰â ¢¿“«–´¥’ ®π Hb ¡“°°«“à 10 g/dl ®–∑”„Àâ QOL ¥¢’ πÈ÷ 15-17 4. º≈µÕà Õµ— √“°“√‡ ¬’ ™«’ µ‘ (mortality rate) ·≈–Õµ— √“°“√√∫— ‰«√â °— …“„π‚√ß欓∫“≈ (hospital admission rate) ¡¢’ Õâ ¡≈Ÿ °“√»°÷ …“‡ª√¬’ ∫‡∑¬’ ∫Õµ— √“°“√‡ ¬’ ™«’ µ‘ √–À«“à ߺªŸâ «É ¬ CKD ∑¡Ë’ ’ Hb <11 g/dl ·≈– Hb >11 g/dl æ∫«“à „πºªâŸ «É ¬∑¡Ë’ √’ –¥∫— Hb <11 g/dl ®–¡Õ’ µ— √“°“√‡ ¬’ ™«’ µ‘  ßŸ °«“à ºªŸâ «É ¬∑¡Ë’ √’ –¥∫— Hb >11 g/ dl18 ‚¥¬ “‡Àµ°ÿ “√‡ ¬’ ™«’ µ‘ ®–‡ªπì ®“° CVD19 ·≈–¡°’ “√»°÷ …“¬Õâ πÀ≈ß— „πºªâŸ «É ¬ dialysis æ∫«“à ºªâŸ «É ¬∑¡Ë’ ’ Hb πÕâ ¬°«“à ®–¡Õ’ µ— √“°“√√∫— √°— …“„π‚√ß欓∫“≈ ßŸ °«“à ºªâŸ «É ¬∑¡Ë’ ’ Hb  ßŸ °«“à 20 5. º≈µÕà °√–∫«π°“√·¢ßÁ µ«— ¢Õ߇≈Õ◊ ¥ (Homeostasis) ºªâŸ «É ¬‰µ‡ ÕË◊ ¡∑¡Ë’ ’ Hb πÕâ ¬°«“à 10 g/dl ®–¡’ bleeding time ¬“«¢÷Èπ ´÷Ë߇¡◊ËÕ·°â‰¢¿“«–´’¥®–∑”„Àâ√–¥—∫ fibrinogen, factor VIII ‡æ‘Ë¡¢÷Èπ ·≈– ‡°√¥Á ‡≈Õ◊ ¥¡°’ “√‡°“–µ«— °π— ¥¢’ πÈ÷ (platelet aggregation)

New Frontiers in Dialysis 102 ∏π‘µ ®‘√π—π∑∏å «™—  ‘√‘¿“ ™â“ß»‘√‘°≈ÿ ™¬— ∏π—𥓠µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ √ªŸ ∑’Ë 2  ¡¡µ∞‘ “π°≈‰°°“√·°‰â ¢¿“«–´¥’ ∑¡’Ë º’ ≈™–≈Õ¿“«–‰µ‡ Õ◊Ë ¡13 3. °“√ª√–‡¡π‘ ¿“«–´¥’ (Evaluation of anemia) ‡πÕË◊ ß®“°ºªŸâ «É ¬ CKD ¡°— ¡¿’ “«–´¥’ ·≈–¿“«–´¥’ ¡º’ ≈°√–∑∫µÕà °“√欓°√≥‚å √§ (prognosis) ¥ß— ππÈ— KDOQI ªï 2006 (Kidney Disease Outcomes Quality Initiative) 21 ·≈– EBPG ªï 2004 (European Best Practice guideline)22 ·π–π”„Àµâ √«®À“¿“«–´¥’ ¥«â ¬°“√«¥— √–¥∫— Hb „πºªŸâ «É ¬ CKD ∑°ÿ √“¬ ‚¥¬‰¡¢à πÈ÷ Õ¬àŸ °∫— √–¬–¢Õß CKD À√Õ◊  “‡Àµ¢ÿ Õß CKD KDOQI ·π–π”„Àµâ √«®À“¿“«–´¥’ „πºªâŸ «É ¬ CKD ∑‰Ë’ ¡‰à ¥√â ∫— ESA (erythropoiesis-stimulating agent) ¥«â ¬°“√«¥— √–¥∫— Hb Õ¬“à ßπÕâ ¬ 1 §√ßÈ— /ªï ‡æ√“–‡¡ÕË◊ Àπ“â ∑‰Ë’ µ≈¥≈ß ¡“°¢π÷È ®–¡¿’ “«–´¥’ √πÿ ·√ߢπ÷È ·µ„à πºªâŸ «É ¬∫“ß√“¬∑¡’Ë ¿’ “«–´¥’ Õ¬°àŸ Õà πÀ√Õ◊ Õ“°“√‰¡§à ß∑§’Ë «√«¥— √–¥∫— Hb ∫Õà ¬¢π÷È ‡°≥±„å π°“√«π‘ ®‘ ©¬— ¿“«–´¥’ KDOQI „™‡â °≥±‡å ¡ÕË◊ Hb <13.5 g/dl „πº™âŸ “¬ ·≈– Hb <12.0 g/dl „πºÀ⟠≠ß‘ EBPG „™‡â °≥±«å π‘ ®‘ ©¬— ¿“«–´¥’ „πºªâŸ «É ¬ CKD ‡¡ÕË◊ √–¥∫— Hb πÕâ ¬°«“à mean - 2 SD À√Õ◊ <95% ¢Õߧ“à Hb „π§πª°µ∑‘ ‡Ë’ æ»·≈–Õ“¬‡ÿ ¥¬’ «°π— (Hb <11.5 g/dl „πºÀ⟠≠ß‘ ; <13.5 g/dl „πº™Ÿâ “¬; <12.0 g/dl „πº™Ÿâ “¬Õ“¬‡ÿ °π‘ 70 ª)ï ´ß÷Ë ‡°≥±°å “√«π‘ ®‘ ©¬— ¿“«–´¥’ µ“¡ World Health Organization ®–∂Õ◊ ‡°≥±å Hb

Update of Intravenous Iron and Anemia Management  √‘ ¿‘ “ ™“â ß»‘√‘°≈ÿ ™¬— 103 <12.0 g/dl „πºÀ⟠≠ß‘ ·≈– Hb <13 g/dl „πº™Ÿâ “¬ °“√·ª≈º≈ Hb §«√§”πß÷ ∂ß÷ ª®í ®¬— ∑¡Ë’ º’ ≈µÕà °“√«¥— Hb ‰¥·â °à §«“¡ ßŸ ¢Õß ∂“π∑ÕË’ ¬ÕàŸ “»¬— (altitude), ‡™ÕÈ◊ ™“µ,‘ °“√ ∫Ÿ ∫Àÿ √,Ë’ ‡æ» ‚¥¬æ∫«“à ºâŸ∑’ËÕ“»—¬Õ¬Ÿà∑’ˠߟ °«“à √–¥∫— π”È ∑–‡≈∑°ÿ 1000 ‡¡µ√®–¡§’ “à Hb ‡æ¡Ë‘ ¢πÈ÷ 0.9 g/dl „𙓬 ·≈–§“à Hb ‡æ¡Ë‘ ¢πÈ÷ 0.6 g/dl „πÀ≠ß‘ „πº∑⟠ Ë’ ∫Ÿ ∫Àÿ √®Ë’ –¡§’ “à Hb  ßŸ ¢πÈ÷ 1.5 g/dl ‚¥¬‰¡‰à ¥¡â °’ “√‡æ¡Ë‘ ¢πÈ÷ ¢Õß°“√·≈°‡ª≈¬Ë’ πÕÕ°´‡‘ ®π23 À≠ß‘ ∑¡Ë’ ’ ª√–®”‡¥Õ◊ πÀ√Õ◊ µßÈ— §√√¿®å –¡’ Hb µ”Ë °«“à ™“¬ ºâŸªÉ«¬ CKD ∑’Ë¡’¿“«–´’¥§«√¡’°“√µ√«®À“ “‡Àµÿ¢Õß¿“«–´’¥¥â«¬°“√µ√«®∑“ßÀâÕߪؑ∫—µ‘ °“√ÕπË◊ ʇæ¡Ë‘ ‡µ¡‘ ®“°°“√«¥— √–¥∫— Hb °Õà π®–殑 “√≥“„Àâ ESA ‡πÕË◊ ß®“° “‡Àµ¿ÿ “«–´¥’ „πºªŸâ «É ¬ CKD Õ“®‡°‘¥®“° “‡ÀµÿÕ◊Ëπ∑’ˉ¡à„™à®“°°“√¢“¥ erythropoietin ‰¥â KDOQI ‰¥â·π–π”°“√µ√«®‡æ‘Ë¡‡µ‘¡‡æ◊ËÕ ª√–‡¡π‘ ¿“«–´¥’ ‰¥·â °à 1. Complete blood count (CBC) ´ßË÷ √«¡∂ß÷ rbc indices (MCH, MCV, MCHC), wbc count ·≈–°“√π∫— ·¬°™π¥‘ , platelet count °“√µ√«® CBC ®–∫Õ°∂ß÷ severity ¢Õß¿“«–´¥’ , bone marrow function, adequacy of nutrient °“√ª√–‡¡π‘ §«“¡√πÿ ·√ߢÕß¿“«–´¥’ §«√¥®Ÿ “°§“à Hb ¡“°°«“à §“à Hct ‡æ√“–§“à Hct ¢π÷È Õ¬°Ÿà ∫— ‡§√Õ◊Ë ß∑„’Ë ™«â ¥— 22  «à π Hb ®–¡°’ “√∑” standardize ¢Õ߇§√Õ◊Ë ß·≈–‰¡¡à º’ ≈®“° storage time À√Õ◊ Õ≥ÿ À¿¡Ÿ ∑‘ ∑Ë’ ” °“√¥Ÿ rbc indices ®–™«à ¬∫Õ°™π¥‘ ¢Õß¿“«–´¥’ (type of anemia) ∂“â ¡®’ ”π«π wbc ·≈– platelet µ”Ë ®–· ¥ß∂ß÷ §«“¡º¥‘ ª°µ¢‘ Õß‚√§‡≈Õ◊ ¥ÕπË◊ Ê 2. Absolute reticulocyte count ‡πÕË◊ ß®“°∂“â rbc morphology ‡ªπì normochromic normocytic Õ“®®–‡ªπì ®“° CKD À√Õ◊ ®“° chronic disease ´ßË÷ ‡°¥‘ ®“° erythropoietic activity µ”Ë °“√«¥— absolute reticulocyte count ®–∫Õ°∂ß÷ erythropoietic activity ‚¥¬π”§“à absolute reticulocyte count ¡“§”π«≥ reticulocyte index ·≈– reticulocyte production index µ“¡ µŸ √ Absolute reticulocyte count = %reticulocyte count x rbc count Reticulocyte index = Observed absolute reticulocyte count Normal absolute reticulocyte count §“à normal absolute reticulocyte count ª√–¡“≥ 40,000-50,000 cell/µL Reticulocyte production index = Reticulocyte index ÷ Expected maturation time ∂“â ¡’ ESA ®–°√–µπâÿ „À‰â ¢°√–¥°Ÿ ª≈Õà ¬ reticulocyte ¡“Õ¬„Ÿà π‡≈Õ◊ ¥‡√«Á ¢πÈ÷ ·≈– reticulocyte ®– Õ¬„Ÿà π‡≈Õ◊ ¥π“π¢π÷È °«“à ®–‡ªπì mature rbc ∑”„À¡â ’ maturation time π“π „π¿“«–ª°µ‘ reticulocyte maturation time „π‡≈◊Õ¥ª√–¡“≥ 1 «—π „π¿“«–´’¥∑’Ë¡’ erythropoietin ‡æ’¬ßæÕ∑’Ë®–µÕ∫ πÕßµàÕ¿“«–´’¥®–¡’ maturation time π“π¢πÈ÷ ‡™πà Hb 10-13 g/dl ®–¡’ maturation time ª√–¡“≥ 1.5 «π— , Hb 7-10 g/dl ®–¡’ maturation time 2 «π— , Hb 3-7 g/dl ®–¡’ maturation time 2.5 «π— ∂“â ºªâŸ «É ¬∑´’Ë ¥’ ·≈–«¥— reticulocyte production index ‰¥¡â “°°«“à 3 · ¥ß«“à ‰¢°√–¥°Ÿ µÕ∫ πÕßµÕà ¿“«–´¥’ ‰¥â ·µ∂à “â reticulocyte production index πÕâ ¬°«“à 2 · ¥ß«“à ‰¢°√–¥°Ÿ µÕ∫ πÕßµÕà ¿“«–´¥’ µ”Ë (hypoproliferative response) 3. Assessment of iron status ºªŸâ «É ¬ CKD ∑¡Ë’ ¿’ “«–´¥’ §«√‰¥√â ∫— °“√ª√–‡¡π‘  ¿“«–‡À≈°Á „π√“à ß°“¬ ‚¥¬ª√–‡¡π‘ iron storage ´ßË÷ ®–¥®Ÿ “° serum ferritin ·≈–ª√–‡¡π‘ iron adequacy  ”À√∫— erythropoiesis ´ßË÷ ¥®Ÿ “° serum transferrin saturation (TSAT) À√Õ◊ ª√¡‘ “≥ Hb „π reticulocyte (reticulocyte

New Frontiers in Dialysis 104 ∏π‘µ ®√‘ ππ— ∑∏å «—™  √‘ ¿‘ “ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π‘™ « π— µå  ÿ‡¡∏°≈ÿ Hb content; CHr) À√Õ◊ percentage of hypochromic rbc (PHRC) 3.1 Ferritin ¡¢’ 𓥂¡‡≈°≈ÿ „À≠ªà √–¡“≥ 450 Kd  √“â ß®“°µ∫— ∑”Àπ“â ∑„’Ë π°“√‡°∫Á  – ¡‡À≈°Á (iron storage) ¡’ªí®®—¬À≈“¬Õ¬à“ß∑’Ë¡’º≈µàÕ√–¥—∫ ferritin §◊Õ¿“«– inflammation, malignancy ‡™àπ neuroblastoma, renal cell carcinoma, malnutrition ®–¡§’ “à serum ferritin ®– ßŸ 24 ®ß÷ ∂Õ◊ «“à ferritin ‡ªπì marker µ«— ÀπßË÷ ¢Õß inflammation ·≈– tumor marker ·µ§à “à serum ferritin µ”Ë · ¥ß«“à ¡¿’ “«–¢“¥‡À≈°Á ¥ß— ππÈ— ∂“â «¥— §“à serum ferritin ‰¥µâ ”Ë ®–¡§’ «“¡®”‡æ“– (specificity)  ßŸ ∑·Ë’  ¥ß«“à ¡¿’ “«–¢“¥‡À≈°Á ·µà ∂“â «¥— serum ferritin ‰¥ â ߟ Õ“®®–¡À’ √Õ◊ ‰¡¡à ¿’ “«–¢“¥‡À≈°Á °‰Á ¥â 3.2 Transferrin saturation Transferrin ‡ªπì globulin ¢π“¥ 90 Kd  √“â ß®“°µ∫— ∑”Àπ“â ∑„Ë’ π°“√ ¢π ßà (transportation) ‡À≈°Á §“à transferrin ∑«Ë’ ¥— ®–„°≈‡â §¬’ ß°∫— §“à TIBC (Total Iron Binding Capacity) §“à ª°µ¢‘ Õß serum transferrin §Õ◊ 170-300 mg/dl ´ßË÷ ®–¡§’ “à  ßŸ °«“à TIBC ª√–¡“≥ 25% ‚¥¬§“à ª°µ¢‘ Õß TIBC §Õ◊ 200-350 µg/L §“à transferrin  “¡“√∂§”π«≥‰¥®â “°§“à TIBC Transferrin (mg/dl) × 1.25 = TIBC (µg/L) TSAT(%) = [serum iron/TIBC] × 100 „π¿“«–¢“¥‡À≈°Á §“à TSAT ®–µ”Ë ‚¥¬¡°— ®–πÕâ ¬°«“à 10% ‡πÕË◊ ß®“° serum iron ≈¥≈ß TIBC  ßŸ ¢πÈ÷ ·µ¡à ¢’ Õâ ®”°¥— „π°“√·ª≈º≈ TSAT §Õ◊ „π¿“«– malnutrition, inflammation ®–¡’ TIBC µ”Ë ¥ß— ππÈ— ·¡«â “à serum iron µ”Ë ‡¡ÕË◊ À“√¥«â ¬ TIBC ∑µË’ ”Ë ¥«â ¬§“à TSAT °ªÁ °µ‰‘ ¥â 3.3 Reticulocyte Hb content ®–‡ªπì °“√«¥— iron „π‡¡¥Á ‡≈Õ◊ ¥‚¥¬µ√ß ¡§’ “à ·ª√ºπ— πÕâ ¬ ∂“â §“à CHr πÕâ ¬°«“à 29-32 pg/cell ¡°— ®–∫ßà ™«’È “à ºªâŸ «É ¬¡¿’ “«–¢“¥‡À≈°Á ·≈–®–‰¥ªâ √–‚¬™π®å “°°“√„À‡â À≈°Á 25, 26 3.4 Percentage of hypochromic rbc ‰¡§à Õà ¬π¬‘ ¡«¥— „π∑“ߪØ∫‘ µ— ‘ ‡æ√“–∂“â sample ‡°∫Á ‰«πâ “π À√Õ◊ „™‡â «≈“π“π„π°“√ ßà ¡“¬ß— ÀÕâ ßµ√«®®–∑”„Àâ PHRC  ßŸ °«“à §“à ·∑®â √ß‘ EBPG πÕ°®“°·π–π”«∏‘ °’ “√ª√–‡¡π‘ ¿“«–´¥’ ¢“â ßµπâ ·≈«â ¬ß— ·π–π”„À¡â °’ “√µ√«® C-reactive protein (CRP) ‡æÕ◊Ë ª√–‡¡π‘  ¿“«– inflammation ·≈–ºªâŸ «É ¬∑∑’Ë ” dialysis §«√ª√–‡¡π‘ frequency ·≈– dialysis dose √«à ¡¥«â ¬ À≈ß— ®“°ª√–‡¡π‘ ¿“«–´¥’ ‡∫Õ◊È ßµπâ EBPG‰¥·â π–π”„À¡â °’ “√µ√«®ºªâŸ «É ¬‡æ¡‘Ë ‡µ¡‘ (extensivework- up) µ“¡Õ“°“√∑“ߧ≈π‘ °‘ ·≈–º≈°“√µ√«®‡∫ÕÈ◊ ßµπâ ‚¥¬§«√§√Õ∫§≈¡ÿ °“√µ√«®µÕà ‰ªπÈ’ - assessment of occult gastrointestinal blood loss - serum B12 and red cell folate concentration - serum/plasma intact parathyroid hormone (iPTH) - differential wbc count and platelet - tests for hemolysis (plasma/serum levels of haptoglobin, lactate dehydrogenase, bilirubin, Coombsû test) - plasma/serum and/or urine protein electrophoresis/immunoblotting - serum aluminium - Hb electrophoresis and bone marrow examination in seleced cases

Update of Intravenous Iron and Anemia Management  ‘√¿‘ “ ™“â ß»‘√°‘ ≈ÿ ™—¬ 105  à«π KDOQI ‰¡à·π–π”„Àâ∑” stool occult blood test „π°“√ª√–‡¡‘π¿“«–¢“¥‡À≈Á° ‡πÕ◊Ë ß®“°¡º’ ≈≈∫≈«ß¡“° 4. ·π«∑“ß°“√√°— …“¿“«–´¥’ (Treatment of renal anemia) EBPG 200422 ‰¥°â ”Àπ¥·π«∑“ß„π°“√√°— …“¿“«–´¥’ ¥ß— πÈ’ 1. ºªŸâ «É ¬ CKD §«√®–¡‡’ ª“Ñ À¡“¬√–¥∫— Hb >11 g/dl (Hct >33%) À√Õ◊ „πºªâŸ «É ¬∑¡Ë’ √’ –¥∫— ‰¡∂à ß÷ ‡ª“Ñ À¡“¬ §«√√°— …“„À¡â √’ –¥∫— Hb ∂ß÷ ‡ª“Ñ À¡“¬„π√–¬–‡«≈“ 4 ‡¥Õ◊ π „πºªŸâ «É ¬∑∑Ë’ ” hemodialysis §«√ «¥— √–¥∫— Hb °Õà π‡√¡‘Ë ∑” dialysis session ·≈–¡¢’ Õâ ·π–π”ÕπË◊ Ê ‡æ¡Ë‘ ‡µ¡‘ ‡°¬Ë’ «°∫— √–¥∫— Hb §Õ◊ - §«√π”ª®í ®¬— ‡√ÕË◊ ßÕ“¬,ÿ ‡æ», °®‘ °√√¡„π™«’ µ‘ ª√–®”«π— ·≈– co-morbid condition ¢Õߺ⟠ª«É ¬¡“√«à ¡æ®‘ “√≥“ª√∫— √–¥∫— Hb  ßŸ °«“à 11.0 g/dl - √–¥∫— Hb °Õà π‡√¡Ë‘ ∑” hemodialysis ‰¡§à «√‡°π‘ 14.0 g/dl ‡æ√“–®–‡ ¬Ë’ ßµÕà º≈¢“â ߇§¬’ ß®“° post-dialysis hemoconcentration - √–¥∫— Hb ∑‡Ë’ À¡“– ¡ Õ“®·µ°µ“à ß°π— „πºªâŸ «É ¬∑¡Ë’ ’ co-morbid condition µ“à ß°π— ‡™πà „π ºªŸâ «É ¬∑¡’Ë ’ cardiovascular disease (CVD) √πÿ ·√ß∑¡’Ë ’ New York Heart Association Classification of Congestive Heart Failure µßÈ— ·µà class III ¢π÷È ‰ª ‰¡§à «√„À¡â √’ –¥∫— Hb >12.0 g/dl ‡πÕË◊ ß®“°¡°’ “√»°÷ …“· ¥ß«“à ºªâŸ «É ¬∑¡Ë’ ’ severe CVD ∑√Ë’ °— …“„À¡â √’ –¥∫— Hb ª°µ‘ ®–¡Õ’ µ— √“°“√‡ ¬’ ™«’ µ‘  ßŸ °«“à ºªŸâ «É ¬∑¡Ë’ √’ –¥∫— Hb 11 g/dl27 ·≈– æ∫Õ∫ÿ µ— °‘ “√≥å thrombosis „π vascular access  ßŸ ¢πÈ÷ „πºªâŸ «É ¬∑¡Ë’ √’ –¥∫— Hb ª°µ‘ ¥ß— ππÈ— ºªâŸ «É ¬∑¡Ë’ ’ severe CVD ·≈– vascular access graft §«√√°— …“√–¥∫— Hb ª√–¡“≥ 11-12 g/dl ∂“â ‰¡¡à Õ’ “°“√‡®∫Á Àπ“â Õ° angina - „πºªâŸ «É ¬‡∫“À«“π∑¡Ë’ ’ peripheral vascular disease (PVD) √«à ¡¥«â ¬ §«√√–«ß— „π°“√‡æ¡Ë‘ Hb >12.0 g/dl „πºªâŸ «É ¬‡∫“À«“π rbc deformability ‡ ¬’ √«à ¡°∫— ¡√’ –¥∫— plasma fibrinogen  ßŸ ®–∑”„À‡â ≈Õ◊ ¥ ¡§’ «“¡Àπ¥◊ 28 ®–∑”„Àâ PVD √πÿ ·√ߢπÈ÷ 29 - ºªâŸ «É ¬∑‡’Ë ªπì chronic hypoxemic pulmonary disease Õ“®®–‰¥ªâ √–‚¬™π®å “°°“√√°— …“√–¥∫— Hb ∑ Ë’ ߟ - „πºªŸâ «É ¬ CKD ·≈–‡ªπì sickle cell disease ´ßË÷ rbc ®–¡’ HbS ‡ªπì  «à π„À≠·à ≈–¡’ HbF ‡≈°Á πÕâ ¬ §«√ª√∫— ¢π“¥ ESA „À√â –¥∫— HbS ‰¡‡à °π‘ 30% ‡æÕË◊ À≈°’ ‡≈¬Ë’ ß°“√‡°¥‘ sickling crisis ‡æ√“– rbc ∑¡’Ë ’ HbS ®–·µ°ß“à ¬ (hemolysis) ∑”„Àºâ ªŸâ «É ¬µÕâ ߉¥√â ∫— ‡≈Õ◊ ¥∫Õà ¬ ºªâŸ «É ¬°≈¡ÿà π·’È ¡«â “à ®–‰¥â ESA „π¢π“¥ ßŸ √–¥∫— Hb ®–Õ¬ªàŸ √–¡“≥ 7-8 g/dl ‡πÕË◊ ß®“°¡°’ “√‡°¥‘ rbc hemolysis °“√„Àâ hydroxyurea √«à ¡‰ª¥«â ¬ Õ“®®–‰ª‡æ¡Ë‘ √–¥∫— HbF ‰¥â 2. ºªâŸ «É ¬ CKD §«√¡‡’ À≈°Á ‡æ¬’ ßæÕ∑®Ë’ –∑”„À√â –¥∫— Hb >11.0 g/dl ‚¥¬‡ª“Ñ À¡“¬∑·Ë’  ¥ß«“à ¡‡’ À≈°Á ‡æ¬’ ßæÕ§Õ◊ - serum ferritin >100 µg/L - PHRC <10% À√Õ◊ TSAT >20% À√Õ◊ CHr >29 pg/cell

New Frontiers in Dialysis 106 ∏π‘µ ®‘√ππ— ∑å∏«—™  √‘ ‘¿“ ™“â ß»√‘ ‘°≈ÿ ™¬— ∏ππ— ¥“ µ√–°“√«π‘™ « π— µå  ‡ÿ ¡∏°ÿ≈ „π∑“ߪØ∫‘ µ— §‘ «√√°— …“√–¥∫— serum ferritin 200-500 µg/L, PHRC <2.5% À√Õ◊ TSAT 30-40% À√Õ◊ CHr 35 pg/cell ‰¡§à «√„À‡â À≈°Á „πºªâŸ «É ¬∑¡Ë’ §’ “à serum ferritin  ßŸ °«“à 800 µg/L ‡æ√“–‡ ¬Ë’ ßµÕà °“√‡°¥‘ iron toxicity KDOQI 200621 ·≈– KDOQI ‡æ¡Ë‘ ‡µ¡‘ „πªï 200730 ‰¥°â ”Àπ¥√–¥∫— Hb ‡æÕË◊ ‡ªπì ·π«∑“ß°“√ 殑 “√≥“„Àâ ESA ·≈–‡À≈°Á ¥ß— πÈ’ 1. °“√√°— …“‡æÕ◊Ë ª√∫— √–¥∫— Hb ‡ª“Ñ À¡“¬§«√殑 “√≥“º≈¥·’ ≈–º≈‡ ¬’ ®“°°“√√°— …“ ‡™πà QOL ∑¥Ë’ ¢’ πÈ÷ , °“√‰¡µà Õâ ߉¥√â ∫— ‡≈Õ◊ ¥, º≈¢“â ߇§¬’ ß®“°√–¥∫— Hb ∑ Ë’ ߟ ‚¥¬ KDOQI 2007 ·π–π”ºªâŸ «É ¬∑‡Ë’ ªπì CKD ∑ßÈ— ∑‰Ë’ ¡‰à ¥√â ∫— °“√∑” dialysis ·≈–∑” dialysis ∑‰Ë’ ¥√â ∫— ESA §«√¡√’ –¥∫— Hb ‡ª“Ñ À¡“¬ (target Hb) „π™«à ß 11.0 -12.0 g/dl ·≈–‰¡§à «√„Àâ Hb ‡ª“Ñ À¡“¬‡°π‘ 13.0 g/dl ‡πÕË◊ ß®“°√–¥∫— Hb ∑¡Ë’ “°°«“à 13.0 g/dl ®– ‡æ¡Ë‘ Õµ— √“°“√‡ ¬’ ™«’ µ‘ ®“° CVD 2. ESA ¡§’ «“¡ ”§≠— „π°“√√°— …“¿“«–´¥’ „πºªŸâ «É ¬ CKD ESA ∑‡Ë’ ªπì long-acting agent À√Õ◊ short-acting agent ®–¡«’ ∏‘ °’ “√„À¬â “·µ°µ“à ß°π— 3. ºŸâªÉ«¬ CKD ¡—°µâÕ߉¥â√—∫‡À≈Á°‡æ◊ËÕ·°â‰¢¿“«–´’¥ ®÷ߧ«√¡’°“√µ√«® ¿“«–‡À≈Á°„π √“à ß°“¬¥ß— π’È 3.1 §«“¡∂„Ë’ π°“√ª√–‡¡π‘  ¿“«–‡À≈°Á (Frequency of iron status test) „π™«à ß·√°¢Õß°“√„Àâ ESA §«√ª√–‡¡‘π ¿“«–‡À≈Á°∑ÿ°‡¥◊Õπ ·µà∂⓺ŸâªÉ«¬∑’ˉ¡à‰¥â√—∫ ESA À√◊Õ‰¥â√—∫ ESA „π¢π“¥§ß∑’Ë·≈â« §«√ª√–‡¡π‘  ¿“«–‡À≈°Á Õ¬“à ßπÕâ ¬∑°ÿ 3‡¥Õ◊ π‡æÕ◊Ë „À¡â ª’ √¡‘ “≥‡À≈°Á ‡æ¬’ ßæÕ„π√–À«“à ß°“√√°— …“¿“«–´¥’ Õ¬“à ߉√°µÁ “¡§«√π”¢Õâ ¡≈Ÿ ‡°¬Ë’ «°∫— √–¥∫— Hb ºªâŸ «É ¬, °“√µÕ∫ πÕßµÕà ¬“ ESA ·≈–°“√√°— …“ÕπË◊ Ê ¡“ √«à ¡æ®‘ “√≥“„π°“√ª√–‡¡π‘ ‡À≈°Á ∂¢Ë’ πÈ÷ ‚¥¬ KDOQI ·π–π”≈°— …≥–∑“ߧ≈π‘ °‘ ∑ºË’ ªŸâ «É ¬§«√®–‰¥√â ∫— °“√ ª√–‡¡π‘  ¿“«–‡À≈°Á ∂¢’Ë π÷È §Õ◊ - À≈ß— ‡√¡Ë‘ ¬“ ESA - √–¥∫— Hb ‡æ¡Ë‘ ‰¡‰à ¥µâ “¡∑§Ë’ “¥À¡“¬À≈ß— ‰¥√â ∫— ¬“ ESA - ¡ª’ ≠í À“®“°‡√ÕË◊ ߇≈Õ◊ ¥ÕÕ° (bleeding) - À≈ß— °“√º“à µ¥— - À≈ß— ®“°√°— …“„π‚√ß欓∫“≈ - ‡æÕ◊Ë µ¥‘ µ“¡º≈°“√„À‡â À≈°Á À≈ß— „À¬â “‡À≈°Á §√∫µ“¡°”Àπ¥ - ‡æÕË◊ ª√–‡¡π‘ °“√‰¡µà Õ∫ πÕßµÕà ¬“ ESA 3.2 §«√π”º≈°“√ª√–‡¡π‘ iron status, Hb ·≈–¢π“¥ ESA ¡“‡ªπì ¢Õâ ¡≈Ÿ ª√–°Õ∫°“√µ¥—  π‘ „® „À‡â À≈°Á ‡™πà ºªŸâ «É ¬∑«Ë’ ¥— √–¥∫— serum ferritin ≈¥≈ß ·µà Hb ‰¡‡à ª≈¬Ë’ π·ª≈ßÀ√Õ◊ ¡§’ “à ≈¥≈ß · ¥ß«“à ºâŸ ª«É ¬Õ“®®–¡°’ “√‡ ¬’ ‡À≈°Á ÕÕ°πÕ°√“à ß°“¬ (external iron loss ‡™πà GI bleeding À√Õ◊ dialysis-associated blood loss „πºªâŸ «É ¬∑∑Ë’ ” hemodialysis) ·µ∂à “â ºªâŸ «É ¬«¥— √–¥∫— serum ferritin ≈¥≈ß ·µà Hb ‡æ¡Ë‘ ¢πÈ÷ „πºâŸ ª«É ¬∑‰’Ë ¥√â ∫— ¬“ ESA · ¥ß«“à ºªâŸ «É ¬¡°’ “√µÕ∫ πÕßµÕà ¬“ ESA ‡æ√“–¡°’ “√ shift ¢Õ߇À≈°Á ®“° iron storage ¡“ √“â ߇¡¥Á ‡≈Õ◊ ¥ 3.3 °”À𥇪“Ñ À¡“¬ iron therapy „π√–À«“à ߉¥â ESA ‡æÕË◊ ®–‰¥√â –¥∫— Hb ∑µË’ Õâ ß°“√‚¥¬„™â

Update of Intravenous Iron and Anemia Management  ‘√‘¿“ ™â“ß»‘√‘°ÿ≈™¬— 107 ¢π“¥¬“ ESA ∑µË’ ”Ë ·≈–ºªŸâ «É ¬‰¡¡à º’ ≈¢“â ߇§¬’ ß®“°¿“«–‡À≈°Á ‡°π‘ ‚¥¬ iron status ‡ª“Ñ À¡“¬§Õ◊ - ºªâŸ «É ¬ CKD ∑∑Ë’ ” hemodialysis: serum ferritin >200 ng/ml ·≈– TSAT >20% À√Õ◊ CHr >29 pg/cell √–¥∫— serum ferritin µ“¡ KDOQI 2006 ®–¡‡’ ª“Ñ À¡“¬ ßŸ °«“à √–¥∫— serum ferritin ‡¥¡‘ ∑Ë’ KDOQI ·π–𔉫â (KDOQI ‡¥¡‘ ·π–𔇪“Ñ À¡“¬ serum ferritin >100 ng/ml) ‡πÕË◊ ß®“°°“√„À‡â À≈°Á ‚¥¬„Àâ serum ferritin ¡√’ –¥∫— ‡ª“Ñ À¡“¬ ßŸ ¢πÈ÷ ®–≈¥¢π“¥¬“ ESA ‰¥¡â “°¢πÈ÷ - ºªâŸ «É ¬ CKD ∑‰Ë’ ¡‰à ¥√â ∫— °“√∑” dialysis À√Õ◊ ∑” peritoneal dialysis: serum ferritin >100 ng/ml ·≈– TSAT >20% ‡πÕË◊ ß®“°„πºªâŸ «É ¬∑‰Ë’ ¡‰à ¥∑â ” hemodialysis ®–‰¡¡à ’ dialysis-related blood loss ·≈– ¢Õâ ¡≈Ÿ ª®í ®∫ÿ π— ¬ß— ‰¡¡à “°æÕ∑®Ë’ – π∫—  ππÿ ª√–‚¬™π®å “°°“√‡æ¡Ë‘ √–¥∫— serum ferritin ‡ª“Ñ À¡“¬ KDOQI ®ß÷ ·π–π”„À√â –¥∫— serum ferritin ‡ª“Ñ À¡“¬„πºªŸâ «É ¬∑‰Ë’ ¡‰à ¥√â ∫— °“√∑” hemodialysis µ”Ë °«“à ºâŸªÉ«¬∑’Ë∑” hemodialysis ‡æÕË◊ ®–‰¥Àâ ≈°’ ‡≈¬Ë’ ߺ≈¢“â ߇§¬’ ß®“°¿“«–‡À≈°Á ‡°π‘ 3.4 ¬—߉¡à¡’À≈—°∞“π‡æ’¬ßæÕ∑’Ë®–„Àâ‡À≈Á°∑“߇ âπ‡≈◊Õ¥∂â“ serum ferritin >500 ng/ml §«√ æ‘®“√≥“ªí®®—¬Õ◊Ëπª√–°Õ∫°àÕπ„Àâ‡À≈Á° §◊Õ°“√µÕ∫ πÕßµàÕ ESA, √–¥—∫ Hb, √–¥—∫ TSAT ·≈– ≈°— …≥–∑“ߧ≈π‘ °‘ ¢ÕߺªŸâ «É ¬ ‡πÕË◊ ß®“°¬ß— ‰¡¡à °’ “√»°÷ …“·∫∫ randomized controlled trial ‡ª√¬’ ∫‡∑¬’ ∫ §«“¡ª≈Õ¥¿¬— ·≈–ª√– ∑‘ ∏¿‘ “æ°“√„À‡â À≈°Á √–À«“à ß√–¥∫— serum ferritin ‡ª“Ñ À¡“¬∑ Ë’ ߟ °«“à 500 ng/ml ·≈–√–¥∫— serum ferritin ∑√Ë’ –¥∫— µ”Ë °«“à πÕ°®“°πæÈ’ ∫«“à ºªŸâ «É ¬∑¡Ë’ √’ –¥∫— serum ferritin >500 ng/ml ®–¡’ iron storage „π tissue ¡“°‡æ¬’ ßæÕ31 „πºªŸâ «É ¬∑¡Ë’ ’ serum ferritin >500 ng/ml ·≈– TSAT <20% Õ“®®–¡’ inflammation À√Õ◊ ¿“«–¢“¥‡À≈°Á §«√µ√«®√–¥∫— CRP ·≈– CHr ‡æ¡Ë‘ ‡µ¡‘ 4. §«√√–«ß— °“√„À‡â ≈Õ◊ ¥„πºªâŸ «É ¬ CKD ‡πÕË◊ ß®“°Õ“® √“â ß antibody µÕà HLA ∑”„À¡â º’ ≈µÕà °“√‡ª≈’Ë¬π‰µ„πÕ𓧵 ·≈–°“√„Àâ‡≈◊Õ¥∫àÕ¬Ê ‡ªìπ‡«≈“π“πÕ“®∑”„À⇰‘¥ iron overload ‰¥â „𧔠·π–π”¢Õß KDOQI ‰¡°à ”Àπ¥√–¥∫— Hb „π°“√„À‡â ≈Õ◊ ¥ ·≈–§“à Hb ‡ª“Ñ À¡“¬‰¡„à ™¢à Õâ ∫ßà ™„È’ π°“√„À‡â ≈Õ◊ ¥ °“√殑 “√≥“„À‡â ≈Õ◊ ¥§«√殑 “√≥“∂ß÷ risk/benefit ®“°°“√„À‡â ≈Õ◊ ¥ ‡™πà Õ“®µÕâ ß„À‡â ≈Õ◊ ¥„π¿“«– acute bleeding ∂“â ®–„À‡â ≈Õ◊ ¥„π¿“«– chronic anemia §«√殑 “√≥“Õ“°“√ºªŸâ «É ¬«“à ‡ªπì º≈®“°¿“«–´¥’ À√Õ◊ ‰¡à Õ“°“√ππÈ— ®–¥¢’ πÈ÷ ¥«â ¬°“√„À‡â ≈Õ◊ ¥À√Õ◊ ‰¡à ¡°’ “√√°— …“ÕπË◊ ·∑π°“√„À‡â ≈Õ◊ ¥‰¥Àâ √Õ◊ ‰¡à „πºªâŸ «É ¬Õ“¬¡ÿ “°∑Ë’ ¡¿’ “«– severe chronic anemia °“√„À‡â ≈Õ◊ ¥µÕâ ß„À™â “â Ê ·≈–„ÀÕâ ¬“à ß√–«ß— ‡æ√“–Õ“®∑”„À‡â °¥‘ congestive heart failure ‰¥3â 2 5. °“√√°— …“¿“«–´¥’ ¥«â ¬ erythropoiesis-stimulating agents (Treatment of anemia with erythropoiesis-stimulating agents) ESA „πª®í ®∫ÿ π— §Õ◊ erythropoietin ‰¥·â °à epoetin alfa, epoetin beta ´ßË÷ ∂Õ◊ «“à ‡ªπì short acting erythropoietin ‡πÕË◊ ß®“°¡§’ “à §√ßË÷ ™«’ µ‘  πÈ— °«“à darbepoetin ∑∂Ë’ Õ◊ ‡ªπì long acting erythropoietin KDOQI ·π–π”°“√„™â ESA ¥ß— πÈ’ 1. „πºªŸâ «É ¬∑‰Ë’ ¥√â ∫— ESA §«√µ¥‘ µ“¡ Hb Õ¬“à ßπÕâ ¬ 1 §√ßÈ— /‡¥Õ◊ π 2. ¢π“¥¬“ ESA (ESA dosing)

New Frontiers in Dialysis 108 ∏𵑠®√‘ ππ— ∑å∏«—™  ‘√‘¿“ ™“â ß»√‘ ‘°ÿ≈™¬— ∏π—𥓠µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ 2.1 ¢π“¥¬“µßÈ— µπâ ¢Õß ESA ·≈–°“√ª√∫— ¢π“¥¬“ ESA §«√殑 “√≥“®“°√–¥∫— Hb ¢≥–ππÈ— ¢ÕߺªâŸ «É ¬, √–¥∫— Hb ‡ª“Ñ À¡“¬, Õµ— √“°“√‡æ¡Ë‘ ¢πÈ÷ ¢Õß Hb À≈ß— ‰¥¬â “ ·≈–Õ“°“√∑“ߧ≈π‘ °‘ ‚¥¬∑«Ë— ‰ª ¢π“¥¬“ ESA µßÈ— µπâ ®–¡‡’ ª“Ñ À¡“¬∑√Ë’ –¥∫— Hb ‡æ¡Ë‘ ª√–¡“≥ 1-2 g/dl/month ·≈–°“√ª√∫— ¢π“¥¬“ ESA ®–‰¡ªà √∫— °Õà π 4  ª— ¥“ÀÀå ≈ß— ®“°‡√¡Ë‘ ¬“ 2.2 ‡¡ÕË◊ √–¥∫— Hb ‡ª“Ñ À¡“¬‰¥µâ “¡µÕâ ß°“√  “¡“√∂≈¥¢π“¥¬“ ESA ≈߉¥â ·µ‰à ¡§à «√À¬¥ÿ ¬“ ‡æ√“–∂“â À¬¥ÿ ¬“®–∑”„À§â “à Hb ≈¥≈ßµ”Ë °«“à ‡ª“Ñ À¡“¬π“π ®“°°“√‡ ¬’ erythropoietic precursor 2.3 ∂“â ‰¡‰à ¥„â À¬â “ ESA µ“¡√–¬–∑°Ë’ ”Àπ¥ (missed ESA schedule) §«√„À¬â “ ESA ∑π— ∑’ ‡æÕË◊ À≈°’ ‡≈¬Ë’ ß°“√≈¥≈ߢÕß Hb µ”Ë °«“à ‡ª“Ñ À¡“¬Õ¬πŸà “π 2.4 §«√„Àâ ESA µÕà „πºªâŸ «É ¬∑®Ë’ ”‡ªπì µÕâ ߉¥√â ∫— ¬“ ESA (ESA-dependent patient) ·≈–‡¢“â √°— …“ „π‚√ß欓∫“≈ 2.5 ºªâŸ «É ¬∑¡Ë’ §’ «“¡¥π— ‚≈Àµ‘  ßŸ , vascular access occlusion, inadequate dialysis, ¡ª’ √–«µ— ™‘ °— À√Õ◊ malnutrition ‰¡‡à ªπì ¢Õâ À“â ¡„π°“√„À¬â “ ESA ‡æ√“–‰¡¡à À’ ≈°— ∞“π«“à °“√À¬¥ÿ ESA ®–∑”„Àºâ ≈°“√ √°— …“¿“«–¥ß— °≈“à «¥¢’ π÷È 3. «∏‘ °’ “√„À¬â “ ESA (Route of administration) 3.1 °“√‡≈Õ◊ °«∏‘ „’ À¬â “ ESA §«√殑 “√≥“ª®í ®¬— Õπ◊Ë ª√–°Õ∫¥«â ¬§Õ◊ CKD stage, treatment setting, efficacy, safety ·≈–™π¥‘ ESA ∑®Ë’ –„Àâ 3.2 „πºªâŸ «É ¬ CKD ∑‰’Ë ¡‰à ¥√â ∫— °“√∑” hemodialysis °“√„Àâ ESA ¥«â ¬«∏‘ ©’ ¥’ „µºâ «‘ Àπß— (subcutaneous administration; SC) ®–¡§’ «“¡ –¥«° 3.3 „πºâŸªÉ«¬ CKD ∑’ˉ¥â√—∫°“√∑” hemodialysis °“√„Àâ ESA ∑“߇ âπ‡≈◊Õ¥ (intravenous administration; IV) ®–¡§’ «“¡ –¥«° „π short acting ESA ª√– ∑‘ ∏¿‘ “æ°“√„À¬â “∑“ß SC ®–¥°’ «“à ∑“ß IV ‡πÕË◊ ß®“°°“√„À¬â “∑“ß SC ®–≈¥¢π“¥¬“ ESA ‰¥3â 3 ·µ∂à “â ‡ªπì long-acting ESA ª√– ∑‘ ∏¿‘ “æ°“√„À¬â “∑“ß SC ·≈–∑“ß IV ®– „°≈‡â §¬’ ß°π— 34, 35 KDOQI 2006 ·π–π”„Àâ ESA ·°ºà ªâŸ «É ¬∑∑Ë’ ” hemodialysis ∑“ß IV ‡πÕË◊ ß®“°≈¥§«“¡ ‡ ¬Ë’ ßµÕà °“√‡°¥‘ pure red cell aplasia (PRCA) ®“°°“√„À¬â “∑“ß SC 4. §«“¡∂„Ë’ π°“√„À¬â “ ESA (Frequency of administration) 4.1 §«“¡∂„Ë’ π°“√„À¬â “ ESA §«√殑 “√≥“®“° CKD stage, treatment setting, efficacy ·≈– ™π¥‘ ¢Õß ESA 4.2 ‡æÕË◊ §«“¡ –¥«°¢ÕߺªâŸ «É ¬„πºªŸâ «É ¬ CKD ∑‰Ë’ ¡‰à ¥√â ∫— °“√∑” hemodialysis ‰¡§à «√‡≈Õ◊ °«∏‘ ∑’ Ë’ µÕâ ß„À¬â “ ESA ∫Õà ¬ ºªŸâ «É ¬∑‰Ë’ ¥√â ∫— short acting ESA ·≈«â ¡√’ –¥∫— Hb  ßŸ ‡°π‘ ‡ª“Ñ À¡“¬ °“√≈¥¬“‚¥¬°“√„À¬â “À“à ß ®–∑”„Àªâ √– ∑‘ ∏¿‘ “欓πÕâ ¬°«“à °“√≈¥ª√¡‘ “≥¬“·µ§à ߧ«“¡∂„’Ë π°“√„À¬â “‡À¡Õ◊ π‡¥¡‘  «à π long acting ESA  “¡“√∂≈¥¬“‚¥¬„À¬â “À“à ßÕÕ°‰¥â KDOQI 200136 ·π–π”„À„â ™¬â “ erythropoietin „π¢π“¥µßÈ— µπâ (initial dose) 80-120 U/kg/week ‡¡ÕË◊ „À¬â “∑“ß SC À√Õ◊ ¢π“¥ 120-180 U/kg/week ‡¡ÕË◊ „À¬â “∑“ß IV

Update of Intravenous Iron and Anemia Management  √‘ ¿‘ “ ™â“ß»√‘ °‘ ÿ≈™—¬ 109 ‡¡ÕË◊ „À¬â “ ESA §«√√–«ß— º≈¢“â ߇§¬’ ß∑æË’ ∫‰¥∫â Õà ¬§Õ◊ hypertension, headache §«√≈¥√–¥∫— ¬“ erythropoietin ≈ß 25% „πºªŸâ «É ¬∑‰Ë’ ¥√â ∫— ¬“·≈«â Hb ‡æ¡Ë‘ ª√–¡“≥ 12 g/dl À√Õ◊ ¡√’ –¥∫— Hb ‡æ¡Ë‘ „πÕµ— √“ ¡“°°«“à 1 g/dl „π√–¬–‡«≈“ 2  ª— ¥“Àå  «à π°“√‡æ¡Ë‘ ¢π“¥¬“°‰Á ¡§à «√‡æ¡Ë‘ ‡°π‘ °«“à 1 §√ßÈ— /‡¥Õ◊ π 6. °“√„À‡â À≈°Á (Iron supplement)  “‡Àµ°ÿ “√¢“¥‡À≈°Á „πºªâŸ «É ¬ CKD ¡‰’ ¥Àâ ≈“¬ª√–°“√§Õ◊ 1. ¡°’ “√≈¥≈ߢÕß iron storage 2. Chronic blood loss ‡™πà dialysis-related blood loss „πºªŸâ «É ¬∑∑Ë’ ” hemodialysis, surgical blood loss, °“√‡®“–‡≈Õ◊ ¥‡æÕË◊  ßà µ√«®µ“à ßÊ, occult gastrointestinal bleeding 3. °“√¥Ÿ¥´÷¡‡À≈Á°®“°∑“߇¥‘πÕ“À“√≈¥≈ß ‡¡◊ËÕ¡’¬Ÿ√’‡¡’¬®–∑”„ÀâÕ“¬ÿ‡¡Á¥‡≈◊Õ¥·¥ß —Èπ≈ß ·≈–¡°’ “√ √“â ߇¡¥Á ‡≈Õ◊ ¥·¥ß≈¥≈߇À≈°Á ®–Õ¬„Ÿà π‡¡¥Á ‡≈Õ◊ ¥·¥ß≈¥≈߇À≈°Á  «à π‡°π‘ ®–∂°Ÿ 𔉪‡°∫Á ‰«‡â ªπì iron storage ∑”„Àâ ferritin  ßŸ ¢πÈ÷ ®ß÷ ‰ª≈¥°“√¥¥Ÿ ´¡÷ ‡À≈°Á ®“°Õ“À“√ À√Õ◊ °“√„™â phosphate binder ®– ≈¥°“√¥¥Ÿ ´¡÷ ‡À≈°Á 4. ¡§’ «“¡µÕâ ß°“√„™‡â À≈°Á ¡“°¢π÷È ‡™πà ‡¡Õ◊Ë „Àâ ESA ®–¡°’ “√¥ß÷ ‡À≈°Á ÕÕ°®“° storage ¡“°¢π÷È À√Õ◊ reticuloendothelial system ª≈Õà ¬‡À≈°Á ‰¥πâ Õâ ¬ (reticuloendothelial blockade) ‰¥¡â °’ “√»°÷ …“„À‡â À≈°Á „πºªâŸ «É ¬ CKD ∑¡Ë’ ¿’ “«–´¥’ √«à ¡°∫— ¡§’ “à ‡©≈¬Ë’ TSAT ≈ 19 -20% æ∫«“à „π ºªŸâ «É ¬∑‰’Ë ¥‡â À≈°Á Õ¬“à ߇¥¬’ «·≈–‰¡‰à ¥â ESA ° Á “¡“√∂®–¡’ Hb ‡æ¡‘Ë ¢π÷È ‰¥3â 7 ®“°°“√µ√«®√–¥∫— serum ferritin ·≈– TSAT ®– “¡“√∂∫Õ°ª√–‡¿∑°“√¢“¥‡À≈°Á ‰¥¥â ß— πÈ’ - Absolute iron deficiency ®–¡’ TSAT <20% ·≈– serum transferrin <100 ng/ml  “‡Àµÿ Õ“®‡°¥‘ ®“° blood loss, ¡°’ “√≈¥≈ߢÕß°“√¥¥Ÿ ´¡÷ ‡À≈°Á - Functional iron deficiency ®–¡’ TSAT <20% ·≈– serum transferrin Õ¬„àŸ π™«à ß 100-700 ng/ ml  “‡ÀµÕÿ “®‡°¥‘ ®“°¡§’ «“¡µÕâ ß°“√„™‡â À≈°Á ¡“°®“°°“√„À¬â “ ESA - Reticuloendothelial blockade ®–¡’ TSAT <20% ·≈– serum transferrin  ßŸ ‡¡ÕË◊ „À‡â À≈°Á ®–¬ßË‘ ∑”„Àâ serum ferritin ¬ßË‘  ßŸ ·µ‰à ¡∑à ”„Àâ Hb ‡æ¡Ë‘ ¢π÷È  “‡ÀµÕÿ “®‡°¥‘ ®“°¡’ inflammation ∑”„Àâ RES ‰¡ à “¡“√∂ª≈Õà ¬‡À≈°Á ÕÕ°¡“„™‰â ¥â º≈°“√µ√«®‡æÕË◊ ®”·π°ª√–‡¿∑°“√¢“¥‡À≈°Á  √ªÿ ¥ß— µ“√“ß∑Ë’ 1 °Õà π®–„À‡â À≈°Á ·°ºà ªŸâ «É ¬ §«√殑 “√≥“∂ß÷ «∏‘ ∑’ ®Ë’ –„À¬â “ (route of iron administration) ¢π“¥ ¬“‡À≈°Á ∑®Ë’ –„À·â ≈–√–¬–‡«≈“∑®Ë’ –„Àâ (duration) ‚¥¬æ®‘ “√≥“®“° iron status, √–¥∫— Hb, ¢π“¥ ESA ‡À≈Á°∑’Ë¡’®”Àπà“¬®–¡’∑—Èß√Ÿª√—∫ª√–∑“π (oral form) À√◊Õ„Àâ∑“߇ âπ‡≈◊Õ¥ (IV iron) °“√„Àâ‡À≈Á°√—∫ ª√–∑“π¡°— ‰¡‡à 欒 ßæÕ·°‰â ¢¿“«–¢“¥‡À≈°Á ‡πÕ◊Ë ß®“°¡ª’ ≠í À“Õ“®¡ª’ ≠í À“„π°“√¥¥Ÿ ´¡÷ ‡À≈°Á ®“°∑“߇¥π‘ Õ“À“√38, 39 IV iron ∑¡Ë’ ®’ ”Àπ“à ¬„πª®í ®∫ÿ π— ¡’ 3 ·∫∫ §Õ◊ iron sucrose, iron gluconate, iron dextran

New Frontiers in Dialysis 110 ∏π‘µ ®‘√π—π∑∏å «™—  √‘ ‘¿“ ™â“ß»√‘ ‘°ÿ≈™¬— ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°ÿ≈ µ“√“ß∑’Ë 1 °“√µ√«® iron status ‡æÕË◊ ®”·π°ª√–‡¿∑°“√¢“¥‡À≈°Á Absolute iron deficiency Functional iron deficiency RES blockade decrease Transferrin increase decrease decrease decrease S. iron decrease decrease decrease increase TIBC increase decrease increase ferritin TSAT decrease decrease none increase S.ferritin decrease normal or increase Response to iron increase Hb increase Hb Response to Epo increase Hb decrease ferritin CRP §≥ÿ ≈°— …≥–¢Õ߇À≈°Á „À∑⠓߇ πâ ‡≈Õ◊ ¥ (IV iron) ≈°— …≥– IV iron ®–¡≈’ °— …≥–‡ªπì spheroid particle ∑¡Ë’ ‡’ À≈°Á Õ¬µàŸ √ß°≈“߇√¬’ ° iron core ´ßË÷ ®–‡ªìπ iron oxyhydroxide ‡ª≈◊Õ°πÕ°ª√–°Õ∫¥â«¬§“√å‚∫‰Œ‡¥√µ‡√’¬° carbohydrate shell IV iron ·µ≈à –™π¥‘ ®–¡’ iron core ‡À¡Õ◊ π°π— ·µ¢à π“¥¢Õß core µ“à ß°π— ·≈– carbohydrate shell ®–¡§’ ≥ÿ  ¡∫µ— µ‘ “à ß°π— iron sucrose ‡ª≈Õ◊ °πÕ°®–‡ªπì sucrose  «à π iron gluconate ‡ª≈Õ◊ °πÕ°®–‡ªπì gluconate ≈Õâ ¡√Õ∫ sucrose Õ°’ ™πÈ— ÀπßË÷ ‚¥¬ iron sucrose ·≈– iron gluconate ®–¡¢’ 𓥄°≈‡â §¬’ ß°π— ·µà iron dextran ®–¡¢’ 𓥄À≠à ·≈–πÈ”Àπ°— ‚¡‡≈°≈ÿ ¡“° ª®í ®¬— ∑¡’Ë º’ ≈µÕà pharmacokinetic ¢Õß IV iron §Õ◊ ¢π“¥¢Õß core ·≈– carbohydrate shell ‚¥¬∂“â ¡¢’ π“¥ core ·≈– carbohydrate shell „À≠à ®–∑”„À¡â π’ ”È Àπ°— ‚¡‡≈°≈ÿ ¡“° ‡¡ÕË◊ „À‡â À≈°Á ∑¡Ë’ ’ πÈ”Àπ°— ‚¡‡≈°≈ÿ ¡“°∑“߇ πâ ‡≈Õ◊ ¥®–¡§’ “à §√ß÷Ë ™«’ µ‘ ¡“°°«“à ‡À≈°Á ∑¡’Ë π’ È”Àπ°— ‚¡‡≈°≈ÿ πÕâ ¬°«“à ‡™πà ironsucrose ®–¡’§à“§√÷Ëß™’«‘µ 6-7 ™—Ë«‚¡ß iron gluconate ®–¡’§à“§√÷Ëß™’«‘µ 1 ™—Ë«‚¡ß iron dextran ¡’πÈ”Àπ—°‚¡‡≈°ÿ≈ ¡“°®–¡§’ “à §√ßË÷ ™«’ µ‘ ¬“« ¥ß— ππÈ— °“√„Àâ iron dextran ∑“߇ πâ ‡≈Õ◊ ¥„πºªâŸ «É ¬∑¢Ë’ “¥‡À≈°Á  “¡“√∂„Àâ 1 §√ßÈ— /  ª— ¥“À‰å ¥â  «à π iron sucrose À√Õ◊ iron gluconate  “¡“√∂„À∂⠢˒ πÈ÷ ‰¥‡â ™πà 3 §√ß—È / ª— ¥“Àå À√Õ◊ Õ“®„À«â π— ≈–§√ß—È ‰¥â ª®í ®¬— ∑¡Ë’ º’ ≈µÕà °“√ª≈Õà ¬‡À≈°Á ®“° IV iron (iron bioactivity) ®–¢πÈ÷ Õ¬°Ÿà ∫—  ¥—  «à π core size ·≈– surface area µÕà volume ¢Õß IV iron ππÈ— ·≈–¢πÈ÷ Õ¬°àŸ ∫— §«“¡·¢ßÁ ·√ߢÕß carbohydrate shell ∑®Ë’ –¬¥÷ iron core ‰«â (strength of carbohydrate-iron bond) ‚¥¬∂“â core size ‡≈°Á surface area ¡“° strength of carbohydrate- iron bond πÕâ ¬ ®–¡°’ “√ª≈Õà ¬ iron ÕÕ°¡“° ‡¡Õ◊Ë „Àâ IV iron 95% ¢Õ߇À≈°Á ®–∂°Ÿ ®∫— ‡¢“â reticuloendothelial system (RES) §Õ◊ liver, spleen ·≈«â ®∫— °∫— transferrin  ßà ‡À≈°Á ‰ª¬ß— ‰¢°√–¥°Ÿ (bone marrow) ‡æÕË◊ π” ‰ª„™â √â“߇¡Á¥‡≈◊Õ¥·¥ßµàÕ‰ª „πºŸâªÉ«¬∑’Ë¢“¥‡À≈Á°·≈–¡’°“√ √â“߇¡Á¥‡≈◊Õ¥‡√Á« (rapid erythropoiesis) ®–„™‡â «≈“ 10-20 «π— À≈ß— ®“°„Àâ IV iron ®π𔉪 √“â ߇¡¥Á ‡≈Õ◊ ¥ ·µ∂à “â ºªâŸ «É ¬¢“¥ erythropoietin ‡À≈°Á ®–‰¡à∂Ÿ° à߉ª¬—߉¢°√–¥Ÿ°∑”„ÀâºâŸªÉ«¬¬—ߧߡ’¿“«–´’¥Õ¬Ÿà Õ’° 5%¢Õ߇À≈Á°∑’Ë„Àâ∑“߇ âπ‡≈◊Õ¥®–®—∫°—∫ transferrin ·≈â« àßµàÕ‰ª¬—߉¢°√–¥°Ÿ ‡æ◊ËÕ„™â √â“߇¡Á¥‡≈◊Õ¥·¥ß‚¥¬‰¡àºà“π RES ‡√’¬° labile iron effect

Update of Intravenous Iron and Anemia Management  ‘√‘¿“ ™â“ß»√‘ °‘ ÿ≈™¬— 111 ´ßË÷ ®–∑”„À‡â °¥‘ oxidative stress, neutrophil function ‡ ¬’ ‰ª, °√–µπâÿ „À¡â ’ bacterial growth ‰¥â ‡πÕË◊ ß®“° bacterial growth µÕâ ßÕ“»¬— ‡À≈°Á «∏‘ °’ “√„À‡â À≈°Á KDOQI 2006 ·π–π”«∏‘ „’ À‡â À≈°Á ¥ß— πÈ’ 1. „πºªŸâ «É ¬∑∑Ë’ ” hemodialysis §«√„À‡â À≈°Á ·∫∫ IV iron ‡πÕË◊ ß®“°¡°’ “√»°÷ …“‡ª√¬’ ∫‡∑¬’ ∫º≈ °“√„À‡â À≈°Á ·∫∫ IV iron ·≈– oral form „πºªâŸ «É ¬∑‰Ë’ ¥â ESA æ∫«“à ºªŸâ «É ¬∑‰Ë’ ¥‡â À≈°Á ·∫∫ IV iron ®–¡§’ “à Hb  ßŸ °«“à ·≈–„™¬â “ ESA „π¢π“¥µ”Ë °«“à ºªâŸ «É ¬∑‰Ë’ ¥â oral iron40-42 ·≈–¡°’ “√»°÷ …“„πºªâŸ «É ¬∑‰Ë’ ¡‰à ¥√â ∫— ESA ‚¥¬‡ª√¬’ ∫‡∑¬’ ∫º≈°“√„Àâ oral iron ‡¡ÕË◊ ‡∑¬’ ∫°∫— °≈¡àÿ ∑‰Ë’ ¡‰à ¥√â ∫— ‡À≈°Á (placebo) æ∫«“à √–¥∫— Hb „π 2 °≈¡ÿà π‰’È ¡·à µ°µ“à ß°π— 43 2. „πºªŸâ «É ¬∑‰Ë’ ¡‰à ¥∑â ” hemodialysis À√Õ◊ ∑” peritoneal dialysis ®–„À‡â À≈°Á Õ“®„À∑â “ß IV iron À√Õ◊ oral form °‰Á ¥â ‡πÕË◊ ß®“°º≈°“√»°÷ …“√–À«“à ß°“√„Àâ IV iron ‡∑¬’ ∫°∫— oral iron ¡§’ «“¡À≈“°À≈“¬, ‰¡à¡’°“√»÷°…“‡ª√’¬∫‡∑’¬∫º≈√–À«à“ß°“√„Àâ oral iron ·≈–°“√‰¡à‰¥â‡À≈Á° πÕ°®“°π’ȺŸâªÉ«¬∑’ˉ¡à‰¥â∑” hemodialysis ®–‡°¥‘ dialysis-related blood loss πÕâ ¬°«“à ºªŸâ «É ¬∑∑Ë’ ” hemodialysis ‡¡ÕË◊ 殑 “√≥“√«à ¡°∫— «∏‘ °’ “√∫√À‘ “√¬“‚¥¬ oral iron ß“à ¬°«“à IV iron „πºªŸâ «É ¬°≈¡àÿ πÈ’ ®ß÷ ·π–π”«“à  “¡“√∂„™‰â ¥∑â ßÈ— oral iron ·≈– IV iron 3. „π√–À«“à ß°“√„À‡â À≈°Á ·∫∫ IV iron §«√¡∫’ §ÿ ≈“°√∑“ß°“√·æ∑¬∑å ™Ë’ ”π“≠·≈–·°‰â ¢¿“«– anaphylaxis ‡πÕË◊ ß®“°°“√„Àâ IV iron ®–¡‚’ Õ°“ ‡°¥‘ hypersensitivity reaction ‚¥¬‡©æ“– iron dextran ®–¡‚’ Õ°“ æ∫∫Õà ¬°«“à IV iron √ªŸ ÕπË◊ KDOQI 200136 ‰¥·â π–π”¢π“¥¬“‡À≈°Á ∑®Ë’ –„À„â πºªâŸ «É ¬∑∑Ë’ ” dialysis µ“¡√–¥∫— TSAT ·≈– serum ferritin §Õ◊ - serum ferritin <100 ng/ml ·≈–/À√Õ◊ TSAT <20% „À‡â À≈°Á ‡æÕË◊ ‡ªπì repletion ‚¥¬„À¢â π“¥ 1000 mg µÕà ‡πÕË◊ ß°π— „π 8-10 dialysis session - serum ferritin 100-800 ng/ml ·≈– TSAT 20-50% „À‡â À≈°Á ‡æÕË◊ ‡ªπì maintenance ‚¥¬„Àâ ¢π“¥ 250-1000 mg „π√–¬–‡«≈“ 12  ª— ¥“Àå ‚¥¬Õ“®„Àâ 1-3 §√ßÈ— / ª— ¥“À°å ‰Á ¥â - serum ferritin >800 ng/ml ·≈– TSAT >50% §«√À¬¥ÿ „À‡â À≈°Á 3 ‡¥Õ◊ π, À“ “‡Àµ∑ÿ ∑Ë’ ”„Àâ serum ferritin  ßŸ ¢πÈ÷ , «¥— √–¥∫— serum ferritin ·≈– TSAT ´”È °“√„À‡â À≈°Á „π√ªŸ iron sucrose ·≈– iron gluconate ∑“ß IV ‰¡®à ”‡ªπì µÕâ ß∑”°“√∑¥ Õ∫ °Õà π„À¬â “ (test dose) ·µà iron dextran µÕâ ß∑”°“√∑¥ Õ∫°Õà π ¢π“¥ ßŸ  ¥ÿ ¢Õß iron sucrose ∑„Ë’ À‰â ¥â ‚¥¬ª≈Õ¥¿¬— §Õ◊ 300 mg/2 hour ¢π“¥ ßŸ  ¥ÿ ¢Õß iron gluconate ∑„Ë’ À‰â ¥‚â ¥¬ª≈Õ¥¿¬— §Õ◊ 250 mg/2 hour  «à π°“√„™â iron dextran ¡‚’ Õ°“ ‡°¥‘ anaphylactic reaction  ßŸ °«“à iron √ªŸ ÕπË◊ ®–„À·â ∫∫ total single dose 1000 mg „π‡«≈“À≈“¬™«—Ë ‚¡ß §«√√–«ß— º≈¢“â ß ‡§¬’ ß®“°°“√„À‡â À≈°Á ∑“ß IV „π√–À«“à ß°“√∑” hemodialysis ‡™πà hypotension, nausea, cramp, pruritus

New Frontiers in Dialysis 112 ∏𵑠®‘√ππ— ∑å∏«™—  ‘√‘¿“ ™â“ß»√‘ ‘°≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°ÿ≈ 7. °“√„™â¬“À√◊Õ«‘∏’√—°…“ÕË◊π√à«¡°—∫°“√„Àâ ESA „πºŸâªÉ«¬∑Ë’∑” hemodialysis (Using pharmacological and nonpharmacological adjuvants to ESA treatment in HD-CKD) KDOQI 200621‰¥¡â §’ ”·π–𔇰¬’Ë «°∫— °“√„™¬â “À√Õ◊ «∏‘ °’ “√√°— …“Õπ◊Ë √«à ¡°∫— °“√„ÀâESA„πºªŸâ «É ¬ ∑∑Ë’ ” hemodialysis ¥ß— πÈ’ 1. ¬ß— ‰¡¡à À’ ≈°— ∞“π‡æ¬’ ßæÕ∑®Ë’ – π∫—  ππÿ °“√„™â L-carnitine (´ßË÷ ‡ªπì  “√∑‡Ë’ °¬Ë’ «¢Õâ ß„π°“√π” long-chain fatty acid ‡¢“â ‰ª„π mitochondria) „π°“√√°— …“¿“«–´¥’ „πºªâŸ «É ¬ CKD 2. ¬ß— ‰¡¡à À’ ≈°— ∞“π‡æ¬’ ßæÕ∑®’Ë – π∫—  ππÿ °“√„™â vitamin C „π°“√√°— …“¿“«–´¥’ „πºªâŸ «É ¬ CKD ·¡â«à“®–¡’°“√»÷°…“«à“ vitamin C ™à«¬‡æ‘Ë¡°“√ª≈àÕ¬‡À≈Á°®“° ferritin ·≈–‡æ‘Ë¡°“√„™â‡À≈Á°„π°“√  √“â ߇¡¥Á ‡≈Õ◊ ¥·¥ß 3. ‰¡à§«√„™â androgen ‡æ◊ËÕ√à«¡°—∫ ESA „π°“√√—°…“¿“«–´’¥„πºŸâªÉ«¬ CKD ‡π◊ËÕß®“°º≈ ¢“â ߇§¬’ ß®“°°“√„™â androgen ¡“° „π¢≥–∑°Ë’ “√»°÷ …“º≈°“√„Àâ androgen ∑‡Ë’ æ¡Ë‘ √–¥∫— Hb ‡ªπì °“√ »°÷ …“¢π“¥‡≈°Á ¬“Õπ◊Ë Ê ∑’Ë KDOQI ‰¡‰à ¥ â √ªÿ ‡ªπì §”·π–π” ·≈–§«√√Õ°“√»°÷ …“‡æ¡‘Ë ‡µ¡‘ „πÕ𓧵 §Õ◊ statins, pentoxyfylline ·≈–°“√„™â vitamin B12 À√◊Õ folate „πºŸâªÉ«¬∑’ˉ¡à‰¥â¢“¥«‘µ“¡‘ππ’È ·≈– KDOQI ¬—߉¡à ·π–π”°“√‡ª≈¬’Ë π·ª≈ßhemodialysisprescription‡æÕ◊Ë √°— …“¿“«–´¥’ ‡æ√“–‰¡¡à °’ “√»°÷ …“∑‡’Ë ªπì randomized control trial ∑’Ë™—¥‡®π«à“°“√ª√—∫ hemodialysis prescription ∫“ßÕ¬à“ß ‡™àπ ™π‘¥ dialyzer membrane, hemodialysis dose, ultrapure dialysate, hemodiafiltration, nocturnal hemodialysis ®–∑”„À°â “√µÕ∫ πÕß µÕà ¬“ ESA ¥¢’ πÈ÷ 8. °“√ª√–‡¡π‘ ºªŸâ «É ¬∑’ˉ¡µà Õ∫ πÕßµÕà °“√√°— …“ (Evaluating failure to respond to treatment) ºªŸâ «É ¬∑‰Ë’ ¥√â ∫— ESA ·≈–‰¡¢à “¥‡À≈°Á ·µà Hb ‰¡‡à æ¡Ë‘ µ“¡∑§Ë’ “¥À¡“¬ · ¥ß«“à ¡°’ “√µÕ∫ πÕß µÕà ¬“ ESA πÕâ ¬ (ESA hyporesponsiveness) KDOQI 200621 ·π–π”„Àªâ √–‡¡π‘ ¥ß— πÈ’ 1. ºªâŸ «É ¬∑∂Ë’ Õ◊ «“à ¡°’ “√µÕ∫ πÕßµÕà ¬“ ESA πÕâ ¬‰¥·â °à - ºªŸâ «É ¬ CKD ∑¡Ë’ ¿’ “«–´¥’ µÕâ ߉¥â ESA ¢π“¥ ßŸ ‡æÕË◊ √°— …“√–¥∫— Hb À√Õ◊ ¡√’ –¥∫— Hb ≈¥≈ß„π ¢π“¥¬“ ESA §ß∑·Ë’ ≈«â - ºªâŸ «É ¬∑‰Ë’ ¥√â ∫— ¬“ ESA „π¢π“¥∑‡Ë’ ¡ÕË◊ ‡∑¬’ ∫°∫— epoetin ·≈«â ¡“°°«“à 500 IU/kg/week §“à Hb πÕâ ¬°«“à 11 g/dl  “‡Àµ∑ÿ ∑’Ë ”„Àâ ESA hyporesponse ‡°¥‘ ‰¥®â “° chronic blood loss, frequent hospitalization, infection/ inflammation, hypoalbuminemia, persistent iron deficiency EBPG 200422 ‰¥·â π–π” “‡Àµÿ ESA hyporesponse ‡æ¡‘Ë ‡µ¡‘ ∑§’Ë «√ ∫◊ §πâ §Õ◊ hyperparathyroidism,

Update of Intravenous Iron and Anemia Management  ‘√‘¿“ ™“â ß»‘√‘°≈ÿ ™¬— 113 aluminium toxicity, hemoglobinopathy, vitamin deficiency, hematologic/nonhematologic malignancy, hemolysis, inadequate dialysis, malnutrition, º≈¢“â ߇§¬’ ß®“°¬“∫“ßÕ¬“à ß ‡™πà immunosuppressive drug, ACE inhibitor 2. §«√ª√–‡¡π‘ ¿“«– PRCA „πºªâŸ «É ¬∑‰Ë’ ¥√â ∫— ¬“ ESA ¡“°°«“à 4  ª— ¥“À·å ≈–¡Õ’ “°“√µÕà ‰ªπÈ’ - ¡°’ “√≈¥≈ߢÕß Hb Õ¬“à ß√«¥‡√«Á „πÕµ— √“ 0.5-1 g/dl/week À√Õ◊ µÕâ ß„À‡â ≈Õ◊ ¥ª√–¡“≥ 1-2 §√ßÈ— / ª— ¥“Àå ·≈– - wbc ·≈– platelet ª°µ‘ ·≈– - absolute reticulocyte count πÕâ ¬°«“à 10,000/µL PRCA ∑‡Ë’ °¥‘ „πºªŸâ «É ¬∑‰Ë’ ¥√â ∫— ESA®–‡ªπì antibody-mediated PRCA ≈°— …≥–Õ“°“√∑“ߧ≈π‘ °‘ §Õ◊ ºªâŸ «É ¬®–´¥’ ¡“°®πµÕâ ߉¥√â ∫— ‡≈Õ◊ ¥‡ªπì ª√–®” „π™«à ß°Õà πªï §».1998 Õ∫ÿ µ— °‘ “√≥å PRCA ®“° ESA æ∫πÕâ ¬¡“° ·µæà ∫¡“°¢πÈ÷ „πªï 1998-2002 ‚¥¬æ∫„πºªâŸ «É ¬∑‰Ë’ ¥√â ∫— ¬“ epoetin alfa ∑‡Ë’ ªπì ·∫∫ prefilled syringe ·≈–„À¬â “∑“ß SC ‚¥¬‰¡æà ∫„πÕ‡¡√°‘ “ ´ßË÷ „πªï 1998 °“√º≈µ‘ epoetin alfa ‰¥„â ™â polysorbate 80 ·∑π human albumin ·≈–®°ÿ syringe ‡ªπì uncoated rubber ´ß÷Ë ‡¡Õ◊Ë polysorbate 80 ∑”ªØ°‘ √‘ ¬‘ “°∫— uncoated rubber ®–‰¥ â “√∑¡Ë’ ≈’ °— …≥–‡ªπì immunoadjuvant §Õ◊ °√–µπâÿ „À‡â °¥‘ °“√ √“â ß antibody ‰¥‡â ¡ÕË◊ „À¬â “∑“ß SC µÕà ¡“„πªï 2003 ‰¥‡â ª≈¬Ë’ π®°ÿ syringe ®“° uncoated rubber ‡ªπì fluoro-resin-coated syringe Õ∫ÿ µ— ‘ °“√≥å antibody-mediated PRCA °≈Á ¥≈ß„°≈‡â §¬’ ß°∫— °Õà πªï 199844, 45 ·µ‰à ¡¡à √’ “¬ß“π°“√‡°¥‘ antibody- mediated PRCA „πºªâŸ «É ¬‰¥â ESA ∑“ß IV46 °“√«π‘ ®‘ ©¬— PRCA „À·â ππà Õπ §Õ◊ µ√«®æ∫ neutralizing antibody µÕà erythropoietin ·≈–µÕâ ß À¬¥ÿ °“√„™â ESA ∑°ÿ ™π¥‘ ‡æ√“– antibody ¡’ cross-reaction °∫— ESA ™π¥‘ ÕπË◊ ‰¥â ∂“â „™µâ Õà Õ“®∑”„À‡â °¥‘ anaphylactic reaction ‰¥â Õ“®æ®‘ “√≥“„Àâ immunosuppressive drug ·µ°à “√‡ª≈¬’Ë π‰µ®–∑”„Àºâ ªâŸ «É ¬À“¬®“° PRCA ‰¥â 9. New erythropoiesis-stimulating agents (ESA) ∑ºË’ «‘ ¢Õß erythropoietic stem cell ®–¡’ erythropoietic receptor ´ßË÷ ‡ªπì ‚ª√µπ’ ∑¡Ë’ ’ 2 ligand Õ¬Ÿà ‡¡ÕË◊ erythropoietin ®∫— °∫— receptor π®È’ –‡°¥‘ °“√‡ª≈¬Ë’ π√ªŸ ‡ªπì dimeric erythropoietin receptor ∑”„Àâ 2 ligand ¡“„°≈°â π— ‡°¥‘ phosphorylation ∑”„À‰â ¥æâ ≈ß— ß“π∑∑Ë’ ”„À‡â °¥‘ translocation §Õ◊ ¥ß÷ kinase enzyme ®“° cytosol ¢Õß erythropoietic stem cell ‡¢“â ‰ª„π nucleus ·≈«â °√–µπâÿ stem cell ππÈ— ·≈–„π∑“ß°≈∫— °π— kinase enzyme ‡À≈“à π®’È –¡’ translocation °≈∫— ‡¢“â ¡“„π cytosol ·≈«â ‡°¥‘ ªØ°‘ √‘ ¬‘ “≈°Ÿ ‚´∑à ∑’Ë ”„À¡â ’ translocation ¢Õß enzyme ÕπË◊ Ê °√–µπâÿ nucleus ¢Õß stem cell „À¡â °’ “√·∫ßà µ«— ®π‡°¥‘ ‡ªπì mature rbc ∂“â erythropoietin ≈¥≈ß ®–‰¡‡à °¥‘ phosphorylation ·≈–‰¡¡à °’ “√ √“â ßæ≈ß— ß“π∑”„À‰â ¡¡à ’ translocation ¢Õß kinase enzyme °≈∫— ‡¢“â „π cytosol ®ß÷ ‰¡¡à °’ “√°√–µπâÿ stem cell ®“°°≈‰°¥ß— °≈“à «¢Õß erythropoietin „π°“√ √“â ߇¡¥Á ‡≈Õ◊ ¥·¥ß ‰¥¡â °’ “√æ≤— 𓬓„À¡¢à πÈ÷ ‡æÕË◊ √°— …“¿“«–´¥’ ®“°¢“¥ erythropoietin §Õ◊

New Frontiers in Dialysis 114 ∏π‘µ ®‘√π—π∑å∏«—™  ‘√‘¿“ ™“â ß»√‘ °‘ ÿ≈™—¬ ∏π—𥓠µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°≈ÿ 1. Continuous erythropoietin receptor activator (CERA)47 ‡ªπì methoxypolyethylene glycol (PEG) peptide ∑¡’Ë ¢’ 𓥄À≠‡à ¢“â ‰ª√«¡„π erythropoietin sequence ®ß÷ ¡’ affinity µÕà °“√®∫— °∫— erythropoietin receptor µË” ∑”„Àâ¡’§à“§√÷Ëß™’«‘µ¢Õ߬“¬“« ‡¡◊ËÕÀ≈ÿ¥®“° erythropoietin receptor ®–¬—ߧßÕ¬àŸ„π æ≈“ ¡“∑”„À®â ∫— °∫— receptor „À¡‰à ¥Õâ °’ ¥ß— ππÈ— ¬“∑¡Ë’ §’ “à §√ßË÷ ™«’ µ‘ ¬“«®–¡’ erythropoietic activity ¡“°¢πÈ÷ ‚¥¬§“à §√ßË÷ ™«’ µ‘ ¢Õß CERA ‡¡Õ◊Ë „À∑â “ß©¥’ „µºâ «‘ Àπß— À√Õ◊ ‡¢“â ‡ πâ ‡≈Õ◊ ¥®–ª√–¡“≥ 140 ™«Ë— ‚¡ß ¢≥–π‰È’ ¥â ¡°’ “√𔬓¡“„™„â π§πæ∫«“à reticulocyte count  ßŸ ¢πÈ÷ ‰¥â 2. EPO-mimetic peptide ‰¥¡â °’ “√»°÷ …“‡æÕË◊  ß— ‡§√“–Àå peptide ∑§Ë’ ≈“â ¬ erythropoietin ‚¥¬ ®∫— ·≈–°√–µπâÿ erythropoietin receptor ‰¥§â Õ◊ Hematide ´ßË÷ ‰¥∑â ”°“√»°÷ …“„Àâ single intravenous dose „πºªâŸ «É ¬ CKD  “¡“√∂‡æ¡Ë‘ √–¥∫— reticulocyte ‰¥â 3. °√–µπâÿ erythropoietin gene expression ‚¥¬À≈°— °“√§Õ◊ „π¿“«– hypoxia ®–¡°’ “√ √“â ß hypoxia inducible factor 1 alpha ®∫— °∫— hypoxia inducible factor 1 beta ‡°¥‘ ‡ªπì dimer ∑¥Ë’ ß÷ transcription factor µ“à ßÊ ‰ª®∫— °∫— erythropoietin gene „π‡´≈ ‡°¥‘ mRNA transcription ·≈– √“â ß erythropoietin ·µ„à π¿“«–∑‰Ë’ ¡¢à “¥ÕÕ°´‡‘ ®π hypoxia inducible factor ®–‡°¥‘ prolyl hydroxylation ·≈–∂°Ÿ inactivate ¥«â ¬ ubiquitin protein ligase complex ‡°¥‘ 26S proteosome degradation µ“¡¡“ ´ßË÷ ‡ªπì negative feedback mechanism ‡æÕË◊ ªÕÑ ß°π— erythrocytosis ∂“â µÕâ ß°“√ √“â ß erythropoietin ®–µÕâ ߬∫— ¬ßÈ— prolyl hydroxylase °√–∫«π°“√ prolyl hydroxylation ®–‰¡‡à °¥‘ ubiquitin protein ligase complex ®–‰¡®à ∫— °∫— hypoxia inducible factor ∑”„À≡ࡒ proteosome degradation µ“¡¡“ „πªí®®ÿ∫—π∑’Ë prolyl hydroxylase inhibitor ∑’Ë¡’°“√  —߇§√“–Àå§◊Õ FG-2216 ‡ªìπ peptide ∑’Ë¡’¢π“¥‡≈Á°·≈–„Àâ∑“ß oral æ∫«à“ “¡“√∂‡æ‘Ë¡ endogenous erythropoietin ‰¥â 3-5 ‡∑“à πÕ°®“°π¬È’ ß— æ∫«“à FG-2216 ¬ß— ¡§’ ≥ÿ  ¡∫µ— „‘ π°“√ modulate iron metabolism ‚¥¬‰ª downregulate hepcidin ∑ ’Ë √“â ß®“°µ∫— ·≈–¡À’ π“â ∑„’Ë π°“√¬∫— ¬ß—È °“√¥¥Ÿ ´¡÷ ‡À≈°Á ®“°∑“߇¥π‘ Õ“À“√ ·≈– FG-2216 ¬ß— ‡æ¡‘Ë ª√– ∑‘ ∏¿‘ “æ°“√„™â iron „π‡´≈ ‰¥¡â °’ “√π” FG-2216 „™„â π§πæ∫«“à ‰¡¡à º’ ≈¢“â ߇§¬’ ß 4. Epo-gene transfer ¬ß— Õ¬„àŸ π¢π—È  µ— «∑å ¥≈Õß ‚¥¬„ à erythropoietin gene ‡¢“â „πÀπ„Ÿ À¡â °’ “√ √“â ß erythropoietin 10.  √ªÿ °“√√°— …“¿“«–´¥’ „πºªŸâ «É ¬CKD®–¡º’ ≈„π°“√‡æ¡‘Ë §≥ÿ ¿“晫’ µ‘ ºªâŸ «É ¬·≈–≈¥Õµ— √“°“√‡ ¬’ ™«’ µ‘ °“√√°— …“¿“«–´¥’ §«√¡√’ –¥∫— Hb ‡ª“Ñ À¡“¬Õ¬„Ÿà π™«à ß 11-12 g/dl ‚¥¬ Hb ‰¡§à «√‡°π‘ 13 g/dl «∏‘ °’ “√ √—°…“¿“«–´’¥πÕ°®“°°“√„Àâ ESA ·≈â« §«√ª√–‡¡‘π ¿“«–‡À≈Á°„π√à“ß°“¬‡æ◊ËÕæ‘®“√≥“„Àâ‡À≈Á°´÷Ëß ®–∑”„À≈â ¥¢π“¥°“√„™¬â “ ESA ≈߉¥â πÕ°®“°π„’È πºªŸâ «É ¬∑‰’Ë ¥√â ∫— ESA ·≈«â Hb ‰¡‡à æ¡‘Ë µ“¡‡ª“Ñ À¡“¬∑§’Ë “¥ §«√®–‰¥µâ √«®À“ “‡Àµ‡ÿ æ¡‘Ë ‡µ¡‘

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New Frontiers in Dialysis 116 ∏𵑠®√‘ ππ— ∑∏å «—™  √‘ ‘¿“ ™“â ß»‘√‘°≈ÿ ™¬— ∏ππ— ¥“ µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ improve quality of life and cognitive function in chronic hemodialysis patients. Am J Kidney Dis. 1989;14:478- 85. 18. Culleton BF, Manns BJ, Zhang J, Tonelli M, Klarenbach S, Hemmelgarn BR. Impact of anemia on hospitalization and mortality in older adults. Blood. 2006 ;107:3841-6. 19. Astor BC, Coresh J, Heiss G, Pettitt D, Sarnak MJ. Kidney function and anemia as risk factors for coronary heart disease and mortality: the Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J. 2006;151:492- 500. 20. Xia H, Ebben J, Ma JZ, Collins AJ. Hematocrit levels and hospitalization risks in hemodialysis patients. J Am Soc Nephrol. 1999;10:1309-16. 21. II. Clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease in adults. Am J Kidney Dis. 2006;47(Suppl 3):S16-85. 22. Locatelli F, Aljama P, Barany P, Canaud B, Carrera F, Eckardt KU, et al. Revised European best practice guidelines for the management of anaemia in patients with chronic renal failure. Nephrol Dial Transplant. 2004;19 Suppl 2:ii1-47. 23. Tirlapur VG, Gicheru K, Charalambous BM, Evans PJ, Mir MA. Packed cell volume, haemoglobin, and oxygen saturation changes in healthy smokers and non-smokers. Thorax. 1983;38:785-7. 24. Kalantar-Zadeh K, Rodriguez RA, Humphreys MH. Association between serum ferritin and measures of inflammation, nutrition and iron in haemodialysis patients. Nephrol Dial Transplant. 2004;19:141-9. 25. Brugnara C. Iron deficiency and erythropoiesis: new diagnostic approaches. Clin Chem. 2003;49:1573-8. 26. Fishbane S, Shapiro W, Dutka P, Valenzuela OF, Faubert J. A randomized trial of iron deficiency testing strategies in hemodialysis patients. Kidney Int. 2001;60:2406-11. 27. Besarab A, Bolton WK, Browne JK, Egrie JC, Nissenson AR, Okamoto DM, et al. The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. N Engl J Med. 1998;339:584-90. 28. Canaud B, Donadieu P, Polito C, Rivory JP, Mathieu-Daude JC, Peterlongo F, et al. Erythropoietin-associated hypertension: what role for blood viscosity changes? Nephron. 1989;51:430-1. 29. Wakeen M, Zimmerman SW. Association between human recombinant EPO and peripheral vascular disease in diabetic patients receiving peritoneal dialysis. Am J Kidney Dis. 1998;32:488-93. 30. KDOQI Clinical Practice Guideline and Clinical Practice Recommendations for anemia in chronic kidney disease: 2007 update of hemoglobin target. Am J Kidney Dis. 2007;50:471-530. 31. Canavese C, Bergamo D, Ciccone G, Longo F, Fop F, Thea A, et al. Validation of serum ferritin values by magnetic susceptometry in predicting iron overload in dialysis patients. Kidney Int. 2004;65:1091-8. 32. Rao SV, Jollis JG, Harrington RA, Granger CB, Newby LK, Armstrong PW, et al. Relationship of blood transfusion and clinical outcomes in patients with acute coronary syndromes. Jama. 2004;292:1555-62. 33. Kaufman JS, Reda DJ, Fye CL, Goldfarb DS, Henderson WG, Kleinman JG, et al. Subcutaneous compared with intravenous epoetin in patients receiving hemodialysis. Department of Veterans Affairs Cooperative

Update of Intravenous Iron and Anemia Management  ‘√¿‘ “ ™â“ß»√‘ °‘ ≈ÿ ™—¬ 117 Study Group on Erythropoietin in Hemodialysis Patients. N Engl J Med. 1998;339:578-83. 34. Locatelli F, Canaud B, Giacardy F, Martin-Malo A, Baker N, Wilson J. Treatment of anaemia in dialysis patients with unit dosing of darbepoetin alfa at a reduced dose frequency relative to recombinant human erythropoietin (rHuEpo). Nephrol Dial Transplant. 2003;18:362-9. 35. Vanrenterghem Y, Barany P, Mann JF, Kerr PG, Wilson J, Baker NF, et al. Randomized trial of darbepoetin alfa for treatment of renal anemia at a reduced dose frequency compared with rHuEPO in dialysis patients. Kidney Int. 2002;62:2167-75. 36. IV. NKF-K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease: update 2000. Am J Kidney Dis. 2001;37(Suppl 1):S182-238. 37. Silverberg DS, Blum M, Agbaria Z, Deutsch V, Irony M, Schwartz D, et al. The effect of i.v. iron alone or in combination with low-dose erythropoietin in the rapid correction of anemia of chronic renal failure in the predialysis period. Clin Nephrol. 2001;55:212-9. 38. Ahsan N. Intravenous infusion of total dose iron is superior to oral iron in treatment of anemia in peritoneal dialysis patients: a single center comparative study. J Am Soc Nephrol. 1998;9:664-8. 39. Wingard RL, Parker RA, Ismail N, Hakim RM. Efficacy of oral iron therapy in patients receiving recombinant human erythropoietin. Am J Kidney Dis. 1995;25:433-9. 40. Fishbane S, Frei GL, Maesaka J. Reduction in recombinant human erythropoietin doses by the use of chronic intravenous iron supplementation. Am J Kidney Dis. 1995;26:41-6. 41. Macdougall IC, Tucker B, Thompson J, Tomson CR, Baker LR, Raine AE. A randomized controlled study of iron supplementation in patients treated with erythropoietin. Kidney Int. 1996;50:1694-9. 42. Van Wyck DB, Roppolo M, Martinez CO, Mazey RM, McMurray S. A randomized, controlled trial comparing IV iron sucrose to oral iron in anemic patients with nondialysis-dependent CKD. Kidney Int. 2005;68:2846- 56. 43. Markowitz GS, Kahn GA, Feingold RE, Coco M, Lynn RI. An evaluation of the effectiveness of oral iron therapy in hemodialysis patients receiving recombinant human erythropoietin. Clin Nephrol. 1997;48:34-40. 44. Boven K, Stryker S, Knight J, Thomas A, van Regenmortel M, Kemeny DM, et al. The increased incidence of pure red cell aplasia with an Eprex formulation in uncoated rubber stopper syringes. Kidney Int. 2005;67:2346- 53. 45. Casadevall N, Nataf J, Viron B, Kolta A, Kiladjian JJ, Martin-Dupont P, et al. Pure red-cell aplasia and antierythropoietin antibodies in patients treated with recombinant erythropoietin. N Engl J Med. 2002;346:469- 75. 46. Rossert J, Casadevall N, Eckardt KU. Anti-erythropoietin antibodies and pure red cell aplasia. J Am Soc Nephrol. 2004;15:398-406. 47. Macdougall IC. CERA (Continuous Erythropoietin Receptor Activator): a new erythropoiesis-stimulating agent for the treatment of anemia. Curr Hematol Rep. 2005;4:436-40.



7 Acute Complications during Hemodialysis ∫≠— ™“  ∂√‘ –æ®πå 1. ¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ (intradialytic hypotension) 2. ¿“«– dialyzer reaction 3. ¿“«–µ–§√«‘ (muscle cramp) 4. ¿“«– dialysis disequilibrium syndrome 5. Õ“°“√ª«¥»√’ …– ·≈–§≈π◊Ë ‰ Õâ “‡®¬’ π (headache, nausea and vomiting) 6. Õ“°“√§π— (uremic pruritus) 7. ¿“«– air embolism 8. ¿“«–¢“¥ÕÕ°´‡‘ ®π (hypoxemia) 9. ¿“«–‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ° (hemolysis) 10. Õ“°“√‰¢â Àπ“« πË— (febrile reaction)

New Frontiers in Dialysis 120 ∏𵑠®√‘ π—π∑å∏«™—  √‘ ‘¿“ ™â“ß»‘√‘°≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π‘™ « —πµå  ‡ÿ ¡∏°ÿ≈ °“√øÕ°‡≈◊Õ¥¥â«¬‡§√◊ËÕ߉µ‡∑’¬¡‡ªìπ°“√∫”∫—¥∑¥·∑π∑“߉µ«‘∏’Àπ÷Ëß ´÷Ëß¡’°“√æ—≤π“ ‡∑§‚π‚≈¬’Õ¬à“ß°â“«≈È” ∑”„Àâ¡’ª√– ‘∑∏‘¿“æ ·≈–ª≈Õ¥¿—¬ Ÿß Õ¬à“߉√°Áµ“¡ºŸâªÉ«¬ à«πÀπ÷Ë߬—ߧ߇°‘¥ ª≠í À“¿“«–·∑√°´Õâ π©∫— æ≈π— √–À«“à ß°“√øÕ°‡≈Õ◊ ¥‰¥â ‚¥¬æ∫Õ∫ÿ µ— °‘ “√≥¢å Õß §«“¡¥π— ‚≈Àµ‘ µË”√Õâ ¬≈– 15-50 µ–§√‘«√âÕ¬≈– 5-20 §≈◊Ëπ‰ âÕ“‡®’¬π√âÕ¬≈– 5-15 ª«¥»’√…–√âÕ¬≈– 5 ‡®Á∫Àπâ“Õ°√âÕ¬≈– 2-5 ª«¥À≈ß— √Õâ ¬≈– 2-5 §π— µ“¡µ«— √Õâ ¬≈– 5 ·≈–‰¢Àâ π“« πË— √Õâ ¬≈– 1 µ“¡≈”¥∫— Õ“®‡ªπì º≈®“°ª®í ®¬— ®“°µ—«ºâŸªÉ«¬‡Õß À√◊Õ°“√ª√—∫°“√√—°…“º‘¥æ≈“¥ „π∫∑§«“¡π’È®–¢Õ°≈à“«∂÷ß¿“«–·∑√°´âÕπ©—∫æ≈—π ¢≥–∑”°“√øÕ°‡≈Õ◊ ¥∑ Ë’ ”§≠— √«¡∑ßÈ— ·π«∑“ß°“√√°— …“欓∫“≈ ‡ªπì ≈”¥∫— ¢Õâ µÕà ‰ªπÈ’ 1. ¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ (intradialytic hypotension) 2. ¿“«– dialyzer reaction 3. ¿“«–µ–§√«‘ (muscle cramp) 4. ¿“«– dialysis disequilibrium syndrome 5. Õ“°“√ª«¥»√’ …– ·≈–§≈πË◊ ‰ Õâ “‡®¬’ π (headache, nausea and vomiting) 6. Õ“°“√§π— (uremic pruritus) 7. ¿“«– air embolism 8. ¿“«–¢“¥ÕÕ°´‡‘ ®π (hypoxemia) 9. ¿“«–‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ° (hemolysis) 10. Õ“°“√‰¢â Àπ“« πË— (febrile reaction) 1. ¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ (Intradialytic hypotension) ‡ªπì ¿“«–·∑√°´Õâ π∑æË’ ∫∫Õà ¬„π°“√øÕ°‡≈Õ◊ ¥¥«â ¬‡§√ÕË◊ ߉µ‡∑¬’ ¡æ∫Õ∫ÿ µ— °‘ “√≥µå ßÈ— ·µ√à Õâ ¬≈– 15-50[1] ª®í ®¬— ‡ ¬’Ë ßµÕà °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥‰¥·â °àºªâŸ «É ¬ ßŸ Õ“¬∑ÿ ¡’Ë À’ ≈Õ¥‡≈Õ◊ ¥·¢ßÁ µ«— ºªâŸ «É ¬‡∫“À«“π ºªŸâ «É ¬√ªŸ √“à ߇≈°Á ‚¥¬‡©æ“–‡æ»À≠ß‘ ºªâŸ «É ¬∑¡Ë’ §’ «“¡º¥‘ ª°µ¢‘ Õß√–∫∫ª√– “∑Õµ— ‚π¡µ— ‘ (autonomic neuropathy) ·≈–ºªâŸ «É ¬‚√§À«— „®∑ßÈ— ™π¥‘ systolic ·≈– diastolic heart failure §”®”°¥— §«“¡ ¿“«–∑¡Ë’ ’ systolic blood pressure µ”Ë °«“à 100 mmHg À√Õ◊ ≈¥≈ß¡“°°«“à 20-30 mmHg ‡¡ÕË◊ ‡∑’¬∫°—∫§«“¡¥—π‚≈À‘µ°àÕπøÕ°‡≈◊Õ¥ √à«¡°—∫‡°‘¥Õ“°“√¢“¥‡≈◊Õ¥‰ª‡≈’Ȭ߇π◊ÈÕ‡¬◊ËÕµà“ßÊ ‡™àπ µ–§√‘« ÕÕà π‡æ≈¬’ ¡π÷ »√’ …–  ¡Õߢ“¥‡≈Õ◊ ¥ °≈“â ¡‡πÕÈ◊ À«— „®¢“¥‡≈Õ◊ ¥ ª«¥∑Õâ ß®“°≈”‰ ¢â “¥‡≈Õ◊ ¥ (mesenteric angina) ‡ªπì µπâ  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ °≈‰°°“√‡°¥‘ ¿“«–§«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥ °“√§«∫§¡ÿ √–¥∫— §«“¡¥π— ‚≈Àµ‘ ¢Õß√“à ß°“¬¢πÈ÷ °∫— 2 ª®í ®¬— À≈°— §Õ◊ 1) cardiac output (CO) ‚¥¬∑Ë’ CO ¢πÈ÷ °∫— Õµ— √“°“√‡µπâ ¢ÕßÀ«— „® (heart rate) ·≈– ª√¡‘ “≥ ‡≈Õ◊ ¥∑∫Ë’ ∫’ ÕÕ°®“°À«— „®·µ≈à –§√ßÈ— (stroke volume) ´ßË÷ stroke volume ‡ªπì º≈¡“®“°À«— „®∫∫’ µ«— (cardiac

Acute Complications during Hemodialysis ∫—≠™“  ∂√‘ –æ®πå 121 contractility) °∫— ª√¡‘ “≥‡≈Õ◊ ¥„πÀ≈Õ¥‡≈Õ◊ ¥ (plasma volume) ‚¥¬∑«—Ë ‰ª√“à ß°“¬®–¡°’ “√µÕ∫ πÕßµÕà ¿“«– hypovolemia ¥«â ¬°“√‡æ¡Ë‘ ¢πÈ÷ CO ®“°À«— „®°“√∫∫’ µ«— ·√ߢπÈ÷ ·≈–‡µπâ ‡√«Á ¢πÈ÷ 2) peripheral vascular resistance (PVR) °“√À¥µ—« ·≈–¢¬“¬µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥  «à πª≈“¬¡º’ ≈‚¥¬µ√ßµÕà ª√¡‘ “≥‡≈Õ◊ ¥ ·≈–§«∫§¡ÿ √–¥∫— §«“¡¥π— ‚≈Àµ‘ ¢ÕߺªŸâ «É ¬ ‚¥¬∑«—Ë ‰ª√“à ß°“¬®– ¡°’ “√µÕ∫ πÕßµÕà ¿“«– hypovolemia ¥«â ¬°“√‡æ¡‘Ë PVR ®“°°“√À¥µ«— ¢ÕßÀ≈Õ¥‡≈Õ◊ ¥ «à π arteriole ·≈– venule ∑”„À‡â ≈Õ◊ ¥∂°Ÿ ¢∫— ‡¢“â À≈Õ¥‡≈Õ◊ ¥ «à π°≈“߇æ¡Ë‘ ¢πÈ÷  “‡Àµ°ÿ “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥  “‡Àµ ÿ «à π„À≠‡à °¥‘ ®“°¢∫«π°“√øÕ°‡≈Õ◊ ¥∑¡Ë’ °’ “√¥ß÷ ‡≈Õ◊ ¥À√Õ◊ plasma volume ¡“°‡°π‘ °«“à √à“ß°“¬®– “¡“√∂ª√—∫µ—« ‚¥¬Õ“»—¬°“√¥÷ßπÈ”πÕ°À≈Õ¥‡≈◊Õ¥„Àâ°≈—∫‡¢â“¡“Õ¬Ÿà„πÀ≈Õ¥‡≈◊Õ¥ ∑¥·∑π (plasma refilling) ´ßË÷ ‡√¬’ ° “‡ÀµÿÀ≈—°πÈ«’ “à volume dependent factors ‡™πà °“√¥ß÷ π”È ª√¡‘ “≥ ¡“°¢≥–øÕ°‡≈Õ◊ ¥ (high ultrafiltration rate) „πºªŸâ «É ¬π”È Àπ°— µ«— ‡æ¡Ë‘ ¡“°√–À«“à ß°“√øÕ°‡≈Õ◊ ¥  “‡Àµÿ √ÕߢÕß°“√‡°‘¥ intradialytic hypotension Õ“®‡°‘¥§«“¡º‘¥ª°µ‘¢Õß°≈‰°°“√§«∫§ÿ¡§«“¡¥—π‚≈À‘µ ‡æ◊ËÕ‡æ‘Ë¡ª√‘¡“≥ plasma volume ‡™àπ ºâŸªÉ«¬∑’Ë¡’ autonomic neuropathy À√◊ÕºŸâªÉ«¬¡’¿“«–‚≈À‘µ®“ß ¡“°®– ≠Ÿ ‡ ¬’ §«“¡ “¡“√∂„π°“√À¥µ«— ¢ÕßÀ≈Õ¥‡≈Õ◊ ¥∑”„À‰â ¡ à “¡“√∂‡æ¡Ë‘ PVR ‰¥â ºªâŸ «É ¬‡ªπì ‚√§ °≈â“¡‡π◊ÕÈ À—«„®¢“¥‡≈◊Õ¥ À√◊Õ pericardial effusion ®–‰¡à “¡“√∂‡æ‘Ë¡ CO ®“°°“√À—«„®∫∫’ µ«— ·√ߢ÷Èπ À√◊Õ‡æ‘Ë¡Õ—µ√“°“√‡µâπ¢ÕßÀ—«„®‰¥â ¥—ßπ—ÈπÀ“°‡°‘¥ªí≠À“°—∫ªí®®—¬„¥ªí®®—¬Àπ÷Ëß„π°“√§«∫§ÿ¡ plasma volume ¥—ß°≈à“«®–¡’º≈∑”„À⇰‘¥¿“«–§«“¡¥—π‚≈À‘µµË”‰¥â ´÷Ëß √ÿª·¬°µ“¡À≈—°µ“¡°≈‰°°“√‡°‘¥ µ“¡µ“√“ß∑Ë’ 1 °“√√°— …“¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ 1. °“√≈¥ À√Õ◊ À¬¥ÿ °“√¥ß÷ π”È (ultrafiltration) 2. ®¥— ∑“à „Àºâ ªŸâ «É ¬πÕπ»√’ …–µ”Ë ·≈–‡∑“â  ßŸ (Trendelenberg position) 3. „À â “√π”È ∑¥·∑π ´ßË÷  «à π„À≠®à –‡≈Õ◊ °„™â 0.9% normal saline §√ßÈ— ≈– 100-200 ¡≈‘ ≈≈‘ µ‘ √ ∑“ß “¬π”‡≈Õ◊ ¥‡¢“â ºªâŸ «É ¬ (venous blood line) ‡πÕË◊ ß®“° 0.9% normal saline „Àºâ ≈°“√√°— …“„°≈‡â §¬’ ß °∫—  “√π”È ™π¥‘ ÕπË◊ Ê ‚¥¬‡©æ“– albumin [2, 3] 4. °“√≈¥Õµ— √“°“√¥ß÷ ‡≈Õ◊ ¥ÕÕ°®“°√“à ß°“¬ [blood flow rate, (BFR)] ‚¥¬∑«—Ë ‰ª‰¡®à ”‡ªπì µÕâ ß≈¥ BFR ¬°‡«πâ °√≥§’ «“¡¥π— ‚≈Àµ‘ µ”Ë Õ¬“à ß√πÿ ·√ß À√Õ◊ ‰¡‰à ¥ºâ ≈µÕà °“√√°— …“ÕπË◊ Ê ‡Àµºÿ ≈¢Õß°“√‰¡µà Õâ ß≈¥ BFR ‡πÕË◊ ß®“° - ‡§√◊ËÕ߉µ‡∑’¬¡„πªí®®ÿ∫—π¡’√–∫∫§«∫§ÿ¡°“√¥÷ßπȔ՗µ‚π¡—µ‘·¡à𬔠Ÿß °“√ª√—∫ BFR ®–‰¡à¡’º≈µàÕÕ—µ√“°“√¥÷ßπÈ” ¥—ßπ—Èπ “¡“√∂‡ªî¥ BFR ‰¥âµ“¡ª°µ‘ ‚¥¬®–‰¡à¡’º≈µàÕ√–¥—∫§«“¡¥—π ‚≈Àµ‘ ¢ÕߺªâŸ «É ¬ - „πÕ¥µ’ „™µâ «— °√Õß™π¥‘ parallel palate ¥ß— ππÈ— °“√ª√∫— ≈¥ BFR ®–≈¥§«“¡¥π— ‡≈Õ◊ ¥„𠵫— °√Õß parallel plate ∑”„Àªâ √¡‘ “≥‡≈Õ◊ ¥∑¥Ë’ ß÷ ÕÕ°®“°√“à ß°“¬≈¥≈ß ·µªà ®í ®∫ÿ π— „™µâ «— °√Õß™π¥‘ hollow fiber ‡ªπì  «à π„À≠à °“√ª√∫— BFR ª°µ®‘ ß÷ ‰¡¡à º’ ≈µÕà §«“¡¥π— ‡≈Õ◊ ¥„𵫗 °√Õß ·≈–Õµ— √“°“√¥ß÷ π”È - „πÕ¥’µ„™âπÈ”øÕ°‡≈◊Õ¥ acetate °“√ª√—∫ BFR  ßŸ ®–‡æ‘Ë¡√–¥—∫ acetate „π√à“ß°“¬¡’

New Frontiers in Dialysis 122 ∏π‘µ ®√‘ π—π∑∏å «™—  √‘ ¿‘ “ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ º≈¢¬“¬À≈Õ¥‡≈◊Õ¥ ∑”„Àâ√–¥—∫§«“¡¥—π‚≈À‘µ≈¥≈ß ·µàªí®®ÿ∫—π„™âπÈ” bicarbonate ‡ªìπ à«π„À≠à®÷ß ‰¡¡à º’ ≈µÕà √–¥∫— §«“¡¥π— ‚≈Àµ‘ 5. °“√√—°…“Õ◊ËπÊ ‰¥â·°à °“√„ÀâÕÕ°´‘‡®π ‡æ◊ËÕ‡æ‘Ë¡ÕÕ°´‘‡®π„Àâ°—∫°≈â“¡‡π◊ÈÕÀ—«„® ·≈– ‡π◊ÈÕ‡¬◊ËÕ à«πµà“ßÊ ¢Õß√à“ß°“¬À«—ߺ≈≈¥°“√À≈—Ëß adenosine ∑”„À⧫“¡¥—π‚≈À‘µ¢ÕߺŸâªÉ«¬‡æ‘Ë¡¢÷Èπ  à«π°“√„™â¬“ vasoconstrictor ‡™àπ norepinephrine, vasopressin æ‘®“√≥“„Àâ„πºâŸªÉ«¬‡ªìπ√“¬Ê À√◊Õ °√≥√’ °— …“µ“¡¢“â ßµπâ ·≈«â §«“¡¥π— ‚≈Àµ‘ ‰¡¥à ¢’ π÷È µ“√“ß∑Ë’ 1  “‡Àµ¢ÿ Õß Intradialytic hypotension 1. Volume related - Large weight gain (high ultrafiltration rate) - Short dialysis (high ultrafiltration rate) - Low target (dry) weight - Nonvolumetric dialysis (inaccurate or erratic ultrafiltration) - Low dialysis solution Na (intracellular fluid shift) 2. Inadequate vasoconstriction - High dialysis solution temperature - Food ingestion (splanchnic vasodilatation) - Tissue ischemia (adenosine-mediated, aggravated by anemia) - Autonomic neuropathy - Antihypertensive medications - Acetate buffer 3. Cardiac factors - Diastolic dysfunction - Arrhythmia (atrial fibrillation) - Ischemia - Pericardial tamponade - Myocardial infarction 4. Uncommon causes - Occult hemorrhage - Septicemia - Dialyzer reaction - Hemolysis - Air embolism

Acute Complications during Hemodialysis ∫—≠™“  ∂√‘ –æ®πå 123 °“√ªÕÑ ß°π— ¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥·¬°µ“¡ “‡Àµÿ 1. º≈¡“®“°°“√‡ª≈¬Ë’ π·ª≈ߢÕßπ”È „πÀ≈Õ¥‡≈Õ◊ ¥ (volume related)  «à π„À≠‡à ªπì º≈¡“®“°Õµ— √“°“√¥ß÷ πÈ” ßŸ (high ultrafiltration rate) ∑”„À°â ≈‰°°“√ª√∫— µ«— ¢Õß√“à ß°“¬‡æ¡‘Ë plasma volume ‰¡à‡æ’¬ßæÕ ¡—°®–‡°‘¥™à«ß√–¬–∑⓬¢Õß°“√øÕ°‡≈◊Õ¥ ´÷ËߧߵâÕßæ‘®“√≥“∂÷ß “‡Àµÿ°“√‡°‘¥µ“¡ µ“√“ß∑Ë’ 1 ·≈–殑 “√≥“·°‰â ¢‡ªπì ≈”¥∫— §Õ◊ 1.1 π”È Àπ°— µ«— ‡æ¡Ë‘ ¢π÷È ¡“°·π–π”ºªŸâ «É ¬§«∫§¡ÿ πÈ”Àπ°— ®”°¥— πÈ”¥¡◊Ë ‡©≈¬’Ë 500-800¡≈‘ ≈≈‘ µ‘ √ µÕà «π— ·≈–®”°¥— ‡°≈Õ◊ „πÕ“À“√√«¡∑ß—È ≈¥§«“¡‡¢¡â ¢πâ ‚´‡¥¬’ ¡„ππÈ”¬“øÕ°‡≈Õ◊ ¥‡æÕ◊Ë ≈¥§«“¡°√–À“¬πÈ” ‚¥¬∑«Ë— ‰ªπ”È Àπ°— µ«— ¢ÕߺªŸâ «É ¬§«√®–‡æ¡Ë‘ ¢πÈ÷ ‡©≈¬Ë’ 0.5-1.0 °‚‘ ≈°√¡— µÕà «π— 1.2 √–¬–‡«≈“°“√øÕ°‡≈Õ◊ ¥ πÈ— ∑”„À‡â °¥‘ high ultrafiltration rate §«√ª√∫— ‡æ¡‘Ë ‡«≈“ °“√øÕ°‡≈Õ◊ ¥ ‡æÕË◊ ≈¥Õµ— √“°“√¥ß÷ π”È „π·µ≈à –™«Ë— ‚¡ß ®–∑”„À√â “à ß“¬¢ÕߺªâŸ «É ¬ª√∫— µ«— ‰¥∑â π— ‡æ¡Ë‘ plasma refilling ‰¥â 1.3 π”È Àπ°— µ«— (dry weight) µË”°«“à §«“¡‡ªπì ®√ß‘ °“√ª√∫— π”È Àπ°— µ«— dry weight „À∂â °Ÿ µÕâ ß ´ßË÷  “¡“√∂ª√–‡¡π‘ ß“à ¬Ê ¥«â ¬«∏‘ ’ trial and error Õ“»¬— °“√µ¥‘ µ“¡Õ“°“√ Õ“°“√· ¥ß¢ÕߺªŸâ «É ¬ §Õ◊ Õ“°“√∫«¡ µ–§√«‘ ÀÕŸ ÕÈ◊ ‡«¬’ π»√’ …– §≈πË◊ ‰ â Õ“‡®¬’ π °“√À¡πË— µ¥‘ µ“¡ ·≈–ª√∫— ‡ª≈¬Ë’ ππ”È Àπ°— µ«— ®√ß‘ „Àâ‡À¡“– ¡ ®–™à«¬ªÑÕß°—π°“√‡°‘¥¿“«–§«“¡¥—π‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥  à«π°“√ª√–‡¡‘π«‘∏’Õ◊ËπÊ Õ“®æ®‘ “√≥“π”¡“„™„â πºªâŸ «É ¬‡ªπì √“¬Ê ‡™πà «∏‘ °’ “√µ√«®Õ≈— µ√“´“«πÀå ≈Õ¥‡≈Õ◊ ¥¥” (inferior vena cava), °“√µ¥‘ µ“¡°“√‡ª≈¬Ë’ π·ª≈ߢÕß plasma volume (plasma volume monitor), °“√«¥— bioelectric impedance analysis (BIA) ‡ªπì µπâ 1.4 ªí≠À“¢Õ߇§√Ë◊Õ߉µ‡∑’¬¡™π‘¥‰¡à¡’√–∫∫§«∫§ÿ¡°“√¥÷ßπȔ՗µ‚π¡—µ‘ (nonvolumetric dialysis) ∑”„ÀÕâ µ— √“°“√¥ß÷ π”È ¡§’ «“¡º¥‘ æ≈“¥ ßŸ ‡πÕË◊ ß®“°Õµ— √“°“√¥ß÷ π”È ®–¢πÈ÷ °∫— §«“¡¥π— ‡≈Õ◊ ¥¿“¬„𵫗 °√Õß ‡¡ÕË◊ ¡°’ “√‡ª≈¬Ë’ π·ª≈ß BFR ®–¡º’ ≈∑”„À°â “√¥ß÷ π”È ‡ª≈¬Ë’ π·ª≈߇°¥‘ ¢πÈ÷ „πª®í ®∫ÿ π— ‡§√ÕË◊ ߉µ‡∑¬’ ¡ «à π„À≠‡à ªπì ™π¥‘ ∑¡Ë’ √’ –∫∫§«∫§¡ÿ °“√¥ß÷ π”È Õµ— ‚π¡µ— ‘ (ultrafiltration controller) ∑”„À§â «∫§¡ÿ °“√¥ß÷ π”È Õ¬“à ß ¡”Ë ‡ ¡Õ ®ß÷ ≈¥Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ 1.5 °“√„™â dialysate ‰¡‡à À¡“– ¡ - °“√„™â dialysate sodium µ”Ë °«“à „π‡≈Õ◊ ¥ ‚´‡¥¬’ ¡‡ªπì ‡°≈Õ◊ ·√∑à §Ë’ «∫§¡ÿ √–¥∫— plasma osmolality À“°ª√∫— §«“¡‡¢¡â ¢πâ ¢ÕßπÈ”¬“ dialysate sodium µË”°«“à „π‡≈Õ◊ ¥®ß÷ ¡º’ ≈∑”„Àâ plasma osmolality ≈¥≈ß ∑”„Àπâ È”„πÀ≈Õ¥‡≈Õ◊ ¥‡§≈Õ◊Ë π¬“â ¬¡“ ¿àŸ “¬„π‡´≈≈å ®ß÷ ≈¥ plasma refilling ∑”„À§â «“¡¥π— ‚≈Àµ‘ ≈¥≈ß · ¥ß¥ß— √ªŸ ∑Ë’ 1 ª®í ®∫ÿ π— ¡√’ “¬ß“π π∫—  ππÿ ™¥— ‡®π«“à ‡¡ÕË◊ „™â dialysate sodium  ßŸ ®–≈¥Õ∫ÿ µ— °‘ “√≥°å “√ ‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥ ¥ß— ππ—È §«√‡≈Õ◊ °„™â dialysate sodium 142-145 mEq/L À√Õ◊ „™«â ∏‘ °’ “√µß—È sodium profiling[4-6] ‡™àπ °“√ª√—∫µ—Èß‚´‡¥’¬¡ Ÿß„π™à«ß·√°Ê ¢Õß°“√øÕ°‡≈◊Õ¥ ·≈–§àÕ¬Ê ª√—∫≈¥ ‡ªìπ≈”¥—∫·∫∫ linear À√◊Õ stepwise À√◊Õµ—Èß ≈—∫√–¥—∫‚´‡¥’¬¡ ŸßµË”„πºŸâªÉ«¬∑’Ë¡’§«“¡‡ ’ˬߠŸßµàÕ°“√ ‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ ·µÕà ¬“à ߉√°µÁ “¡Õ“®‡°¥‘ º≈¢“â ߇§¬’ ߢÕß°“√„™â dialysate sodium  Ÿß®“°°√–µÿâπ„ÀâºâŸªÉ«¬¡’°“√°√–À“¬πÈ”¡“° Õ“®®–‡°‘¥ªí≠À“πÈ”Àπ—°µ—«‡æ‘Ë¡¡“°√–À«à“ß°“√øÕ° ‡≈Õ◊ ¥·µ≈à –§√ß—È µ“¡¡“

New Frontiers in Dialysis 124 ∏π‘µ ®√‘ ππ— ∑∏å «™—  ‘√‘¿“ ™â“ß»‘√°‘ ≈ÿ ™¬— ∏π—𥓠µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°ÿ≈ Intracellular fluid Extracellular fluid Dialyzer Step 3 Step 1 Osmolality 320 mosmol/kg Water movement 280 Osmolality 320 mosmol/kg Loss of urea falling to 290 mosmol/kg as and water diffusion occurs Step 2 √ªŸ ∑Ë’ 1 °“√øÕ°‡≈Õ◊ ¥¢®¥— ¢Õ߇ ¬’ ®“°√“à ß°“¬ ‚¥¬‡©æ“–¬‡Ÿ √¬’ ∑”„Àâ plasma osmolality ≈¥≈ß®“° 320 ‡ªπì 290mOsm/kg ßà º≈„Àπâ È”¿“¬πÕ°‡´≈≈‡å §≈Õ◊Ë πµ«— ‡¢“â ¿“¬„π‡´≈≈µå “¡§«“¡·µ°µ“à ߢÕß√–¥∫— plasma osmolality - °“√„™â dialysate calcium µË” (2.5 mEq/L) ®–¡‚’ Õ°“ ‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë °«“à °“√„™â dialysate calcium  Ÿß (3.5 mEq/L) ‡™◊ËÕ«à“√–¥—∫·§≈‡´’¬¡µË”¡’º≈∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¥”¢¬“¬µ—« ·≈– °≈“â ¡‡πÕ◊È À«— „®∫∫’ µ«— ≈¥≈ߥߗ ππ—È ºªâŸ «É ¬∑¡’Ë ª’ ≠í À“§«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥·π–π”„À„â ™âdialysate calcium  Ÿß (3.0-3.5 mEq/L) ·µàÕ¬à“߉√µâÕßæ÷ß√–«—ߺ≈¢â“߇§’¬ß§◊Õ ¿“«– hypercalcemia ‡π◊ËÕß®“°ºâŸ ªÉ«¬øÕ°‡≈◊Õ¥ à«π„À≠à®–‰¥â√—∫¬“®—∫øÕ ‡øµ„πÕ“À“√∑’Ë¡’·§≈‡´’¬¡‡ªìπ à«πª√–°Õ∫ ·≈–‰¥â√—∫¬“ «µ‘ “¡π‘ ¥’´ß÷Ë ®–¡·’ π«‚π¡â ®–‡°¥‘ ¿“«–hypercalcemiaÕ¬‡àŸ ¥¡‘ §«√µ¥‘ µ“¡¥√Ÿ –¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥‡ªπì √–¬– - °“√„™â dialysate potassium µË” (1-2 mEq/L) ¡‚’ Õ°“ ‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë °«“à °“√„™â dialysate potassium  Ÿß (3.0 mEq/L) ‡™◊ËÕ«à“√–¥—∫‚ª·µ ‡´’¬¡µË”∑”„Àâ¡’§«“¡º‘¥ª°µ‘¢Õß√–∫∫ ª√– “∑Õµ— ‚π¡µ— ‘ ·≈–°“√∫∫’ µ«— ¢ÕßÀ«— „® Õ¬“à ߉√°µÁ “¡À“°‡≈Õ◊ °„™â dialysate potassium  ßŸ ®–∑”„Àâ ‡°‘¥º≈¢â“߇§’¬ß∑’Ë ”§—≠§◊Õ¿“«– hyperkalemia ‰¥â ¥—ßπ—Èπ‚¥¬∑—Ë«‰ª®÷߉¡à·π–π”„Àâ‡≈◊Õ°„™â dialysate potassium  ßŸ 1.6 °“√ª√∫— ‡∑§π§‘ °“√øÕ°‡≈Õ◊ ¥ ¥«â ¬«∏‘ µ’ “à ßÊ ‡™πà °“√ª√∫— √–¥∫— ‚´‡¥¬’ ¡ ßŸ „π™«à ß·√° ¢Õß°“√øÕ°‡≈Õ◊ ¥ ·≈–§Õà ¬Ê ≈¥≈߇ªπì ≈”¥∫— (sodium profile) °“√ª√∫— °“√¥ß÷ π”È ¥«â ¬Õµ— √“‡√«Á „π™«à ß ·√°¢Õß°“√øÕ°‡≈Õ◊ ¥ ·≈«â §Õà ¬≈¥≈ß„π™«à ß∑“â ¬ (ultrafiltration profile) °“√¥ß÷ π”È ‡æ¬’ ßÕ¬“à ߇¥¬’ «„π™«à ß 1-2 ™—Ë«‚¡ß·√°µàե⫬°“√øÕ°‡≈◊Õ¥ª°µ‘ (sequential ultrafiltration dialysis) æ∫«à“ “¡“√∂≈¥Õÿ∫—µ‘ °“√≥å°“√‡°‘¥§«“¡¥—π‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥ √«¡∑—ÈßÕ“°“√º‘¥ª°µ‘Õ◊ËπÊ ‡™àπ µ–§√‘« ‡«’¬π»’√…– ÕàÕπ‡æ≈’¬  à«π°“√®–‡≈◊Õ°„™â‡∑§π‘§°“√øÕ°‡≈◊Õ¥·∫∫„¥ ‡æ◊ËÕ≈¥Õÿ∫—µ‘°“√≥å°“√‡°‘¥§«“¡¥—π‚≈À‘µ µË”¢≥–øÕ°‡≈◊Õ¥¬—߉¡à™—¥‡®π ·µà®“°°“√»÷°…“‡ª√’¬∫‡∑’¬∫‡∑§π‘§°“√øÕ°‡≈◊Õ¥·∫∫µà“ßÊ æ∫

Acute Complications during Hemodialysis ∫≠— ™“  ∂√‘ –æ®πå 125 √ªŸ ∑Ë’ 2 Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë „π·µ≈à –‡∑§π§‘ ¢Õß°“√øÕ°‡≈Õ◊ ¥ æ∫«“à sodium profile (NaM), high sodium dialysate (HNa) ·≈– cool dialysate (35°C) ¡Õ’ ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë πÕâ ¬ °«“à «∏‘ ’ sequential ultrafiltration (UF) ·≈– standard dialysis (Standard) Õ¬“à ß¡π’ ¬—  ”§≠— ∑“ß ∂µ‘ ‘ [* <0.05] «“à °“√øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ ’ sodium profile (Na+ 152 ≈¥‡ªπì 136 mEq/L), high sodium dialysate (Na+ 143 mEq/L) ·≈– cool dialysate (35 Õß»“‡´≈‡´¬’  ) ¡ª’ √– ∑‘ ∏¿‘ “æ„π°“√√°— …“„°≈‡â §¬’ ß°π— ·≈–∑ßÈ— 3 «∏‘ ¡’ ’ ª√– ∑‘ ∏¿‘ “楰’ «“à °“√øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ ’ sequential ultrafiltration ·≈–«∏‘ ¡’ “µ√µ√“∞“π (Na+ 138 mEq/ L)[7] · ¥ß¥ß— √ªŸ ∑Ë’ 2 πÕ°®“°π„È’ πª®í ®∫ÿ π— ¥«â ¬‡∑§‚π‚≈¬∑’ °Ë’ “â «Àπ“â ¡“°¢πÈ÷ ¡°’ “√„™‡â ∑§π§‘ °“√‡Ω“Ñ √–«ß— ·≈–µ¥‘ µ“¡ºªŸâ «É ¬¢≥–øÕ°‡≈Õ◊ ¥µ“à ßÊ ¡“„™ â “¡“√∂≈¥Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ° ‡≈Õ◊ ¥ ‰¥·â °à √–∫∫µ√«®°“√‡ª≈¬Ë’ π·ª≈ßÕ≥ÿ À¿¡Ÿ ¢‘ ≥–øÕ°‡≈Õ◊ ¥ (online temperature sensors), √–∫∫ µ‘¥µ“¡°“√‡ª≈’ˬπ·ª≈ßπÈ”„πÀ≈Õ¥‡≈◊Õ¥ (plasma volume monitor) À√◊Õ CRIT-LINE monitor, √–∫∫ °“√µ‘¥µ“¡°“√‡ª≈’ˬπ·ª≈ß conductivity (online conductivity measurement), √–∫∫°“√§«∫§ÿ¡√«¡ ∑—Èß°“√‡ª≈’ˬπ·ª≈ßπÈ”„πÀ≈Õ¥‡≈◊Õ¥ °“√‡ª≈’ˬπ·ª≈ß conductivity ·≈–°“√‡ª≈’ˬπ·ª≈ßÕÿ≥À¿Ÿ¡‘ ¢≥–øÕ°‡≈Õ◊ ¥„À‡â °¥‘ §«“¡ ¡¥≈ÿ (closed loop biofeedback system)[8] ‡ªπì µπâ 2) §«“¡º¥‘ ª°µ¢‘ Õß°“√À¥µ«— ¢ÕßÀ≈Õ¥‡≈Õ◊ ¥ (Inadequate vasoconstriction) 2.1 º≈®“°°“√ª√∫— Õ≥ÿ À¿¡Ÿ π‘ ”È ¬“ dialysate  ßŸ (¡“°°«“à 36 Õß»“‡´≈‡´¬’  ) ·≈–º≈ ®“°¢∫«π°“√øÕ°‡≈◊Õ¥®–‡æ‘Ë¡Õÿ≥À¿Ÿ¡‘¿“¬„π√à“ß°“¬ Õ∏‘∫“¬®“°°“√¢“¥ “√πÈ”¢≥–øÕ°‡≈◊Õ¥ ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥∫√‘‡«≥º‘«Àπ—߇°‘¥°“√À¥µ—« °“√√–∫“¬§«“¡√âÕπ¢Õß√à“ß°“¬≈¥≈ß ¡’Õÿ≥À¿Ÿ¡‘ ¿“¬„π√“à ß°“¬‡æ¡‘Ë ¢π÷È ∑”„ÀÀâ ≈Õ¥‡≈Õ◊ ¥¥”·≈–À≈Õ¥‡≈Õ◊ ¥·¥ß¢¬“¬µ«— ·≈–‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”µ“¡¡“ ¥—ßπ—Èπ§«√ª√—∫Õÿ≥À¿Ÿ¡‘πÈ”¬“ dialysate µË”°«à“Õÿ≥À¿Ÿ¡‘√à“ß°“¬ºŸâªÉ«¬ª√–¡“≥ 1-2 Õß»“‡´≈‡´’¬  À√◊Õª√—∫Õÿ≥À¿Ÿ¡‘ª√–¡“≥ 34-36 Õß»“‡´≈‡´’¬  ‡æ◊Ëՙ૬§«∫§ÿ¡Õÿ≥À¿Ÿ¡‘√à“ß°“¬„Àâ§ß∑’Ë ¡’º≈≈¥

New Frontiers in Dialysis 126 ∏π‘µ ®‘√ππ— ∑å∏«—™  ‘√‘¿“ ™â“ß»√‘ ‘°ÿ≈™—¬ ∏ππ— ¥“ µ√–°“√«π‘™ « π— µå  ‡ÿ ¡∏°≈ÿ ¿“«–§«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥º≈‡ ¬’ ¢Õß°“√ª√∫— Õ≥ÿ À¿¡Ÿ µ‘ Ë”‡°π‘ ‰ª®–∑”„Àºâ ªŸâ «É ¬√ Ÿâ °÷ ‰¡ à ∫“¬µ«— Àπ“« —Ëπ ·≈–Õ“®¡’º≈‡ ’¬µàÕ°“√∑”ß“π¢ÕßÀ—«„® ªí®®ÿ∫—πæ—≤π“„™â‡§√◊ËÕ߉µ‡∑’¬¡∑’Ë¡’√–∫∫ online temperature sensors  “¡“√∂§«∫§¡ÿ Õ≥ÿ À¿¡Ÿ ¢‘ Õß√“à ß°“¬„À§â ß∑Ë’ (isothermic dialysis) æ∫«“à  “¡“√∂ ≈¥Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ·≈–º≈¢“â ߇§¬’ ߥߗ °≈“à «[9-11] 2.2 °“√√—∫ª√–∑“πÕ“À“√¢≥–øÕ°‡≈◊Õ¥ ®–¡’º≈∑”„ÀâÀ≈Õ¥‡≈◊Õ¥‡≈’Ȭß≈”‰ â¡“°¢÷Èπ (splanchnic sequestration) ·≈–¡°’ “√¢¬“¬µ«— ¢ÕßÀ≈Õ¥‡≈Õ◊ ¥‡≈¬È’ ß≈”‰ â (splanchnic vasodilatation) ®ß÷ ¡°’ “√≈¥≈ߢÕß peripheral vascular resistance (PVR) ∑”„À‡â °¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ‰¥ßâ “à ¬[12] º≈‡ ¬’ ¥ß— °≈à“«®–‡°‘¥¿“¬„π 30 π“∑’ ·≈–‡°‘¥π“πª√–¡“≥ 2 ™—Ë«‚¡ß ¥—ßπ—Èπ„π°√≥’ºŸâªÉ«¬¡’§«“¡‡ ’ˬߠŸßµàÕ °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ §«√ߥ√∫— ª√–∑“πÕ“À“√∑π— ∑°’ Õà π À√Õ◊ ¢≥–øÕ°‡≈Õ◊ ¥ 2.3 °“√¢“¥‡≈◊Õ¥ √à«¡°—∫ªí®®—¬°√–µâÿπ®“°¿“«–´’¥„Àâ¡’°“√À≈—Ëß “√ adenosine [Tissue ischemia (adenosine-mediated, aggravated by anemia)]  “√ adenosine ®–¡ƒ’ ∑∏¢Ï‘ ¬“¬À≈Õ¥‡≈Õ◊ ¥ ·≈–¬—∫¬—Èß°“√À≈—Ëß norepinephrine ∑”„À⇰‘¥§«“¡¥—π‚≈À‘µµË”Õ¬à“ß©—∫æ≈—π‰¥â „πºŸâªÉ«¬‡°‘¥§«“¡¥—π ‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥®–¡’°“√¢“¥‡≈◊Õ¥¢Õ߇π◊ÈÕ‡¬◊ËÕ‡°‘¥¢÷Èπ ¥—ßπ—Èπ®÷߇ªìπ‡ ¡◊Õπ«ß®√°√–µÿâπ„ÀâÀ≈—Ëß adenosine ‡æ‘Ë¡¢÷ÈπÕ’° ·≈–‡°‘¥§«“¡¥—π‚≈À‘µµË”Õ¬à“ß©—∫æ≈—πµ“¡¡“ ¥—ßπ—Èπ°“√„™â¬“°≈ÿà¡ adenosine receptorblocker‰¥·â °àcaffeine “¡“√∂≈¥Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”Õ¬“à ß©∫— æ≈π— ®“°adenosine ¢≥–øÕ°‡≈◊Õ¥‰¥â[13] °“√·°â‰¢ªí®®—¬°√–µÿâπ°“√¢“¥‡≈◊Õ¥¢Õ߇π◊ÈÕ‡¬◊Ëե⫬°“√‡æ‘Ë¡√–¥—∫ hematocrit ¥â«¬°“√„Àâ‡≈◊Õ¥ À√◊Õ¬“ erythropoietin  “¡“√∂≈¥Õÿ∫—µ‘°“√≥å°“√‡°‘¥§«“¡¥—π‚≈À‘µµË”¢≥–øÕ° ‡≈Õ◊ ¥‰¥[â 14] 2.4 §«“¡º¥‘ ª°µ¢‘ Õß√–∫∫ª√– “∑Õµ— ‚π¡µ— ‘ (autonomic neuropathy) æ∫‰¥∫â Õà ¬„πºªâŸ «É ¬ ‰µ«“¬‡√Õ◊È √ß— ‚¥¬‡©æ“–°≈¡ÿà ºªŸâ «É ¬‡∫“À«“𠇪πì º≈¡“®“°§«“¡º¥‘ ª°µ¢‘ Õß√–∫∫ autonomic sympathetic nervous system (SNS) „π°“√µÕ∫ πÕßµÕà ¿“«–¢“¥π”È ¢Õß√“à ß°“¬§Õ◊ ‰¡¡à °’ “√À≈ßË—  “√ catecholamine ‡æ◊Ëՙ૬„π°“√À¥µ—«¢ÕßÀ≈Õ¥‡≈◊Õ¥ ·≈–°“√∫’∫µ—«¢ÕßÀ—«„®‡æ‘Ë¡¢÷Èπ À√◊Õ‡°‘¥°“√µÕ∫ πÕߺ‘¥ª°µ‘ ¢Õß√“à ß°“¬∑‡’Ë √¬’ °«“à Bezold-Jarisch reflex §Õ◊ °“√µÕ∫ πÕߢÕß√–∫∫ SNS ≈¥≈ß ·µ¡à °’ “√°√–µπÿâ √–∫∫ parasympathetic nervous system ‡æ¡Ë‘ ¢πÈ÷ ·∑π ∑”„À‡â °¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥‰¥â À≈°— °“√ «‘π‘®©—¬Õ“»—¬°“√µ√«®æ‘‡»…‡æ‘Ë¡‡µ‘¡µà“ßÊ ¢≥–∑’Ë°“√«‘π‘®©—¬‡∫◊ÈÕßµâπ®“°Õ—µ√“°“√‡µâπ¢ÕßÀ—«„®®– ™“â ¢≥–‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ´ßË÷ ∫ßà ∫Õ°∂ß÷ °“√µÕ∫ πÕߢÕß√–∫∫ SNS ¢ÕߺªŸâ «É ¬º¥‘ ª°µ‘ °“√√°— …“ §«“¡¥π— ‚≈Àµ‘ µ”Ë ®“°§«“¡º¥‘ ª°µ¢‘ Õß√–∫∫ª√– “∑Õµ— ‚π¡µ— ‘ §Õ◊ 2.4.1 Selective alpha-1 adrenergic agonist À√Õ◊ midodrine (Gutron) √∫— ª√–∑“π 2.5-10 ¡‘≈≈‘°√—¡ °àÕπ∑”°“√øÕ°‡≈◊Õ¥ 30-120 π“∑’ ®–™à«¬°√–µÿâπ°“√∑”ß“π¢Õß√–∫∫ SNS ∑”„Àâ À≈Õ¥‡≈Õ◊ ¥À¥µ«— ¡º’ ≈‡æ¡Ë‘ PVR  “¡“√∂‡æ¡Ë‘ √–¥∫— §«“¡¥π— ‚≈Àµ‘ ¢ÕߺªŸâ «É ¬ ·≈–¬“¡º’ ≈¢“â ߇§¬’ ßπÕâ ¬ ¡“°[15] ‡™à𠪫¥»’√…– §—πµ“¡º‘«Àπ—ß °≈—Èπªí  “«–‰¡àÕ¬Ÿà Õ¬à“߉√°Áµ“¡§«√À≈’°‡À≈’ˬ߰“√„™â¬“ ¢≥–ºªŸâ «É ¬°≈“â ¡‡πÕÈ◊ À«— „®¢“¥‡≈Õ◊ ¥°”‡√∫‘ ·≈–§«√ߥ°“√√∫— ª√–∑“π¬“≈¥§«“¡¥π— ‚≈Àµ‘ °≈¡àÿ alpha- adrenergic blocker √«à ¡ ‡πÕË◊ ß®“°®–≈¥ª√– ∑‘ ∏¿‘ “æ°“√‡æ¡Ë‘ §«“¡¥π— ‚≈Àµ‘ ¢Õ߬“ midodrine

Acute Complications during Hemodialysis ∫≠— ™“  ∂√‘ –æ®πå 127 2.4.2 Serotonin uptake inhibitor (SRIs, sertraline) ®–ÕÕ°ƒ∑∏≈‘Ï ¥ postsynaptic serotonin receptor ¡º’ ≈‡æ¡‘Ë √–¥∫— serotonin ¡º’ ≈∑”„À√â “à ß°“¬µÕ∫ πÕßµÕà catecholamine ‰¥¥â ¢’ π÷È °“√√∫— ª√–∑“𬓠sertraline 50-100 ¡≈‘ ≈°‘ √¡— µÕà «π— µ¥‘ µÕà °π— π“π 4-6  ª— ¥“Àå  “¡“√∂≈¥Õµ— √“°“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”¢≥– øÕ°‡≈Õ◊ ¥ √«¡∑ßÈ— ™«à ¬·°‰â ¢§«“¡º¥‘ ª°µ√‘ –∫∫ª√– “∑Õµ— ‚π¡µ— „‘ πºªâŸ «É ¬øÕ°‡≈Õ◊ ¥‰¥[â 16, 17] 2.5 º≈®“°¬“≈¥§«“¡¥π— ‚≈Àµ‘  ßŸ ·π–π”„Àßâ ¥¬“≈¥§«“¡¥π— ‚≈Àµ‘ ¡Õ◊È °Õà π°“√øÕ°‡≈Õ◊ ¥ „πºŸâªÉ«¬∑’Ë¡’§«“¡‡ ’ˬߠŸß À√◊Õ‡°‘¥§«“¡¥—π‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥ ‡æ√“–«à“¬“≈¥§«“¡¥—π‚≈À‘µ∑ÿ° ™π¥‘ ®–ÕÕ°ƒ∑∏„Ï‘ π¢≥–∑”°“√øÕ°‡≈Õ◊ ¥ ·≈–∑”„À°â ≈‰°°“√ª√∫— µ«— ªÕÑ ß°π— §«“¡¥π— ‚≈Àµ‘ µ”Ë ‡ ¬’ ‰ª 2.6 º≈®“°πÈ”¬“ dialysate acetate ®–∑”„Àæâ ∫Õ∫ÿ µ— °‘ “√≥°å “√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”‰¥ â ߟ Õ∏∫‘ “¬®“°°“√ ≈“¬µ«— ¢Õß acetate ‡ªπì bicarbonate ™“â ®ß÷ ‡°¥‘ °“√ – ¡ acetate „π√“à ß°“¬ ¡º’ ≈ ∑”„ÀâÀ≈Õ¥‡≈◊Õ¥¢¬“¬µ—« ·≈–À—«„®∫’∫µ—«≈¥≈ß[18] ¥—ßπ—Èπ®÷߉¡à§«√‡≈◊Õ°„™âπÈ”¬“ dialysate acetate „πºªŸâ «É ¬∑¡Ë’ ª’ ≠í À“§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ ´ßË÷ „πª®í ®∫ÿ π—  «à π„À≠®à –‡≈°‘ „™â dialysate acetate ·≈–‡ª≈¬Ë’ π¡“„™â bicarbonate ·∑π 3) ‚√§À«— „® ‡ªπì ª≠í À“∑æË’ ∫‰¥∫â Õà ¬„πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— Õ“®‡°¥‘ ®“°°≈“â ¡‡πÕÈ◊ À«— „®¢“¥ ‡≈Õ◊ ¥ (myocardial infraction) À«— „®‡µπâ º¥‘ ®ß— À«– (arrhythmia) ‡¬ÕË◊ À¡âÿ À«— „®Õ°— ‡ ∫ (pericarditis) ∑”„Àâ À«— „®∫’∫µ—«≈¥≈ß À√Õ◊ ∑“ßµ√ß°—π¢“â ¡‡°‘¥°≈â“¡‡πÈÕ◊ À—«„®‚µ (left ventricular hypertrophy) ∑”„ÀÀâ «— „® §≈“¬µ—«√—∫‡≈◊Õ¥≈¥≈߇°‘¥‡ªìπ diastolic heart failure ¥—ßπ—È𮔇ªìπµâÕß√—°…“µ“¡ “‡Àµÿ‚√§ À√◊Õ ª√°÷ …“Õ“¬·ÿ æ∑¬‚å √§À«— „®√«¡¥·Ÿ ≈√°— …“ 4)  “‡ÀµÿÕË◊πÊ ‰¥â·°à °“√ Ÿ≠‡ ’¬‡≈◊Õ¥ (occult hemorrhage), °“√µ‘¥‡™◊ÈÕ„π°√–· ‚≈À‘µ (septicemia), hemolysis ·≈– air embolism ´÷ËߧߵâÕ߉ª√—°…“µ“¡ “‡Àµÿ¢Õß‚√§®÷ß®–·°â‰¢§«“¡¥—π ‚≈Àµ‘ µ”Ë ‰¥â ·≈– ¥ÿ ∑“â ¬Õ“®‡°¥‘ ®“° dialyzer reaction À√Õ◊ ‡√¬’ °«“à bioincompatible membrane ‡™ÕË◊ «“à ¡’∫∑∫“∑µàÕ°“√‡°‘¥§«“¡¥—π‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥ ‡ªìπº≈®“°°“√°√–µÿâπ√–∫∫ complement ∑”„À‡â ¡¥Á ‡≈Õ◊ ¥¢“«‰ªÕ¥ÿ µπ— „π‡ πâ ‡≈Õ◊ ¥ªÕ¥‡°¥‘ intrapulmonaryleukoagglutination‡°¥‘ ¿“«–¢“¥ÕÕ°´‡‘ ®π ·≈–°“√°√–µπÿâ cytokine µ“à ßÊ ∑”„ÀÀâ ≈Õ¥‡≈Õ◊ ¥¢¬“¬µ«— ¥ß— ππ—È §«√‡≈Õ◊ °„™â membrane ∑¡’Ë ’ biocompatibility  ßŸ Ê ‡æÕË◊ ªÕÑ ß°π— °“√‡°¥‘ ¿“«–¥ß— °≈“à «  √ªÿ ·π«∑“ߪÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥ À≈°—  ”§≠— ¢Õß°“√ªÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥§Õ◊ °“√·°‰â ¢µ“¡ “‡Àµ¥ÿ ß— °≈“à «¢“â ßµπâ ‚¥¬ “‡Àµ∑ÿ æ’Ë ∫∫Õà ¬‡ªπì º≈¡“®“°πÈ”Àπ°— µ«— ∑‡’Ë æ¡‘Ë ¡“°¢π÷È √–À«“à ß°“√øÕ°‡≈Õ◊ ¥·µ≈à –§√ß—È √à«¡°—∫ªí≠À“‚√§À—«„®¢ÕߺªâŸ «É ¬ ·≈–¿“«– autonomic neuropathy  “¡“√∂ √ªÿ ‡ªπì ·π«∑“ߪÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë „πºªŸâ «É ¬øÕ°‡≈Õ◊ ¥¥«â ¬‡§√ÕË◊ ߉µ‡∑¬’ ¡ ¥ß— µ“√“ß∑Ë’ 2

New Frontiers in Dialysis 128 ∏𵑠®√‘ ππ— ∑∏å «™—  √‘ ‘¿“ ™â“ß»‘√‘°ÿ≈™¬— ∏π—𥓠µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°≈ÿ µ“√“ß∑Ë’ 2 ·π«∑“ß°“√ªÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”¢≥–øÕ°‡≈Õ◊ ¥ 1. ‡≈Õ◊ °„™‡â §√ÕË◊ ߉µ‡∑¬’ ¡∑¡Ë’ °’ ≈‰°§«∫§¡ÿ ª√¡‘ “≥°“√¥ß÷ π”È (ultrafiltration controller) 2. ®”°¥— ª√¡‘ “≥π”È ¥¡Ë◊ ·≈–‡°≈Õ◊ ‚¥¬π”È Àπ°— µ«— ¢ÕߺªâŸ «É ¬ §«√‡æ¡Ë‘ ¢πÈ÷ πÕâ ¬°«“à 1 °‚‘ ≈°√¡— µÕà «π— 3. ª√∫— π”È Àπ°— µ«— ®√ß‘ (dry weight) „À‡â À¡“– ¡ 4. ‡≈Õ◊ °„™πâ ”È ¬“ dialysate ∑¡Ë’ √’ –¥∫— sodium  ßŸ °«“à „π‡≈Õ◊ ¥ (142-145 mEq/L) À√Õ◊ Õ“®‡≈Õ◊ °„™«â ∏‘ ’ °“√ª√∫— sodium profile 3) ߥ√∫— ª√–∑“𬓧«∫§¡ÿ §«“¡¥π— ‚≈Àµ‘ °Õà πøÕ°‡≈Õ◊ ¥ 4) ‡≈Õ◊ °„™πâ ”È ¬“ dialysate ‡ªπì bicarbonate 5) ª√∫— Õ≥ÿ À¿¡Ÿ π‘ ”È ¬“ dialysate Õ¬„Ÿà π™«à ß 34-36 Õß»“‡´≈‡´¬’   6) √°— …“√–¥∫— hemoglobin ¢ÕߺªâŸ «É ¬¡“°°«“à 11 g/dL 7) ߥ°“√√∫— ª√–∑“πÕ“À“√¢≥–∑”°“√øÕ°‡≈Õ◊ ¥ 8) 殑 “√≥“‡≈Õ◊ °°“√µ¥‘ µ“¡°“√‡ª≈¬Ë’ π·ª≈ßπ”È „πÀ≈Õ¥‡≈Õ◊ ¥ (plasma volume monitor) 9) 殑 “√≥“‡≈Õ◊ °„™¬â “ midodrine √∫— ª√–∑“π 2.5-10 ¡≈‘ ≈°‘ √¡— °Õà π∑”°“√øÕ°‡≈Õ◊ ¥ 10) 殑 “√≥“‡≈Õ◊ °„™¬â “ sertraline 11) ‡æ¡Ë‘ √–¬–‡«≈“°“√øÕ°‡≈Õ◊ ¥Õ°’ 30 π“∑’ 2. ¿“«– dialyzer reaction[19] Dialyzer reaction À√Õ◊ acute allergic reaction ‡ªπì ªØ°‘ √‘ ¬‘ “Õ“°“√·æ∑⠇˒ °¥‘ ®“°‡≈Õ◊ ¥ ¡— º — µ«— °√Õß„π¢≥–øÕ°‡≈Õ◊ ¥ æ∫‰¥∫â Õà ¬„πºªŸâ «É ¬∑„Ë’ ™µâ «— °√Õß„À¡‡à ªπì §√ßÈ— ·√° „πÕ¥µ’ ‡√¬’ °¿“«–π«È’ “à first use syndrome  “¡“√∂·¬°ÕÕ°‡ªπì 2 °≈¡àÿ µ“¡§«“¡√πÿ ·√ߢÕß‚√§ 1. Type A reaction (Anaphylactic type)  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ 1.1 Ethylene oxide µ°§“â ßÕ¬¿Ÿà “¬„𵫗 °√ÕßÀ≈ß— °“√∑”§«“¡ –Õ“¥µ«— °√Õß ‡ªπì  “‡Àµÿ  «à π„À≠¢à Õß type A reaction ‡¡ÕË◊ ethylene oxide ‡¢“â ‰ª„π√“à ß°“¬®–°√–µπâÿ „À√â “à ß°“¬ √“â ß antibodies ™π¥‘ IgE ·≈–¡°’ “√°√–µπÿâ „À¡â °’ “√À≈ß—Ë  “√ histamine ÕÕ°¡“°Õà „À‡â °¥‘ ªØ°‘ √‘ ¬‘ “Õ“°“√·æ™â 𥑠anaphylaxis · ¥ß¥—ß√Ÿª∑’Ë 3[20] °“√µ√«®‡≈◊Õ¥®–æ∫ hypereosinophilia ·≈–¡’√–¥—∫ IgE  Ÿß¢÷Èπ „π√“¬∑’Ë¡’Õ“°“√ √πÿ ·√ß®–æ∫ specific IgE-antibodies µÕà ethylene oxide[21] 1.2 µ«— °√Õß polyacrylonitrile membrane (AN69) °∫— ¬“ ACE inhibitor ¡√’ “¬ß“π °“√‡°¥‘ ªØ°‘ √‘ ¬‘ “Õ“°“√·æ™â 𥑠anaphylactoid ‡°¥‘ ¢πÈ÷ ‡ªπì ªØ°‘ √‘ ¬‘ “°“√·æ∑⠉˒ ¡ºà “à π IgE ‡™ÕË◊ «“à ‡°¥‘ ®“° æπÈ◊ º«‘ ¢Õßµ«— °√Õß AN69 ‡ªπì ª√–®≈ÿ ∫‡¡ÕË◊  ¡— º — °∫— ‡≈Õ◊ ¥‡°¥‘ °“√®∫— µ«— ¢Õß Hageman factor (factor XII)

Acute Complications during Hemodialysis ∫—≠™“  ∂‘√–æ®πå 129 √ªŸ ∑Ë’ 3  √ªÿ °≈‰°°“√‡°¥‘ ªØ°‘ √‘ ¬‘ “·æ∑â ß—È ™π¥‘ anaphylactic reaction ·≈– anaphylactoid reaction „πºªŸâ «É ¬øÕ° ‡≈Õ◊ ¥¥«â ¬‡§√Õ◊Ë ß‰µ‡∑¬’ ¡[20] ·≈– prekallikrein ·≈«â ‡°¥‘ °“√‡ª≈¬’Ë π prekallikrein ‡ªπì kallikrein ´ß÷Ë ¡º’ ≈µ“¡¡“§Õ◊ kininogen ®–·∫ßà µ«— ‡ªπì bradykinin ‡æ¡Ë‘ ¢πÈ÷ „π‡≈Õ◊ ¥ ·≈–‡¡ÕË◊ ºªâŸ «É ¬‰¥√â ∫— ¬“ ACE inhibitor ®–¬∫— ¬ßÈ— °“√ÕÕ°ƒ∑∏¢Ï‘ Õ߇ÕπÁ ‰´¡å kinase II ®–¬ßË‘ ∑”„À√â –¥∫— bradykinin „π‡≈Õ◊ ¥‡æ¡Ë‘ ¢πÈ÷ Õ°’ ´ßË÷ √–¥∫— bradykinin ∑§Ë’ ßË— ®–∑”„ÀÀâ ≈Õ¥‡≈Õ◊ ¥¢¬“¬µ«— ·≈–‡™ÕË◊ «“à ∑”„Àâ anaphylactoid reaction µ“¡¡“[22, 23] Õ¬“à ߉√°µÁ “¡ª®í ®∫ÿ π— æ∫«“à °“√„™µâ «— °√Õß AN69 √«à ¡°∫— ‰¥√â ∫— ¬“ angiotensin receptor blocker (ARB)  “¡“√∂∑”„À‡â °¥‘ anaphylactoid reaction ‰¥â ‚¥¬∑¬Ë’ “ ARB ‰¡¡à º’ ≈µÕà √–¥∫— bradykinin „π‡≈Õ◊ ¥ ¥ß— ππÈ— Õ“®®–¡°’ ≈‰°ÕπË◊ Ê ∑¬Ë’ ß— ‰¡∑à √“∫∑”„À‡â °¥‘ anaphylactoid reaction ‰¥[â 24, 25] 1.3  “‡ÀµÕÿ π◊Ë Ê ∑¡Ë’ √’ “¬ß“π°“√‡°¥‘ ªØ°‘ √‘ ¬‘ “°“√·æâ anaphylaxis ‰¥·â °à ®“°°“√„™â formaldehyde¶“à ‡™Õ◊È „𵫗 °√Õß∑¡’Ë π’ ”°≈∫— ¡“„™´â È”[26]®“°°“√„™âhighfluxdialysis√«¡°∫— πÈ”¬“bicarbonate dialysate ‡™Õ◊Ë «“à Õ“®‡°¥‘ ®“°°“√ªπ‡ªÕóô π¢Õ߇™Õ◊È ·∫§∑‡’ √¬’ ·≈– endotoxin ®“°°“√„™â heparin[27] ®“°°“√„™â iron dextran[28] À√Õ◊ π”È ¬“ dialysate acetate[29] ‡™ÕË◊ «“à ‡ªπì ª®í ®¬— °√–µπâÿ „À‡â °¥‘ type A reaction ·≈–¢≥– ‡¥¬’ «°π— ¡º’ ªâŸ «É ¬À≈“¬√“¬‰¡∑à √“∫∂ß÷  “‡Àµ¢ÿ Õߪذ‘ √‘ ¬‘ “°“√·æ∑â ·’Ë ∑®â √ß‘ Õ“°“√ ·≈–Õ“°“√· ¥ß Õ“°“√·æ®â –‡°¥‘ ¿“¬„π 2-3 π“∑·’ √°À≈ß— ®“°‡√¡‘Ë øÕ°‡≈Õ◊ ¥ ¡∫’ “ß√“¬‡∑“à ππ—È Õ“®®–‡°¥‘ ™“â µÕâ ß

New Frontiers in Dialysis 130 ∏𵑠®√‘ π—π∑∏å «™—  ‘√¿‘ “ ™“â ß»√‘ °‘ ÿ≈™¬— ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°≈ÿ „™â‡«≈“π“π∂÷ß 30 π“∑’À≈—ß®“°‡√‘Ë¡øÕ°‡≈◊Õ¥ §«“¡√ÿπ·√ߢÕß‚√§æ∫À≈“°À≈“¬®“°πâÕ¬∂÷ß¡“°§◊Õ ºπË◊ §π— µ“¡º«‘ Àπß— ∫«¡µ“¡µ«— §≈πË◊ ‰ â Õ“‡®¬’ 𠪫¥∑Õâ ß ∂“à ¬‡À≈« ‰¢â Àπ“« πË— ‡ÀßÕË◊ ÕÕ°¡“° µ«— ‡¬πÁ ‡®∫Á ·ππà Õ° À“¬„®ÀÕ∫‡ÀπÕË◊ ¬®“°À≈Õ¥≈¡µ∫’ µ«— §«“¡¥π— ‚≈Àµ‘ µ”Ë ·≈–À«— „®À¬¥ÿ ‡µπâ ®π‡ ¬’ ™«’ µ‘ ‰¥â °“√«‘π‘®©—¬Õ“»—¬ª√–«—µ‘°“√‰¥â√—∫ “√ ´÷Ëߧ“¥«à“‡ªì𠓇Àµÿ¢Õß°“√‡°‘¥ªØ‘°‘√‘¬“°“√·æâ¥—ß °≈“à «¢“â ßµπâ √«à ¡°∫— Õ“®æ®‘ “√≥“µ√«®¬π◊ ¬π— °“√«π‘ ®‘ ©¬— ¥«â ¬ Skin test, Serum specific IgE, Lymphocyte transformation, Basophil activation assays À√Õ◊ °“√∑” In vivo challenge tests °“√√°— …“ Type A reaction À≈°— °“√√°— …“§Õ◊ À¬¥ÿ °“√øÕ°‡≈Õ◊ ¥∑π— ∑’ À“â ¡§π◊ ‡≈Õ◊ ¥°≈∫—  µàŸ «— ºªâŸ «É ¬ ·≈–∑ßÈ‘ µ«— °√Õß ‰¡πà ” °≈—∫¡“„™âÕ’° Õ“®æ‘®“√≥“„À⬓Õ◊ËπÊ µ“¡§«“¡√ÿπ·√ߢÕß‚√§ ‰¥â·°à ºŸâªÉ«¬‡°‘¥§«“¡¥—π‚≈À‘µµË” À√Õ◊ À“¬„®ÀÕ∫‡ÀπÕË◊ ¬®“°À≈Õ¥≈¡µ∫’ µ«— §«√©¥’ ¬“ epinephrine 0.2-0.5 ¡≈‘ ≈°‘ √¡— „µºâ «‘ Àπß— À√Õ◊ ‡¢“â °≈â“¡‡π◊ÈÕ ·≈–§«√©’¥¬“ epinephrine ´È”À≈—ß®“°ºà“π‰ª 5 π“∑’·≈â«Õ“°“√ºŸâªÉ«¬‰¡à¥’¢÷Èπ ºŸâªÉ«¬‡°‘¥ ºπË◊ §π— µ“¡º«‘ Àπß— Õ¬“à ߇¥¬’ «Õ“®©¥’ ‡æ¬’ ߬“ antihistamine À√Õ◊ corticosteroids °“√ªÕÑ ß°π— °“√‡°¥‘ Type A reaction §«√À≈°’ ‡À≈¬Ë’ ß°“√„™ â “√ ethylene oxide ¶“à ‡™ÕÈ◊ µ«— °√Õß À√Õ◊  “¬π”‡≈Õ◊ ¥ ·µ„à π√“¬∑®Ë’ ”‡ªπì µÕâ ß„™ â “√ ethylene oxide §«√¡°’ “√≈“â ߥ«â ¬π”È ‡°≈Õ◊ Õ¬“à ßπÕâ ¬ 2-3 ≈µ‘ √¢πÈ÷ ‰ª°Õà π°“√øÕ°‡≈Õ◊ ¥ ‡æÕË◊ °”®¥—  “√ ethylene oxide À√Õ◊  “√µ°§“â ßÕπ◊Ë Ê „𵫗 °√Õß ·≈– “¬π”‡≈Õ◊ ¥ À“°ºªŸâ «É ¬‰¥√â ∫— ¬“ ACE inhibitor À√Õ◊ ARB §«√À≈°’ ‡À≈¬Ë’ ß°“√„™µâ «— °√Õß™π¥‘ AN 69 ·≈–°√≥º’ ªŸâ «É ¬‡§¬¡ª’ √–«µ— ‡‘ °¥‘ type A reaction ¡“°Õà 𠧫√„™µâ «— °√Õß∑º’Ë “à π°“√¶“à ‡™Õ◊È ¥«â ¬«∏‘ ’ stream À√Õ◊ gamma irradiation ·∑π„™ â “√ ethylene oxide ·≈–Õ“®æ®‘ “√≥“„À¬â “ anti-histamine À√Õ◊ corticosteroids °Õà π∑”°“√øÕ°‡≈Õ◊ ¥ 2. Type B reaction  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ ‡™◊ËÕ«à“‡°‘¥®“°‡≈◊Õ¥ —¡º— °—∫ free hydroxy group ∫πº‘«µ—«°√Õß ¡’°“√°√–µÿâπºà“π√–∫∫ complement ‡°¥‘ anaphylatoxin C3a ·≈– C5a ´ßË÷ C5a ®–™°— π”„À‡â ¡¥Á ‡≈Õ◊ ¥¢“« (neutrophil) «ßË‘ ‰ªÕ¥ÿ µπ— „πÀ≈Õ¥‡≈Õ◊ ¥ªÕ¥[30] ¥ß— ππÈ— ™«à ߇«≈“¿“¬„π 15 π“∑À’ ≈ß— ‡√¡Ë‘ °“√øÕ°‡≈Õ◊ ¥ ®–¡√’ –¥∫— neutrophil „π‡≈Õ◊ ¥≈¥≈ß À≈ß— ®“°ππ—È neutrophil ®–‡æ¡‘Ë °≈∫— ¡“‡ªπì ª°µ„‘ π‡«≈“ 60 π“∑’ √«à ¡°∫— ‡¡¥Á ‡≈Õ◊ ¥¢“«µ«— ÕÕà π (band neutrophil) ®–¡√’ –¥∫— ‡æ¡Ë‘ ¡“°¢πÈ÷ ‡ªπì 3 ‡∑“à ¢Õߧ“à ª°µ‘ µ«— °√Õß·µ≈à –™π¥‘ ¡°’ “√°√–µπÿâ √–∫∫ complement ·µ°µ“à ß°π— µ“¡ biocompatible membrane ¢Õßµ«— °√Õß ‚¥¬‡√¬’ ß≈”¥∫— °“√°√–µπâÿ √–∫∫ complement ®“°¡“°‰ªπÕâ ¬§Õ◊ cellulose (cuprophane), substituted cellulose (cellulose acetate), cellulo-synthetic (Hemophan), reused cellulose ·≈– synthetic membranes ¥ß— ππÈ— À“°‡≈Õ◊ °„™µâ «— °√Õß™π¥‘ cellulose ®–‡°¥‘ §«“¡‡ ¬Ë’ ßµÕà °“√‡°¥‘ type B reaction ‰¥ â ߟ ·≈–À“°‡≈Õ◊ °„™µâ «— °√Õß¢π“¥„À≠¡à æ’ π◊È ∑º’Ë «‘ ¡“°®–‡æ¡‘Ë §«“¡‡ ¬’Ë ßµÕà °“√‡°¥‘ typeBreaction¡“°¢π÷È µ“¡ Õ“°“√ ·≈–Õ“°“√· ¥ß °“√‡°¥‘ type B reaction æ∫‰¥∫â Õà ¬°«“à type A reaction ¡°— ‡°¥‘ ¿“¬„π‡«≈“ 15-60 π“∑À’ ≈ß—

Acute Complications during Hemodialysis ∫—≠™“  ∂‘√–æ®πå 131 ‡√¡Ë‘ ∑”°“√øÕ°‡≈Õ◊ ¥ ®–¡Õ’ “°“√‡®∫Á ·ππà Õ° ª«¥À≈ß— ‡ÀπÕË◊ ¬ ´ß÷Ë ®–¡√’ πÿ ·√ß‚√§πÕâ ¬°«“à type A reaction °“√«π‘ ®‘ ©¬— ·¬°®“° type A reaction §Õ◊ √–¬–‡«≈“°“√‡°¥‘ ‚√§®–™“â °«“à ·≈–¢≥–∑”°“√øÕ°‡≈Õ◊ ¥µÕà Õ“°“√¢Õß‚√§®–§Õà ¬Ê ¥¢’ πÈ÷ ‡Õß °“√√°— …“ Type B reaction ‡ªπì °“√√°— …“µ“¡Õ“°“√¢ÕߺªâŸ «É ¬ ‰¥·â °à °“√„ÀÕâ Õ°´‡‘ ®π °“√„À¬â “ anti-histamine ‡ªπì µπ⠺⟠ª«É ¬ “¡“√∂∑”°“√øÕ°‡≈Õ◊ ¥µÕà ‰ª‰¥â Õ“°“√¡°— ®–‡ªπì ª°µ„‘ π√–¬–‡«≈“ 1 ™«Ë— ‚¡ß °“√ªÕÑ ß°π— °“√‡°¥‘ Type B reaction °“√„™µâ «— °√Õß´”È (Reused dialysis) ®–™«à ¬≈¥ªØ°‘ √‘ ¬‘ “°“√·æâ ‡πÕË◊ ß®“°µ«— °√Õ߇≈Õ◊ ¥®–∂°Ÿ ‡§≈◊Õ∫¥â«¬‚ª√µ’π„π‡≈◊Õ¥ ®÷ß≈¥‚Õ°“ ∑’ˇ≈◊Õ¥ —¡º— °—∫ free hydroxyl group ∫πº‘«µ—«°√Õß °√≥’ºŸâ ª«É ¬¬ß— ‡°¥‘ Õ“°“√ªØ°‘ √‘ ¬‘ “°“√·æ§â «√殑 “√≥“‡ª≈¬’Ë πµ«— °√Õ߇ªπì ™π¥‘ ∑¡’Ë ’biocompatibility ßŸ ¢π÷È ∑¥·∑𠇙πà synthetic membranes, cellulo-synthetic membranes  √ªÿ °“√ “‡Àµÿ 欓∏°‘ ”‡π¥‘ ·π«∑“ß°“√√°— …“ ·≈–ªÕÑ ß°π— °“√‡°¥‘ dialyzer reactions ¥ß— µ“√“ß∑Ë’ 3 µ“√“ß∑Ë’ 3 Development and prevention of dialysis reactions Timescale Pathogenesis Etiology Management Prevention First use Ethylene oxide Rinse dialyzer before use Use gamma-ray or steam anaphylaxis IgE -Stop HD sterilized dialyzers Reuse Formaldehyde -Do not return Discontinue reuse (Rare) extracorporeal 5-20 min Glutaraldehyde blood to patient Avoid AN69 dialyzerswith into HD Renalin ACEi -Epinephrine Discontinue reuse with 20-40 min Bradykinin AN69 membrane with ACEi renalin into HD anaphylactoid Reused membrane -Corticosteroids Use test dose for iron dextran Histamine -Antihistamines Use noncellulose Iron dextran dialyzers Desferoxamine Heparin (Rare) Mild reaction Complement Cellulose membranes ContinoueHD Symptoms usually settle in 1 hr 3. µ–§√«‘ (Muscle cramp) ‡ªπì ¿“«–·∑√°´Õâ π¢≥–øÕ°‡≈Õ◊ ¥æ∫∫Õà ¬√Õâ ¬≈–33-86¡º’ ≈∑”„Àµâ Õâ ßÀ¬¥ÿ °“√øÕ°‡≈Õ◊ ¥°Õà π °”À𥇫≈“∑”„Àºâ ªâŸ «É ¬‰¥√â ∫— °“√øÕ°‡≈Õ◊ ¥‰¡‡à 欒 ßæÕ¿“«–µ–§√«‘ ¡°— ‡°¥‘ „π™«à ß∑“â ¬¢Õß°“√øÕ°‡≈Õ◊ ¥ ‚¥¬¡“°®– —¡æ—π∏å°—∫°“√¥÷ßπÈ”ª√‘¡“≥¡“° ·≈–°“√‡ª≈’Ë¬π ¡¥ÿ≈¢Õß·§≈‡´’¬¡ ·≈–‚ª·µ ‡´’¬¡„π

New Frontiers in Dialysis 132 ∏𵑠®√‘ ππ— ∑∏å «™—  √‘ ‘¿“ ™â“ß»‘√‘°ÿ≈™—¬ ∏π—𥓠µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°≈ÿ √à“ß°“¬ ∑”„À⇰‘¥§«“¡º‘¥ª°µ‘¢Õß√–∫∫ª√– “∑ à«πª≈“¬ ‡°‘¥°“√À¥µ—«¢Õß°≈â“¡‡π◊ÈÕ∑”„À⇰‘¥ µ–§√«‘ µ“¡¡“  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘  “‡Àµ∑ÿ ·Ë’ ∑®â √ß‘ ¬ß— ‰¡∑à √“∫™¥— ‡®π ‡™ÕË◊ «“à ¡§’ «“¡‡°¬Ë’ «¢Õâ ß°∫— ª®í ®¬— ¥ß— µÕà ‰ªπ’È 1. °“√‡ª≈¬’Ë π·ª≈ߢÕߪ√¡‘ “≥‡≈Õ◊ ¥ °“√‡°¥‘ µ–§√«‘ ¡°— ‡°¥‘ √«à ¡°∫— §«“¡¥π— ‚≈Àµ‘ µË”¢≥– øÕ°‡≈Õ◊ ¥ ‡ªπì º≈¡“®“°°“√¥ß÷ πÈ”ª√¡‘ “≥¡“° À√Õ◊ °“√„™πâ È”¬“ dialysate ‚´‡¥¬’ ¡µË” ∑”„Àâ vascular refilling ‰¡‡à 欒 ßæÕ ‡≈Õ◊ ¥ «à π∑‰’Ë ª‡≈¬’È ß°≈“â ¡‡πÕ◊È ≈¥≈ß ‡°¥‘ °≈“â ¡‡πÕ◊È ¢“¥‡≈Õ◊ ¥ ®“°°“√»°÷ …“ π∫—  ππÿ ™¥— ‡®π«“à °“√¥ß÷ π”È √–À«“à ßøÕ°‡≈Õ◊ ¥¡“° ·≈–°“√≈¥≈ߢÕß plasma osmolality ®“°°“√„™πâ ”È ¬“ dialysate sodium µË”®–‡æ¡‘Ë §«“¡‡ ¬’Ë ßµÕà °“√‡°¥‘ µ–§√«‘  ßŸ ¢π÷È 2. °“√‡ª≈¬’Ë π ¡¥≈ÿ ¢Õ߇°≈Õ◊ ·√à ‰¥·â °à ¿“«–·§≈‡´¬’ ¡ ·¡°π‡’ ´¬’ ¡ ·≈–‚ª·µ ‡´¬’ ¡„π ‡≈Õ◊ ¥µ”Ë ∑”„À‡â °¥‘ §«“¡·µ°µ“à ߢÕ߇°≈Õ◊ ·√¿à “¬„π ·≈–¿“¬πÕ°‡´≈≈å ®–°√–µπâÿ „À‡â ´≈≈°å ≈“â ¡‡πÕÈ◊ ‡°¥‘ action potential ‡°¥‘ °“√À¥µ«— ¢Õß°≈“â ¡‡πÕÈ◊ ·≈–∑”„À‡â °¥‘ Õ“°“√µ–§√«‘ µ“¡¡“ 3. °“√¢“¥ÕÕ°´‡‘ ®π¢Õß°≈“â ¡‡πÕ◊È ºªâŸ «É ¬øÕ°‡≈Õ◊ ¥ «à πÀπß÷Ë ®–¡°’ “√≈¥≈ߢÕß “√2,3DPG „π‡≈◊Õ¥ √à«¡°—∫¿“«–‡≈◊Õ¥‡ªìπ¥à“ß ®–∑”„ÀâÕÕ°´‘‡®π®—∫µ—«°—∫‡¡Á¥‡≈◊Õ¥·¥ß·πàπ ¡’°“√ª≈àÕ¬ ÕÕ°´‡‘ ®π„À‡â πÕÈ◊ ‡¬ÕË◊ µ“à ßÊ ·≈–°≈“â ¡‡πÕÈ◊ ≈¥≈ß ∑”„À‡â °¥‘ Õ“°“√µ–§√«‘ 4. °“√¢“¥ “√ carnitine ºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— ®–¡°’ “√¢“¥ “√ carnitine ‡°¥‘ ¢πÈ÷ ‡πÕË◊ ß®“°¡’ °“√√∫— ª√–∑“πÕ“À“√ª√–‡¿∑‡πÕÈ◊  µ— «≈å ¥≈ß √«à ¡°∫— °“√ ≠Ÿ ‡ ¬’  “√ carnitine ‰ª°∫— °“√øÕ°‡≈Õ◊ ¥  “√ carnitine ∑”Àπ“â ∑™Ë’ «à ¬‡√ßà °“√ √“â ßæ≈ß— ß“π ATP ¿“¬„π‡´≈≈å ™«à ¬„π¢∫«π°“√¢π ßà °√¥‰¢¡π— ‡¢“â ‡´≈≈å ·≈–‡ªìπ cofactor „π¢∫«π°“√ oxidation ¢Õ߉¢¡—π¿“¬„π‡´≈≈å ¥—ßπ—Èπ°“√¢“¥ “√ carnitine ®–≈¥ °“√ √“â ßæ≈ß— ß“π√–¥∫— ‡´≈≈å ‡°¥‘ Õ“°“√· ¥ßµ“à ßÊ µ“¡¡“ ‚¥¬‡©æ“–Õ“°“√µ–§√«‘ °“√√°— …“Õ“°“√µ–§√«‘ 1. Hypertonic solutions ‰¥·â °à glucose, mannitol, saline ¡°— ®–‡≈Õ◊ °„™‡â ¡ÕË◊ ‡°¥‘ µ–§√«‘ √«à ¡ °∫— §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥  “√π”È hypertonic solutions ∑”Àπ“â ∑‡Ë’ ªπì osmotic agent ™«à ¬¥ß÷ πÈ”®“°‡π◊ÈÕ‡¬◊ËÕµà“ßÊ ‡¢â“ ŸàÀ≈Õ¥‡≈◊Õ¥ ®÷߇æ‘Ë¡ª√‘¡“≥‡≈◊Õ¥‰ª‡≈’Ȭ߰≈â“¡‡π◊ÈÕ  “¡“√∂≈¥°“√‡°‘¥ µ–§√‘«¢Õߺ⟪ɫ¬‰¥â[31] ªí®®ÿ∫—π·π–π”„Àâ‡≈◊Õ°„™â glucose „πºŸâªÉ«¬øÕ°‡≈◊Õ¥∑’ˉ¡à‰¥â‡ªìπ‡∫“À«“π ‡πÕË◊ ß®“°°“√‡≈Õ◊ °„™â mannitol Õ“®¡°’ “√µ°§“â ß„π√“à ß°“¬‰¥â ·≈–°“√„™â hypertonic saline Õ“®∑”„Àâ ‡°¥‘ ‚´‡¥¬’ ¡‡°π‘ „π√“à ß°“¬ π”È Àπ°— µ«— ‡æ¡Ë‘ ¢πÈ÷ ·≈–‡°¥‘ §«“¡¥π— ‚≈Àµ‘  ßŸ 2. Nifedipine √∫— ª√–∑“π¢π“¥ 10 ¡≈‘ ≈°‘ √¡—  “¡“√∂≈¥°“√‡°¥‘ µ–§√«‘ ‰¥â ®“°°“√¢¬“¬ ‡ πâ ‡≈Õ◊ ¥ «à π∑‡Ë’ ≈¬È’ ß°≈“â ¡‡πÕÈ◊ ·π–π”«“à §«√‡≈Õ◊ °„™ºâ ªâŸ «É ¬°≈¡àÿ ∑¡Ë’ §’ «“¡¥π— ‚≈Àµ‘ ª°µ‘ ¢≥–‡°¥‘ µ–§√«‘ °“√ªÕÑ ß°π— Õ“°“√µ–§√«‘ ¡À’ ≈°— °“√ ”§≠— ‡À¡Õ◊ π°∫— ·π«∑“ß°“√ªÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈À‘µµË”¢≥–øÕ°‡≈◊Õ¥¥—ßµ“√“ß∑’Ë 2 ‡π◊ËÕß®“°∑—Èß Õß¿“«–¡—°®–‡°‘¥√à«¡°—π‡ ¡Õ¢≥–øÕ°‡≈◊Õ¥ Õ¬“à ߉√°µÁ “¡·π«∑“ß°“√ªÕÑ ß°π— ¿“«–µ–§√«‘ ÕπË◊ Ê ∑¡Ë’ ¢’ Õâ ¡≈Ÿ „πª®í ®∫ÿ π— ¡¥’ ß— µÕà ‰ªπÈ’ 1. Quinine sulfate ÕÕ°ƒ∑∏≈Ï‘ ¥ excitability ¢Õ߇ πâ ª√– “∑∑‡Ë’ ≈¬È’ ß°≈“â ¡‡πÕÈ◊ ∑”„Àâ muscle refractory period π“π¢πÈ÷ ®ß÷ ≈¥°“√‡°¥‘ µ–§√«‘ [32] ª®í ®∫ÿ π— ·π–π”„À¬â “¢π“¥ 250-325 ¡≈‘ ≈°‘ √¡— °Õà π

Acute Complications during Hemodialysis ∫—≠™“  ∂‘√–æ®πå 133 øÕ°‡≈Õ◊ ¥ 1-2 ™«Ë— ‚¡ß ‡πÕË◊ ß®“°¬“ quinine sulfate √°— …“‡æ¬’ ßÕ“°“√‡∑“à ππÈ— ·≈–¬“¡º’ ≈¢“â ߇§¬’ ß ‰¥·â °à §≈πË◊ ‰ â Õ“‡®¬’ π ÀÕŸ ÕÈ◊ ®Õª√– “∑µ“ΩÕÉ (optic atrophy) ¥ß— ππÈ— §«√殑 “√≥“„™„â πºªŸâ «É ¬∑‡Ë’ °¥‘ µ–§√«‘ ∫Õà ¬ ·≈–‰¡∑à √“∫ “‡Àµ∑ÿ ·’Ë ∑®â √ß‘ 2. Vitamin E ¢π“¥ 400 IU µÕà «π—  “¡“√∂≈¥°“√‡°¥‘ µ–§√«‘ „°≈‡â §¬’ ß°∫— ¬“ quinine sulfate[33] ·≈–°“√„À¬â “ vitamin E √«à ¡°∫— vitamin C ®–‡æ¡Ë‘ ª√– ∑‘ ∏¿‘ “æ„π°“√√°— …“[34] ·µÕà ¬“à ߉√°µÁ “¡º≈ °“√√°— …“¢Õß vitamin E „π√–¬–¬“«¬ß— ‰¡™à ¥— ‡®π ·≈–§«√µ¥‘ µ“¡º≈¢“â ߇§¬’ ß√–¬–¬“«¢Õ߬“∑®’Ë –‡°¥‘ ¢π÷È 3. Serotonin uptake inhibitor (SRIs, sertraline) ®–ÕÕ°ƒ∑∏≈Ï‘ ¥ postsynaptic serotonin receptor ¡º’ ≈‡æ¡‘Ë √–¥∫— serotonin ·≈–¡º’ ≈∑”„À√â “à ß°“¬µÕ∫ πÕßµÕà catecholamine ‰¥¥â ¢’ π÷È ¬“ sertraline  “¡“√∂ªÕÑ ß°π— °“√‡°¥‘ µ–§√«‘ √«¡∑ßÈ— °“√‡°¥‘ ¿“«–§«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥¥ß— °≈“à «¢“â ßµπâ 4. Carnitine supplement ®“°°“√»°÷ …“æ∫«“à °“√„À â “√ carnitine ∑¥·∑π “¡“√∂™«à ¬ ≈¥°“√‡°¥‘ µ–§√«‘ ¢ÕߺªŸâ «É ¬‰¥â ·≈–≈¥°“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µ”Ë ¢≥–øÕ°‡≈Õ◊ ¥[35] Õ¬“à ߉√°µÁ “¡∫“ß °“√»÷°…“°≈—∫‰¡à‰¥âª√–‚¬™π宓°°“√„Àâ carnitine ∑¥·∑π ªí®®ÿ∫—π¢âÕ¡Ÿ≈ π—∫ πÿπº≈°“√√—°…“¢Õß carnitine ¬ß— ‰¡‡à 欒 ßæÕ ¥ß— ππÈ— KDOQI guideline ·π–π”„™â carnitine ¡“√°— …“¿“«–µ–§√«‘ ‡©æ“–°√≥’ ∑’˺⟪ɫ¬√—°…“¥â«¬«‘∏’¡“µ√∞“πÕ◊ËπÊ ·≈â«Õ“°“√‰¡à¥’¢÷Èπ ·≈–·π–π”«à“§«√µ‘¥µ“¡º≈°“√√—°…“¿“¬„π 9-12 ‡¥Õ◊ π À“°‰¡‰à ¥ºâ ≈§«√À¬¥ÿ °“√√°— …“[36] 5. Benzodiazepines ‰¥·â °à oxazepam ¢π“¥ 5-10 ¡≈‘ ≈°‘ √¡— √∫— ª√–∑“π 2 ™«Ë— ‚¡ß°Õà π øÕ°‡≈Õ◊ ¥ “¡“√∂ªÕÑ ß°π— °“√‡°¥‘ µ–§√«‘ ‰¥â 6. Stretching exercise  “¡“√∂™«à ¬≈¥°“√‡°¥‘ µ–§√«‘ ¢ÕߺªŸâ «É ¬øÕ°‡≈Õ◊ ¥‰¥â 4. ¿“«– Dialysis Disequilibrium Syndrome (DDS)[37] ‡ªπì ¿“«–·∑√°´Õâ π∑“ß√–∫∫ª√– “∑ æ∫∫Õà ¬„πºªŸâ «É ¬øÕ°‡≈Õ◊ ¥§√ßÈ— ·√° ª®í ®¬— ‡ ¬Ë’ ßµÕà °“√ ‡°¥‘ DDS §Õ◊ ºªâŸ «É ¬∑¡Ë’ √’ –¥∫— ¬‡Ÿ √¬’ „π‡≈Õ◊ ¥ ßŸ ¡“°Ê (blood urea nitrogen, [BUN] > 175 mg/dL) ºªŸâ «É ¬  ßŸ Õ“¬ÿ ºªâŸ «É ¬‡¥°Á ºªŸâ «É ¬∑¡Ë’ §’ «“¡º¥‘ ª°µ¢‘ Õß ¡Õß ·≈–ºªŸâ «É ¬∑¡Ë’ ¿’ “«– metabolic acidosis Õ¬“à ß√πÿ ·√ß Õ¬“à ߉√°µÁ “¡ “¡“√∂æ∫„πºªŸâ «É ¬øÕ°‡≈Õ◊ ¥¡“π“π „π°√≥∑’ ºË’ ªŸâ «É ¬∑”°“√øÕ°‡≈Õ◊ ¥‰¡ à ¡”Ë ‡ ¡Õ  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ ¬ß— ‰¡∑à √“∫ “‡Àµ∑ÿ ·Ë’ ∑®â √ß‘ ¡∑’ ƒ…ص’ “à ßÊ æ¬“¬“¡Õ∏∫‘ “¬∂ß÷ °≈‰°°“√‡°¥‘ DDS §Õ◊ 1. °“√øÕ°‡≈Õ◊ ¥≈¥√–¥∫— BUN Õ¬“à ß√«¥‡√«Á ‚¥¬∑√Ë’ –¥∫— ¬‡Ÿ √¬’ „π ¡Õ߬ߗ §ß ßŸ ‡√¬’ °∑ƒ…Æπ’ È’ «“à reverse urea hypothesis ‡°¥‘ §«“¡·µ°µ“à ߢÕß√–¥∫— osmolality ¡°’ “√¥ß÷ π”È ‡¢“â ‰ª„π ¡Õß ∑”„Àâ ‡°¥‘  ¡Õß∫«¡ ´ßË÷ ¡°’ “√»°÷ …“¬π◊ ¬π— „π µ— «∑å ¥≈ÕßÀ≈ß— ®“°≈¥√–¥∫— BUN Õ¬“à ß√«¥‡√«Á æ∫«“à ª√¡‘ “≥ πÈ”„π ¡Õß‡æ¡‘Ë ¢π÷È Õ¬“à ß™¥— ‡®π[38] 2. °“√øÕ°‡≈◊Õ¥‡°‘¥°“√‡ª≈’ˬπ·ª≈ß ¡¥ÿ≈°√¥¥à“ß„π‡≈◊Õ¥Õ¬à“ß√«¥‡√Á« ‚¥¬∑’ËπÈ”„π  ¡Õ߬ߗ §ß§«“¡‡ªπì °√¥Õ¬Ÿà ®ß÷ ‡°¥‘ ¿“«–∑‡Ë’ √¬’ °«“à paradoxical cerebrospinal fluid acidosis ∑”„À¡â °’ “√ ·µ°µ«— ¢Õß cation ‰¥·â °à ‚´‡¥¬’ ¡ ‚ª·µ ‡´¬’ ¡ ·≈–°“√ √“â ß organic acids ¡º’ ≈∑”„À‡â æ¡Ë‘ osmolality

New Frontiers in Dialysis 134 ∏π‘µ ®√‘ ππ— ∑å∏«—™  ‘√‘¿“ ™â“ß»‘√‘°ÿ≈™¬— ∏π—𥓠µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°ÿ≈ „π‡´≈≈ å ¡Õß ¡°’ “√¥ß÷ π”È ‡¢“â ‰ª„π‡´≈≈ å ¡Õß ∑”„À‡â °¥‘  ¡Õß∫«¡µ“¡¡“[37] Õ“°“√ ·≈–Õ“°“√· ¥ß Õ“°“√¡‰’ ¥µâ ßÈ— ·µà §≈πË◊ ‰ â Õ“‡®¬’ 𠪫¥»√’ …–  ∫—  π °≈“â ¡‡πÕÈ◊ °√–µ°ÿ §«“¡¥π— ‚≈Àµ‘  ßŸ µ“ ¡—« ®π∂÷ߢ—Èπ√ÿπ·√߇°‘¥ ´÷¡ ™—° À¡¥ µ‘ ·≈–Õ“®‡ ’¬™’«‘µ‰¥â Õ“°“√‡À≈à“π’ÈÕ“®‡°‘¥¢≥–øÕ°‡≈◊Õ¥ À√◊ÕÀ≈—ß®“°°“√øÕ°‡≈◊Õ¥¿“¬„π 24 ™—Ë«‚¡ß °“√«‘π‘®©—¬Õ“»—¬®“°ª√–«—µ‘ °“√‡°‘¥Õ“°“√ —¡æ—π∏å°—∫ ª√‘¡“≥°“√øÕ°‡≈◊Õ¥ ‚¥¬‡©æ“–„π°“√øÕ°‡≈◊Õ¥§√—Èß·√° ·µàÕ¬à“߉√°Áµ“¡®”‡ªìπµâÕß«‘π‘®©—¬·¬° ‚√§°≈¡àÿ ÕπË◊ Ê √«à ¡¥«â ¬‡ ¡Õ ‰¥·â °à ¿“«– uremia, subdural hematoma, cerebral infarction, intracerebral hemorrhage, meningitis, §«“¡º‘¥ªµ‘¢Õ߇°≈◊Õ·√à„π√à“ß°“¬ (hyponatremia, hypoglycemia) ·≈–¬“ °√–µπâÿ „À‡â °¥‘ encephalopathy °“√√°— …“¿“«– DDS 1. °“√„À â “√π”È hypertonic solutions ‰¥·â °à mannitol, glucose, saline ∑”Àπ“â ∑‡Ë’ ªπì osmotic agent ™«à ¬≈¥§«“¡·µ°µ“à ߢÕß√–¥∫— osmolality √–À«“à ßπ”È „πÀ≈Õ¥‡≈Õ◊ ¥ ·≈–„π ¡Õß 2. °√≥º’ ªâŸ «É ¬¡Õ’ “°“√√πÿ ·√߇°¥‘ ™°— °√–µ°ÿ ´¡÷ À√Õ◊ À¡¥ µ‘ §«√À¬¥ÿ °“√øÕ°‡≈Õ◊ ¥ ·≈– „À¬â “√°— …“Õ“°“√™°— ‰¥·â °à diazepam ∑“ßÀ≈Õ¥‡≈Õ◊ ¥¥” ‚¥¬∑«Ë— ‰ªÕ“°“√¢Õß DDS À≈ß— °“√√°— …“¡°— ®–¥¢’ πÈ÷ ¿“¬„π 24 ™«Ë— ‚¡ß °“√ªÕÑ ß°π— ¿“«– DDS °“√øÕ°‡≈Õ◊ ¥§√ßÈ— ·√° À√Õ◊ „πºªâŸ «É ¬∑¡Ë’ §’ «“¡‡ ¬Ë’ ßµÕà °“√‡°¥‘ DDS §«√‡≈Õ◊ °°“√√°— …“¥ß— µÕà ‰ªπ’È 1. °“√øÕ°‡≈◊Õ¥ª√– ‘∑∏‘¿“æµË” ‰¥â·°à °“√ª√—∫ BFR µË” (150-200 ml/min) °“√„™âµ—« °√Õߪ√– ∑‘ ∏¿‘ “æµ”Ë À√Õ◊ µ«— °√Õß∑¡Ë’ æ’ πÈ◊ ∑ºË’ «‘ 0.9-1.2 µ“√“߇¡µ√ °“√øÕ°‡≈Õ◊ ¥π“π‡æ¬’ ß 2-3 ™«Ë— ‚¡ß 2. °“√„™πâ ”È ¬“ dialysate ∑¡Ë’ √’ –¥∫— ‚´‡¥¬’ ¡ ßŸ (Õ¬“à ßπÕâ ¬ 140 mEq/L) À√Õ◊ ·µ°µ“à ß®“°„π ‡≈Õ◊ ¥‰¡‡à °π‘ 2-3 mEq/L 3. °“√„À â “√πÈ” hypertonic solutions ‰¥·â °à mannitol, glucose, saline ·π–π”„À‡â ≈Õ◊ °„™â glucose „πºªâŸ «É ¬øÕ°‡≈Õ◊ ¥∑‰Ë’ ¡‰à ¥‡â ªπì ‡∫“À«“π ‡πÕË◊ ß®“°°“√‡≈Õ◊ °„™â mannitol Õ“®¡°’ “√µ°§“â ß„π√“à ß°“¬‰¥â ·≈–°“√„™â hypertonic saline Õ“®∑”„À‡â °¥‘ ‚´‡¥¬’ ¡‡°π‘ „π√“à ß°“¬ π”È Àπ°— µ«— ‡æ¡Ë‘ ¢πÈ÷ ·≈–‡°¥‘ §«“¡¥π— ‚≈Àµ‘  ßŸ 5. ª«¥»√’ …– ·≈–§≈π◊Ë ‰ Õâ “‡®¬’ π (Headache, nausea and vomiting) ‡ªπì ¿“«–·∑√°´Õâ π∑æ’Ë ∫‰¥∫â Õà ¬¢≥–øÕ°‡≈Õ◊ ¥ Õ“°“√ª«¥»√’ …–·≈–§≈π◊Ë ‰ Õâ “‡®¬’ π‡°¥‘ ®“° À≈“¬ “‡Àµ‰ÿ ¥·â °à §«“¡¥π— ‚≈Àµ‘ µË” À√Õ◊ §«“¡¥π— ‚≈Àµ‘  ßŸ ¿“«– blood membrane bioincompatibility ¿“«– dialysis disequilibrium syndrome ¿“«–‡°≈◊Õ·√à„π‡≈◊Õ¥º‘¥ª°µ‘‰¥â·°à hypoglycemia, hypernatremia, hyponatremia À√◊ÕÕ“®‡°‘¥®“°≈¥√–¥—∫ caffeine „π‡≈◊Õ¥Õ¬à“ß√«¥‡√Á«„πºŸâªÉ«¬¥◊Ë¡°“·ø‡ªìπª√–®”  ÿ¥∑⓬§«√æ÷ß√–«—ߧ«“¡º‘¥ª°µ‘„π ¡Õß ‡™àπ ‡≈◊Õ¥ÕÕ°„π ¡Õß ‡¬◊ËÕÀÿâ¡ ¡ÕßÕ—°‡ ∫ ¥—ßπ—È𮔇ªìπ

Acute Complications during Hemodialysis ∫—≠™“  ∂√‘ –æ®πå 135 µÕâ ß°“√´°— ª√–«µ— ‘ ·≈–µ√«®√“à ß°“¬ √«¡∑ßÈ— µ√«®∑“ßÀÕâ ߪØ∫‘ µ— °‘ “√‡æÕË◊ ™«à ¬À“°“√«π‘ ®‘ ©¬—  “‡Àµÿ °“√√°— …“Õ“°“√ª«¥»√’ …–·≈–§≈πË◊ ‰ Õâ “‡®¬’ π √°— …“µ“¡Õ“°“√¢ÕߺªŸâ «É ¬ ‡™πà ª«¥»√’ …–„À¬â “·°ªâ «¥°≈¡àÿ ¬“æ“√“‡´µ“¡Õ≈ ¬“°≈¡àÿ non steroidal anti-inflammatory drugs (NSAIDs) §≈πË◊ ‰ Õâ “‡®¬’ π„À¬â “·°Õâ “‡®¬’ π°≈¡àÿ metoclopramide °“√ªÕÑ ß°π— Õ“°“√ª«¥»√’ …–·≈–§≈π◊Ë ‰ Õâ “‡®¬’ π °“√ªÕÑ ß°π— °“√‡°¥‘ Õ“°“√ª«¥»√’ …–·≈–§≈π◊Ë ‰ Õâ “‡®¬’ π‡ππâ ·°‰â ¢µ“¡ “‡Àµ¥ÿ ß— °≈“à «¢“â ßµπâ ‰¥·â °à°“√ªÕÑ ß°π— °“√‡°¥‘ §«“¡¥π— ‚≈Àµ‘ µË”À√Õ◊ §«“¡¥π— ‚≈Àµ‘  ßŸ ¢≥–øÕ°‡≈Õ◊ ¥°“√‡≈Õ◊ °„™µâ «— °√Õß™π¥‘ biocompatible membrane  ßŸ °“√ªÕÑ ß°π— ¿“«– dialysis disequilibrium syndrome °“√‡≈Õ◊ °„™πâ È”¬“ dialysate Õ¬“à ߇À¡“– ¡°∫— ºªâŸ «É ¬·µ≈à –√“¬ ·≈–·π–π”ߥ°“√¥¡Ë◊ °“·ø‡ªπì ª√–®” 6. Õ“°“√§π— (Uremic pruritus) [39, 40] ‡ªπì ¿“«–·∑√°´Õâ π∑æ’Ë ∫‰¥∫â Õà ¬¡“°°«“à √Õâ ¬≈–50∑”„Àºâ ªŸâ «É ¬√ Ÿâ °÷ √”§“≠√∫°«πµÕà §≥ÿ ¿“æ ™«’ µ‘ ¢ÕߺªŸâ «É ¬ ºªŸâ «É ¬ «à π„À≠®à –¡Õ’ “°“√§π— √πÿ ·√ß¡“°¢πÈ÷ ¢≥–øÕ°‡≈Õ◊ ¥  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ ¬—߉¡à∑√“∫ “‡Àµÿ∑’Ë·∑â®√‘ß ·µà§“¥«à“¡’ªí®®—¬À≈“¬Õ¬à“ß√à«¡°—π∑”„À⇰‘¥Õ“°“√§—π ¥ß— µÕà ‰ªπ’È 1. º«‘ ·Àßâ (xerosis) ∑”„Àºâ «‘ Àπß— ™π—È ∫π ¥ÿ (stratum corneum) ¢“¥πÈ” º«‘ Àπß— ™π—È π‡’È ª√¬’ ∫‡ ¡Õ◊ π  ‘Ëß·ª≈°ª≈Õ¡ ®÷ß∑”„À⇰‘¥Õ“°“√§—π πÕ°®“°π’ȺŸâªÉ«¬‰µ«“¬‡√◊ÈÕ√—ß®–¡’√–¥—∫ histamine „π‡≈◊Õ¥ Ÿß ‡πÕË◊ ß®“°¡®’ ”π«π mast cell ‡æ¡Ë‘ ¢πÈ÷ ·≈–¡°’ “√°√–µπâÿ „ÀÀâ ≈ßË— histamine ¡“°¢πÈ÷ ¢≥–øÕ°‡≈Õ◊ ¥ 2. §«“¡º¥‘ ª°µ¢‘ Õ߇°≈Õ◊ ·√„à π‡≈Õ◊ ¥ ‰¥·â °à ¿“«– hyperparathyroidism, hypermagnesemia, hypercalcemia, hyperphosphatemia ‡™◊ËÕ«à“‡°‘¥®“°·§≈‡´’¬¡®—∫°—∫øÕ°‡øµ∫√‘‡«≥º‘«Àπ—ß ·≈–Õ“® ‡°¥‘ ®“°¿“«– aluminum „π‡≈Õ◊ ¥ ßŸ . 3. ¿“«– uremia ®“°°“√øÕ°‡≈Õ◊ ¥‰¡‡à 欒 ßæÕ[41] 4. ¿“«–‚≈Àµ‘ ®“ß À√Õ◊ Õ“®®–‡ªπì º≈¡“®“°°“√¢“¥ŒÕ√‚å ¡π erythropoietin 5. °“√·æ â “√µ“à ßÊ ∑„Ë’ ™„â π°“√øÕ°‡≈Õ◊ ¥ ‡™πà heparin, ethylene oxide, formaldehyde, renalin ·≈–Õ“®‡°¥‘ ®“°¿“«– blood membrane bioincompatibility °“√√°— …“Õ“°“√§π— 1. °“√„™¬â “°≈¡àÿ µ“à ßÊ ∑¡Ë’ √’ “¬ß“π«“à  “¡“√∂°“√√°— …“Õ“°“√§π— ‡™πà §√¡’ À√Õ◊ ‚≈™πË— ™«à ¬ ‡æ¡‘Ë ™¡ÿà ™π◊Ë ¢Õߺ«‘ Àπß— À√Õ◊ ¬“∑“ capsaicin, ¬“√∫— ª√–∑“π anti-histamine, cholestyramine, activated charcoal, ketotifen ´ßË÷ ¬“ÕÕ°ƒ∑∏¬Ï‘ ∫— ¬ßÈ— mast cell ∑”„ÀÀâ ≈ßË— histamine ≈¥≈ß ·≈– erythropoietin  “¡“√∂≈¥√–¥∫— histamine „π‡≈Õ◊ ¥‰¥â ´ßË÷ ¬ß— ‰¡∑à √“∫∂ß÷ °≈‰°∑·Ë’ ∑®â √ß‘ ¢Õ߬“ erythropoietin [42] ª®í ®∫ÿ π— ¡°’ “√»°÷ …“·∫∫ randomized control trial æ∫«à“¬“°≈ÿà¡ gabapentin[43] ·≈– nalfurafine (kappa-opioid agonist)[44]  “¡“√∂≈¥°“√‡°‘¥Õ“°“√§—π ·≈–§«“¡√ÿπ·√ߢÕßÕ“°“√§—π‰¥â ·µàÕ¬à“߉√°Áµ“¡¬—ߧߵâÕß°“√°“√

New Frontiers in Dialysis 136 ∏𵑠®√‘ π—π∑å∏«™—  ‘√‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°ÿ≈ »°÷ …“‡æ¡Ë‘ ‡µ¡‘ ∂ß÷ ª√–‚¬™π∑å ™Ë’ ¥— ‡®π¢Õ߬“°≈¡àÿ µ“à ßÊ ¥ß— ∑°Ë’ ≈“à «¡“ 2. °“√√°— …“¿“«– hyperparathyroidism ·≈–§«∫§¡ÿ √–¥∫— ·§≈‡´¬’ ¡ øÕ ‡øµ ·¡°π‡’ ´¬’ ¡ „ÀÕâ ¬„àŸ π‡°≥±ªå °µ‘ 3. °“√øÕ°‡≈Õ◊ ¥„À‡â 欒 ßæÕ ·≈–°“√‡ª≈¬Ë’ π¡“„™µâ «— °√Õß™π¥‘ high flux membrane  “¡“√∂ ≈¥°“√‡°¥‘ Õ“°“√§π— ·≈–§«“¡√πÿ ·√ߢÕßÕ“°“√§π— ‰¥[â 41] 4. °“√©“¬√ß—  ’ ultraviolet B (UVB)  ª— ¥“À≈å – 2 §√ßÈ—  “¡“√∂∑”≈“¬ “√∑∑Ë’ ”„À‡â °¥‘ Õ“°“√ §π— ‡ªπì °“√√°— …“∑ÕË’ Õ°ƒ∑∏‡Ï‘ √«Á ·≈–¡ª’ √– ∑‘ ∏¿‘ “æ§Õà π¢“â ߠߟ 7. ¿“«– Air embolism ‡ªπì ¿“«–·∑√°´Õâ πÕ¬“à ß√πÿ ·√ß “¡“√∂∑”„Àºâ ªŸâ «É ¬‡ ¬’ ™«’ µ‘ À“°«π‘ ®‘ ©¬— ·≈–√°— …“™“â „πª®í ®∫ÿ π— ‡§√◊ËÕ߉µ‡∑’¬¡¡’√–∫∫ªÑÕß°—πª≈Õ¥¿—¬ Ÿß ¡’√–∫∫°“√¥—∫®—∫øÕßÕ“°“»∑’ËÀ≈ÿ¥‡¢â“‰ª„𠓬π”‡≈◊Õ¥ æ√Õâ ¡ ≠— ≠“≥‡µÕ◊ π ¥ß— ππÈ— Õ∫ÿ µ— °‘ “√≥¢å Õß air embolism ®ß÷ ≈¥≈ßÕ¬“à ß¡“°  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ √–∫∫¥∫— ®∫— øÕßÕ“°“»∑À’Ë ≈¥ÿ ‡¢“â ‰ª„𠓬π”‡≈Õ◊ ¥¢Õ߇§√Õ◊Ë ß‰µ‡∑¬’ ¡∑”„À°â “√‡°¥‘ øÕßÕ“°“» ·≈«â À≈¥ÿ º“à 𠓬π”‡≈Õ◊ ¥‡¢“â ºªâŸ «É ¬ (venous blood line) ¡π’ Õâ ¬¡“° ¥ß— ππÈ— °“√‡°¥‘ air embolism ¡°— ®– ‡°¥‘ ®“°µ”·Àπßà °Õà π blood pump §Õ◊ °“√¥¥Ÿ Õ“°“»‡¢“â ‰ª∑“ߥ“â π arterial ®“°µ”·Àπßà °“√·∑߇¢¡Á ®“°°“√„Àâ “√πÈ”∑“ß “¬π”‡≈◊Õ¥ÕÕ°®“°ºâŸªÉ«¬ (arterial line) À√◊Õ®“°°“√‡≈◊ËÕπÀ≈ÿ¥¢Õß “¬π” ‡≈Õ◊ ¥„π√–∫∫ Õ“°“√ ·≈–Õ“°“√· ¥ß Õ“°“√∑“ߧ≈π‘ °‘ ®–√πÿ ·√ß¡“°πÕâ ¬¢π÷È °∫— ª√¡‘ “≥Õ“°“»∑‡’Ë ¢“â  √Ÿà “à ß°“¬·≈–∑“à ¢ÕߺªâŸ «É ¬¢≥– ‡°‘¥‡Àµÿ°“√≥å§◊Õ ∂⓺⟪ɫ¬Õ¬Ÿà„π∑à“π—Ëß»’√…– Ÿß øÕßÕ“°“»®–≈Õ¬À≈ÿ¥ºà“πÀ—«„®‡¢â“ àŸ√–∫∫À≈Õ¥ ‡≈◊Õ¥·¥ß‰ªÕÿ¥µ—π∫√‘‡«≥ ¡Õß ∑”„À⇰‘¥ ¡Õߢ“¥‡≈◊Õ¥‡°‘¥Õ“°“√™—° ´÷¡ ÕàÕπ·√ß·¢π¢“§√÷Ëß´’° ·≈– —∫ π‰¥â[45] À√◊Õ∂⓺ŸâªÉ«¬Õ¬àŸ„π∑à“πÕπ øÕßÕ“°“»®–≈Õ¬À≈ÿ¥ºà“πÀ—«„®´’°¢«“ ·≈–‰ªÕÿ¥µ—π ∫√‡‘ «≥‡ πâ ‡≈Õ◊ ¥¿“¬„πªÕ¥ ∑”„À‡â °¥‘ Õ“°“√ÀÕ∫‡ÀπÕË◊ ¬ ‡®∫Á ·ππà Õ° ‰Õ À«— „®‡µπâ º¥‘ ®ß— À«– ·≈–∂“â √πÿ ·√ß¡“°‡≈Õ◊ ¥®“°ªÕ¥‰¡‡à 欒 ßæÕ‰ª¬ß— À«— „®´°’ ´“â ¬∑”„À‡â °¥‘ §«“¡¥π— ‚≈Àµ‘ µË”µ“¡¡“ °“√«π‘ ®‘ ©¬— air embolism Õ“»¬— °“√µ√«®æ∫øÕßÕ“°“»¿“¬„𠓬π”‡≈Õ◊ ¥¥”‡¢“â ºªŸâ «É ¬ (venous blood line) °“√√°— …“¿“«– air embolism À≈°— °“√√°— …“¢π—È ·√°§Õ◊ À¬¥ÿ °“√øÕ°‡≈Õ◊ ¥∑π— ∑’À“â ¡§π◊ ‡≈Õ◊ ¥°≈∫—  µàŸ «— ºªŸâ «É ¬·≈«â ®¥— „Àºâ ªŸâ «É ¬ πÕπ»√’ …–µ”Ë µ–·§ßµ«— ¢“â ß´“â ¬≈ß ‡æÕË◊ „Àøâ ÕßÕ“°“»‡¢“â ¡“√«¡°π— „πÀ«— „®´°’ ¢«“ ‰¡Àà ≈¥ÿ ‰ª∫√‡‘ «≥ÕπË◊ ´ß÷Ë „π√“¬∑¡’Ë Õ’ “°“√√πÿ ·√ß¡ª’ √¡‘ “≥øÕßÕ“°“»¡“°Õ“®æ®‘ “√≥“¥¥Ÿ Õ“°“»®“°À«— „®´°’ ¢«“º“à π°“√„  à “¬ central venous catheter (CVP line) °“√„Àâ hyperbaric oxygen therapy[46] À√Õ◊ 殑 “≥“„ÀÕâ Õ°´‡‘ ®π 100 ‡ªÕ√凴Áπµå®–™à«¬¢®—¥øÕßÕ“°“»ÕÕ°®“°‡≈◊Õ¥‰¥â‡√Á«¢÷Èπ „π√“¬∑’ËÕ“°“√√ÿπ·√ß®”‡ªìπµâÕß„ à‡§√◊ËÕß ™«à ¬À“¬„®§«√„™Õâ Õ°´‡‘ ®π¢π“¥ ßŸ (FiO2 100%)

Acute Complications during Hemodialysis ∫≠— ™“  ∂√‘ –æ®πå 137 °“√ªÕÑ ß°π— ¿“«– air embolism 1. ‰¡§à «√©¥’ ¬“ À√Õ◊ „Àπâ È”‡°≈Õ◊ ∑“ß “¬π”‡≈Õ◊ ¥ÕÕ°®“°ºªâŸ «É ¬ (arterial line) ·≈– blood pump ‡πÕË◊ ß®“°øÕßÕ“°“»®–¡‚’ Õ°“ À≈¥ÿ º“à π‡¢“â √“à ß°“¬∑“ß∫√‡‘ «≥·∑߇¢¡Á ‰¥â (arterial needle track) 2. °“√‡µ√¬’ ¡‡§√ÕË◊ ß ·≈–Õªÿ °√≥„å π√–∫∫°“√øÕ°‡≈Õ◊ ¥„Àæâ √Õâ ¡ ‰¡„à À¡â °’ “√‡≈ÕË◊ πÀ≈¥ÿ ‰¡¡à ’ øÕßÕ“°“»„𠓬π”‡≈Õ◊ ¥ ·≈–µ«— °√Õß 8. ¿“«–¢“¥ÕÕ°´‡‘ ®π (Hypoxemia) °“√øÕ°‡≈Õ◊ ¥®–¡º’ ≈≈¥√–¥∫— ÕÕ°´‡‘ ®π„π‡≈Õ◊ ¥ (PaO2) ‡©≈¬Ë’ 5-30 ¡≈‘ ≈‡‘ ¡µ√ª√Õ∑∑π— ∑À’ ≈ß— ‡√¡Ë‘ °“√øÕ°‡≈Õ◊ ¥ ≈¥µ”Ë  ¥ÿ „π‡«≈“ 30-60 π“∑’ ·≈–°≈∫— ¡“ª°µ„‘ π‡«≈“ 60-120 π“∑À’ ≈ß— À¬¥ÿ øÕ°‡≈Õ◊ ¥ ‚¥¬∑«Ë— ‰ªºªŸâ «É ¬¡°— ®–‰¡¡à Õ’ “°“√®“°°“√≈¥≈ߢÕßÕÕ°´‡‘ ®π ¬°‡«πâ °√≥º’ ªâŸ «É ¬¡‚’ √§À«— „® À√Õ◊ ‚√§ªÕ¥ √«à ¡  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ ª®í ®¬— À≈“¬Õ¬“à ߧ“¥«“à ‡ªπì  “‡Àµ°ÿ “√‡°¥‘ ¿“«–¢“¥ÕÕ°´‡‘ ®π ¥ß— µÕà ‰ªπÈ’ 1. ¿“«– blood membrane bioincompatibility[19] ®–°√–µπâÿ complement º“à π∑“ß alternative pathway „π‡«≈“‡æ¬’ ß 2-3 π“∑’ À≈ß— ®“°‡≈Õ◊ ¥ºªâŸ «É ¬ ¡— º — °∫— µ«— °√Õß™π¥‘ bioincompatible membrane  ßŸ ‰¥·â °à cuprophane ¡º’ ≈∑”„À‡â ¡¥Á ‡≈Õ◊ ¥¢“«™π¥‘ neutrophil ‡°“–°≈¡ÿà °π— (leukoagglutination) ‡°¥‘ °“√Õ¥ÿ µπ— „πÀ≈Õ¥‡≈Õ◊ ¥ªÕ¥ ∑”„À°â “√·≈°‡ª≈¬Ë’ πÕÕ°´‡‘ ®π¿“¬„πªÕ¥≈¥≈ß ( A-a oxygen gradient °«“â ߢπ÷È ) 2. ¿“«– hypoventilation 2.1 π”È ¬“ dialysate ™π¥‘ acetate ®–‰¡‰à ¥™â ¥‡™¬ carbon dioxide ´ßË÷ ®– ≠Ÿ ‡ ¬’ ‰ª°∫— ¢∫«π°“√ øÕ°‡≈◊Õ¥ ¥—ßπ—Èπ®–∑”„Àâ√–¥—∫ carbon dioxide „π‡≈◊Õ¥≈¥≈ß √à“ß°“¬µÕ∫ πÕߥ⫬≈¥°“√°√–µÿâπ »πŸ ¬Àå “¬„®„π ¡Õß ‡°¥‘ °“√À“¬„®™“â ≈ß ·≈–¡¿’ “«–¢“¥ÕÕ°´‡‘ ®πµ“¡¡“ ¢≥–‡¥¬’ «°π— ¢∫«π°“√‡ª≈¬’Ë π acetate ‡ªπì bicarbonate „πµ∫— ®–„™Õâ Õ°´‡‘ ®π„π‡≈Õ◊ ¥ ¥ß— ππ—È ‡ªπì ª®í ®¬— ‡ √¡‘ µÕà °“√‡°¥‘ ¿“«–¢“¥ÕÕ°´‡‘ ®π 2.2 π”È ¬“ dialysate ™π¥‘ bicarbonate  ßŸ ‚¥¬‡©æ“–¡“°°«“à 35 mEq/L ®–‡°¥‘ ¿“«–‡≈Õ◊ ¥‡ªπì ¥“à ß ¡°’ “√°¥»πŸ ¬Àå “¬„®„π ¡Õß ∑”„À√â –¥∫— ÕÕ°´‡‘ ®π„π‡≈Õ◊ ¥≈¥≈ß °“√√°— …“¿“«–¢“¥ÕÕ°´‡‘ ®π ºªŸâ «É ¬øÕ°‡≈Õ◊ ¥∑«—Ë ‰ª‰¡®à ”‡ªπì µÕâ ß„À°â “√√°— …“®–‡≈Õ◊ °„À°â “√√°— …“¥«â ¬°“√„ÀÕâ Õ°´‡‘ ®π‰¥·â °à nasal oxygen À√Õ◊ ‡æ¡Ë‘ ÕÕ°´‡‘ ®π„πºªâŸ «É ¬∑„Ë’  ‡à §√ÕË◊ ß™«à ¬À“¬„® „πºªŸâ «É ¬¡‚’ √§À«— „®°”‡√∫‘ ºªâŸ «É ¬‚√§ªÕ¥ À√Õ◊ ºªŸâ «É ¬∑¡Ë’ Õ’ “°“√¢“¥ÕÕ°´‡‘ ®π‡°¥‘ ¢πÈ÷ °“√ªÕÑ ß°π— ¿“«–¢“¥ÕÕ°´‡‘ ®π 1. °“√‡≈Õ◊ °„™µâ «— °√Õß∑¡Ë’ ’ biocompatible membrane  ßŸ ‰¥·â °à synthetic membrane 2. À≈°’ ‡≈¬Ë’ ß°“√„™πâ ”È ¬“ dialysate ™π¥‘ acetate 3. À≈°’ ‡≈¬Ë’ ß°“√„™πâ ”È ¬“ dialysate ™π¥‘ bicarbonate  ßŸ ‚¥¬‡©æ“–¡“°°«“à 35 mEq/L