New Frontiers in Dialysis

New Frontiers in Dialysis 138 ∏π‘µ ®√‘ π—π∑∏å «—™  √‘ ‘¿“ ™“â ß»‘√‘°≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π‘™ « —πµå  ‡ÿ ¡∏°≈ÿ 9. ¿“«–‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ° (Hemolysis) °“√øÕ°‡≈Õ◊ ¥®–¡°’ “√·µ°¢Õ߇¡¥Á ‡≈Õ◊ ¥‡≈°Á πÕâ ¬√«à ¡¥«â ¬‡ ¡Õ®“° “¡“√∂µ√«®‡≈Õ◊ ¥æ∫free hemoglobin·µ¡à °— ®–‰¡‡à °¥‘ Õ“°“√√πÿ ·√ß„¥ÊºªâŸ «É ¬√“¬∑‡’Ë °¥‘ Õ“°“√√πÿ ·√ß®”‡ªπì µÕâ ßÀ“ “‡Àµÿ·≈–·°‰â ¢ ‡πÕ◊Ë ß®“°ºªâŸ «É ¬°≈¡ÿà π¡’È ‚’ Õ°“ ‡ ¬’ ™«’ µ‘ ‰¥®â “°¿“«–‚ª·µ ‡´¬’ ¡ ßŸ „π‡≈Õ◊ ¥  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ 1. Mechanical trauma ®“°°“√æ∫— ßÕ¢Õß “¬π”‡≈Õ◊ ¥ ‚¥¬‡©æ“–∫√‡‘ «≥°Õà π∂ß÷ blood pump ·≈–¡√’ “¬ß“π‡°¥‘ ‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ°®“°°“√„™â BFR  ßŸ √«à ¡°∫— °“√„™‡â ¢¡Á ·∑ßøÕ°‡≈Õ◊ ¥¢π“¥‡≈°Á 2.  “√ªπ‡ªÕôó π¢Õßπ”È ¬“ dialysate 2.1 Chloramines‡ªπì  “√¶“à ‡™Õ◊È ·∫§∑‡’ √¬’ „ππÈ”ª√–ª“µ°§“â ß®“°§«“¡∫°æ√Õà ߢÕߢ∫«π°“√ ‡µ√¬’ ¡π”È ∫√ ‘ ∑ÿ ∏Ï‘ ‡æÕË◊ °“√øÕ°‡≈Õ◊ ¥ 2.2 Zinc, copper, fluoride, nitrate, aluminum ªπ‡ªÕôó π 2.3  “√∑”§«“¡ –Õ“¥µ«— °√Õ߉¥·â °à hydrogen peroxide, formaldehyde, hypochlorite ´ßË÷ ‡°¥‘ ®“°°“√µ°§“â ß¿“¬„𵫗 °√Õß°Õà π¡“„™„â À¡à 3. §«“¡º¥‘ æ≈“¥¢Õ߇§√Õ◊Ë ß‰µ‡∑¬’ ¡∑”„Àπâ È”¬“ dialysate ¡’ osmolality µË”‡°π‘ ‰ª À√Õ◊ ¡Õ’ ≥ÿ À¿¡Ÿ ‘  ßŸ ‡°π‘ ‰ª 4. ‚√§‡≈◊Õ¥‡¥‘¡¢Õߺ⟪ɫ¬ √à«¡°—∫ªí®®—¬°√–µÿâπ®“°¢∫«π°“√øÕ°‡≈◊Õ¥ ‡™àπ ºâŸªÉ«¬‡¡Á¥ ‡≈Õ◊ ¥·¥ß·µ°ß“à ¬®“° glucose 6-phosphate dehydrogenase deficiency (G6PD) ‰¥√â ∫— ¬“ quinine À√Õ◊ ¬“°≈¡àÿ µ“à ßÊ °√–µπâÿ oxidant ¢≥–øÕ°‡≈Õ◊ ¥ À√Õ◊ ®“°¬“ quinine ∑”„À‡â °¥‘ ‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ°·∫∫ drug induced microangiopathy Õ“°“√ ·≈–Õ“°“√· ¥ß °“√‡°¥‘ Õ“°“√µ“¡√–¥∫— §«“¡√πÿ ·√ߢÕ߇¡¥Á ‡≈Õ◊ ¥·¥ß·µ° ‰¥·â °à ª«¥À≈ß— ·ππà Õ° °≈“â ¡‡πÕ◊È ÕÕà π·√ß À“¬„®ÀÕ∫‡ÀπÕ◊Ë ¬ À«— „®«“¬ ·≈–À¬¥ÿ ‡µπâ ‰¥â ‚¥¬§«“¡√πÿ ·√߇°¥‘ ®“°°“√·µ°¢Õ߇¡¥Á ‡≈Õ◊ ¥·¥ß ∑”„À¡â ‚’ ª·µ ‡´¬’ ¡ ßŸ „π‡≈Õ◊ ¥ µ√«®√“à ß°“¬æ∫ º«‘ §≈È”¢π÷È ‡≈Õ◊ ¥„𠓬π”‡≈Õ◊ ¥‡¢“â ºªâŸ «É ¬ (venous blood line) ¡ ’ ¡’ «à ߧ≈”È (port-wine stain) À“°π”‡≈Õ◊ ¥¡“ªπòí  «à π∑‡Ë’ ªπì plasma ¥“â π∫π®–‡ªπì  ™’ ¡æŸ ·≈–√–¥∫— hematocrit ≈¥≈ß §«√ ßà ‡≈Õ◊ ¥‡æ¡‘Ë ‡µ¡‘ ‡æÕ◊Ë °“√«π‘ ®‘ ©¬— ¿“«–‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ° ‰¥·â °à complete blood count (CBC), lactate dehydrogenase (LDH), haptoglobin, methemoglobin ·≈–§«√ ßà µ√«®π”È ¬“ dialysate ‰¥·â °à chloramines, zinc, copper, nitrate √«¡∑ß—È ª√–‡¡π‘ «“à µ«— °√Õß¡’ hydrogen peroxide, formaldehyde, hypochlorite µ°§“â ßÀ√Õ◊ ‰¡à °“√√°— …“¿“«–‡¡¥Á ‡≈Õ◊ ¥·µ° À¬¥ÿ °“√øÕ°‡≈Õ◊ ¥∑π— ∑’ À“â ¡§π◊ ‡≈Õ◊ ¥°≈∫—  µŸà «— ºªâŸ «É ¬ ‡πÕË◊ ß®“°‡≈Õ◊ ¥∑§Ë’ “â ßÕ¬®Ÿà –¡ª’ √¡‘ “≥‚ª ·µ ‡´¬’ ¡ ßŸ ‡æ¡‘Ë §«“¡‡ ¬’Ë ßµÕà ¿“«–À«— „®À¬¥ÿ ‡µπâ ‰¥âÀ≈ß— ®“°·°‰â ¢ “‡Àµ¢ÿ Õß¿“«–‡¡¥Á ‡≈Õ◊ ¥·¥ß·µ°·≈«â §«√∑”°“√øÕ°‡≈◊Õ¥´È”∑—π∑’ ‡æ◊ËÕ·°â‰¢¿“«–‚ª·µ ‡´’¬¡ Ÿß„π‡≈◊Õ¥ ·≈–§«√„ÀâºâŸªÉ«¬πÕ𵑥µ“¡ Õ“°“√„π‚√ß欓∫“≈

Acute Complications during Hemodialysis ∫≠— ™“  ∂‘√–æ®πå 139 °“√ªÕÑ ß°π— ¿“«–‡¡¥Á ‡≈Õ◊ ¥·µ° 殑 “√≥“ªÕÑ ß°π— ·°‰â ¢µ“¡ “‡Àµÿ ¥ß— °≈“à «¢“â ßµπâ ‰¥·â °à µ√«®µ¥‘ µ“¡√–¥∫—  “√ªπ‡ªÕôó π„π π”È ¬“ dialysate  ¡”Ë ‡ ¡Õ °“√≈“â ß∑”§«“¡ –Õ“¥µ«— °√ÕßÕ¬“à ß∂°Ÿ µÕâ ßµ“¡«∏‘ ¡’ “µ√∞“π 10. Õ“°“√‰¢â Àπ“« π—Ë (Febrile reaction)  “‡Àµ·ÿ ≈–欓∏°‘ ”‡π¥‘ 1.  “√ endotoxin ªπ‡ªÕôó π„ππ”È ¬“ dialysate[47] ‡ªπì  “‡Àµ ÿ «à π„À≠¢à ÕßÕ“°“√‰¢Àâ π“« πË— ¢≥–øÕ°‡≈Õ◊ ¥  “√ endotoxin ‡ªπì lipopolysaccharide ®“°‡ª≈Õ◊ °πÕ°¢Õ߇™ÕÈ◊ ·∫§∑‡’ √¬’ ·°√¡≈∫ ´ßË÷ À≈¥ÿ ≈Õ¥®“°√–∫∫°“√‡µ√¬’ ¡π”È ∫√ ‘ ∑ÿ ∏Ï‘ ‰¥·â °à ∂ß— ‡°∫Á π”È ∫√ ‘ ∑ÿ ∏Ï‘ ∂ß— π”È ¬“ dialysate bicarbonate º“à π ºπ—ßµ—«°√Õ߇¢â“√à“ß°“¬ °√–µÿâπ°“√À≈—Ëß cytokines ®“°‡¡Á¥‡≈◊Õ¥¢“« ∑”„À⇰‘¥Õ“°“√‰¢âÀπ“« —Ë𠪫¥µ“¡µ«— 2. °“√µ¥‘ ‡™Õ◊È „π√“à ß°“¬¢ÕߺªâŸ «É ¬‚¥¬ “‡Àµ ÿ «à π„À≠‡à °¥‘ ®“°°“√µ¥‘ ‡™Õ◊È ¢Õßvascularaccess À√Õ◊ ®“° “¬ «π (catheter) ¡°— ‡°¥‘ ®“°‡™ÕÈ◊ Staphylococcus aureus À√Õ◊ Staphylococcus epidermidis °“√ µ√«®æ∫º«‘ Àπß— ∫√‡‘ «≥√Õ∫Ê catheter À√Õ◊ vascular access ‡°¥‘ ∫«¡ ·¥ß √Õâ π ®–™«à ¬„π°“√«π‘ ®‘ ©¬— ¿“«–µ¥‘ ‡™Õ◊È Õ¬“à ߉√°µÁ “¡º«‘ Àπß— ∫√‡‘ «≥ vascular access ‡ªπì ª°µ„‘ πºªŸâ «É ¬®”π«π¡“°∑¡’Ë °’ “√µ¥‘ ‡™Õ◊È ¢Õß vascular access Õ“°“√‰¢â Àπ“« —Ëπ®–√ÿπ·√ß¡“°¢÷Èπ¢≥–øÕ°‡≈◊Õ¥ ‡π◊ËÕß®“°°“√øÕ°‡≈◊Õ¥®– °√–®“¬‡™ÕÈ◊ ®“° vascular access ‡¢“â °√–· ‡≈Õ◊ ¥¡“°¢πÈ÷ [48] °“√√°— …“ °“√°”®¥— ·À≈ßà ¢Õ߇™ÕÈ◊ ·∫§∑‡’ √¬’ ‰¥·â °à ‡Õ“ “¬ catheter À√Õ◊ vascular access ÕÕ° ·°‰â ¢ ª√∫— ª√ßÿ √–∫∫°“√‡µ√¬’ ¡π”È ∫√ ‘ ∑ÿ ∏„Ï‘ À¥â ¢’ πÈ÷ √«à ¡°∫— °“√„À¬â “ªØ™‘ «’ 𖵓¡‡™ÕÈ◊  “‡Àµÿ ‡Õ° “√Õ“â ßÕß‘ 1. Orofino L, Marcen R, Quereda C, Villafruela JJ, Sabater J, Matesanz R, et al. Epidemiology of symptomatic hypotension in hemodialysis: is cool dialysate beneficial for all patients? Am J Nephrol. 1990;10(3):177-80. 2. Emili S, Black NA, Paul RV, Rexing CJ, Ullian ME. A protocol-based treatment for intradialytic hypotension in hospitalized hemodialysis patients. Am J Kidney Dis. 1999 Jun;33(6):1107-14. 3. Knoll GA, Grabowski JA, Dervin GF, OûRourke K. A randomized, controlled trial of albumin versus saline for the treatment of intradialytic hypotension. J Am Soc Nephrol. 2004 Feb;15(2):487-92. 4. Mann H, Stiller S. Sodium modeling. Kidney Int Suppl. 2000 Aug;76:S79-88. 5. Locatelli F, Andrulli S, Di Filippo S, Pozzoli U, Tetta C. Effect of sodium pool changes on blood pressure in patients undergoing PFD: design of a prospective randomized multicenter trial. J Nephrol. 2001 May- Jun;14(3):157-61. 6. Tang HL, Wong SH, Chu KH, Lee W, Cheuk A, Tang CM, et al. Sodium ramping reduces hypotension and symptoms during haemodialysis. Hong Kong Med J. 2006 Feb;12(1):10-4.

New Frontiers in Dialysis 140 ∏π‘µ ®√‘ π—π∑å∏«—™  ‘√‘¿“ ™â“ß»‘√°‘ ≈ÿ ™¬— ∏ππ— ¥“ µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°≈ÿ 7. Dheenan S, Henrich WL. Preventing dialysis hypotension: a comparison of usual protective maneuvers. Kidney Int. 2001 Mar;59(3):1175-81. 8. Garzoni D, Keusch G, Kleinoeder T, Martin H, Dhondt A, Cremaschi L, et al. Reduced complications during hemodialysis by automatic blood volume controlled ultrafiltration. Int J Artif Organs. 2007 Jan;30(1):16-24. 9. Maggiore Q, Pizzarelli F, Santoro A, Panzetta G, Bonforte G, Hannedouche T, et al. The effects of control of thermal balance on vascular stability in hemodialysis patients: results of the European randomized clinical trial. Am J Kidney Dis. 2002 Aug;40(2):280-90. 10. Schneditz D, Ronco C, Levin N. Temperature control by the blood temperature monitor. Semin Dial. 2003 Nov-Dec;16(6):477-82. 11. Pergola PE, Habiba NM, Johnson JM. Body temperature regulation during hemodialysis in long-term patients: is it time to change dialysate temperature prescription? Am J Kidney Dis. 2004 Jul;44(1):155-65. 12. Barakat MM, Nawab ZM, Yu AW, Lau AH, Ing TS, Daugirdas JT. Hemodynamic effects of intradialytic food ingestion and the effects of caffeine. J Am Soc Nephrol. 1993 May;3(11):1813-8. 13. Shinzato T, Nakai S, Odani H, Nakane K, Takai I, Maeda K. Relationship between dialysis induced hypotension and adenosine released by ischemic tissue. Asaio J. 1992 Jul-Sep;38(3):M286-90. 14. Sherman RA, Torres F, Cody RP. The effect of red cell transfusion on hemodialysis-related hypotension. Am J Kidney Dis. 1988 Jan;11(1):33-5. 15. Prakash S, Garg AX, Heidenheim AP, House AA. Midodrine appears to be safe and effective for dialysis- induced hypotension: a systematic review. Nephrol Dial Transplant. 2004 Oct;19(10):2553-8. 16. Yalcin AU, Kudaiberdieva G, Sahin G, Gorenek B, Akcar N, Kuskus S, et al. Effect of sertraline hydrochloride on cardiac autonomic dysfunction in patients with hemodialysis-induced hypotension. Nephron Physiol. 2003 Jan;93(1):P21-8. 17. Dheenan S, Venkatesan J, Grubb BP, Henrich WL. Effect of sertraline hydrochloride on dialysis hypotension. Am J Kidney Dis. 1998 Apr;31(4):624-30. 18. Jacob AD, Elkins N, Reiss OK, Chan L, Shapiro JI. Effects of acetate on energy metabolism and function in the isolated perfused rat heart. Kidney Int. 1997 Sep;52(3):755-60. 19. Salem M, Ivanovich PT, Ing TS, Daugirdas JT. Adverse effects of dialyzers manifesting during the dialysis session. Nephrol Dial Transplant. 1994;9 Suppl 2:127-37. 20. Ebo DG, Bosmans JL, Couttenye MM, Stevens WJ. Haemodialysis-associated anaphylactic and anaphylactoid reactions. Allergy. 2006 Feb;61(2):211-20. 21. Rockel A, Wahn V, Hertel J, Fiegel P. Ethylene oxide hypersensitivity in dialysis patients. Lancet. 1986 Feb 15;1(8477):382-3. 22. Schulman G, Hakim R, Arias R, Silverberg M, Kaplan AP, Arbeit L. Bradykinin generation by dialysis membranes: possible role in anaphylactic reaction. J Am Soc Nephrol. 1993 Mar;3(9):1563-9. 23. Verresen L, Fink E, Lemke HD, Vanrenterghem Y. Bradykinin is a mediator of anaphylactoid reactions during hemodialysis with AN69 membranes. Kidney Int. 1994 May;45(5):1497-503.

Acute Complications during Hemodialysis ∫≠— ™“  ∂√‘ –æ®πå 141 24. John B, Anijeet HK, Ahmad R. Anaphylactic reaction during haemodialysis on AN69 membrane in a patient receiving angiotensin II receptor antagonist. Nephrol Dial Transplant. 2001 Sep;16(9):1955-6. 25. Krieter DH, Canaud B. Anaphylactic reaction during haemodialysis on AN69 membrane in a patient receiving angiotensin II receptor antagonist. Nephrol Dial Transplant. 2002 May;17(5):943-4. 26. Maurice F, Rivory JP, Larsson PH, Johansson SG, Bousquet J. Anaphylactic shock caused by formaldehyde in a patient undergoing long-term hemodialysis. J Allergy Clin Immunol. 1986 Apr;77(4):594- 7. 27. Tejedor Alonso MA, Lopez Revuelta K, Garcia Bueno MJ, Casas Losada ML, Rosado Ingelmo A, Gruss Vergara E, et al. Thrombocytopenia and anaphylaxis secondary to heparin in a hemodialysis patient. Clin Nephrol. 2005 Mar;63(3):236-40. 28. Fishbane S, Ungureanu VD, Maesaka JK, Kaupke CJ, Lim V, Wish J. The safety of intravenous iron dextran in hemodialysis patients. Am J Kidney Dis. 1996 Oct;28(4):529-34. 29. Papadakis JT, Patrikarea A, Saradi S, Papakostas K, Leondi A, Kravaritis A, et al. Hypersensitivity reactions during hemodialysis related to the use of acetate dialysate. A case report. Clin Nephrol. 1991 May;35(5):224- 6. 30. Hakim RM, Breillatt J, Lazarus JM, Port FK. Complement activation and hypersensitivity reactions to dialysis membranes. N Engl J Med. 1984 Oct 4;311(14):878-82. 31. Sherman RA, Goodling KA, Eisinger RP. Acute therapy of hemodialysis-related muscle cramps. Am J Kidney Dis. 1982 Sep;2(2):287-8. 32. Kaji DM, Ackad A, Nottage WG, Stein RM. Prevention of muscle cramps in haemodialysis patients by quinine sulphate. Lancet. 1976 Jul 10;2(7976):66-7. 33. Roca AO, Jarjoura D, Blend D, Cugino A, Rutecki GW, Nuchikat PS, et al. Dialysis leg cramps. Efficacy of quinine versus vitamin E. Asaio J. 1992 Jul-Sep;38(3):M481-5. 34. Khajehdehi P, Mojerlou M, Behzadi S, Rais-Jalali GA. A randomized, double-blind, placebo-controlled trial of supplementary vitamins E, C and their combination for treatment of haemodialysis cramps. Nephrol Dial Transplant. 2001 Jul;16(7):1448-51. 35. Ahmad S, Robertson HT, Golper TA, Wolfson M, Kurtin P, Katz LA, et al. Multicenter trial of L-carnitine in maintenance hemodialysis patients. II. Clinical and biochemical effects. Kidney Int. 1990 Nov;38(5):912-8. 36. Eknoyan G, Latos DL, Lindberg J. Practice recommendations for the use of L-carnitine in dialysis-related carnitine disorder. National Kidney Foundation Carnitine Consensus Conference. Am J Kidney Dis. 2003 Apr;41(4):868-76. 37. Arieff AI. Dialysis disequilibrium syndrome: current concepts on pathogenesis and prevention. Kidney international. 1994 Mar;45(3):629-35. 38. Silver SM, Sterns RH, Halperin ML. Brain swelling after dialysis: old urea or new osmoles? Am J Kidney Dis. 1996 Jul;28(1):1-13.

New Frontiers in Dialysis 142 ∏𵑠®‘√ππ— ∑å∏«™—  ‘√‘¿“ ™â“ß»‘√°‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°ÿ≈ 39. Mettang T, Pauli-Magnus C, Alscher DM. Uraemic pruritus--new perspectives and insights from recent trials. Nephrol Dial Transplant. 2002 Sep;17(9):1558-63. 40. Lugon JR. Uremic pruritus: a review. Hemodialysis international. 2005 Apr;9(2):180-8. 41. Hiroshige K, Kabashima N, Takasugi M, Kuroiwa A. Optimal dialysis improves uremic pruritus. Am J Kidney Dis. 1995 Mar;25(3):413-9. 42. De Marchi S, Cecchin E, Villalta D, Sepiacci G, Santini G, Bartoli E. Relief of pruritus and decreases in plasma histamine concentrations during erythropoietin therapy in patients with uremia. The New England journal of medicine. 1992 Apr 9;326(15):969-74. 43. Gunal AI, Ozalp G, Yoldas TK, Gunal SY, Kirciman E, Celiker H. Gabapentin therapy for pruritus in haemodialysis patients: a randomized, placebo-controlled, double-blind trial. Nephrol Dial Transplant. 2004 Dec;19(12):3137- 9. 44. Wikstrom B, Gellert R, Ladefoged SD, Danda Y, Akai M, Ide K, et al. Kappa-opioid system in uremic pruritus: multicenter, randomized, double-blind, placebo-controlled clinical studies. J Am Soc Nephrol. 2005 Dec;16(12):3742-7. 45. Yu AS, Levy E. Paradoxical cerebral air embolism from a hemodialysis catheter. Am J Kidney Dis. 1997 Mar;29(3):453-5. 46. Dunbar EM, Fox R, Watson B, Akrill P. Successful late treatment of venous air embolism with hyperbaric oxygen. Postgraduate medical journal. 1990 Jun;66(776):469-70. 47. Hindman SH, Favero MS, Carson LA, Petersen NJ, Schonberger LB, Solano JT. Pyrogenic reactions during haemodialysis caused by extramural endotoxin. Lancet. 1975 Oct 18;2(7938):732-4. 48. Singh B, Depner TA. Catheter related bacterial infections mimic reactions to exogenous pyrogens during hemodialysis. Asaio J. 1994 Jul-Sep;40(3):M674-7.

8 Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  π‘ ’ ¥…‘ ∞∫√√®ß 1. ∫∑π” 2. º≈°√–∑∫µÕà °√–¥°Ÿ ∑‡’Ë°¥‘ ¢πÈ÷ ®“°¿“«–§«“¡º¥‘ ª°µ¢‘ Õß·§≈‡´¬’ ¡·≈–øÕ ‡øµ„πºªâŸ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— 3. °≈‰°°“√‡°¥‘ ¿“«– secondary hyperparathyroidism 4. °“√√°— …“¿“«–øÕ ‡øµ„π‡≈Õ◊ ¥ ßŸ ·≈– secondary hyperparathyroidism 5.  √ªÿ

New Frontiers in Dialysis 144 ∏π‘µ ®√‘ π—π∑∏å «™—  ‘√‘¿“ ™â“ß»√‘ °‘ ÿ≈™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°ÿ≈ 1. ∫∑π” ª≠í À“ ”§≠— Õ°’ Õ¬“à ßÀπßË÷ ∑‡Ë’ °¥‘ ¢πÈ÷ „πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— §Õ◊ °“√§ßË— ¢ÕßøÕ ‡øµ ´ßË÷ πÕ°®“° ®–‰ª°√–µπâÿ „À¡â °’ “√À≈ßË— æ“√“‰∏√Õ¬¥Œå Õ√‚å ¡π (PTH) ÕÕ°¡“‡æ¡Ë‘ ¢πÈ÷ (secondary hyperparathyroidism) ∑”„À‡â °¥‘ ¿“«–°√–¥°Ÿ º∑ÿ ‡Ë’ √¬’ °«“à osteitis fibrosa À√Õ◊ high bone turnover renal osteodystrophy ·≈«â „πªí®®ÿ∫—π¬—ßæ∫«à“°“√§—ËߢÕßøÕ ‡øµ¡’§«“¡‡°’ˬ«‚¬ß°—∫Õ—µ√“°“√µ“¬∑’ˇæ‘Ë¡ Ÿß¢÷Èπ ‚¥¬‡©æ“–  “‡Àµ°ÿ “√µ“¬∑‡’Ë °¥‘ ®“°‚√§À«— „®1∑ß—È π ’È «à πÀπß÷Ë ‡ªπì ‡æ√“–øÕ ‡øµ∑§’Ë ß—Ë Õ¬„Ÿà π°√–· ‡≈Õ◊ ¥‡ªπì √–¬–‡«≈“ π“πÊ  “¡“√∂ÕÕ°ƒ∑∏‘Ï‚¥¬µ√ßµàÕ vascular smooth muscle cells ∑”„À⇰‘¥°“√‡ª≈’ˬπ·ª≈߉ª‡ªìπ ‡´≈≈°å √–¥°Ÿ (osteoblasts) ´ßË÷ ‡´≈≈å osteoblast π®È’ –∑”°“√ √“â ß‚ª√µπ’ ´ßË÷ ‡ªπì  «à πª√–°Õ∫¢Õß°√–¥°Ÿ ¿“¬„πÀ≈Õ¥‡≈Õ◊ ¥ ‚¥¬‡©æ“–∑À’Ë ≈Õ¥‡≈Õ◊ ¥À«— „® ∑”„À‡â °¥‘ ¿“«– vascular calcification2 ¢π÷È ¿“«–¥ß— °≈“à « ¡º’ ≈∑”„Àºâ ªŸâ «É ¬‡À≈“à π‡’È ªπì ‚√§À≈Õ¥‡≈Õ◊ ¥À«— „®µß—È ·µÕà “¬πÿ Õ⠬ʷ≈–¡Õ’ µ— √“°“√µ“¬∑ ’Ë ßŸ ¢π÷È °“√√°— …“¿“«– secondary hyperparathyroidism ‚¥¬„™â calcium-containing phosphate binders ·≈– vitamin D ‡æ◊ËÕ √—°…“„Àâ√–¥—∫ PTH Õ¬Ÿà„π‡°≥±å∑’ˇÀ¡“– ¡¬—ß¡’º≈¢â“߇§’¬ß∑’Ë ”§—≠ §◊Õ °“√‡æ‘Ë¡¢÷Èπ¢Õß√–¥—∫ ·§≈‡´’¬¡·≈–øÕ ‡øµ„π‡≈◊Õ¥ ∑”„Àâº≈§Ÿ≥¢Õß·§≈‡´’¬¡·≈–øÕ ‡øµ„π‡≈◊Õ¥ (calcium-phosphate product) ‡æ¡Ë‘  ßŸ ¢πÈ÷ ®“°°“√»°÷ …“æ∫«“à ª√¡‘ “≥·§≈‡´¬’ ¡∑ºË’ ªŸâ «É ¬√∫— ª√–∑“π ·≈–º≈§≥Ÿ ¢Õß calcium- phosphate product ∑ Ë’ ߟ ¡º’ ≈‡æ¡Ë‘ Õµ— √“‡ ¬Ë’ ߢÕß°“√‡°¥‘ vascular calcification ·≈–Õµ— √“°“√µ“¬3 ¥ß— ππÈ— „πªí®®ÿ∫—π®÷ß¡’·π«‚πâ¡∑’Ë®–„À⧫“¡ ”§—≠„π°“√√—°…“øÕ ‡øµ·≈– calcium-phosphate product „Àâ Õ¬Ÿà„π‡°≥±åª°µ‘ ‚¥¬„À⺟âªÉ«¬√—∫ª√–∑“π·§≈‡´’¬¡„πª√‘¡“≥∑’ËπâÕ¬∑’Ë ÿ¥ ¡“°°«à“°“√„À⧫“¡  ”§≠— „π°“√√°— …“√–¥∫— PTH ¥ß— ππÈ— ‡æÕË◊ „À°â “√√°— …“√–¥∫— ¢Õß·§≈‡´¬’ ¡ øÕ ‡øµ ·≈– PTH ‡ªπì ‰ª Õ¬“à ߇À¡“– ¡·≈–¡ª’ √– ∑‘ ∏¿‘ “æ ®ß÷ ¡§’ «“¡®”‡ªπì ∑®Ë’ –µÕâ ߺ≈µ‘ ¬“„À¡Êà ÕÕ°¡“ ‡™πà ¬“„π°≈¡àÿ non- calcium containing phosphate binders ∑ Ë’ “¡“√∂®∫— °∫— øÕ ‡øµ‰¥‚â ¥¬∑‰Ë’ ¡‡à æ¡Ë‘ ª√¡‘ “≥ calcium intake ·≈–/À√Õ◊ √–¥∫— ¢Õß calcium-phosphate product ·≈– ¬“„π°≈¡àÿ ¢Õß vitamin D analogs ´ßË÷  “¡“√∂≈¥ PTH ‰¥â ‚¥¬‰¡à‡æ‘Ë¡°“√¥Ÿ¥´÷¡¢Õß·§≈‡´’¬¡·≈–øÕ ‡øµ„π∑“߇¥‘πÕ“À“√ πÕ°®“°π’È°“√√—°…“¿“«– secondary hyperparathyroidism ¡“°®π‡°‘π‰ª®π°√–∑—Ëß√–¥—∫ PTH ≈¥µË”°«à“‡°≥±å∑’ˇÀ¡“– ¡¬—ß ∑”„À⇰‘¥¿“«–°√–¥°Ÿ ºÿÕ’°™π‘¥Àπ÷Ëß∑’ˇ√’¬°«à“ adynamic bone disease À√◊Õ low bone turnover renal osteodystrophy ‰¥â‡™àπ°—π ¥—ßπ—Èπ®÷ß¡’§«“¡®”‡ªìπ∑’Ë®–µâÕß∑”§«“¡‡¢â“„®∂÷ߧ«“¡º‘¥ª°µ‘¢Õß ·§≈‡´¬’ ¡·≈–øÕ ‡øµ„πºªâŸ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— ·≈–„À°â “√√°— …“ºªŸâ «É ¬‡À≈“à πÕÈ’ ¬“à ß∂°Ÿ µÕâ ß 2. º≈°√–∑∫µàÕ°√–¥Ÿ°∑’ˇ°‘¥¢÷Èπ®“°¿“«–§«“¡º‘¥ª°µ‘¢Õß·§≈‡´’¬¡·≈–øÕ ‡øµ„π ºªŸâ «É ¬‰µ«“¬‡√Õ◊È √ß— º≈°√–∑∫¢Õߧ«“¡º¥‘ ª°µ¢‘ Õß·§≈‡´¬’ ¡·≈–øÕ ‡øµµÕà °√–¥°Ÿ „πºªŸâ «É ¬‰µ«“¬‡√Õ◊È √ß—  “¡“√∂ ·∫ßà ÕÕ°‰¥â ‡ªπì 2 °≈¡àÿ „À≠Êà §Õ◊

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥…‘ ∞∫√√®ß 145 1. High-bone turnover renal osteodystrophy ‰¥·â °à ºªŸâ «É ¬∑¡’Ë ¿’ “«– secondary hyperparathyroidism ¡√’ –¥∫— PTH  ßŸ ∑”„À¡â °’ “√∑”≈“¬°√–¥°Ÿ ‡æ¡Ë‘ ¡“°¢πÈ÷ Õ¬µàŸ ≈Õ¥‡«≈“ √“à ß°“¬æ¬“¬“¡ª√∫— µ«— ‚¥¬°“√  √â“ß°√–¥Ÿ°„À¡àÕÕ°¡“∑¥·∑π°√–¥Ÿ°∑’Ë∂Ÿ°∑”≈“¬‰ª ·µà‰¡à “¡“√∂ √â“ß°√–¥Ÿ°„À¡àÕÕ°¡“‰¥â∑—π ‡°‘¥¿“«–°√–¥°Ÿ º∑ÿ ˇ’ √’¬°«“à osteitis fibrosa ¿“«–¥ß— °≈“à «æ∫‰¥âª√–¡“≥ 30% ¢ÕߺŸâªÉ«¬∑’ˉ¥â√—∫°“√ øÕ°‡≈Õ◊ ¥ (hemodialysis) ·≈– 10-15% „πºªâŸ «É ¬∑∑Ë’ ”°“√øÕ°‰µ∑“ß™Õà ß∑Õâ ß (peritoneal dialysis)4,5 2. Low-bone turnover renal osteodystrophy ‰¥·â °à ºªŸâ «É ¬∑¡Ë’ √’ –¥∫— PTH µ”Ë ºªâŸ «É ¬„π°≈¡àÿ π®È’ – ¡∑’ ßÈ— °“√ √“â ß·≈–°“√∑”≈“¬°√–¥°Ÿ πÕâ ¬°«“à §πª°µ‘ ¡®’ ”π«π osteoblast ·≈– osteoclast πÕâ ¬ ‚¥¬ º≈≈æ— ∏∑å ‰Ë’ ¥§â Õ◊ °“√ √“â ßπÕâ ¬°«“à °“√∑”≈“¬∑”„À‡â °¥‘ ¿“«–°√–¥°Ÿ º∑ÿ Ë’ ‡√¬’ °«“à adynamic bone disease ºªŸâ «É ¬„π°≈¡ÿà π¡’È Õ’ µ— √“‡ ¬’Ë ßµÕà °“√‡°¥‘ °√–¥°Ÿ º·ÿ ≈–°√–¥°Ÿ À°— ‰¥‡â ™πà ‡¥¬’ «°∫— °≈¡ÿà ∑‡’Ë ªπì highboneturnover6  “‡ÀµÿÕ“®‡°‘¥®“° uremic toxins ∑’ËÕ¬àŸ„π°√–· ‡≈◊Õ¥∑”„Àâ°√–¥Ÿ°¡’°“√µÕ∫ πÕßµàÕ PTH πâÕ¬≈ß À√◊Õ®“°°“√√—°…“¿“«– secondary hyperparathyroidism ¡“°®π‡°‘π‰ª®π∑”„Àâ PTH ¡’√–¥—∫µË”°«à“ ‡°≥±∑å ‡Ë’ À¡“– ¡ ¿“«–πæÈ’ ∫‰¥∫â Õà ¬„πºªŸâ «É ¬∑‡Ë’ ªπì ‡∫“À«“π ·≈–ª√–¡“≥ 50% ¢ÕߺªŸâ «É ¬ peritoneal dialysis „π¢≥–∑ºË’ ªâŸ «É ¬ hemodialysis æ∫‰¥ªâ √–¡“≥ 30%5 πÕ°®“°π„È’ π°≈¡àÿ low bone turnover ¬ß— ¡’ §«“¡º‘¥ª°µ‘¢Õß°√–¥Ÿ°Õ’°™π‘¥∑’ˇ√’¬°«à“ osteomalacia ´÷Ë߇ªìπ¿“«–∑’Ë¡’°“√≈¥≈ߢÕß°“√®—∫¢Õß ·§≈‡´¬’ ¡·≈–øÕ ‡øµ°∫— ‚ª√µπ’ ∑‡Ë’ ´≈≈°å √–¥°Ÿ  √“â ߢπÈ÷ ¡“∑”„À°â √–¥°Ÿ ºÿ „π ¡¬— °Õà πæ∫¿“«–π‰È’ ¥∫â Õà ¬  “‡Àµÿ‡°‘¥®“°°“√∑’˺ŸâªÉ«¬‰¥â√—∫¬“ aluminum hydroxide ∑’Ë„™â ”À√—∫≈¥√–¥—∫øÕ ‡øµ„π‡≈◊Õ¥ ®“° °“√»°÷ …“ºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— „πª√–‡∑»‰∑¬„πªï 2543 æ∫¿“«–πªÈ’ √–¡“≥ 4%4 3. °≈‰°°“√‡°¥‘ ¿“«– secondary hyperparathyroidism ¿“«– secondary hyperparathyroidism ‡°‘¥®“°°“√∑’˵àÕ¡æ“√“‰∏√Õ¬¥åÀ≈—Ëß PTH ÕÕ°¡“ ¡“°°«“à ª°µ‘ ‚¥¬ª®í ®¬— ∑ Ë’ ”§≠— „À≠Êà 3 ª®í ®¬— ‰¥·â °à 1. °“√§Ë—ߢÕßøÕ ‡øµ ‡¡◊ËÕ‡π◊ÈÕ‰µ∂Ÿ°∑”≈“¬∑”„À⢗∫∂à“¬øÕ ‡øµ‰¥â≈¥≈ß °“√§—ËߢÕß øÕ ‡øµπ¡È’ º’ ≈‚¥¬µ√ß„π°“√°√–µπâÿ „À¡â °’ “√À≈ßË— PTH 2. °“√≈¥≈ߢÕß calcitriol (À√Õ◊ 1,25 dihydroxycholecalciferol, 1,25 dihydroxyvitaminD3 ೷PTH ೷Phosphate ೹Calcitriol ೹Calcium √ªŸ ∑’Ë 1  “‡Àµ¢ÿ Õß secondary hyperparathyroidism

New Frontiers in Dialysis 146 ∏𵑠®‘√π—π∑å∏«—™  √‘ ‘¿“ ™“â ß»√‘ °‘ ÿ≈™—¬ ∏π—𥓠µ√–°“√«π‘™ « π— µå  ÿ‡¡∏°ÿ≈ ´ßË÷ ‡ªπì active form ¢Õß vitamin D) °“√ √“â ß calcitriol ‡°¥‘ ¢πÈ÷ ∑‰Ë’ µ ‚¥¬Õ“»¬— ‡ÕπÁ ‰´¡å 1-alpha hydroxylase ´ßË÷ ∑”Àπ“â ∑‡Ë’ ª≈¬Ë’ π 25 hydroxycholecalciferol À√Õ◊ 25 hydroxyvitaminD3 ∑ Ë’ – ¡Õ¬∑àŸ µË’ ∫— „À°â ≈“¬‰ª‡ªπì calcitriol ‡¡ÕË◊ ‰µ∂°Ÿ ∑”≈“¬‰ª ‡ÕπÁ ‰´¡å 1-alpha hydroxylase ¡ª’ √¡‘ “≥≈¥≈ß ∑”„À â √“â ß calcitriol ‰¥≈â ¥≈ß calcitriol π¡È’ º’ ≈‚¥¬µ√ß„π°“√¬∫— ¬ßÈ— °“√ √“â ß·≈–°“√À≈ßË— PTH ¥ß— ππ—È √–¥∫— ¢Õß PTH ®ß÷ ‡æ¡Ë‘  ßŸ ¢πÈ÷ 3. √–¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥≈¥≈ß´ß÷Ë ‡ªπì º≈®“°°“√∑ø’Ë Õ ‡øµ„π‡≈Õ◊ ¥¡√’ –¥∫—  ßŸ ·≈«â ‰ª®∫— µ«— °∫— ·§≈‡´¬’ ¡ ‡¡Õ◊Ë √–¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥≈¥µË”≈ß calcium sensing receptor (CaSR) ∑µ’Ë Õà ¡æ“√“‰∏√Õ¬¥å ®– ßà  ≠— ≠“≥„À‡â ´≈≈µå Õà ¡æ“√“‰∏√Õ¬¥ å √“â ß·≈–À≈ßË— PTH ‡æ¡Ë‘ ¢πÈ÷ PTH ∑‡Ë’ æ¡Ë‘ ¢πÈ÷ ¡∫’ ∑∫“∑„π°“√ª√∫— √–¥∫— ·§≈‡´¬’ ¡·≈–øÕ ‡øµ„π‡≈Õ◊ ¥„À‡â ªπì ª°µ‘ ‚¥¬ 1. °√–µÿâπ„Àâ¡’°“√∑”≈“¬°√–¥Ÿ° (bone resorption) ‡æ◊ËÕª≈¥ª≈àÕ¬·§≈‡´’¬¡·≈–øÕ ‡øµ ‡¢“â  °Ÿà √–· ‡≈Õ◊ ¥ 2. ‡æ¡‘Ë °“√¥¥Ÿ ´¡÷ °≈∫— ¢Õß·§≈‡´¬’ ¡∑“߉µ 3. ‡æ‘Ë¡°“√¢—∫∂à“¬øÕ ‡øµÕÕ°∑“߉µ ‚¥¬ºà“π∑“ß°“√≈¥≈ߢÕß sodium-phosphate cotransporter type II ∑∫Ë’ √‡‘ «≥ luminal membrane ¢Õß proximal tubule7 ∑”„À°â “√¥¥Ÿ ´¡÷ °≈∫— ¢ÕßøÕ ‡øµ ≈¥≈ß º≈√–¬– —Èπ∑’ˇ°‘¥¢÷Èπ®“°°“√‡æ‘Ë¡¢÷Èπ¢Õß PTH §◊Õ √–¥—∫·§≈‡´’¬¡„π‡≈◊Õ¥‡æ‘Ë¡¢÷Èπ·≈–√–¥—∫ øÕ ‡øµ≈¥≈ß °“√∑’Ë PTH  Ÿß¢÷ÈπÕ¬à“ßµàÕ‡π◊ËÕ߇ªìπ√–¬–‡«≈“π“π ®–∑”„À⇰‘¥°“√∑”≈“¬°√–¥Ÿ° Õ¬“à ߉¡Àà ¬¥ÿ ¬ßÈ— ®π‡°¥‘ ¿“«–°√–¥°Ÿ „π√–¬–·√°ºªâŸ «É ¬¡°— ®–‰¡¡à Õ’ “°“√Õ–‰√ ·µ‡à ¡ÕË◊ ‡ªπì π“πÊ ºªŸâ «É ¬ ®–‡√‘Ë¡¡’Õ“°“√ª«¥µ“¡°√–¥Ÿ° ·≈–°≈â“¡‡π◊ÈÕ ¡’°≈â“¡‡π◊ÈÕÕàÕπ·√ß ∫“ߧ√—Èß¡’°√–¥Ÿ°À—° ‡Õ°´‡√¬å®– æ∫«“à ¡°’ √–¥°Ÿ º‚ÿ ¥¬∑«Ë— ‰ª ‡™πà subperiosteal erosion ∑πË’ «È‘ ¡Õ◊ (√ªŸ ∑Ë’ 2a), distal end ¢Õß clavicle, ‰µ°â √–¥°Ÿ ischium °∫— pubis, ∫√‡‘ «≥ sacroiliac joint ·≈–∑√Ë’ Õ¬µÕà ¢Õß metaphysis °∫— diaphysis ¢Õß long bone πÕ°®“°π¬È’ ß— æ∫ patchy osteosclerosis ∑∫Ë’ √‡‘ «≥°√–¥°Ÿ  π— À≈ß— (çrugger jerseyé spine) (√ªŸ ∑Ë’ 2b) ·≈– Õ“®æ∫≈°— …≥–¢Õß çsalt and pepperé ∑∫Ë’ √‡‘ «≥°–‚À≈°»√’ …–‰¥â (√ªŸ ∑Ë’ 2c) πÕ°®“°º≈∑“ß°√–¥°Ÿ ·≈–°≈“â ¡‡πÕÈ◊ ·≈«â ∂“â √–¥∫— øÕ ‡øµÀ√Õ◊ calcium-phosphate product  ßŸ ¡“°‡°π‘ ‰ª Õ“®∑”„À¡â °’ “√‡°“–µ«— ¢Õß·§≈‡´¬’ ¡·≈–øÕ ‡øµµ“¡‡πÕÈ◊ ‡¬ÕË◊ (soft tissue calcification) ‚¥¬‡©æ“–∂“â ¡°’ “√‡°“–µ«— ∫√‡‘ «≥√Õ∫Ê¢Õâ Õ“®∑”„À‡â °¥‘ ¢Õâ Õ°— ‡ ∫‰¥â∂“â ¡°’ “√‡°“–µ«— „π‡ πâ ‡≈Õ◊ ¥(vascular calcification) Õ“®∑”„À¡â ¿’ “«–À«— „®¢“¥‡≈Õ◊ ¥ ‡≈Õ◊ ¥‰ª‡≈¬È’ ß∫√‡‘ «≥º«‘ Àπß— °≈“â ¡‡πÕÈ◊ ·≈– subcutaneous tissue πÕâ ¬≈ß ‡°¥‘ tissue necrosis (calcific uremic arteriolopathy) ¿“«–¥ß— °≈“à «¡°— æ∫„πºªŸâ «É ¬∑‡Ë’ ªπì ‡∫“À«“π ∂Ⓡհ´‡√¬å∫√‘‡«≥¡◊Õ·≈–‡∑â“Õ“®™à«¬„Àâ‡ÀÁπ√àÕß√Õ¬¢Õß vascular calcification ‰¥â ¿“«– ·∑√°´Õâ π‡À≈“à π∑’È ”„ÀÕâ µ— √“°“√µ“¬¢ÕߺªŸâ «É ¬‡æ¡‘Ë  ßŸ ¢π÷È 8 °“√√°— …“¿“«– secondary hyperparathyroidism §«√∑”µß—È ·µ‡à ππ‘Ë Ê ‡æ√“–¡©‘ –ππ—È ∂“â µÕà ¡æ“√“ ‰∏√Õ¬¥å‰¥â√—∫°“√°√–µÿâπ‡ªìπ√–¬–‡«≈“π“πÊ µàÕ¡®–¡’¢π“¥„À≠à¢÷Èπ (parathyroid gland hyperplasia) ·≈– ¥ÿ ∑“â ¬°≈“¬‰ª‡ªπì parathyroid adenoma ´ßË÷ parathyroid adenoma πªÈ’ √–惵µ‘ «— ‡À¡Õ◊ π°∫— ‡πÕÈ◊ ßÕ° (tumor) ∑‰’Ë ¡Õà ¬„àŸ π°“√§«∫§¡ÿ ¢Õß calcium-phosphate-calcitriol axis Õ°’ µÕà ‰ª À≈ß—Ë PTH ÕÕ°¡“Õ¬“à ߉¡Àà ¬¥ÿ ¬ß—È ∑—ÈßÊ ∑’Ë√–¥—∫·§≈‡´’¬¡„π‡≈◊Õ¥ Ÿß ·≈–‰¥â√—∫«‘µ“¡‘π¥’„πª√‘¡“≥¡“°  “‡Àµÿ∑’ˇªìπ¥—ßπ’ȇæ√“–«à“µàÕ¡ æ“√“‰∏√Õ¬¥∑å °Ë’ ≈“¬‡ªπì adenoma ‰ª·≈«â ®–¡ª’ √¡‘ “≥¢Õß vitamin D receptor (VDR)9,10 ·≈– CaSR ≈¥

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥‘…∞∫√√®ß 147 √ªŸ ∑’Ë 2 Hyperparathyroid bone disease a) subperiosteal bone resorption ∑∫Ë’ √‡‘ «≥°√–¥°Ÿ π«È‘ ¡Õ◊ ®–‡ÀπÁ «“à ∑Ë’ ∫√‡‘ «≥¢Õ∫°√–¥°Ÿ π«È‘ ¡≈’ °— …≥–¢√¢ÿ √–·≈–‰¡‡à √¬’ ∫ b) Rugger Jersey spine ¡≈’ °— …≥–‡ªπì band-like regions of increased opacity ∑∫Ë’ √‡‘ «≥ superior ·≈– inferior margins ¢Õß vertebral bodies c) salt and pepper appearance ¢Õß°√–‚À≈°»√’ …– ≈ß11 ∑”„À‰â ¡µà Õ∫ πÕßµÕà ·§≈‡´¬’ ¡·≈–«µ‘ “¡π‘ ¥Õ’ °’ µÕà ‰ª ¥ß— ππÈ— ®ß÷ §«√∑”°“√√°— …“°Õà π∑µË’ Õà ¡æ“√“ ‰∏√Õ¬¥å®–°≈“¬‰ª‡ªìπ adenoma ‡æ√“–‡¡◊ËÕ∂÷߇«≈“π—ÈπÕ“®®–µâÕß àߺŸâªÉ«¬‰ª∑”°“√ºà“µ—¥µàÕ¡æ“√“ ‰∏√Õ¬¥å °“√§ßË— ¢ÕßøÕ ‡øµ „πª®í ®∫ÿ π— ‡√“∑√“∫«“à √–¥∫— øÕ ‡øµ„π‡≈Õ◊ ¥∂°Ÿ §«∫§¡ÿ ¥«â ¬ŒÕ√‚å ¡π 3 µ«— §Õ◊ PTH, calcitriol ·≈– FGF-2312 °“√§ßË— ¢ÕßøÕ ‡øµ‡√¡Ë‘ µßÈ— ·µ‡à ¡ÕË◊ glomerular filtration rate (GFR) πÕâ ¬°«“à 60 ml/min À√Õ◊ serum creatinine ª√–¡“≥ 2 mg/dl ‚¥¬„π√–¬–·√°√“à ß°“¬®–ª√∫— µ«— ‚¥¬‡æ¡Ë‘ °“√À≈ßË— ŒÕ√‚å ¡π FGF-23 ´ßË÷  √“â ß¡“®“°‡´≈≈å osteoblast ¡º’ ≈∑”„À¡â °’ “√¢∫— øÕ ‡øµÕÕ°∑“ߪ í  “«–‡æ¡Ë‘ ¡“°¢πÈ÷ 13 ŒÕ√‚å ¡ππÈ’ ¬ß—  “¡“√∂¬∫— ¬ßÈ— °“√ √“â ß calcitriol14  ßà º≈„À°â “√¥¥Ÿ ´¡÷ ¢ÕßøÕ ‡øµ®“°∑“߇¥π‘ Õ“À“√≈¥≈ߥ«â ¬ ®“° °“√»÷°…“„πºâŸªÉ«¬‰µ«“¬‡√◊ÈÕ√—ßæ∫«à“√–¥—∫¢ÕߌÕ√å‚¡π FGF-23 ®–·ª√º—πµ“¡√–¥—∫¢ÕßøÕ ‡øµ∑’Ë ‡æ¡Ë‘ ¢πÈ÷ „π‡≈Õ◊ ¥·≈–°“√¢∫— øÕ ‡øµÕÕ°∑“ߪ í  “«– ·≈–·ª√º°ºπ— °∫— √–¥∫— ¢Õß GFR15 „π√–¬–·√°Ê ¢Õß¿“«–‰µ«“¬‡√◊ÈÕ√—ß (CKD stage 2-3) √–¥—∫¢ÕßøÕ ‡øµ„π‡≈◊Õ¥Õ“®Õ¬Ÿà„π‡°≥±åª°µ‘‰¥â ‡√“¡—°®– ‡√¡Ë‘ ‡ÀπÁ °“√‡æ¡Ë‘ ¢πÈ÷ ¢ÕßøÕ ‡øµ‡¡ÕË◊ ºªŸâ «É ¬‡¢“â  √Ÿà –¬– CKD stage 4-5 ∑ßÈ— π‡È’ ªπì ‡æ√“–‰µ∂°Ÿ ∑”≈“¬‰ª¡“° ·≈– FGF-23 ∑’ˇæ‘Ë¡¡“°¢÷Èπ‰¡à “¡“√∂∑”„À≵¢—∫øÕ ‡øµÕÕ°‰¥â‡æ’¬ßæÕ ·µà‡¥‘¡‡§¬‡™◊ËÕ«à“°“√‡æ‘Ë¡ ¢π÷È ¢ÕßøÕ ‡øµ„π‡≈Õ◊ ¥¡º’ ≈∑”„À√â –¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥≈¥≈ß®“°°“√®∫— µ«— ¢ÕßøÕ ‡øµ°∫— ·§≈‡´¬’ ¡ ·≈«â √–¥∫— ·§≈‡´¬’ ¡∑≈’Ë ¥≈ßπ’È°√–µπÿâ „À¡â °’ “√À≈ß—Ë ¢ÕßPTH16 ·µ°à “√»°÷ …“√–¬–µÕà ¡“„π µ— «∑å ¥≈Õß∑‡’Ë ªπì

New Frontiers in Dialysis 148 ∏π‘µ ®‘√ππ— ∑∏å «™—  √‘ ¿‘ “ ™“â ß»√‘ °‘ ÿ≈™—¬ ∏π—𥓠µ√–°“√«π‘™ « π— µå  ÿ‡¡∏°≈ÿ ‰µ«“¬‡√◊ÈÕ√—ßæ∫«à“‡¡◊ËÕ§«∫§ÿ¡√–¥—∫¢Õß·§≈‡´’¬¡„π‡≈◊Õ¥„À⇪ìπª°µ‘‚¥¬°“√„ÀâÕ“À“√∑’Ë¡’ª√‘¡“≥ ·§≈‡´’¬¡ ßŸ ·°à —µ«å∑¥≈Õß æ∫«à“√–¥—∫ PTH ·ª√º—πµ“¡√–¥—∫¢ÕßøÕ ‡øµ∑’ˇæ‘Ë¡¢÷Èπ„π‡≈◊Õ¥ „π°“√ »÷°…“‡¥’¬«°—ππ’È∑“ߧ≥–ºâŸ»÷°…“‰¥â∑”°“√∑¥≈Õß‚¥¬‡≈’Ȭ߇´≈≈åæ“√“‰∏√Õ¬¥å„πÕ“À“√‡≈’Ȭ߇´≈≈å∑’Ë¡’ ª√‘¡“≥øÕ ‡øµ Ÿß‡æ◊ËÕæ‘ Ÿ®πå«à“øÕ ‡øµ “¡“√∂°√–µÿâπ°“√À≈—Ëß PTH ‰¥â‚¥¬µ√ß º≈ª√“°Ø«à“ Õ“À“√‡≈’Ȭ߇´≈≈å∑’Ë¡’øÕ ‡øµ Ÿß “¡“√∂°√–µÿâπ„À⇴≈≈åæ“√“‰∏√Õ¬¥åÀ≈—Ëß PTH ÕÕ°¡“¡“°¢÷Èπ · ¥ß „À‡â ÀπÁ «“à øÕ ‡øµ “¡“√∂°√–µπâÿ °“√À≈ßË— PTH ‰¥‚â ¥¬∑‰Ë’ ¡¢à πÈ÷ °∫— °“√‡ª≈¬Ë’ π·ª≈ߢÕß calcium17 ¥ß— ππÈ— °“√§«∫§¡ÿ Õ“À“√‚¥¬„Àºâ ªâŸ «É ¬√∫— ª√–∑“πÕ“À“√∑¡’Ë ª’ √¡‘ “≥øÕ ‡øµµË”µß—È ·µ‡à ππ‘Ë Ê “¡“√∂ªÕÑ ß°π— ¿“«– secondary hyperparathyroidism ‰¥1â 6, 18πÕ°®“°π¬’È ß— æ∫«“à Õ“À“√∑¡’Ë ø’ Õ ‡øµµË” “¡“√∂‡æ¡‘Ë ª√¡‘ “≥¢Õß CaSR „πµÕà ¡æ“√“‰∏√Õ¬¥¢å Õß µ— «∑å ¥≈Õß™«à ¬„À â µ— «∑å ¥≈ÕßµÕ∫ πÕßµÕà ·§≈‡´¬’ ¡‰¥¥â ¢’ πÈ÷ 19 πÕ°®“°º≈µÕà °“√À≈ßË— PTH ·≈«â °“√§ß—Ë ¢ÕßøÕ ‡øµ¬ß— ¡§’ «“¡ ”§≠— µÕà °“√‡°¥‘ vascular calcification ®“°°“√»÷°…“¢Õß Goodman ·≈–§≥–æ∫«à“ºâŸªÉ«¬øÕ°‡≈◊Õ¥¡’Õ—µ√“°“√‡°‘¥ coronary calcification  ßŸ °«à“ºâŸªÉ«¬ ÿ¢¿“楒∑’Ë¡’Õ“¬ÿ‡∑à“°—πÕ¬à“ß¡’π—¬ ”§—≠ §≥–ºâŸ∑”°“√»÷°…“¬—ß· ¥ß„Àâ‡ÀÁπ ∂ß÷ §«“¡ ¡— æπ— ∏„å π‡™ß‘ ∫«°¢Õß°“√‡°¥‘ coronary calcification °∫— √–¥∫— øÕ ‡øµ, calcium-phosphate product ·≈–ª√¡‘ “≥·§≈‡´¬’ ¡∑º’Ë ªâŸ «É ¬√∫— ª√–∑“π3 µÕà ¡“ Ganesh ·≈–§≥–æ∫§«“¡ ¡— æπ— ∏¢å Õß√–¥∫— øÕ ‡øµ „π‡≈Õ◊ ¥∑ Ë’ ߟ °«“à 6.5 mg/dl À√Õ◊ calcium-phosphate product ∑ Ë’ ߟ ¢πÈ÷ ∑°ÿ Ê 10 mg2/dl2 °∫— °“√‡æ¡Ë‘ ¢πÈ÷ ¢Õß ¢Õß cardiovascular mortality1 °“√≈¥≈ߢÕß√–¥∫— calcitriol Calcitriol ‡ªπì active hormone ¢Õß vitamin D ´ßË÷  √“â ß∑‰Ë’ µ‚¥¬°“√ hydroxylation ¢Õß 25- hydroxyvitaminD3 ∑‡Ë’ °∫Á  – ¡„πµ∫— ‚¥¬ calcitriol ¡À’ π“â ∑√Ë’ «à ¡°∫— PTH „π°“√ª√∫— √–¥∫— ·§≈‡´¬’ ¡„π ‡≈◊Õ¥„À⇪ìπª°µ‘ °≈à“«§◊Õ‡¡◊ËÕ√–¥—∫·§≈‡´’¬¡„π‡≈◊Õ¥µË”≈ß°√–µÿâπ„Àâ¡’°“√À≈—Ëß PTH ´÷Ëß¡’º≈„π°“√ ‡æ¡‘Ë √–¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥„À‡â ªπì ª°µ¥‘ ß— °≈‰°∑‰’Ë ¥°â ≈“à «¡“·≈«â PTH¬ß—  “¡“√∂°√–µπÿâ °“√ √“â ßcalcitriol ∑‰Ë’ µ‰¥Õâ °’ ¥«â ¬ calcitriol ∑‡Ë’ æ¡Ë‘ ¢πÈ÷ ‡¡ÕË◊ ®∫— °∫— VDR ∑¡Ë’ Õ’ ¬„àŸ π∑“߇¥π‘ Õ“À“√ °√–¥°Ÿ ·≈–µÕà ¡æ“√“‰∏√Õ¬¥å ೷Phosphate ೷Vascular ೷Cardiovascular ೷PTH Calcification Mortality √ªŸ ∑Ë’ 2 º≈°√–∑∫¢Õß°“√§ß—Ë ¢ÕßøÕ ‡øµ

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  π‘ ’ ¥‘…∞∫√√®ß 149 ®–™à«¬‡æ‘Ë¡°“√¥Ÿ¥´÷¡¢Õß·§≈‡´’¬¡·≈–øÕ ‡øµ∑’Ë≈”‰ â‡≈Á° ·≈–∑”„Àâ°√–¥Ÿ°¡’°“√ª≈¥ª≈àÕ¬ ·§≈‡´¬’ ¡ÕÕ°¡“„π√–∫∫‰À≈‡«¬’ π‡æ¡‘Ë ¢π÷È ª√∫— √–¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥„À‡â ªπì ª°µ‘ ¢≥–‡¥¬’ «°π— calcitriol ¬ß— ¡º’ ≈‚¥¬µ√ß„π°“√¬∫— ¬ßÈ— °“√ √“â ß·≈–°“√À≈ßË— PTH °“√»°÷ …“„π µ— «∑å ¥≈Õß∑‡Ë’ ªπì ‰µ«“¬æ∫§«“¡  ¡— æπ— ∏¢å Õß°“√≈¥≈ߢÕß√–¥∫— calcitriol °∫— °“√≈¥≈ߢÕß GFR ·≈– √–¥∫— ¢Õß calcitriol ®–≈¥≈ßµ”Ë °«“à ª°µÕ‘ ¬“à ß¡π’ ¬—  ”§≠— ‡¡Õ◊Ë GFR πÕâ ¬°«“à 60 ml/min20,21 „πªï §.».1984 Slatopolsky ·≈–§≥–‰¥∑â ”°“√ »°÷ …“‚¥¬°“√„Àâ calcitriol ·°ºà ªâŸ «É ¬øÕ°‡≈Õ◊ ¥∑¡’Ë ¿’ “«– secondary hyperparathyroidism º≈ª√“°Ø«“à calcitriol  “¡“√∂≈¥√–¥∫— ¢Õß PTH ‰¥°â Õà π∑®Ë’ –∑”„À¡â °’ “√‡æ¡Ë‘ ¢πÈ÷ ¢Õß√–¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥22 · ¥ß„À‡â ÀπÁ «“à calcitriol  “¡“√∂¬—∫¬—Èß°“√À≈—Ëß PTH ‚¥¬µ√ß (‚¥¬‰¡à¢÷Èπ°—∫ª√‘¡“≥·§≈‡´’¬¡∑’ˇæ‘Ë¡ Ÿß¢÷Èπ) ∑ƒ…Æ’¥—ß °≈“à «‰¥√â ∫— °“√ π∫—  ππÿ ®“°°“√»°÷ …“ in vitro ‚¥¬°“√‡≈¬’È ß‡´≈≈æå “√“‰∏√Õ¬¥„å πÕ“À“√‡≈¬’È ß‡´≈≈∑å º’Ë  ¡ calcitriol „𧫓¡‡¢¡â ¢πâ µ“à ßÊ æ∫«“à calcitriol  “¡“√∂¬∫— ¬ßÈ— PTH mRNA transcription ∑”„À¡â °’ “√À≈ßË— PTH ≈¥≈ß23-25 πÕ°®“°π’È calcitriol À√Õ◊ analog ¢Õß calcitriol ¬ß—  “¡“√∂°√µπÿâ „À¡â °’ “√‡æ¡‘Ë ¢π÷È ¢Õß VDR 25,26 ·≈– CaSR27 ™«à ¬„Àµâ Õà ¡æ“√“‰∏√Õ¬¥µå Õ∫ πÕßµÕà ·§≈‡´¬’ ¡·≈– calcitriol ‰¥¥â ¢’ πÈ÷ ·≈–∑ Ë’ ”§≠— ‰¥¡â °’ “√ æ ‘ ®Ÿ π·å ≈«â «“à °“√„Àâ calcitriol „πºªŸâ «É ¬ secondary hyperparathyroidism  “¡“√∂™«à ¬√°— …“¿“«– osteitis fibrosa ‰¥2â 8 °“√»°÷ …“„π√–¬–À≈ß— æ∫§«“¡ ”§≠— ¢Õß 25-hydroxyvitaminD ‚¥¬æ∫«“à 86% ¢ÕߺªŸâ «É ¬ CKD 3-4 ·≈– 97% ¢ÕߺªâŸ «É ¬ CKD 5 ¡√’ –¥∫— ¢Õß 25-hydroxyvitaminD µ”Ë °«“à ª°µ‘ ·≈–¬ß— æ∫«“à „π CKD 3-4 √–¥∫— ¢Õß 25-hydroxyvitaminD ·ª√ºπ— µ“¡√–¥∫— ¢Õß calcitriol ·≈– ·ª√º°ºπ— °∫— PTH29 ¿“«–·§≈‡´¬’ ¡µ”Ë „π‡≈Õ◊ ¥ „πª®í ®∫ÿ π— ‡√“¡°— ®–æ∫«“à ºªâŸ «É ¬∑‰’Ë ¥√â ∫— °“√øÕ°‡≈Õ◊ ¥¡√’ –¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥§Õà π¢“â ߠߟ À√Õ◊  ßŸ °«“à ª°µ‘∑‡’Ë ªπì ‡™πà π‡’È æ√“–ºªŸâ «É ¬‡À≈“à π‰’È ¥√â ∫— ·§≈‡´¬’ ¡·≈–«µ‘ “¡π‘ ¥„’ πª√¡‘ “≥ ßŸ ª√–°Õ∫°∫— ¡¿’ “«– hyperparathyroidism ·≈–/À√◊Õ parathyroid adenoma ∑”„ÀâµàÕ¡æ“√“‰∏√Õ¬¥å¡’°“√µÕ∫ πÕßµàÕ ·§≈‡´¬’ ¡·≈–«µ‘ “¡¥‘ ≈’ ¥≈ߥߗ ∑‰Ë’ ¥°â ≈“à «¡“·≈«â ·µ¬à ß— ¡º’ ªâŸ «É ¬ «à ππÕâ ¬∑æË’ ∫«“à ¡√’ –¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥ µË” ‡™àπ ºŸâªÉ«¬∑’ˉ¡à‰¥â√—∫°“√√—°…“Õ¬à“ßµàÕ‡π◊ËÕß ¡’√–¥—∫øÕ ‡øµ„π‡≈◊Õ¥ Ÿß∑”„Àâ·§≈‡´’¬¡µË”  àߺ≈ „Àâ¡’°“√À≈—Ëß PTH ‰¥â ®“°°“√»÷°…“„π —µ«å∑¥≈Õß∑’ˇªìπ‰µ«“¬æ∫«à“ Õ“À“√∑’Ë¡’·§≈‡´’¬¡ Ÿß∑”„Àâ¡’ °“√º≈µ‘ ·≈–°“√À≈ßË— PTH πÕâ ¬≈ß ·≈–√–¥∫— ·§≈´¬’ ¡„π‡≈Õ◊ ¥∑ Ë’ ߟ  “¡“√∂‡æ¡Ë‘ ª√¡‘ “≥ VDR ‰¥3â 0 ‡À≈“à π’È· ¥ß„Àâ‡ÀÁπ∂÷ߧ«“¡ ”§—≠„π°“√§«∫§ÿ¡√–¥—∫·§≈‡´’¬¡„π‡≈◊Õ¥„À⇪ìπª°µ‘ Õ¬à“߉√°Áµ“¡„π°“√ √°— …“§«√√–«ß— ‰¡„à À√â –¥∫— ·§≈‡´¬’ ¡ ßŸ ‡°π‘ ‰ª ‡æ√“–®–∑”„Àâ calcium-phosphate product  ßŸ µ“¡‰ª¥«â ¬ ‡ ¬Ë’ ßµÕà °“√‡°¥‘ vascular calcification πÕ°®“°π¬È’ ß— ¡ª’ ®í ®¬— ÕπË◊ Ê ∑¡Ë’ º’ ≈µÕà √–¥∫— PTH ‡™πà ¿“«– metabolic acidosis °“√»°÷ …“„π  µ— «∑å ¥≈Õß·≈–„πºªâŸ «É ¬®”π«π‰¡¡à “°æ∫«“à ºªâŸ «É ¬∑¡’Ë ¿’ “«–metabolicacidosis®–¡√’ –¥∫— PTH ßŸ °«“à 31,32 ·≈– metabolic acidosis  “¡“√∂‡æ¡Ë‘ ®”π«π PTH receptor „π‡´≈≈°å √–¥°Ÿ ‰¥3â 3 À≈°— ∞“π¥ß— °≈“à «∫ßà ™«È’ “à ¿“«– metabolic acidosis Õ“®¡º’ ≈‡æ¡Ë‘ §«“¡√πÿ ·√ߢÕß secondary hyperparathyroidism

New Frontiers in Dialysis 150 ∏π‘µ ®√‘ ππ— ∑∏å «™—  ‘√¿‘ “ ™â“ß»‘√‘°ÿ≈™¬— ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°ÿ≈ 4. °“√√°— …“¿“«–øÕ ‡øµ„π‡≈Õ◊ ¥ ßŸ ·≈– secondary hyperparathyroidism °“√§ßË— ¢ÕßøÕ ‡øµ ·≈– °“√≈¥≈ߢÕß√–¥∫— ¢Õß calcitriol ‡√¡Ë‘ µßÈ— ·µ‡à ¡ÕË◊ GFR πÕâ ¬°«“à 60 ml/ min ¥—ßπ—Èπ®÷ß®”‡ªìπµâÕß„Àâ°“√√—°…“µ—Èß·µà‡π‘ËπÊ „π°“√√—°…“‡√“欓¬“¡∑’Ë®–≈¥°“√§—ËߢÕßøÕ ‡øµ ·≈–√°— …“√–¥∫— ·§≈‡´¬’ ¡·≈– PTH „ÀÕâ ¬„àŸ π√–¥∫— ∑‡Ë’ À¡“– ¡ ºªâŸ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— ‰¡®à ”‡ªπì ®–µÕâ ß¡¿’ “«– secondary hyperparathyroidism ∑°ÿ §π °“√»°÷ …“‚¥¬°“√∑” bone biopsy „πºªŸâ «É ¬µ“à ߪ√–‡∑»∑¡Ë’ ‰’ µ «“¬‡√ÕÈ◊ √ß— √–¬– ¥ÿ ∑“â ¬ æ∫«“à ¡º’ ªâŸ «É ¬‡æ¬’ ß 50% ‡∑“à ππÈ— ∑¡Ë’ ’ osteitis fibrosa „π¢≥–∑ºË’ ªâŸ «É ¬ 27% æ∫ ≈°— …≥–∑‡’Ë ¢“â ‰¥°â ∫— adynamic bone disease  ”À√∫— ºªŸâ «É ¬‰∑¬æ∫«“à ¡Õ’ ∫ÿ µ— °‘ “√≥¢å Õß adynamic bone disease ∂ß÷ 41%4 ¥ß— ππÈ— „π°“√√°— …“®ß÷ ®”‡ªπì ∑®Ë’ –µÕâ ß¡°’ “√‡®“– intact PTH Õ¬“à ß ¡”Ë ‡ ¡Õ πÕ°®“°®–‡æÕË◊ ª√—∫°“√„À⬓լà“߇À¡“– ¡·≈â« ¬—߇æ◊ËÕÀ≈’°‡≈’ˬ߰“√√—°…“∑’Ë¡“°‡°‘𮔇ªìπ (over treatment) ®π ∑”„À‡â °¥‘ ¿“«– adynamic bone disease ·≈– vascular calcification ®“°°“√»°÷ …“æ∫§«“¡º¥‘ ª°µ¢‘ Õß°√–¥°Ÿ „π 75-85% ¢ÕߺªŸâ «É ¬∑¡Ë’ ’ GFR 20-50 ml/min34 ¥ß— π—Èπ®÷ߧ«√·π–π”„Àºâ ªŸâ «É ¬§«∫§¡ÿ Õ“À“√∑¡Ë’ ª’ √¡‘ “≥øÕ ‡øµ ßŸ µßÈ— ·µ‡à ππË‘ Ê Õ“À“√®”æ«°πÈ’ ‰¥·â °à ∂«—Ë π”È ‡µ“â À⟠‡µ“â ‡®¬È’ « π¡ ¥ ‡π¬ ‰Õ»°√¡’ ‰¢·à ¥ß ≈°Ÿ ‡°¥ ≈°Ÿ æ√πÿ °ßâÿ ·Àßâ ™Õ°‚°·≈µ ·≈– π”È Õ¥— ≈¡ ∂“â °“√§«∫§¡ÿ Õ“À“√‰¡‰à ¥ºâ ≈§«√„À¬â “™«à ¬ ¬“∑ ’Ë “¡“√∂§«∫§¡ÿ √–¥∫— ¢ÕßøÕ ‡øµ„π‡≈Õ◊ ¥ ·≈– ™«à ¬≈¥ PTH ‰¥â ª√–°Õ∫‰ª¥«â ¬¬“°≈¡àÿ µ“à ßÊ ¥ß— µÕà ‰ªπÈ’ 1. Calcium-containing phosphate binders ‰¥·â °à calcium carbonate (CaCO3) À√Õ◊ calcium acetate (CaAc) CaCO3 À√Õ◊ CaAc ‡¡ÕË◊ √∫— ª√–∑“πÀ≈ß— Õ“À“√∑π— ∑®’ –®∫— °∫— øÕ ‡øµ„πÕ“À“√ ¬∫— ¬ßÈ— °“√ ¥Ÿ¥´÷¡¢ÕßøÕ ‡øµ®“°∑“߇¥‘πÕ“À“√ ·≈â«¢—∫∂à“¬ÕÕ°¡“∑“ßÕÿ®®“√–35 ·µà¡’º≈¢â“߇§’¬ß∑’Ë ”§—≠§◊Õ ·§≈‡´’¬¡∑’Ë√—∫ª√–∑“π‡¢â“‰ªÕ“®∂Ÿ°¥Ÿ¥´÷¡‚¥¬≈”‰ â ‚¥¬‡©æ“–∂⓺ŸâªÉ«¬√—∫ª√–∑“𬓵Õπ∑âÕß«à“ß À√Õ◊ √∫— ª√–∑“πª√¡‘ “≥¡“°‡°π‘ ‰ª∑”„À·â §≈‡´¬’ ¡ ßŸ  ßà º≈„À¡â °’ “√‡æ¡‘Ë ¢π÷È ¢Õßcalcium-phosphateproduct ®“°°“√ª√–‡¡π‘ º≈°“√»°÷ …“·∫∫ post hoc „πºªâŸ «É ¬„À¡∑à ‡Ë’ √¡Ë‘ ∑” hemodialysis æ∫«“à °“√„™â calcium- containing phosphate binders ‡ªπì strongest predictor ¢ÕßÕµ— √“°“√µ“¬36 Õ¬“à ߉√°µÁ “¡§ß®–µÕâ ß√Õ °“√»°÷ …“·∫∫ prospective randomized control trials µÕà ‰ª CaAc  “¡“√∂®∫— °∫— øÕ ‡øµ‰¥¥â °’ «“à CaCO3 „πª√¡‘ “≥ elemental calcium ∑‡Ë’ ∑“à °π— 37 Õ¬“à ߉√°µÁ “¡‡¡ÕË◊ ‡ª√¬’ ∫‡∑¬’ ∫Õµ— √“°“√‡°¥‘ hypercalcemia „π ºªŸâ «É ¬‰µ«“¬∑‰’Ë ¥√â ∫— CaCO3 °∫— CaAc „π√–¥∫— ∑®’Ë ∫— °∫— øÕ ‡øµ‰¥„â °≈‡â §¬’ ß°π— (´ß÷Ë µÕâ ß„™â CaCO 3 „π¢π“¥ ¡“°°«“à ) æ∫«“à ¡Õ’ µ— √“°“√‡°¥‘ hypercalcemia ‰¡·à µ°µ“à ß°π— ·≈–¬ß— æ∫«“à º≈¢“â ߇§¬’ ß∑“ß√–∫∫∑“ß ‡¥π‘ Õ“À“√¢Õß CaAc ¡¡’ “°°«“à ®π∑”„Àºâ ªâŸ «É ¬∫“ß√“¬µÕâ ßÀ¬¥ÿ „™¬â “38-40 Õ¬“à ߉√°µÁ “¡ CaAc ¡ª’ √–‚¬™πå „πºŸâªÉ«¬∑’ˇ ’ˬߵàÕ°“√‡°‘¥ vascular calcification ‡æ√“–™à«¬≈¥ª√‘¡“≥ calcium intake ≈߉¥â °“√„Àâ ·§≈‡´¬’ ¡§«√‡√¡Ë‘ ∑¢Ë’ π“¥µ”Ë °Õà π 2-3 §√ßÈ— µÕà «π— À≈ß— Õ“À“√∑π— ∑’ ∂“â ºªâŸ «É ¬∑“πÕ“À“√¡ÕÈ◊ „¥¡“°°„Á À√â ∫— ª√–∑“π¬“À≈ß— Õ“À“√¡ÕÈ◊ ππÈ— ¢π“¥¬“‡æ¡Ë‘ ‰¥∑â °ÿ 2-3  ª— ¥“Àå ‚¥¬‡√“®–欓¬“¡√°— …“ serum calcium ‰¡„à À‡â °π‘ 10.2 mg/dl ·≈– serum phosphate ‰¡„à À‡â °π‘ 5.5 mg/dl (µ“√“ß∑Ë’ 1) K/DOQI ·π–π”«“à ‰¡à §«√„Àªâ √¡‘ “≥¢Õß elemental calcium ‡°π‘ °«“à 1.5 °√¡— /«π— (CaCO3 1250 ¡≈‘ ≈°‘ √¡— ¡’ elemental calcium 500 ¡≈‘ ≈°‘ √¡— , CaAc 667 ¡≈‘ ≈°‘ √¡— ¡’ elemental calcium 169 ¡≈‘ ≈°‘ √¡— )

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥…‘ ∞∫√√®ß 151 2. Non-calcium containing phosphate binders ‰¥·â °à aluminum hydroxide, lanthanum carbonate ·≈– sevelamer hydrochloride Aluminum hydroxide ∑’Ë„™â°—πÕ¬à“ß·æ√àÀ≈“¬¡“‡ªìπ‡«≈“π“π„πÕ¥’µ  “¡“√∂®—∫°—∫ øÕ ‡øµ„π∑“߇¥π‘ Õ“À“√‰¥¥â °’ «“à ·§≈‡´¬’ ¡ ·≈–‰¡∑à ”„À√â –¥∫— ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥ ßŸ ¢πÈ÷ 35 Õ¬“à ߉√°µÁ “¡ aluminum  “¡“√∂ – ¡„π à«πµà“ßÊ ¢Õß√à“ß°“¬‰¥â ‡™àπ „π‰¢°√–¥Ÿ°∑”„À⇰‘¥¿“«–´’¥ ·≈– osteomalacia41 ∂“â  – ¡„π ¡Õß®–∑”„À¡â Õ’ “°“√ ∫—  π, hallucination ·≈– ™°— ‰¥â42 ¥ß— ππÈ— ®ß÷ §«√À≈°’ ‡≈¬Ë’ ß°“√„Àâ aluminum hydroxide ∂“â ®”‡ªπì Õ“®„À‰â ¥„â π√–¬– πÈ— ‰¡‡à °π‘ 2  ª— ¥“Àå ¿“«– aluminum toxicity  “¡“√∂«π‘ ®‘ ©¬— ‰¥®â “°°“√«¥— √–¥∫— ¢Õß aluminum „π‡≈Õ◊ ¥À≈ß— °“√„Àâ desferoxamine À√Õ◊ °“√∑” aluminum staining ®“° bone biopsy specimen °“√√°— …“‰¥·â °°à “√„Àâ desferoxamine Lanthanum carbonate ¢≥–π’ÈÕ¬Ÿà√–À«à“ß°“√π”‡¢â“¡“„™â„πª√–‡∑»‰∑¬ ¡’ª√– ‘∑∏‘¿“æ„π °“√®∫— °∫— øÕ ‡øµ‰¥‡â ™πà ‡¥¬’ «°∫— ·§≈‡´¬’ ¡ ≈¥√–¥∫— øÕ ‡øµ·≈– calcium-phosphate product ‚¥¬‰¡à ∑”„À·â §≈‡´¬’ ¡‡æ¡‘Ë  ßŸ ¢π÷È 43,44 °“√»°÷ …“‚¥¬ bone biopsy „πºªŸâ «É ¬øÕ°‡≈Õ◊ ¥‰¡æà ∫¿“«– osteomalacia „πºªâŸ «É ¬∑‰’Ë ¥√â ∫— lanthanum carbonate ´ß÷Ë „πÕ¥µ’ æ∫‰¥∫â Õà ¬„πºªŸâ «É ¬∑‰’Ë ¥√â ∫— aluminum hydroxide45 Õ¬“à ߉√ °µÁ “¡°“√»°÷ …“„π µ— «∑å ¥≈Õßæ∫¡°’ “√ – ¡¢Õß lanthanum „πªÕ¥ ‰µ °√–¥°Ÿ  ¡Õß ·≈–µ∫— ‚¥¬  —µ«å∑¥≈Õß∑’ˉµ«“¬®–¡’°“√ – ¡¡“°°«à“ —µ«å∑¥≈Õ¥∑’Ë¡’‰µª°µ‘  “‡Àµÿ‡ªìπ®“°¿“«–‰µ«“¬∑”„Àâ¡’ °“√¥¥Ÿ ´¡÷ ¢Õß lanthanum ‡æ¡Ë‘ ¢πÈ÷ „π∑“߇¥π‘ Õ“À“√46  ”À√∫— °“√ – ¡„πµ∫— ππÈ— ‡¡ÕË◊ π”‡≈Õ◊ ¥¢Õß µ— «å ∑¥≈Õß¡“µ√«®¥‰Ÿ ¡æà ∫§«“¡º¥‘ ª°µ¢‘ Õ߇ÕπÁ ‰´¡µå ∫— ·≈–πÈ”Àπ°— ¢Õßµ∫— ‰¡·à µ°µ“à ß®“° µ— «∑å ¥≈Õß∑‰’Ë ¡à ‰¥√â ∫— ¬“ ‡¡ÕË◊ µ√«®µ∫— ¥«â ¬ MRI ·≈–∑“ß°≈Õâ ß®≈ÿ ∑√√»π‰å ¡æà ∫«“à ¡§’ «“¡º¥‘ ª°µ4‘ 7  «à π°“√ – ¡„π  ¡Õß®“°°“√»°÷ …“„πºªŸâ «É ¬øÕ°‡≈Õ◊ ¥®”π«π 360 §π µ¥‘ µ“¡º≈‡ªπì √–¬–‡«≈“ 2 ªï ‰¡æà ∫§«“¡º¥‘ ª°µ¢‘ Õß cognitive function ·µÕà ¬“à ß„¥48 Sevelamer hydrochloride ‡ªπì non-absorbed, calcium free ·≈– metal free phosphate binder ∑Ë’ ¡’„™â„πµà“ߪ√–‡∑» sevelamer ≈¥°“√¥Ÿ¥´÷¡¢ÕßøÕ ‡øµ‚¥¬‰¡à∑”„Àâ√–¥—∫·§≈‡´’¬¡ Ÿß¢÷Èπ  “¡“√∂ ≈¥√–¥∫— cholesterol ·≈– LDL ·≈–≈¥°“√‡°¥‘ coronary ·≈– aortic calcification „πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— √–¬–°Õà π·≈–À≈ß— ‡√¡‘Ë µπâ øÕ°‡≈Õ◊ ¥49,50 °“√»°÷ …“∑‰Ë’ ¥√â ∫— °“√µæ’ ¡‘ æ‡å √«Á Ê πæÈ’ ∫«“à sevelamer Õ“®¡º’ ≈ „π°“√≈¥Õµ— √“°“√µ“¬‰¥Õâ °’ ¥«â ¬51,52 Õ¬“à ߉√°µÁ “¡®“°°“√»°÷ …“ CARE study æ∫«“à CaAc  “¡“√∂ §«∫§¡ÿ √–¥∫— ¢ÕßøÕ ‡øµ·≈– calcium-phosphate product „π‡≈Õ◊ ¥‰¥¥â °’ «“à sevelamer53 º≈¢“â ߇§¬’ ߢÕß sevelamer ∑æË’ ∫∫Õà ¬§Õ◊ ¿“«– metabolic acidosis54 3. Vitamin D √“à ¬°“¬‰¥√â ∫— «µ‘ “¡π‘ ¥¡’ “®“° 2 ∑“ß §Õ◊ º≈µ‘ ¿“¬„π√“à ß°“¬‚¥¬Õ“»¬— · ß ultraviolet ·≈– ®“°Õ“À“√∑’ˇªìπº≈‘µ¿—≥±å®“° —µ«å Õ“À“√∑’Ë¡’«‘µ“¡‘π¥’„πª√‘¡“≥ Ÿß ‰¥â·°à π¡ ‡π¬ ·≈– ‰¢à·¥ß À≈—ß®“°∑’Ë√à“ß°“¬‰¥â√—∫«‘µ“¡‘π¥’·≈â«®–∂Ÿ°‡ª≈’ˬπ·ª≈߉ª‡ªìπ 25-hydroxycholecalciferol À√◊Õ 25- hydroxyvitaminD3  – ¡∑’˵—∫ ‡¡◊ËÕ„¥∑’Ë√à“ß°“¬µâÕß°“√„™â«‘µ“¡‘π¥’ ‰µ®–∑”Àπâ“∑’ˇª≈’ˬπ 25- hydroxycholecalciferol ‡ªπì 1,25- dihydroxycholecalciferol (1,25-dihydroxyvitaminD3 À√Õ◊ calcitriol) ‚¥¬ Õ“»¬— ‡ÕπÁ ‰´¡å 1 alpha-hydroxylase ª®í ®¬— À≈°— 2 ª®í ®¬— ∑ Ë’ “¡“√∂°√–µπâÿ °“√ √“â ß calcitriol ‰¥â §Õ◊ PTH

New Frontiers in Dialysis 152 ∏π‘µ ®√‘ ππ— ∑∏å «—™  √‘ ‘¿“ ™“â ß»‘√°‘ ≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π‘™ « —πµå  ÿ‡¡∏°ÿ≈ ·≈– ¿“«–øÕ ‡øµ„π‡≈Õ◊ ¥µ”Ë calcitriol ®–‰ª¡’ º ≈ ° √ – µÿâ π „ Àâ ¡’ ° “ √ ¥Ÿ ¥ ´÷ ¡ · § ≈ ‡ ´’ ¬ ¡ · ≈ – øÕ ‡øµ‡æ‘Ë¡¡“°¢÷Èπ„π∑“߇¥‘πÕ“À“√ ∑”„Àâ √–¥—∫øÕ ‡øµ°≈—∫¡“‡ªìπª°µ‘ ·≈– ≈¥°“√  √“â ß·≈–À≈ßË— PTH «‘ µ “ ¡‘ π ¥’ ∑’Ë „ ™â „ π ° “ √ √— ° … “ ¿ “ « – secondary hyperparathyroidism ·∫ßà ÕÕ°‰¥‡â ªπì 2 °≈¡ÿà „À≠Êà §Õ◊ calcitriol ·≈– analog ¢Õß calcitriol ‰¥·â °à alfacalcidol, doxercalciferol ·≈– paricalcitol  ”À√∫— doxercalciferol ·≈– paricalcitol ππÈ— ¡„’ ™â ·µ„à πµ“à ߪ√–‡∑» °“√„Àâ calcitriol À√Õ◊ analog ¢Õß calcitriol  “¡“√∂™à«¬≈¥√–¥—∫¢Õß PTH √ªŸ ∑’Ë 3 ªÑÕß°—π°“√‡°‘¥ high bone turnover renal °“√ √“â ß·≈–ª®í ®¬— ∑§’Ë «∫§¡ÿ °“√ √“â ß«µ‘ “¡π‘ ¥’ osteodystrophy ‰¥â ®“°°“√»÷°…“æ∫«à“„πºâŸ ª«É ¬∑¡Ë’ ’ GFR 20-60 ml/min °“√„Àâ calcitriol À√Õ◊ alfacalcidol (1-alpha hydroxycholcalciferol À√Õ◊ 1-alpha hydroxyvitaminD3 ‡ªπì vitamin D derivative ´ßË÷ ®–µÕâ ߉¥√â ∫— 25 hydroxylation ∑µË’ ∫— °Õà π®ß÷ ®–‡ªπì active form)  “¡“√∂∑”„Àâ bone histology ¥¢’ πÈ÷ ‰¥5â 5,56 calcitriol À√Õ◊ alfacalcidol ·¡®â – “¡“√∂≈¥√–¥∫— PTH ‰¥â ¥’ ·µà¡’º≈¢â“߇§’¬ß§◊Õ∑”„Àâ·§≈‡´’¬¡·≈–øÕ ‡øµ„π‡≈◊Õ¥‡æ‘Ë¡ ßŸ ¢÷Èπ®“°°“√‡æ‘Ë¡°“√¥¥Ÿ ´÷¡„π∑“߇¥‘π Õ“À“√´÷Ë߇ªìπªí®®—¬∑”„Àâ∫“ߧ√—È߉¡à “¡“√∂„À⬓„π¢π“¥ Ÿß‰¥â „π√–¬–µàÕ¡“®÷ß¡’°“√§âπ§«â“º≈‘µ vitamin D analog µ«— „À¡Êà ∑¡Ë’ §’ ≥ÿ  ¡∫µ— „‘ π°“√≈¥√–¥∫— PTH ‚¥¬‰¡‡à æ¡Ë‘ °“√¥¥Ÿ ´¡÷ ¢Õß·§≈‡´¬’ ¡·≈– øÕ ‡øµ ¬“µ—«π’È™◊ËÕ paricalcitol ªí®®ÿ∫—π¡’„™â·µà„πµà“ߪ√–‡∑» calcitriol À√◊Õ alfacalcidol π’È®“°°“√ »°÷ …“æ∫«“à °“√„Àâ intermittent À√Õ◊ pulse therapy 3 §√ßÈ— / ª— ¥“ÀÕå “®‰¥ºâ ≈¥°’ «“à °“√„À∑â °ÿ «π— ·≈–„π ºªâŸ «É ¬∑‰’Ë ¥√â ∫— pulse therapy ¡Õ’ µ— √“°“√‡°¥‘ ¿“«–·§≈‡´¬’ ¡·≈–øÕ ‡øµ ßŸ ·≈–¡√’ –¥∫— calcium-phosphate productµË”°«“à ºªŸâ «É ¬∑‰’Ë ¥√â ∫— ¬“∑°ÿ «π— 28,57 °“√√°— …“µß—È ·µ‡à ππ‘Ë Ê ®–™«à ¬‡æ¡‘Ë °“√µÕ∫ πÕߢÕ߬“∑”„À‰â ¡à µÕâ ß„™¬â “„π¢π“¥∑ Ë’ ߟ  ”À√∫— ¢π“¥¢Õß calcitriol ππÈ— §«√‡√¡Ë‘ ®“° 0.25-0.5 µg 3 §√ßÈ— / ª— ¥“Àå „π¢≥–∑Ë’ alfacalcidol Õ“®‡√¡Ë‘ µπâ „π¢π“¥∑ Ë’ ߟ °«“à §Õ◊ 0.5 -1 µg ·≈«â §Õà ¬Ê ‡æ¡Ë‘ ¢πÈ÷ ∑°ÿ 2-3 ‡¥Õ◊ π ¢π“¥ ßŸ  ¥ÿ ∑„Ë’ À¬â “ ‰¥§â Õ◊ 4-6 µg 3 §√ßÈ— / ª— ¥“Àå ∑ßÈ— π‚’È ¥¬ª√∫— µ“¡√–¥∫— intact PTH, ·§≈‡´¬’ ¡, øÕ ‡øµ ·≈– calcium- phosphate product  «à π doxercalciferol ππ—È §Õ◊ 1-alpha hydroxyvitaminD2 ¡≈’ °— …≥–„°≈‡â §¬’ ß°∫— alfacalcidol ®÷ß¡’º≈¢â“߇§’¬ß∑’˧≈⓬§≈÷ß°—∫ alfacalcidol ¬“µ—«π’È¡’„™â·µà„πµà“ߪ√–‡∑» °“√»÷°…“∑’Ëæ÷Ëß®–≈ßµ’æ‘¡æå ‡√«Á Ê π‡È’ ª√¬’ ∫‡∑¬’ ∫°“√„À«â µ‘ “¡π‘ ¥™’ 𥑠µ“à ßÊ ‰¥·â °à paricalcitol, doxercalciferol ·≈– calcitriol æ∫¿“«– vascular calcification „π  —µ«å∑¥≈Õß∑’ˉ¥â√—∫ doxercalciferol ·≈– calcitriol ·µà‰¡àæ∫¿“«–¥—ß°≈à“«„π  µ— «∑å ¥≈Õß∑‰Ë’ ¥√â ∫— paricalcitol58,59 ª®í ®∫ÿ π— ‡ªπì ∑∑’Ë √“∫°π— ¥«’ “à °“√„Àâ active vitamin D Õ“®¡º’ ≈¥„’ π°“√≈¥Õµ— √“°“√µ“¬∑‡’Ë °¥‘ ®“° ‚√§À≈Õ¥‡≈Õ◊ ¥À«— „®·≈–Õµ— √“°“√µ“¬‚¥¬√«¡60,61 °“√»°÷ …“¬Õâ πÀ≈ß— „πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— 70,000 §π

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  π‘ ’ ¥…‘ ∞∫√√®ß 153 ‡ª√’¬∫‡∑’¬∫√–À«à“ß°≈ÿࡺ⟪ɫ¬∑’ˉ¥â√—∫ paricalcitol ·≈– calcitriol æ∫«à“Õ—µ√“°“√µ“¬„πºŸâªÉ«¬∑’ˉ¥â√—∫ paricalcitol µ”Ë °«“à „π°≈¡àÿ ∑‰Ë’ ¥√â ∫— calcitriol Õ¬“à ß¡π’ ¬—  ”§≠— 62 °“√»°÷ …“„πÕ°’ cohort ÀπßË÷ æ∫«“à ºªâŸ «É ¬∑Ë’ ‰¡à‰¥â√—∫«‘µ“¡‘π¥’¡’Õ—µ√“°“√µ“¬ Ÿß°«à“ºâŸªÉ«¬∑’ˉ¥â√—∫ active vitamin D ∑ÿ°™π‘¥ ·µà‰¡àæ∫§«“¡·µ° µ“à ߢÕßÕµ— √“°“√µ“¬‡¡ÕË◊ ‡ª√¬’ ∫‡∑¬’ ∫√–À«“à ߺªâŸ «É ¬∑‰Ë’ ¥√â ∫— paricalcitol °∫— ºªŸâ «É ¬∑‰Ë’ ¥√â ∫— active vitamin D ™π‘¥Õ◊Ë𠇙àπ calcitriol ·≈– doxercalciferol63 πÕ°®“°π’Ȭ—ß¡’°“√»÷°…“∂÷ߧ«“¡ —¡æ—π∏å¢Õß°“√¢“¥ 25-hydroxyvitaminD ·≈– 1,25-dihydroxyvitaminD °∫— Õµ— √“°“√µ“¬¢ÕߺªâŸ «É ¬øÕ°‡≈Õ◊ ¥æ∫«“à ºªâŸ «É ¬∑¢’Ë “¥ 25-hydroxyvitaminD Õ¬“à ß√πÿ ·√ß¡Õ’ µ— √“°“√µ“¬‚¥¬√«¡ ßŸ °«“à °≈¡ÿà ºªŸâ «É ¬∑¢’Ë “¥ 1,25-dihydroxyvitaminD64 · ¥ß„À‡â ÀπÁ §«“¡ ”§≠— ¢Õß°“√√°— …“√–¥∫— «µ‘ “¡π‘ ¥„’ π√“à ß°“¬„À‡â ªπì ª°µ‘¥ß— ∑‰’Ë ¥°â ≈“à «¡“·≈«â «“à 86% ¢ÕߺªŸâ «É ¬ CKD 3-4 ·≈– 97% ¢ÕߺªŸâ «É ¬ CKD 5 ¡√’ –¥∫— ¢Õß 25-hydroxyvitaminD µ”Ë °«“à ª°µ2‘ 9 ¥ß— ππÈ— K/DOQI ®ß÷ ·π–π”„Àâ vitamin D „π√ªŸ ¢Õß ergocalciferol „πºªŸâ «É ¬∑¡Ë’ √’ –¥∫— 25-hydroxyvitaminD µ”Ë °«“à 30 ng/mL ‚¥¬„À√â ∫— ª√–∑“π„π¢π“¥ 50,000 ¬πŸ µ‘ ∑°ÿ ‡¥Õ◊ π‡ªπì ‡«≈“ 6 ‡¥Õ◊ π ·µ∂à “â √–¥∫— µ”Ë °«“à 15 ng/mL „À√â ∫— ª√–∑“π 50,000 ¬πŸ µ‘ ∑°ÿ  ª— ¥“Àå π“π 4  ª— ¥“Àå ®“°ππÈ— „À√â ∫— ª√–∑“π∑°ÿ ‡¥Õ◊ πµÕà ‰ªÕ°’ 4 ‡¥Õ◊ π °“√»÷°…“∂÷ßÕÿ∫—µ‘°“√≥å¢Õß°“√¢“¥ 25-hydroxyvitaminD3 „πºŸâªÉ«¬øÕ°‡≈◊Õ¥„πª√–‡∑»‰∑¬∑’Ë‚√ß æ¬“∫“≈«™√‘ –„Àºâ ≈‡™πà ‡¥¬’ «°π— ‚¥¬æ∫«“à 78.2% ¢ÕߺªŸâ «É ¬ predialysis CKD stage 3-5 ¡√’ –¥∫— ¢Õß 25- hydroxyvitaminD3 µË”°«“à 30 ng/mL (¢Õâ ¡≈Ÿ ¬ß— ‰¡‰à ¥√â ∫— °“√µæ’ ¡‘ æ)å ¥ß— ππ—È ‡√“®ß÷ §«√殑 “√≥“„Àâ ergocalciferol „πºŸâªÉ«¬°≈ÿà¡¥—ß°≈à“« º≈„π‡™‘ß∫«°¢Õß«‘µ“¡‘π¥’µàÕÕ—µ√“°“√µ“¬π—Èπ à«πÀπ÷ËßÕ“®Õ∏‘∫“¬‰¥â®“° ª√– ∑‘ ∏¿‘ “æ¢Õß active vitamin D „π°“√≈¥ inflammation ·≈– thrombosis ¬∫— ¬ß—È vascular smooth muscle cell proliferation ≈¥ vascular stiffening ·≈– left ventricular hypertrophy πÕ°®“°π’Ȭ—ß¡’ƒ∑∏‘Ï„π°“√ downregulate renin-angiotensin system ·≈– “¡“√∂≈¥§«“¡¥π— ‚≈Àµ‘ ‰¥6â 5 4. Calcimimetics ¬“„π°≈¡ÿà calciminetic (cinacalcet) ¡ƒ’ ∑∏™‘Ï «à ¬‡æ¡‘Ë °“√µÕ∫ πÕߢÕß CaSR µÕà ·§≈‡´¬’ ¡  “¡“√∂ ≈¥°“√· ¥ßÕÕ°¢Õß PTH mRNA ·≈–≈¥°“√À≈ß—Ë PTH ‰¥6â 6 °“√»°÷ …“≈“à  ¥ÿ ´ß÷Ë ‡ªπì multicenterrandomized control trial „πºªâŸ «É ¬ secondary hyperparathyroidism ®”π«π 740 §π ∑‰Ë’ ¥√â ∫— °“√√°— …“¥«â ¬¬“ÕπË◊ Õ¬·Ÿà ≈«â ·µà√–¥—∫ intact PTH ¬—ß Ÿß°«à“ 300 pg/ml ‡¡◊ËÕπ”ºâŸªÉ«¬°≈ÿà¡¥—ß°≈à“«¡“ randomize „Àâ cinacalcet ‡ª√¬’ ∫‡∑¬’ ∫°∫— placebo æ∫«“à 43% ¢ÕߺªŸâ «É ¬∑‰Ë’ ¥√â ∫— cinacalcet ¡√’ –¥∫— intact PTH ≈¥≈ßµ”Ë °«“à 250 pg/ml67 ¢Õâ ¡≈Ÿ ¥ß— °≈“à «· ¥ß„À‡â ÀπÁ «“à cinacalcet  “¡“√∂„™√â «à ¡°∫— «µ‘ “¡π‘ ¥’ ·≈– ·§≈‡´¬’ ¡„π°“√√°— …“ ¿“«– secondary hyperparathyroidism ‰¥â πÕ°®“°π°’È “√»°÷ …“„π µ— «∑å ¥≈Õ߉¡æà ∫«“à cinacalcet ∑”„À‡â °¥‘ vascular calcification68 ·≈– cinacalcet ¬ß— Õ“®¡ª’ √–‚¬™π„å πºªŸâ «É ¬∑¡Ë’ ’ persistent hyperparathyroidism À≈ß— ®“°‡ª≈¬’Ë π‰µ‰ª·≈«â 69,70º≈¢ÕßcinacalcetµÕà Õµ— √“°“√µ“¬„πºªŸâ «É ¬‰µ«“¬‡√Õ◊È √ß— ¢≥–π°’È ”≈ß— Õ¬„àŸ π√–À«“à ß °“√»°÷ …“71 ¬“ cinacalcet ¢≥–π¡È’ „’ ™·â µ„à πµ“à ߪ√–‡∑»‡∑“à ππÈ— °“√≈¥ª√¡‘ “≥·§≈‡´¬’ ¡„π dialysate „ÀÕâ ¬∑àŸ Ë’ 2.5 mEq/L ™«à ¬≈¥Õµ— √“°“√‡°¥‘ hypercalcemia ∑”„À â “¡“√∂„À¬â “ phosphate binders ·≈– active vitamin D ‰¥„â π¢π“¥∑ Ë’ ߟ ¢πÈ÷ ·≈–™«à ¬≈¥°“√‡°¥‘ ¿“«– adynamic bone disease ‰¥â Õ¬“à ߉√°µÁ “¡°“√„™â dialysate calcium µ”Ë °«“à 3.5 mEq/L Õ“®∑”„À¡â ’ negative calcium balance ·≈–‡æ¡Ë‘ Õ∫ÿ µ— °‘ “√≥¢å Õß°“√‡°¥‘ intradialytic hypotension72 ®“°°“√∑°Ë’ ≈“â ¡‡πÕÈ◊

New Frontiers in Dialysis 154 ∏π‘µ ®‘√π—π∑å∏«—™  ‘√‘¿“ ™“â ß»‘√‘°≈ÿ ™¬— ∏π—𥓠µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°ÿ≈ À—«„®∫’∫µ—«‰¥â≈¥≈ß °“√»÷°…“„πºâŸªÉ«¬∑’ˇªìπ‚√§À—«„®æ∫«à“°“√„™â dialysate calcium 3.5 mEq/L  “¡“√∂≈¥°“√‡°¥‘ intradialytic hypotension ‰¥7â 3 Õ¬“à ߉√°µÁ “¡°“√»°÷ …“·≈–µ¥‘ µ“¡º≈‡ªπì ‡«≈“ 3 ªï „πºŸâªÉ«¬∑’ˉ¥â√—∫ dialysate calcium 3 mEq/L æ∫§«“¡ —¡æ—π∏å¢Õß°“√‡æ‘Ë¡¢÷Èπ¢Õß√–¥—∫·§≈‡´’¬¡À≈—ß øÕ°‡≈Õ◊ ¥°∫— °“√‡æ¡‘Ë ¢π÷È ¢Õß aortic calcification74 ·≈–¢Õâ ¡≈Ÿ ®“° DOPPS (Dialysis Outcomes and Practice Patterns Study) æ∫«à“°“√„™â dialysate calcium ∑’Ë¡’§«“¡‡¢â¡¢âπ Ÿß¡’§«“¡ —¡æ—π∏å°—∫Õ—µ√“°“√µ“¬ ‚¥¬√«¡¢ÕߺªâŸ «É ¬75 ¥ß— ππ—È °“√µ¥—  π‘ „®«“à ®–„™ªâ √¡‘ “≥ dialysate calcium ‡∑“à ‰√§«√殑 “√≥“¥µŸ “¡§«“¡ ‡À¡“– ¡¢ÕߺªŸâ «É ¬·µ≈à –√“¬ °“√øÕ°‡≈◊Õ¥‡æ◊ËÕ¢®—¥øÕ ‡øµÕÕ°π—Èπ æ∫«à“øÕ ‡øµ®–∂Ÿ°¢—∫ÕÕ°®“° intravascular compartment¡“°„π™«à ß2™«—Ë ‚¡ß·√°¡ø’ Õ ‡øµ‡æ¬’ ß «à ππÕâ ¬∑∂’Ë °Ÿ ¢∫— ÕÕ°„π™«à ß‚¡ß ¥ÿ ∑“â ¬¥ß— ππ—È °“√∑” short daily hemodialysis ´÷Ë߇ªìπ∑’Ëπ‘¬¡¡“°¢÷Èπ„πµà“ߪ√–‡∑»¢≥–π’È ®÷ß “¡“√∂§«∫§ÿ¡√–¥—∫¢Õß øÕ ‡øµ‰¥¥â °’ «“à °“√∑” hemodialysis 2-3 §√ßÈ— µÕà  ª— ¥“À7å 6 PTHππ—È πÕ°®“°®–¡º’ ≈µÕà °“√∑”≈“¬°√–¥°Ÿ ·≈«â ¬ß— ¡§’ «“¡®”‡ªπì „π°“√ √“â ß°√–¥°Ÿ Õ°’ ¥«â ¬ ¥—ßπ—Èπ®÷ß®”‡ªìπ∑’Ë®–µâÕß√—°…“ PTH „ÀâÕ¬Ÿà„π√–¥—∫∑’ˇÀ¡“– ¡‡æ◊ËÕ§«“¡ ¡¥ÿ≈¢Õß°“√ √â“ß·≈– ∑”≈“¬°√–¥°Ÿ  ”À√∫— „πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß— ®“°°“√∑” bone biopsy „πºªâŸ «É ¬µ“à ߪ√–‡∑»æ∫«“à ºªŸâ «É ¬ ∑¡Ë’ √’ –¥∫— intact PTH πÕâ ¬°«“à 100 pg/ml ‡°Õ◊ ∫∑ßÈ— À¡¥®–¡’ bone histology ‡ªπì ·∫∫ adynamic bone „π¢≥–∑√Ë’ –¥∫— intact PTH √–À«“à ß 100-400 pg/ml bone histology Õ“®‡ªπì ‰¥∑â ßÈ— ª°µ,‘ osteitis fibrosa À√◊Õ adynamic bone ·≈–∂â“¡“°°«à“ 400 pg/ml  à«π¡“°®–¡’≈—°…≥–¢Õß osteitis fibrosa Õ¬à“߉√ °Áµ“¡„π√–¬–À≈—ßæ∫«à“¢Õߧ«“¡ —¡æ—π∏å√–À«à“ß√–¥—∫¢Õß PTH °—∫ bone histology ¡’§«“¡‰¡à ·ππà Õπ‡æ¡‘Ë ¡“°¢π÷È °«“à ·µ°à Õà π∑ß—È πÕ’È “®‡ªπì ‡æ√“–¬“∑„’Ë ™„â π°“√√°— …“¿“«–secondaryhyperparathyroidism ¡§’ «“¡À≈“°À≈“¬¡“°¢πÈ÷ ¡º’ ≈µÕà °“√‡ª≈¬Ë’ π·ª≈ߢÕß bone remodeling ¥ß— ππ—È °“√∑®Ë’ –«π‘ ®‘ ©¬— ¿“«– renal osteodystrophy „À‰â ¥·â ππà Õ𮔇ªπì ®–µÕâ ß∑” bone biopsy ‡∑“à ππ—È ·µ‡à πÕË◊ ß®“°°“√∑” bone biopsy ‡ªπì invasive procedure ‰¡‡à À¡“–∑®Ë’ –„™ â ”À√∫— routine diagnosis ¥ß— ππÈ— ‡√“®ß÷ ¬ß— µÕâ ßÕ“»¬— ¢Õâ ¡≈Ÿ ‡°“à Õ¬Ÿà ®“°°“√»°÷ …“æ∫«“à ºªâŸ «É ¬°≈¡àÿ ∑¡Ë’ √’ –¥∫— intact PTH Õ¬√àŸ –À«“à ß 150-300 pg/ml (2-3 ‡∑“à ¢Õß√–¥∫— ª°µ)‘ ¡’ bone formation rate „°≈‡â §¬’ ß°∫— ª°µ¡‘ “°∑ Ë’ ¥ÿ 77,78 ¥ß— ππÈ— „πµ“à ߪ√–‡∑»®ß÷ ·π–π”„À§â «∫§¡ÿ intact PTH „ÀâÕ¬Ÿà„π√–¥—∫¥—ß°≈à“«  “‡Àµÿ∑’Ë√–¥—∫π’È Ÿß°«à“ª°µ‘ 2-3 ‡∑à“‡ªìπ‡æ√“–ªí®®—¬µà“ßÊ „π√à“ß°“¬¢ÕߺŸâ ªÉ«¬∑”„À⇴≈≈å°√–¥°Ÿ ¡’°“√µÕ∫ πÕßµàÕ PTH ≈¥≈ß ªí®®—¬‡À≈à“π’ȉ¥â·°à °“√§—ËߢÕßøÕ ‡øµ, ¿“«– metabolic acidosis79, °“√§ßË— ¢Õß uremic toxins, §«“¡º¥‘ ª°µ¢‘ Õß vitamin D metabolism ·≈– °“√≈¥≈ß ¢Õß®”π«π PTH receptor80,81 ¥ß— ππÈ— √“à ß°“¬®ß÷ ®”‡ªπì µÕâ ßÕ“»¬— √–¥∫— ¢Õß PTH ∑ Ë’ ߟ ¢πÈ÷ ‡æÕË◊ √°— …“ bone remodeling „À‡â ªπì ª°µ‘ πÕ°®“°π¬È’ ß— æ∫«“à intact PTH assay ∑„Ë’ ™°â π— Õ¬“à ß·æ√Àà ≈“¬∑«Ë— ‚≈° πÕ°®“° ®–«¥— √–¥∫— full length-PTH (1-84, PTH ¡’ °√¥Õ–¡‚‘ π∑ßÈ— À¡¥ 84 µ«— ) Õ¬“à ß∑‡’Ë √“∑√“∫°π— ·≈«â ¬ß— ¡’ cross reactivity °∫— c-terminal fragments (7-84) ¢Õß PTH ´ß÷Ë  – ¡„πºªŸâ «É ¬‰µ«“¬‡√Õ◊È √ß— √–¬– ¥ÿ ∑“â ¬¥«â ¬ ∑”„À§â “à PTH ∑«Ë’ ¥— ‰¥®â “° intact PTH assay  ßŸ °«“à ∑§Ë’ «√®–‡ªπì ∂ß÷ 30-50%82,83 ·≈– c-terminal fragments PTH πÈ’ ¬ß— Õ“®¡º’ ≈µ“â π (antagonize) °“√ÕÕ°ƒ∑∏¢Ï‘ Õß full length-PTH Õ°’ ¥«â ¬84 ª®í ®¬— ¥ß— °≈“à « ßà ‡ √¡‘ „À√â –¥∫— intact PTH ∑‡Ë’ À¡“– ¡„πºªŸâ «É ¬‰µ«“¬‡√ÕÈ◊ √ß—  ßŸ °«“à §πª°µ‘ ·≈–°“√√°— …“„Àâ intact PTH Õ¬„àŸ π√–¥∫— ∑Ë’

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥‘…∞∫√√®ß 155 ‡À¡“– ¡‰¡µà ”Ë ®π‡°π‘ ‰ª®–™«à ¬ªÕÑ ß°π— °“√‡°¥‘ adynamic bone disease ‰¥â  ”À√∫— ¢Õâ ¡≈Ÿ ¢Õߧπ‰∑¬ æ∫«à“√–¥—∫ intact PTH ∑’Ë¡“°°«à“ 200 pg/ml  “¡“√∂∑”𓬰“√‡°‘¥ high bone turnover renal osteodystrophy ‰¥Õâ ¬“à ß¡§’ «“¡®”‡æ“–‡®“–®ß∂ß÷ 96%4 ´ßË÷ √–¥∫— ¥ß— °≈“à «µ”Ë °«“à „π°“√»°÷ …“¢Õßµ“à ß ª√–‡∑» De Boer ·≈–§≥–‰¥∑â ”°“√»°÷ …“√–¥∫— intact PTH „πºªŸâ «É ¬‰µ«“¬∑¡Ë’ ‡’ ™ÕÈ◊ ™“µµ‘ “à ßÊ°π— æ∫ «“à §π‡Õ‡™¬’ ¡√’ –¥∫— intact PTH µË”°«“à §πº«‘ ¥” §πº«‘ ¢“« ·≈–§π hispanic Õ¬“à ß¡π’ ¬—  ”§≠— 85 ‡πÕ◊Ë ß®“° ¬ß— ‰¡¡à °’ “√»°÷ …“√–¥∫— intact PTH ∑‡’Ë À¡“– ¡„π§π‰∑¬ ·≈–®“°¢Õâ ¡≈Ÿ ¥ß— °≈“à «· ¥ß„À‡â ÀπÁ «“à √–¥∫— intact PTH ∑‡’Ë À¡“– ¡„π§π‰∑¬À√Õ◊ §π‡Õ‡™¬’ π“à ®–µË”°«“à „πµ“à ߪ√–‡∑» º‡Ÿâ ¢¬’ π®ß÷ ·π–π”„À√â °— …“√–¥∫— intact PTH ‰«∑â √Ë’ –¥∫— µ”Ë °«“à „πµ“à ߪ√–‡∑»‡≈°Á πÕâ ¬§Õ◊ 150-250 pg/ml* (µ“√“ß∑Ë’ 1)  ¥ÿ ∑“â ¬π„’È πºªâŸ «É ¬∑¡’Ë ¿’ “«– secondary hyperparathyroidism ¡“‡ªπì ‡«≈“π“π ®π°≈“¬‡ªπì tertiary hyperparathyroidism ∑‰Ë’ ¡µà Õ∫ πÕßµÕà °“√√°— …“µ“à ßÊ ¥ß— ∑‰Ë’ ¥°â ≈“à «¡“·≈«â ∑“߇≈Õ◊ ° ¥ÿ ∑“â ¬§Õ◊ °“√∑” parathyroidectomy °“√ºà“µ—¥µàÕ¡æ“√“‰∏√Õ¬¥å‡ªìπ°“√ºà“µ—¥∑’˧àÕπ¢â“߬“° µâÕßÕ“»—¬»—≈¬·æ∑¬å∑’Ë¡’ ª√– ∫°“√≥·å ≈–§«“¡™”π“≠ πÕ°®“°º≈¢“â ߇§¬’ ß∑“ß°“√º“à µ¥— ‡™πà recurrent laryngeal nerve palsy ·≈«â °“√∑µ’Ë Õà ¡æ“√“‰∏√Õ¬¥∂å °Ÿ µ¥— ÕÕ°‰ª∑π— ∑∑’ π— „¥ ∑”„Àâ PTH ¡√’ –¥∫— ≈¥µË”≈ßÕ¬“à ß¡“°„π‡«≈“Õπ—  π—È Õ“®∑”„À√â “à ß°“¬ª√∫— µ«— ‰¡∑à π— ·≈–‡°¥‘ ¿“«– hungry bone syndrome µ“¡¡“  “‡Àµ¢ÿ Õß hungry bone syndrome ‡°‘¥®“°°“√∑’Ë·§≈‡´’¬¡·≈–øÕ ‡øµ„π°√–· ‡≈◊Õ¥°≈—∫‡¢â“ àŸ°√–¥Ÿ°Õ¬à“ß√«¥‡√Á« ∑”„Àâ ·§≈‡´’¬¡·≈–øÕ ‡øµ„π‡≈◊Õ¥¡’√–¥—∫µË”≈ß „π√–¬–À≈—߉¥â¡’°“√欓¬“¡√—°…“¿“«– tertiary hyperparathyroidism ‚¥¬°“√©¥’ ·Õ≈°ÕŒÕ≈å (ethanol) ‡¢“â ‰ª„πµÕà ¡æ“√“‰∏√Õ¬¥å (percutaneous ethanol injection therapy (PEIT)) ‡æÕË◊ ∑”≈“¬µÕà ¡æ“√“‰∏√Õ¬¥·å ∫∫™“â Ê ·∑π°“√∑” surgical parathyroidectomy °“√»°÷ …“„πª√–‡∑»≠ª’Ë πÿÉ æ∫«“à ‰¥ºâ ≈§Õà π¢“â ߥ8’ 6 ·≈–¡º’ ≈¢“â ߇§¬’ ßπÕâ ¬ ·µ¡à °— ®–µÕâ ß©¥’ ¡“°°«“à 1 §√ß—È ¢πÈ÷ ‰ª °“√µ¥‘ µ“¡º≈„π√–¬–¬“«À≈ß— 3 ªæï ∫«“à  “¡“√∂√°— …“√–¥∫— PTH ‰«‰â ¥„â π‡°≥±∑å ‡Ë’ À¡“– ¡‰¥8â 7 µ“√“ß∑’Ë 1 ‡°≥±·å ≈–§«“¡∂„Ë’ π°“√µ√«®·§≈‡´¬’ ¡ øÕ ‡øµ ·≈– PTH „πºªâŸ «É ¬‰µ«“¬ CKD stage 5 √–¥∫— ∑‡Ë’ À¡“– ¡ §«“¡∂¢Ë’ Õß°“√µ√«® Serum calcium 8.4-9.5 mg/dL ∑°ÿ ‡¥Õ◊ π Serum phosphorus 3.5-5.5 mg/dL ∑°ÿ ‡¥Õ◊ π Ca x PO4 product < 55 mg2/dL2 ∑°ÿ 3 ‡¥Õ◊ π PTH ∑°ÿ 3 ‡¥Õ◊ π 150-300 pg/mL* ¥—¥·ª≈ß¡“®“° K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease

New Frontiers in Dialysis 156 ∏π‘µ ®√‘ ππ— ∑∏å «™—  √‘ ¿‘ “ ™“â ß»√‘ °‘ ÿ≈™¬— ∏π—𥓠µ√–°“√«π‘™ « —πµå  ‡ÿ ¡∏°≈ÿ 5.  √ªÿ ¿“«– secondary hyperparathyroidism ‡°‘¥®“°°“√§—ËߢÕßøÕ ‡øµ °“√¢“¥ calcitriol ·≈– ·§≈‡´¬’ ¡„π‡≈Õ◊ ¥¡√’ –¥∫— µ”Ë  ßà º≈„À¡â °’ “√°√–µπâÿ °“√À≈ßË— PTH ∑”„À‡â °¥‘ ¿“«– high bone turnover renal osteodystrophy °“√√°— …“§«√∑”·µ‡à ππË‘ Ê ‡æÕË◊ ≈¥°“√‡°¥‘ parathyroid gland hyperplasia ·≈– parathyroid adenoma ´ß÷Ë ®–∑”„À°â “√µÕ∫ πÕßµÕà °“√√°— …“≈¥≈ß °“√§«∫§¡ÿ Õ“À“√∑¡’Ë ø’ Õ ‡øµ ßŸ °“√„Àâ phosphate binders ·≈– active vitamin D  “¡“√∂™«à ¬§«∫§¡ÿ √–¥∫— ¢ÕßøÕ ‡øµ ·≈– PTH ‰¥â ·µÕà ¬“à ߉√°µÁ “¡ º≈¢â“߇§’¬ß∑’ˇ°‘¥¢÷Èπ®“°√—°…“∑’Ë¡“°®π‡°‘π‰ªÕ“®∑”„À⇰‘¥ adynamic bone disease ‰¥â °“√√—∫ ª√–∑“π·§≈‡´¬’ ¡ ·≈– °“√‰¥√â ∫— «µ‘ “¡π‘ ¥„’ πª√¡‘ “≥∑ Ë’ ߟ ¬ß— ¡º’ ≈∑”„À‡â °¥‘ vascular calcification ´ßË÷ ¿“«–¥ß— °≈“à «¡§’ «“¡ ¡— æπ— ∏°å ∫— cardiovascular mortality ´ß÷Ë ‡ªπì  “‡Àµ°ÿ “√µ“¬∑¡’Ë “°∑ ’Ë ¥ÿ „πºªâŸ «É ¬°≈¡ÿà π’È ‡Õ° “√Õ“â ßÕß‘ 1. Ganesh SK, Stack AG, Levin NW, Hulbert-Shearon T, Port FK. Association of elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol. 2001;12:2131-8. 2. Jono S, McKee MD, Murry CE, Shioi A, Nishizawa Y, Mori K, et al. Phosphate regulation of vascular smooth muscle cell calcification. Circ Res. 2000;87:E10-7. 3. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med. 2000;342:1478-83. 4. Changsirikulchai S, Domrongkitchaiporn S, Sirikulchayanonta V, Ongphiphadhanakul B, Kunkitti N, Stitchantrakul W, et al. Renal osteodystrophy in Ramathibodi Hospital: histomorphometry and clinical correlation. J Med Assoc Thai. 2000;83:1223-32. 5. Torres A, Lorenzo V, Hernandez D, Rodriguez JC, Concepcion MT, Rodriguez AP, et al. Bone disease in predialysis, hemodialysis, and CAPD patients: evidence of a better bone response to PTH. Kidney Int. 1995;47:1434-42. 6. Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis. 2000;36:1115-21. 7. Kempson SA, Lotscher M, Kaissling B, Biber J, Murer H, Levi M. Parathyroid hormone action on phosphate transporter mRNA and protein in rat renal proximal tubules. Am J Physiol. 1995;268(4 Pt 2):F784-91. 8. Goodman WG. Renal Osteodystrophy in Adults and Children. In: Favus MJ, editor. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 3 ed. Chicago: Lippincott-Raven; 1996. p. 341-52. 9. Brown AJ, Dusso A, Lopez-Hilker S, Lewis-Finch J, Grooms P, Slatopolsky E. 1,25-(OH)2D receptors are decreased in parathyroid glands from chronically uremic dogs. Kidney Int. 1989;35:19-23. 10. Tokumoto M, Tsuruya K, Fukuda K, Kanai H, Kuroki S, Hirakata H. Reduced p21, p27 and vitamin D receptor in the nodular hyperplasia in patients with advanced secondary hyperparathyroidism. Kidney Int. 2002;62:1196- 207.

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥…‘ ∞∫√√®ß 157 11. Gogusev J, Duchambon P, Hory B, Giovannini M, Goureau Y, Sarfati E, et al. Depressed expression of calcium receptor in parathyroid gland tissue of patients with hyperparathyroidism. Kidney Int. 1997;51:328- 36. 12. Burnett SA, Gunawardene SC, Bringhurst FR, Juppner H, Lee H, Finkelstein JS. Regulation of C-terminal and intact FGF-23 by dietary phosphate in men and women. Journal of Bone & Mineral Research. 2006;21:1187- 96. 13. Larsson T, Nisbeth U, Ljunggren O, Juppner H, Jonsson KB. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int. 2003;64:2272-9. 14. Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. Journal of Bone & Mineral Research. 2004;19:429-35. 15. Gutierrez O, Isakova T, Rhee E, Shah A, Holmes J, Collerone G, et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol. 2005;16:2205-15. 16. Slatopolsky E, Caglar S, Pennell JP, Taggart DD, Canterbury JM, Reiss E, et al. On the pathogenesis of hyperparathyroidism in chronic experimental renal insufficiency in the dog. J Clin Invest. 1971;50:492-9. 17. Slatopolsky E, Finch J, Denda M, Ritter C, Zhong M, Dusso A, et al. Phosphorus restriction prevents parathyroid gland growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest. 1996;97:2534-40. 18. Naveh-Many T, Rahamimov R, Livni N, Silver J. Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D. J Clin Invest. 1995 ;96:1786-93. 19. Ritter CS, Martin DR, Lu Y, Slatopolsky E, Brown AJ. Reversal of secondary hyperparathyroidism by phosphate restriction restores parathyroid calcium-sensing receptor expression and function. J Bone Miner Res. 2002;17:2206-13. 20. Martin-Malo A, Rodriguez M, Martinez ME, Torres A, Felsenfeld AJ. The interaction of PTH and dietary phosphorus and calcium on serum calcitriol levels in the rat with experimental renal failure. Nephrol Dial Transplant. 1996;11:1553-8. 21. Holick MF. Vitamin D: Photobiology, Metabolism, Mechanism of Action, and Clinical Applications. In: Favus MJ, editor. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 3 ed. Chicago: Lippincott-Raven; 1996. p. 74. 22. Slatopolsky E, Weerts C, Thielan J, Horst R, Harter H, Martin KJ. Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients. J Clin Invest. 1984;74:2136-43. 23. Slatopolsky E, Lopez-Hilker S, Delmez J, Dusso A, Brown A, Martin KJ. The parathyroid-calcitriol axis in health and chronic renal failure. Kidney Int Suppl. 1990;29:S41-7. 24. Silver J, Naveh-Many T, Mayer H, Schmelzer HJ, Popovtzer MM. Regulation by vitamin D metabolites of

New Frontiers in Dialysis 158 ∏π‘µ ®‘√ππ— ∑∏å «™—  ‘√¿‘ “ ™“â ß»√‘ ‘°≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°≈ÿ parathyroid hormone gene transcription in vivo in the rat. J Clin Invest. 1986;78:1296-301. 25. Naveh-Many T, Marx R, Keshet E, Pike JW, Silver J. Regulation of 1,25-dihydroxyvitamin D3 receptor gene expression by 1,25-dihydroxyvitamin D3 in the parathyroid in vivo. J Clin Invest. 1990;86:1968-75. 26. Denda M, Finch J, Brown AJ, Nishii Y, Kubodera N, Slatopolsky E. 1,25-dihydroxyvitamin D3 and 22- oxacalcitriol prevent the decrease in vitamin D receptor content in the parathyroid glands of uremic rats. Kidney Int. 1996;50:34-9. 27. Brown AJ, Zhong M, Finch J, Ritter C, McCracken R, Morrissey J, et al. Rat calcium-sensing receptor is regulated by vitamin D but not by calcium. Am J Physiol. 1996;270(3 Pt 2):F454-60. 28. Andress DL, Norris KC, Coburn JW, Slatopolsky EA, Sherrard DJ. Intravenous calcitriol in the treatment of refractory osteitis fibrosa of chronic renal failure. N Engl J Med. 1989; 321:274-9. 29. Gonzalez EA, Sachdeva A, Oliver DA, Martin KJ. Vitamin D insufficiency and deficiency in chronic kidney disease. A single center observational study. Am J Nephrol. 2004;24:503-10. 30. Russell J, Bar A, Sherwood LM, Hurwitz S. Interaction between calcium and 1,25-dihydroxyvitamin D3 in the regulation of preproparathyroid hormone and vitamin D receptor messenger ribonucleic acid in avian parathyroids. Endocrinology. 1993;132:2639-44. 31. Lopez I, Aguilera-Tejero E, Felsenfeld AJ, Estepa JC, Rodriguez M. Direct effect of acute metabolic and respiratory acidosis on parathyroid hormone secretion in the dog. J Bone Miner Res. 2002;17:1691-700. 32. Movilli E, Zani R, Carli O, Sangalli L, Pola A, Camerini C, et al. Direct effect of the correction of acidosis on plasma parathyroid hormone concentrations, calcium and phosphate in hemodialysis patients: a prospective study. Nephron. 2001;87:257-62. 33. Disthabanchong S, Martin KJ, McConkey CL, Gonzalez EA. Metabolic acidosis up-regulates PTH/PTHrP receptors in UMR 106-01 osteoblast-like cells. Kidney Int. 2002;62: 1171-7. 34. Elder G. Pathophysiology and recent advances in the management of renal osteodystrophy. J Bone Miner Res. 2002;17:2094-105. 35. Ramirez JA, Emmett M, White MG, Fathi N, Santa Ana CA, Morawski SG, et al. The absorption of dietary phosphorus and calcium in hemodialysis patients. Kidney Int. 1986; 30:753-9. 36. Spiegel DM, Raggi P, Smits G, Block GA. Factors associated with mortality in patients new to haemodialysis. Nephrol Dial Transplant. 2007;22:3568-72. 37. Moriniere P, Djerad M, Boudailliez B, el Esper N, Boitte F, Westeel PF, et al. Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia. Nephron. 1992;60:6-11. 38. Almirall J, Veciana L, Llibre J. Calcium acetate versus calcium carbonate for the control of serum phosphorus in hemodialysis patients. Am J Nephrol. 1994;14:192-6. 39. Ben Hamida F, el Esper I, Compagnon M, Moriniere P, Fournier A. Long-term (6 months) cross-over comparison of calcium acetate with calcium carbonate as phosphate binder. Nephron. 1993;63:258-62. 40. Delmez JA, Tindira CA, Windus DW, Norwood KY, Giles KS, Nighswander TL, et al. Calcium acetate as a

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  π‘ ’ ¥…‘ ∞∫√√®ß 159 phosphorus binder in hemodialysis patients. J Am Soc Nephrol. 1992; 3:96-102. 41. Touam M, Martinez F, Lacour B, Bourdon R, Zingraff J, Di Giulio S, et al. Aluminium-induced, reversible microcytic anemia in chronic renal failure: clinical and experimental studies. Clin Nephrol. 1983;19:295-8. 42. Alfrey AC, LeGendre GR, Kaehny WD. The dialysis encephalopathy syndrome. Possible aluminum intoxication. N Engl J Med. 1976;294:184-8. 43. Finn WF, Joy MS, Hladik G. Efficacy and safety of lanthanum carbonate for reduction of serum phosphorus in patients with chronic renal failure receiving hemodialysis. Clin Nephrol. 2004;62:193-201. 44. Al-Baaj F, Speake M, Hutchison AJ. Control of serum phosphate by oral lanthanum carbonate in patients undergoing haemodialysis and continuous ambulatory peritoneal dialysis in a short-term, placebo-controlled study. Nephrol Dial Transplant. 2005;20:775-82. 45. DûHaese PC, Spasovski GB, Sikole A, Hutchison A, Freemont TJ, Sulkova S, et al. A multicenter study on the effects of lanthanum carbonate (Fosrenol) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int Suppl. 2003;85:S73-8. 46. Lacour B, Lucas A, Auchere D, Ruellan N, de Serre Patey NM, Drueke TB. Chronic renal failure is associated with increased tissue deposition of lanthanum after 28-day oral administration. Kidney Int. 2005;67:1062-9. 47. Ben-Dov IZ, Pappo O, Sklair-Levy M, Galitzer H, Ilan Y, Naveh-Many T, et al. Lanthanum carbonate decreases PTH gene expression with no hepatotoxicity in uraemic rats. Nephrol Dial Transplant. 2007;22:362-8. 48. Altmann P, Barnett ME, Finn WF. Cognitive function in Stage 5 chronic kidney disease patients on hemodialysis: no adverse effects of lanthanum carbonate compared with standard phosphate-binder therapy. Kidney Int. 2007;71:252-9. 49. Chertow GM, Burke SK, Raggi P. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int. 2002;62:245-52. 50. Russo D, Miranda I, Ruocco C, Battaglia Y, Buonanno E, Manzi S, et al. The progression of coronary artery calcification in predialysis patients on calcium carbonate or sevelamer. Kidney Int. 2007;72:1255-61. 51. Block GA, Raggi P, Bellasi A, Kooienga L, Spiegel DM. Mortality effect of coronary calcification and phosphate binder choice in incident hemodialysis patients. Kidney Int. 2007;71:438-41. 52. Suki WN, Zabaneh R, Cangiano JL, Reed J, Fischer D, Garrett L, et al. Effects of sevelamer and calcium- based phosphate binders on mortality in hemodialysis patients. Kidney Int. 2007;72:1130-7. 53. Qunibi WY, Hootkins RE, McDowell LL, Meyer MS, Simon M, Garza RO, et al. Treatment of hyperphosphatemia in hemodialysis patients: The Calcium Acetate Renagel Evaluation (CARE Study). Kidney Int. 2004;65:1914- 26. 54. Brezina B, Qunibi WY, Nolan CR. Acid loading during treatment with sevelamer hydrochloride: mechanisms and clinical implications. Kidney Int Suppl. 2004 Sep(90):S39-45. 55. Baker LR, Abrams SM, Roe CJ, Faugere MC, Fanti P, Subayti Y, et al. Early therapy of renal bone disease with calcitriol: a prospective double-blind study. Kidney Int Suppl. 1989;27:S140-2. 56. Hamdy NA, Kanis JA, Beneton MN, Brown CB, Juttmann JR, Jordans JG, et al. Effect of alfacalcidol on

New Frontiers in Dialysis 160 ∏π‘µ ®‘√π—π∑∏å «—™  ‘√‘¿“ ™â“ß»‘√°‘ ≈ÿ ™¬— ∏π—𥓠µ√–°“√«π‘™ « —πµå  ‡ÿ ¡∏°≈ÿ natural course of renal bone disease in mild to moderate renal failure. Bmj. 1995;310:358-63. 57. Gu Y, Ding F, Chen N, Mei CL, Qian JQ, Wang XY, et al. Comparisons between oral pulse alfacalcidol therapy and daily therapy in maintenance hemodialysis patients with secondary hyperparathyroidism: a randomized, controlled, and multicenter study. Ren Fail. 2005;27:205-12. 58. Cardus A, Panizo S, Parisi E, Fernandez E, Valdivielso JM. Differential effects of vitamin D analogs on vascular calcification. J Bone Miner Res. 2007;22:860-6. 59. Mizobuchi M, Finch JL, Martin DR, Slatopolsky E. Differential effects of vitamin D receptor activators on vascular calcification in uremic rats. Kidney Int. 2007;72:709-15. 60. Teng M, Wolf M, Ofsthun MN, Lazarus JM, Hernan MA, Camargo CA, Jr., et al. Activated injectable vitamin D and hemodialysis survival: a historical cohort study. J Am Soc Nephrol. 2005;16:1115-25. 61. Shoji T, Shinohara K, Kimoto E, Emoto M, Tahara H, Koyama H, et al. Lower risk for cardiovascular mortality in oral 1alpha-hydroxy vitamin D3 users in a haemodialysis population.[see comment]. Nephrology Dialysis Transplantation. 2004;19:179-84. 62. Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med. 2003;349:446-56. 63. Tentori F, Hunt WC, Stidley CA, Rohrscheib MR, Bedrick EJ, Meyer KB, et al. Mortality risk among hemodialysis patients receiving different vitamin D analogs. Kidney Int. 2006;70:1858-65. 64. Wolf M, Shah A, Gutierrez O, Ankers E, Monroy M, Tamez H, et al. Vitamin D levels and early mortality among incident hemodialysis patients. Kidney Int. 2007;72:1004-13. 65. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest. 2002;110:229-38. 66. Levi R, Ben-Dov IZ, Lavi-Moshayoff V, Dinur M, Martin D, Naveh-Many T, et al. Increased Parathyroid Hormone Gene Expression in Secondary Hyperparathyroidism of Experimental Uremia Is Reversed by Calcimimetics: Correlation with Posttranslational Modification of the Trans Acting Factor AUF1. J Am Soc Nephrol. 2006;17:107-12. 67. Block GA, Martin KJ, de Francisco AL, Turner SA, Avram MM, Suranyi MG, et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med. 2004;350:1516-25. 68. Henley C, Colloton M, Cattley RC, Shatzen E, Towler DA, Lacey D, et al. 1,25-Dihydroxyvitamin D3 but not cinacalcet HCl (Sensipar/Mimpara) treatment mediates aortic calcification in a rat model of secondary hyperparathyroidism.[see comment]. Nephrology Dialysis Transplantation. 2005;20:1370-7. 69. Leca N, Laftavi M, Gundroo A, Kohli R, Min I, Karam J, et al. Early and severe hyperparathyroidism associated with hypercalcemia after renal transplant treated with cinacalcet. American Journal of Transplantation. 2006;6:2391-5. 70. Serra AL, Savoca R, Huber AR, Hepp U, Delsignore A, Hersberger M, et al. Effective control of persistent hyperparathyroidism with cinacalcet in renal allograft recipients. Nephrology Dialysis Transplantation. 2007;22:577-83.

Hyperphosphatemia and Hyperparathyroidism in Hemodialysis  ‘π’ ¥‘…∞∫√√®ß 161 71. Chertow GM, Pupim LB, Block GA, Correa-Rotter R, Drueke TB, Floege J, et al. Evaluation of Cinacalcet Therapy to Lower Cardiovascular Events (EVOLVE): rationale and design overview. Clinical Journal of The American Society of Nephrology: CJASN. 2007;2:898-905. 72. van Kuijk WH, Mulder AW, Peels CH, Harff GA, Leunissen KM. Influence of changes in ionized calcium on cardiovascular reactivity during hemodialysis. Clinical Nephrology. 1997;47:190-6. 73. van der Sande FM, Cheriex EC, van Kuijk WH, Leunissen KM. Effect of dialysate calcium concentrations on intradialytic blood pressure course in cardiac-compromised patients. American Journal of Kidney Diseases. 1998;32:125-31. 74. Yamada K, Fujimoto S, Nishiura R, Komatsu H, Tatsumoto M, Sato Y, et al. Risk factors of the progression of abdominal aortic calcification in patients on chronic haemodialysis. Nephrol Dial Transplant. 2007;22:2032- 7. 75. Young EW, Albert JM, Satayathum S, Goodkin DA, Pisoni RL, Akiba T, et al. Predictors and consequences of altered mineral metabolism: the Dialysis Outcomes and Practice Patterns Study. Kidney Int. 2005;67:1179- 87. 76. Achinger SG, Ayus JC. The role of daily dialysis in the control of hyperphosphatemia. Kidney Int Suppl. 2005 Jun(95):S28-32. 77. Wang M, Hercz G, Sherrard DJ, Maloney NA, Segre GV, Pei Y. Relationship between intact 1-84 parathyroid hormone and bone histomorphometric parameters in dialysis patients without aluminum toxicity. Am J Kidney Dis. 1995;26:836-44. 78. Qi Q, Monier-Faugere MC, Geng Z, Malluche HH. Predictive value of serum parathyroid hormone levels for bone turnover in patients on chronic maintenance dialysis. Am J Kidney Dis. 1995;26:622-31. 79. Drueke TB. Abnormal skeletal response to parathyroid hormone and the expression of its receptor in chronic uremia. Pediatr Nephrol. 1996;10:348-50. 80. Picton ML, Moore PR, Mawer EB, Houghton D, Freemont AJ, Hutchison AJ, et al. Down-regulation of human osteoblast PTH/PTHrP receptor mRNA in end-stage renal failure. Kidney Int. 2000;58:1440-9. 81. Disthabanchong S, Hassan H, McConkey CL, Martin KJ, Gonzalez EA. Regulation of PTH1 receptor expression by uremic ultrafiltrate in UMR 106-01 osteoblast-like cells. Kidney Int. 2004;65:897-903. 82. Lepage R, Roy L, Brossard JH, Rousseau L, Dorais C, Lazure C, et al. A non-(1-84) circulating parathyroid hormone (PTH) fragment interferes significantly with intact PTH commercial assay measurements in uremic samples. Clin Chem. 1998;44:805-9. 83. Gao P, Scheibel S, DûAmour P, John MR, Rao SD, Schmidt-Gayk H, et al. Development of a novel immunoradiometric assay exclusively for biologically active whole parathyroid hormone 1-84: implications for improvement of accurate assessment of parathyroid function. J Bone Miner Res. 2001;16:605-14. 84. Slatopolsky E, Finch J, Clay P, Martin D, Sicard G, Singer G, et al. A novel mechanism for skeletal resistance in uremia. Kidney Int. 2000;58:753-61. 85. De Boer IH, Gorodetskaya I, Young B, Hsu CY, Chertow GM. The severity of secondary hyperparathyroidism

New Frontiers in Dialysis 162 ∏π‘µ ®√‘ π—π∑∏å «—™  ‘√¿‘ “ ™“â ß»‘√‘°ÿ≈™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ‡ÿ ¡∏°≈ÿ in chronic renal insufficiency is GFR-dependent, race-dependent, and associated with cardiovascular disease. J Am Soc Nephrol. 2002;13:2762-9. 86. Kakuta T, Fukagawa M, Fujisaki T, Hida M, Suzuki H, Sakai H, et al. Prognosis of parathyroid function after successful percutaneous ethanol injection therapy guided by color Doppler flow mapping in chronic dialysis patients. Am J Kidney Dis. 1999;33:1091-9. 87. Tanaka R, Kakuta T, Fujisaki T, Tanaka S, Sakai H, Kurokawa K, et al. Long-term (3 years) prognosis of parathyroid function in chronic dialysis patients after percutaneous ethanol injection therapy guided by colour Doppler ultrasonography. Nephrol Dial Transplant. 2003;18 Suppl 3:III58-III61.

9 Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π™‘ 1. ∫∑π” 2. ∑¡’Ë “ 3. ™π¥‘ ¢Õß Daily dialysis 4. Urea kinetic ·≈– dose ¢Õß daily dialysis 5. Standard Kt/V „π daily dialysis 6. °“√§”π«≥§“à Standard Kt/V 7. Standard Kt/V model 8. ¢Õâ ¥¢’ Õß Short daily hemodialysis 9. º≈µÕà  ¿“«–‚¿™π“°“√ 10. °“√§«∫§¡ÿ ª√¡‘ “µ√ “√π”È ·≈–§«“¡¥π— ‚≈Àµ‘ 11. Calcium-phosphorus balance 12. Model ¢Õß phosphate balance in daily dialysis 13. °“√¢∫— Middle molecules 14. ¿“«–´¥’ 15. Vascular access 16. Hospitalization 17. §≥ÿ ¿“晫’ µ‘ 18. ¢Õâ ®”°¥— ¢Õß Daily dialysis 19.  √ªÿ

New Frontiers in Dialysis 164 ∏π‘µ ®√‘ π—π∑∏å «™—  √‘ ¿‘ “ ™â“ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°ÿ≈ 1. ∫∑π” ª®í ®∫ÿ π— °“√∫”∫¥— √°— …“∑¥·∑π‰µ‚¥¬∑«Ë— ‰ª®–„™«â ∏‘ ø’ Õ°‡≈Õ◊ ¥ ª— ¥“À≈å – 3 §√ßÈ— ·≈–¡°— ∑”„π »Ÿπ¬åøÕ°‰µÀ√◊Õ„π‚√ß欓∫“≈ Õ¬à“߉√°Á¥’æ∫«à“°“√øÕ°‡≈◊Õ¥¥â«¬«‘∏’π’ȉ¡à‰¥â¢®—¥¢Õ߇ ’¬Õ¬à“ߥ’æÕ ‡æ√“–¢Õ߇ ¬’ „π√“à ß°“¬∂°Ÿ º≈µ‘ ¢π÷È Õ¬“à ßµÕà ‡πÕ◊Ë ßµ≈Õ¥‡«≈“¥ß— ππ—È æ∫«“à ºªâŸ «É ¬‰µ«“¬‡√Õ◊È √ß— √–¬– ¥ÿ ∑“â ¬ (End stage renal disease, ESRD) ®–¡§’ ≥ÿ ¿“晫’ µ‘ ¥Õâ ¬°«“à ª°µ‘ ·≈–¡™’ «’ µ‘ ‡©≈¬Ë’ Õ¬‰àŸ ¥πâ “π 5 ª‡ï ∑“à ππÈ— 1 ´÷Ëßπ—∫«à“πâÕ¬°«à“ºŸâ∑’ˇªìπ¡–‡√ÁߢÕß≈”‰ â„À≠à πÕ°®“°π—Èπ°“√øÕ°‡≈◊Õ¥·∫∫§√—Èߧ√“« (Intermittent hemodialysis, IHD) ®–∑”„À√â –¥∫— ¢Õß solute ·≈– “√π”È „π√“à ß°“¬·°«ßà ¢πÈ÷ ≈ßÕ¬“à ß√«¥‡√«Á °Õà „À‡â °¥‘ Õπ— µ√“¬¡“°¢π÷È 2 ¥ß— ππ—È ®ß÷ ‰¥¡â °’ “√欓¬“¡¥¥— ·ª≈ß·°‰â ¢¢∫«π°“√øÕ°‡≈Õ◊ ¥·∫∫‡¥¡‘ ‚¥¬°≈¡ÿà ¢Õß Tassin ‰¥‡â æ¡Ë‘ ®”π«π™«Ë— ‚¡ß¢Õß°“√øÕ°‡≈Õ◊ ¥®“°§√ßÈ— ≈– 4 ™«Ë— ‚¡ß‡ªπì 8 ™«Ë— ‚¡ß  ª— ¥“À≈å – 3 §√ßÈ— 3 æ∫«“à ∑”„Àâ °“√§«∫§¡ÿ §«“¡¥π— ‚≈Àµ‘ ¥¢’ πÈ÷ ·≈–Õµ— √“µ“¬≈¥≈ß ‡¡ÕË◊ ‡∑¬’ ∫°∫— ºªŸâ «É ¬∑øË’ Õ°‡≈Õ◊ ¥¥«â ¬«∏‘ ‡’ ¥¡‘ Pierratos ·≈–§≥–4‰¥∑â ¥≈Õß‡æ¡‘Ë §«“¡∂¢’Ë Õß°“√øÕ°‡≈Õ◊ ¥´ß÷Ë ®“°√“¬ß“πÀ≈“¬√“¬ß“πµÕà ¡“‰¥æâ ∫«“à ¡¢’ Õâ ¥¢’ Õß metabolic control À≈“¬ª√–°“√ ‡™àπ ¿“«–´’¥ ·√à∏“µÿ ·§≈‡´’¬¡ øÕ øÕ√—  °“√¢®—¥¢Õ߇ ’¬ §à“ §«“¡‡¢¡â ¢πâ ‡≈Õ◊ ¥ ·≈–√–¥∫— B2 microglobulin ∑”„À§â «∫§¡ÿ §«“¡¥π— ‚≈Àµ‘ ¥¢’ πÈ÷ ·≈–∑“â ¬∑ Ë’ ¥ÿ §≥ÿ ¿“æ ™«’ µ‘ ‚¥¬√«¡¥¢’ π÷È 5 ®ß÷ ‰¥¡â º’ ÀâŸ π— ¡“ π„®‡∑§π§‘ °“√øÕ°‡≈Õ◊ ¥„À∂⠢˒ πÈ÷ ‡æ¡Ë‘ ¢πÈ÷ Õ¬“à ߉√°¥Á √’ “¬ß“π «à π„À≠à ¬—߉¡à‰¥â¡’°≈ÿࡧ«∫§ÿ¡·≈–‰¡à‰¥â√–∫ÿ‡«≈“∑’Ë„™â„π°“√øÕ°‡≈◊Õ¥Õ¬à“ß·πà™—¥  à«π„À≠à®–‡æ‘Ë¡§«“¡∂’Ë¢Õß °“√øÕ°‡≈Õ◊ ¥‚¥¬∑®’Ë ”π«π™«—Ë ‚¡ßµÕà  ª— ¥“À¬å ß— §ß∑’Ë ´ß÷Ë ‡ªπì ∑¡’Ë “¢Õߧ”«“à Short daily hemodialysis (SDHD) 2. ∑¡’Ë “ „π™«à ß 18 ª∑ï ºË’ “à π¡“ ¡√’ “¬ß“πæ∫°“√∑” SDHD „πºªŸâ «É ¬ª√–¡“≥ 150 √“¬ ‚¥¬øÕ°‡≈Õ◊ ¥ ∑°ÿ «π— 5-6 §√ß—È / ª— ¥“Àå ·µ®à ”π«πºªŸâ «É ¬„π·µ≈à –·Àßà ∑„Ë’ ™«â ∏‘ π’ ¡È’ ‰’ ¡¡à “° ª√–¡“≥ 7-10 √“¬/·Àßà 6 ·≈–º≈ ¢Õß·µà≈–·Ààß¡—°√“¬ß“πæ∫«à“ ºâŸªÉ«¬¡’§«“¡ ÿ¢ ∫“¬¡“°¢÷Èπ √—∫ª√–∑“πÕ“À“√‰¥â‡æ‘Ë¡¢÷È𠧫∫§ÿ¡ §«“¡¥π— ‚≈Àµ‘ ‰¥¥â ¢’ πÈ÷ §≥ÿ ¿“晫’ µ‘ ¥¢’ πÈ÷ ≈¥√–¥∫— øÕ øÕ√ — ·≈– β2-microglobulin ‰¥‡â æ¡Ë‘ ¢πÈ÷ ∂ß÷ 4 ‡∑“à ¢≥–πÕ’È ß§°å √ The National Institute of Diabetes and Kidney Disease (NIDDK) °”≈ß— ®–‡√¡‘Ë ∑”°“√»°÷ …“·∫∫ prospective multicenter ¢Õß°“√øÕ°‡≈Õ◊ ¥·∫∫ daily dialysis πÕÈ’ ¬7Ÿà 3. ™π¥‘ ¢Õß Daily dialysis ·∫ßà ™π¥‘ ¢Õß daily dialysis ‰¥‡â ªπì 1. ™π¥‘ ∑∑Ë’ ”‡«≈“ πÈ— (short treatment time) ‚¥¬„™‡â «≈“‰¡‡à °π‘ 2 ™«Ë— ‚¡ß/§√ßÈ— ¡°— ∑”„π»πŸ ¬å øÕ°‡≈Õ◊ ¥À√Õ◊ „π‚√ß欓∫“≈ ‡™πà „πª√–‡∑»·∂∫Õ‡¡√°‘ “‡ÀπÕ◊ 2. ™π¥‘ ∑∑Ë’ ”‡«≈“¬“« (long treatment time) ¡°— ∑”‡«≈“°≈“ߧπ◊ ‡©≈¬Ë’ 7 ™«Ë— ‚¡ß ‡√¬’ °Õ°’

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏π—𥓠µ√–°“√«π™‘ 165 ™ÕË◊ ÀπßË÷ «“à Long nighttime hemodialysis (LNHD) À√Õ◊ nocturnal home HD ‡πÕË◊ ß®“°∑”‡ªπì √–¬–‡«≈“π“π ®÷ßµâÕß∑”µÕπ°≈“ߧ◊π‡¡◊ËÕºŸâªÉ«¬πÕπÀ≈—∫·≈–∑”∑’Ë∫â“𠇙àπ„πª√–‡∑»·∂∫¬ÿ‚√ª æ∫«à“„Àâ°“√¢®—¥ ¢Õ߇ ’¬ Ÿß∑’Ë ÿ¥ ·≈–∑”„ÀâºâŸªÉ«¬¡’‡«≈“√–À«à“ß«—π„π°“√∑”°‘®°√√¡Õ◊ËπÊ ‡æ‘Ë¡¢÷Èπ ‡À¡“–„πºâŸªÉ«¬∑’Ë¡’ √Ÿª√à“ß¢π“¥„À≠à ·µà¢âÕ®”°—¥§◊Õ µâÕß∑”‡Õß∑’Ë∫â“π·≈–µâÕß¡’§«“¡√Ÿâ§«“¡™”π“≠„π°“√∑” HD ‡Õß ‡ªπì Õ¬“à ߥ8’ ¥ß— ππ—È °“√殑 “√≥“‡≈Õ◊ °«∏‘ °’ “√√°— …“§«√µÕâ ßÕ∏∫‘ “¬¢Õâ ¥¢’ Õâ ‡ ¬’ ¢Õß·µ≈à –«∏‘ ’√«¡∑ß—È º≈∑µ’Ë “¡ ¡“¥«â ¬ ‡æ√“–∑ß—È 2 «∏‘ ’ ‡ªπì «∏‘ ∑’ ¬’Ë ß— „À¡¡à “° ”À√∫— ª√–‡∑»‰∑¬ ·≈–¬ß— ‰¡‰à ¥·â æ√Àà ≈“¬¡“°„πµ“à ߪ√–‡∑» ·µà„π∑“ß∑ƒ…Æ’π—Èπ¡’¢âÕ¥’°«à“«‘∏’‡¥‘¡·πàπÕπ ‡æ√“–‰¡à∑”„Àâ√–¥—∫¢Õ߇ ’¬µà“ßÊ „π√à“ß°“¬·°«àß¡“° ·≈–„À§â «“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥¡“°°«“à ®–‡ÀÁπ‰¥â®“°µ“√“ß∑’Ë 1 «à“°“√øÕ°‡≈◊Õ¥∑—Èß 3 «‘∏’ ¡’¢âÕ·µ°µà“ß°—πÀ≈“¬ª√–°“√ ‚¥¬¢âÕ ·µ°µ“à ß∑ ’Ë ”§≠— §Õ◊ √–¬–‡«≈“∑„’Ë ™â πÕ°®“°ππ—È ¬ß— ¡§’ «“¡·µ°µ“à ߢÕß ultrafiltration rate, diffusive clearance ·≈–Õµ— √“°“√¢®¥— middlemolecules°“√‡≈Õ◊ °«∏‘ °’ “√øÕ°‡≈Õ◊ ¥∑¥’Ë ∑’  ’Ë ¥ÿ Õ“®‰¡‰à ¥æâ ®‘ “√≥“®“°§“à Kt/VÕ¬“à ß ‡¥¬’ «9 ·µ‡à ¥¡‘ 𬑠¡„™«â ¥— Õµ— √“°“√¢®¥— ¢Õ߬‡Ÿ √¬’ ´ßË÷ ∂Õ◊ ‡ªπì µ«— Õ¬“à ߢÕß “√∑¡Ë’ ¢’ 𓥂¡‡≈°≈ÿ ‡≈°Á ·≈–‡ªπì µ«— ·∑π„π°“√‡ª√¬’ ∫‡∑¬’ ∫§«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥ ‚¥¬«¥— ‡ªπì Kt/V urea æ∫«“à §“à Kt/V urea ∑ ’Ë ßŸ ¢π÷È  ¡— æπ— ∏°å ∫— Õµ— √“µ“¬∑≈’Ë ¥≈ß10 „π∑“ßµ√ߢ“â ¡ º≈°“√»°÷ …“¢Õß The HEMO Study æ∫«“à °“√‡æ¡‘Ë §“à Kt/V urea ∑ ’Ë ßŸ ¢π÷È „π°“√øÕ°‡≈Õ◊ ¥ ª— ¥“À≈å – 3 §√ß—È ‰¡‰à ¥™â «à ¬„ÀÕâ µ— √“°“√√Õ¥™«’ µ‘ ¥¢’ π÷È √«¡∑ß—È °“√„™â high flux dialyzer°¡Á ‰‘ ¥¡â º’ ≈µÕà Õµ— √“°“√√Õ¥™«’ µ‘ ‡™πà °π— 10¥ß— ππ—È ®ß÷ ¡§’ «“¡æ¬“¬“¡∑®’Ë –À“·π«∑“ß°“√√°— …“„À¡Êà ∑®Ë’ –™«à ¬¬¥◊ Õ“¬ºÿ ªŸâ «É ¬ ESRD „Àπâ “π¢πÈ÷ µ“√“ß∑Ë’ 1  √ªÿ §«“¡·µ°µ“à ߢÕß«∏‘ ø’ Õ°‡≈Õ◊ ¥·∫∫µ“à ßÊ Dialysis type IHD SDHD LNHD 1.5-2.5 h 6-8 h Dialysis time 2.5-5 h In-center Home 9.0-77.5 h 36-56 h Setting In-center 400-500 ml/min 200-300 ml/min High Flux Any Weekly dialysis time 7.5-15 h Any Any 6-7 d/wk Bood flow 300-500 ml/min 6-7 d/wk 200-300 ml/min 500-800 ml/min 0.1-1.2 Dialyzer Any 0.2-0.8 Access Any Dialysis frequency 3 d/wk Dialysate flow 500-800 ml/min Sp Kt/V (per HD) 1.2-1.8

New Frontiers in Dialysis 166 ∏𵑠®√‘ ππ— ∑å∏«™—  √‘ ‘¿“ ™â“ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π‘™ « π— µå  ‡ÿ ¡∏°≈ÿ 4. Urea kinetic ·≈– dose ¢Õß daily dialysis ¥™— π∑’  Ë’ ”§≠— ∑„Ë’ ™«â ¥— §«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥§Õ◊ Õµ— √“°“√¢®¥—  “√‚¡‡≈°≈ÿ ‡≈°Á (small molecular weight substance) ·≈– “√‚¡‡≈°ÿ≈¢π“¥°≈“ß (middle molecule) ªí®®—¬µà“ßÊ ∑’Ë¡’º≈µàÕ Õµ— √“°“√¢®¥—  “√µ“à ßÊ ¥ß— · ¥ß„πµ“√“ß∑Ë’ 2 µ«— Õ¬“à ߇™πà blood ·≈– dialysate flow ¡º’ ≈µÕà °“√¢®¥—  “√‚¡‡≈°≈ÿ ‡≈°Á ¡“°°«“à „π¢≥–∑Ë’ √–¬–‡«≈“„π°“√øÕ°‡≈◊Õ¥·≈–æ◊Èπ∑’˺‘«¢Õßµ—«°√Õß¡’º≈µàÕÕ—µ√“¢®—¥ “√‚¡‡≈°ÿ≈„À≠à¡“°°«à“ ≈—°…≥–¢Õ߇¡¡‡∫√π (Membrane flux) ‰¡à§àÕ¬¡’º≈°√–∑∫µàÕ°“√¢®—¥ “√‚¡‡≈°ÿ≈„À≠à¡“°π—° ·≈– ∑”„À≡ࡒº≈µàÕÕ—µ√“√Õ¥™’«‘µ„π HEMO Study ·µà membrane flux ®–¡’º≈∂Ⓡæ‘Ë¡√–¬–‡«≈“„π°“√ øÕ°‡≈Õ◊ ¥„Àπâ “π¢πÈ÷ (6-8 ™«Ë— ‚¡ß) ´ßË÷ ‡ªπì ∑¡Ë’ “¢Õß°“√»°÷ …“¢Õß the National Cooperative Dialysis Study (NCDS) ∑·Ë’ π–π”„À„â ™¬â ‡Ÿ √¬’ ‡ªπì  “√µ«— Õ¬“à ß∑πË’ ”¡“„™«â ¥— Õµ— √“§«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥ ¬ß— ‰¡¡à ·’ π«∑“ß∑™Ë’ ¥— ‡®π„π°“√«¥— çª√¡‘ “≥é ¢Õß°“√øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ ’ daily dialysis °“√«¥— single-pool (sp Kt/V) ·≈– equilibrated Kt/V (eKt/V) „™„â π°“√øÕ°‡≈Õ◊ ¥·∫∫‡¥¡‘  ª— ¥“À≈å – 3 §√ßÈ— ‡∑“à ππÈ— 11-12 ·≈– model ‡À≈“à π‰È’ ¡‰à ¥§â ”π«≥√«¡‰ª∂ß÷ §«“¡∂¢Ë’ Õß°“√øÕ°‡≈Õ◊ ¥∑‡Ë’ æ¡Ë‘ ¢πÈ÷ ¥«â ¬ Gotch ·≈–§≥– ®ß÷ ‰¥·â π–π”„À„â ™â Standard Kt/V (std Kt/V) ·∑π ”À√∫— º∑⟠∑Ë’ ”°“√øÕ°‡≈Õ◊ ¥·∫∫ daily dialysis (∑ßÈ— SDHD ·≈– LNHD)13 ‡™ÕË◊ «“à °“√‡æ¡Ë‘ §«“¡∂¢Ë’ Õß°“√øÕ°‡≈Õ◊ ¥ ‚¥¬∑§Ë’ “à eKt/V ·µ≈à –§√—ßÈ ≈¥≈ߧ√ßË÷ ÀπßË÷ ∑”„Àºâ ≈√«¡ ¢Õߪ√¡‘ “≥°“√øÕ°‡≈Õ◊ ¥¡“°°«“à °“√‡æ¡‘Ë eKt/v ·µ≈à –§√ß—È ‡ªπì 2 ‡∑“à ·µ„à Àøâ Õ° 3 §√ß—È µÕà  ª— ¥“À‡å ∑“à ‡¥¡‘ ‚¥¬§”π«≥®“° ¡°“√ J = KC J = solute removal rate K = dialyzer clearance C = solute concentration ‡πÕË◊ ß®“° C ≈¥≈ßÕ¬“à ß√«¥‡√«Á √–À«“à ß°“√øÕ°‡≈Õ◊ ¥·µ≈à –§√ßÈ— ∑”„Àâ J ≈¥≈߇™πà °π— ·µà eKt/ V ®–‡æ¡Ë‘ ¢πÈ÷ (‡æ√“–¡°’ “√¢®¥— ¢Õ߇ ¬’ ÕÕ°‰ª¡“°) µ“√“ß∑’Ë 2 ª®í ®¬— ∑¡Ë’ º’ ≈µÕà dialyzer clearance (‡√¬’ ßµ“¡≈”¥∫— §«“¡ ”§≠— ) Small molecules Large molecules Blood flow Dialysis time Dialysate flow Surface area Surface area Membrane flux Dialysis time Blood and dialysate flow Membrane flux

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π‘™ 167 °“√«¥— urea kinetic modeling ®– µâÕ߇ª≈’Ë¬π®“°‡¥‘¡∑’Ë«—¥ª√– ‘∑∏‘¿“æµàÕ §√—ÈߢÕß°“√øÕ°‡≈◊Õ¥‡ªìπ°“√«—¥·∫∫‚¥¬ √«¡µ≈Õ¥ ª— ¥“À·å ∑π ‡√¬’ °«“à standard Kt/V (std Kt/V) model ¢Õß std Kt/V ¥ß— · ¥ß„π√ªŸ ∑’Ë 1 ´ßË÷ · ¥ß§“à weekly std Kt/V ‡∑¬’ ∫°∫— eKt/V ·≈–®”π«π°“√øÕ°‡≈◊Õ¥µàÕ —ª¥“Àå æ∫«à“ ®“°°√“ø §à“ std Kt/V ‡æ‘Ë¡¢÷Èπ‡ªìπ‡ âπµ√ß ‡¡◊ËÕ®”π«π°“√øÕ°‡≈◊Õ¥µàÕ —ª¥“Àå‡æ‘Ë¡¢÷Èπ √ªŸ ∑Ë’ 1 ·µà§à“ std Kt/V ®–‡æ‘Ë¡‡ªìπ —¥ à«π·∫∫ Model ¢Õß Standard Kt/V ‚¥¬§¥‘ ‡ªπì function ¢Õß Logarithmic „π°√≥’∑’Ë eKt/V · ¥ß«à“°“√ eKt/V µàÕ°“√øÕ°‡≈◊Õ¥·µà≈–§√—Èß·≈–®”π«π°“√ ‡æ‘Ë¡®”π«π§«“¡∂’Ë¢Õß°“√øÕ°‡≈◊Õ¥¡’º≈ øÕ°‡≈◊Õ¥µàÕ —ª¥“Àå æ∫«à“ std Kt/V ‡æ‘Ë¡‡ªìπ µàÕ§à“ std Kt/V ¡“°°«à“°“√‡æ‘Ë¡ eKt/v „π ‡ âπµ√߇¡◊ËÕ®”π«π°“√øÕ°‡≈◊Õ¥‡æ‘Ë¡¢÷Èπ·≈–‡æ‘Ë¡ ·µà≈–§√—Èß ¥—ß∑’ˉ¥â°≈à“«‰ª·≈â« ‡ âπ CAPD ·∫∫ logarithmic ‡¡ÕË◊ eKt/V ‡æ¡Ë‘ ¢πÈ÷ ´ß÷Ë ‡ªπì °“√≈“â ߉µ·∫∫µÕà ‡πÕ◊Ë ßµ≈Õ¥‡«≈“®–¡’ slope ‡∑“à °∫— 7 §“à weekly std Kt/V ‡∑“à °∫— 2  ”À√∫— ºªŸâ «É ¬ CAPD ®–‡∑¬’ ∫‡∑“à °∫— eKt/V ¢Õß°“√øÕ° ‡≈Õ◊ ¥·∫∫∏√√¡¥“ 3 §√ßÈ— / ª— ¥“Àå ∑§Ë’ “à 1.05 ´ß÷Ë ∂Õ◊ ‡ªπì ¢π“¥¢Õß°“√øÕ°‡≈Õ◊ ¥∑‡Ë’ 欒 ßæÕ¢Õß∑ßÈ— 2 «∏‘ ’ 5. Standard Kt/V „π daily dialysis §“à std Kt/V ¢Õß SDHD „π·µ≈à – √ªŸ ∑’Ë 2 √“¬ß“π ¥—ß· ¥ß„π√Ÿª∑’Ë 2 §à“ 1,2,3 „π ¢π“¥¢Õß°“√øÕ°‡≈Õ◊ ¥„π Daily hemodialysis: model √Ÿª· ¥ßº≈°“√øÕ°‡≈◊Õ¥·∫∫∏√√¡¥“ π„È’ ™ºâ ªâŸ «É ¬¢π“¥ V = 32 L, SDHD = 2 ™«Ë— ‚¡ß ·≈– (conventional HD, CHD) §“à 1û,2û ,3û · ¥ß§“à LNHD = 8.5 ™«Ë— ‚¡ß SDHD ·≈– LNHD §“à (1,1û,1é) 1 · ¥ß∂ß÷ baseline therapy 1û,1é · ¥ß∂ß÷ LNHD ∑Ë’ √“¬ß“π‚¥¬ Pierratos ·≈–§≥–14 §“à 1û „™â µ«— °√Õß F40 Polysulfone dialyzer ∑Ë’ blood flow rate 100 ml/min, dialysate flow rate 300 ml/min ·≈–‡«≈“ 8-9 ™«Ë— ‚¡ß „π¢≥– ∑§Ë’ “à 1é „™µâ «— °√Õß F80, dialysate flow 800 ml/min ∑”„À§â “à std Kt/V  ßŸ ¡“°°«“à 6-7 ¥ß— ππÈ— §“à std Kt/V ®–·ª√ºπ— §Õà π¢“â ß¡“° „πº∑Ÿâ ” LNHD ¢π÷È °∫— ™π¥‘ µ«— °√Õß ·≈– blood

New Frontiers in Dialysis 168 ∏π‘µ ®‘√π—π∑å∏«—™  √‘ ‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°≈ÿ flow ∑‡Ë’ ≈Õ◊ °„™‚â ¥¬¡§’ “à µßÈ— ·µà 4-7 „π°≈¡àÿ SDHD §“à 2 §Õ◊ baseline therapy ∑¡Ë’ §’ “à std Kt/V = 2.0 ‡ªπì √“¬ß“π®“° Kooistra ·≈– §≥–15 ‡¡ÕË◊ ‡ª≈¬Ë’ π°“√√°— …“‡ªπì SDHD ‚¥¬§ß§“à ÕπË◊ ‰«·â µ®à –≈¥ t ≈ߧ√ßË÷ ÀπßË÷ ·≈–‡æ¡Ë‘ §«“¡∂®Ë’ “° 3 §√ßÈ— / ª— ¥“À‡å ªπì 6 §√ß—È / ª— ¥“Àå ∑”„À§â “à std Kt/V ‡æ¡Ë‘ ®“° 2.0 ‡ªπì 2.5 (µ”·Àπßà 2û) ·µ∂à “â ‡ª≈¬Ë’ 𵫗 °√Õß„À¡â ¢’ 𓥄À≠¢à πÈ÷ ‡™πà ¡§’ “à KoA urea 1600 ml/min, blood flow 400 ml/min, dialysate flow 800 ml/min ·≈– t = 2 ™«Ë— ‚¡ß §“à std Kt/V ®–‡æ¡Ë‘ ‡ªπì 4.0 (µ”·Àπßà 2é) µ”·Àπßà 3,3û ‡ªπì °“√»°÷ …“∑°Ë’ ”≈ß— ∑” Õ¬∑àŸ Ë’ Renal Research Institute ∑πË’ «‘ ¬Õ√°å  À√∞— Õ‡¡√°‘ “ ´ßË÷ π”ºªŸâ «É ¬ 12 √“¬ ∑¡Ë’ §’ “à baseline std Kt/V 2.3 µÕà °“√øÕ°‡≈Õ◊ ¥ 3 §√ßÈ— / ª— ¥“Àå ¡“‡ª≈¬Ë’ π‡ªπì SDHD 6 §√ß—È / ª— ¥“Àå ‚¥¬„™‡â «≈“§√ßÈ— ≈– 2.0 ± 0.5 ™«Ë— ‚¡ß ·≈–¡§’ “à std Kt/V 3.0 ± 0.5 º≈°”≈ß— Õ¬„àŸ π√–À«“à ß°“√»°÷ …“ ¥ß— ππÈ— „πª®í ®∫ÿ π— §“à std Kt/ V „π SDHD ®–¡§’ “à ª√–¡“≥ 2.5-3.0 ·µ à “¡“√∂‡æ¡Ë‘ ‰¥∂â ß÷ 4.0 ∂“â ª√∫— ‡ª≈¬Ë’ π dialysis prescription´ßË÷ ‡∑¬’ ∫‡∑“à °∫— LNHD Suri ·≈–§≥–‰¥â∑”°“√‡ª√’¬∫‡∑’¬∫¢π“¥¢Õß°“√øÕ°‡≈◊Õ¥√–À«à“ß SDHD ·≈– LNHD ‡∑¬’ ∫°∫— «∏‘ ∏’ √√¡¥“ ‚¥¬·∫ßà ºªâŸ «É ¬‡ªπì 3 °≈¡àÿ °≈¡àÿ ∑Ë’ 1 SDHD (11 §π) °≈¡àÿ ∑Ë’ 2 LNHD 12 §π ·≈– °≈¡àÿ ∑Ë’ 3 conventional HD (CHD 22 §π) √–¬–‡«≈“»°÷ …“ 18 ‡¥Õ◊ π ∑”°“√‡ª√¬’ ∫‡∑¬’ ∫§“à sp Kt/V, eKt/V, std Kt/ V ·≈– normalized protein equivalent of nitrogen appearance (nPNA) ∑°ÿ ‡¥Õ◊ π√–À«“à ß°≈¡àÿ æ∫«“à §“à weekly HD doses ®– Ÿß„π°≈ÿà¡ daily HD ∑—Èß 2 °≈ÿà¡°«à“°≈ÿࡧ«∫§ÿ¡Õ¬à“ß¡’π—¬ ”§—≠ ·µà§à“§«“¡ ·µ°µ“à ߢπÈ÷ °∫— «∏‘ ∑’ §Ë’ ”π«≥ ‚¥¬æ∫«“à §“à sp Kt/V ·≈– eKt/V ‡æ¡Ë‘ ¢πÈ÷ πÕâ ¬°«“à ∑§Ë’ «√ ·≈–πÕâ ¬°«“à std Kt/ V (√ªŸ ∑Ë’ 3) º∑⟠∑Ë’ ” SDHD ®–¡§’ “à sp Kt/V µÕà §√ßÈ— µ”Ë ≈ß (‡æ√“– t  πÈ— ≈ß ) (√ªŸ ∑Ë’ 4) ·µ∂à “â §”π«≥µÕà √ªŸ ∑Ë’ 3 ‡ª√¬’ ∫‡∑¬’ ∫§«“¡‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥‚¥¬„™°â “√§”π«≥ 3 «∏‘ ’ æ∫«“à ¡§’ «“¡·µ°µ“à ß°π— Õ¬“à ß ¡π’ ¬—  ”§≠— √–À«“à ß 3 «∏‘ π’ È’ (p<0.05) °“√‡ª≈¬Ë’ π·ª≈ߢÕß weekly spKt/V ®–¡“°°«“à weekly eKt/V ·≈– weekly stdKt/V

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π™‘ 169  ª— ¥“À§å “à ®– ßŸ °«“à control ·µ°à ¬Á ß— πÕâ ¬°«“à LNHD §“à weekly sp Kt/V  ßŸ ∑ Ë’ ¥ÿ „π°≈¡àÿ LNHD (9.08 ± 0.33) √Õß≈ß¡“§Õ◊ daily HD (5.55 ± 0.23) ·≈– control HD (5.18 ± 0.12 , p<0.05 ) ∑°ÿ §∑Ÿà ”°“√‡ª√¬’ ∫ ‡∑¬’ ∫‡¡ÕË◊ §”π«≥§“à std Kt/V æ∫«“à ¡·’ π«‚π¡â ‡™πà ‡¥¬’ «°π— §Õ◊ ®– ßŸ ∑ Ë’ ¥ÿ „π°≈¡àÿ LNHD (4.65 ± 0.28) √Õß ≈ß¡“§Õ◊ daily HD (3.01 ± 0.27) ·≈– 2.36 ± 0.05 „π°≈¡àÿ §«∫§¡ÿ (p<0.001) §“à nPNA ¡·’ π«‚π¡â ‡æ¡Ë‘ ¢πÈ÷ ∑—Èß„π°≈ÿà¡ daily HD ·≈– LNHD (√Ÿª∑’Ë 5) ®“°√“¬ß“ππ’È √ÿª«à“ §«√„™â§à“ std Kt/V „π°“√«—¥§«“¡ ‡æ¬’ ßæÕ¢Õß°“√øÕ°‡≈Õ◊ ¥„π°≈¡àÿ daily HD °“√„™§â “à eKt/V §“à ®–µ”Ë ‡°π‘ ®√ß‘ ·≈–§“à sp Kt/V ° Á ߟ ‡°π‘ ®√ß‘ §“à std Kt/V  ßŸ ∑ Ë’ ¥ÿ „π°≈¡àÿ LNHD (‡æ¡Ë‘ ¢πÈ÷  Õ߇∑“à ‡∑¬’ ∫°∫— «∏‘ ∏’ √√¡¥“) „π¢≥–∑Ë’ daily HD ¡§’ “à std Kt/V ‡æ¡Ë‘ ¢πÈ÷ √Õâ ¬≈– 20 6. °“√§”π«≥§“à Standard Kt/V (Std Kt/V) À≈°— °“√øÕ°‡≈Õ◊ ¥„πºªŸâ «É ¬‰µ«“¬√–¬– ¥ÿ ∑“â ¬§Õ◊ °“√¢®¥—  “√æ…‘ ÕÕ° ‚¥¬„™â General mass balance equation ¥ß— πÈ’ V (dc/dt) = G - K x C ––––– 1 V = solute distribution volume G = generation rate K = clearance √ªŸ ∑Ë’ 4 °“√»°÷ …“√–¬–¬“«π“π 18 ‡¥Õ◊ π (A) · ¥ß single-session sp Kt/V, (B) · ¥ß weekly sp Kt/V * · ¥ß§“à §«“¡·µ°µ“à ß∑“ß ∂µ‘ ‡‘ ¡ÕË◊ p < 0.05 ‡¡ÕË◊ ‡∑¬’ ∫°∫— baseline O · ¥ß§«“¡·µ°µ“à ßÕ¬“à ß¡π’ ¬—  ”§≠— √–À«“à ß 2 °≈¡àÿ ∑∑Ë’ ”°“√»°÷ …“

New Frontiers in Dialysis 170 ∏π‘µ ®√‘ π—π∑å∏«™—  √‘ ‘¿“ ™“â ß»‘√°‘ ÿ≈™¬— ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°≈ÿ „π¿“«– steady state ‡™πà chronic kidney disease À√Õ◊ CAPD ´ßË÷ V (dc/dt) = 0 0 = G - (Kr+Kp) C ––––– 2 À√Õ◊ G = (Kr+Kp) C ––––– 3 Kr = Renal function Kp = peritoneal clearance  ¡°“√ 3 À¡“¬∂ß÷ urea kinetic ‡¡ÕË◊ °“√∑”ß“π¢Õ߉µª°µ‘ À√Õ◊ CKD ∑¬Ë’ ß— ‰¡‰à ¥øâ Õ°‡≈Õ◊ ¥ À√Õ◊ º∑⟠∑Ë’ ” CAPD ®¥—  ¡°“√ 3 „À¡‡à ªπì C = G ––––– 4 Kr + Kp ´ßË÷ · ¥ß«“à C ‡ªπì function ¢Õß 1 Kr + Kp §“à C  ¡— æπ— ∏°å ∫— Kr ·∫∫ parabola ·≈–ºπ— ·ª√µ“¡ G §“à C, G ·≈– K ¡§’ «“¡ ¡— æπ— ∏´å ÷ßË °π— ·≈–°π— ‡¡ÕË◊ ¡’ continuous clearance ·µ∂à “â ‡ªπì °“√øÕ° √ªŸ ∑Ë’ 5 (C) · ¥ß∂ß÷ §“à nPNA (g/kg/day), (D) · ¥ß∂ß÷ §“à predialysis BUN (mmol/L)

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π‘™ 171 ‡≈Õ◊ ¥·∫∫§√ßÈ— §√“« (intermittent) §“à C ®–·°«àߢ÷Èπ≈߇ªìπ≈—°…≥–øíπª≈“ §◊Õ§à“¢Õ߇ ’¬®– ŸßµÕπ‡√‘Ë¡µâπ (Co) ·≈–≈¥≈ß (Ct) µÕπª≈“¬ (√ªŸ ∑Ë’ 6) ®“°√ªŸ ∑Ë’ 6 Profile 1 · ¥ß ∂ß÷ °“√øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ ∏’ √√¡¥“ 3 §√ß—È /  ª— ¥“Àå ·≈– Kr = 0 ®–‡ÀπÁ «“à √–¥∫— solute ®–≈¥≈ßÕ¬à“ß√«¥‡√Á«À≈—ß°“√ øÕ°‡≈◊Õ¥·µà≈–§√—Èß ·≈–®–¡’°“√ √ªŸ ∑Ë’ 6  √“â ߢπ÷È „À¡°à Õà π°“√øÕ°§√ß—È µÕà ‰ª · ¥ß∂ß÷ concentration profile 3 «∏‘ ’ (1) Intermittent dialysis Profile 2 ‡ªπì °“√√°— …“·∫∫ (2) Continuous dialysis CAPD ´ßË÷ æ∫«“à §“à average BUN (TAC) (3) Combined intermittent plus continuous dialysis ®– Ÿß°«à“°“√∑” HD ·µà°Á¡‘‰¥â¡’º≈ µàÕ√à“ß°“¬‡æ√“– clinical outcome ¡‰‘ ¥¢â πÈ÷ °∫— §“à BUN Profile 3 · ¥ß∂ß÷ °“√øÕ°‡≈Õ◊ ¥«∏‘ ∏’ √√¡¥“ ·µ¬à ß— ¡§’ “à °“√∑”ß“π¢Õ߉µ‡À≈Õ◊ Õ¬àŸ (Kr À√Õ◊ Kp) ®“° model πÈ’ °“√§”π«≥§“à std Kt/V ®–§”π«≥®“°°“√¢®¥— ¢Õ߇ ¬’ µ≈Õ¥‡«≈“‡¡ÕË◊ Co = CSS 7. Standard Kt/V model ·ª≈ß ¡°“√ 1 „À‡â ªπì √ªŸ ·∫∫∑„Ë’ ™‰â ¥∑â ßÈ— °“√øÕ°‡≈Õ◊ ¥·∫∫ intermittent ·≈– continuous V (dc/dc) = G - (Kd+Kp+Kr) C ––––– 5 ∂“â ‡ªπì °“√øÕ°‡≈Õ◊ ¥·∫∫§√ß—È §√“«æ∫«“à Ct = Co exp [- Kd or Kp+Kr) t/v]+[G/(Kd or Kp+Kr)]x(1-exp[-(Kd or Kp+Kr)t/v]) ––––– 6 ‡¡ÕË◊ Co = predialysis Bun Ct = post dialysis Bun Kd = dialyser urea clearance Kr = renal urea clearance T = treatment time V = urea distribution volume °“√·° â ¡°“√ ➄ ‡¡ÕË◊ ¡°’ “√‡æ¡Ë‘ ¢Õß BUN „π√–À«“à ß°“√øÕ°‡≈Õ◊ ¥·µ≈à –§√ßÈ— Co = Ct exp [-Kp+Kr)ti/v]+[G/(Kp+Kr)][1-exp[-(Kp+Kr)ti/v)] ––––– 7 À√Õ◊

New Frontiers in Dialysis 172 ∏π‘µ ®‘√π—π∑å∏«—™  ‘√‘¿“ ™â“ß»√‘ ‘°ÿ≈™¬— ∏π—𥓠µ√–°“√«π™‘ « —πµå  ÿ‡¡∏°ÿ≈ Co = Ct+Gxti/v ––––– 8 ‡¡ÕË◊ Ct = post dialysis Bun Co = pre daialysis BUN °Õà π°“√øÕ°‡≈Õ◊ ¥§√ßÈ— µÕà ‰ª Ti = interdialysis time interval  ¡°“√ 7 „™‡â ¡ÕË◊ Kp À√Õ◊ Kr ¡§’ “à ¡“°°«“à 0 „π¢≥–∑ Ë’ ¡°“√ 8 „™‡â ¡ÕË◊ Kp À√Õ◊ Kr ¡§’ “à ‡ªπì »πŸ ¬„å π √–À«“à ß°“√øÕ°‡≈Õ◊ ¥ °“√§”π«≥§“à Co µÕâ ßÀ“§“à G °Õà π·≈«â ®ß÷ ¡“‡¢“â  µŸ √¥ß—  ¡°“√ 9 Co = 0.184(PCRn − 0.17)V (1− exp[−eKt /V ]* x exp[-(Kp + Kr)((7 / N)1440 - t) / V]   [spKt /V ] *V / t + 0.184(PCRn − 0.17)V * (1− exp[−Kp + Kr Kp + Kr x ((7/N)1440-t)/V] / [1-exp[-eKt/V] x exp[-(Kp+Kr)((7/N)1440-t)/V]] ´ßË÷ ‡ªπì  µŸ √∑„Ë’ ™‰â ¥ â ”À√∫— intermittent hemodialysis, continuous dialysis eKt/v = spKt/v [1-0.6/(t/60)]+0.03 ––––– 0 ∂“â Kp ·≈– Kr = »πŸ ¬å „π√–À«“à ߢÕß intermittent hemodialysis Co = 0.184(PCRn − 0.17)V * (1− exp[−eKt /V ]) ––––– ¡   spKt /V *V / t +(0.184(PCRn-0.17)V)(7/N)1440-t)/V   /[1-exp[-eKt/V]] „π°√≥∑’ ‡Ë’ ªπì °“√øÕ°‡≈Õ◊ ¥·∫∫µÕà ‡πÕË◊ ß À√Õ◊ CKD ∑¬Ë’ ß— ‰¡‰à ¥øâ Õ°‡≈Õ◊ ¥ À√Õ◊ CAPD  ¡°“√ 9-11 ®– “¡“√∂√«∫‡ªπì CSS = (0.184 [nPCR-0.17]v)/(Kp+Kr) ––––– ™ CSS = steady-state BUN „π¢≥–∑¡Ë’ ’ continuous clearance ‡√“ “¡“√∂·∑π§“à Co ∑‰Ë’ ¥®â “°°“√·∑π§“à „π ¡°“√ 9-11 ≈ß„π ¡°“√ 12 ·≈–§”π«≥ standard Kt/V ´ßË÷ §¥‘ „Àâ Co = CSS Standard K = 0.184 [nPCR › 0.17]v/Co ––––– £ ‡¡ÕË◊ Co = Kp+Kr π”§“à ®“° ¡°“√ 13 À“√¥«â ¬ V ·≈–§≥Ÿ ¥«â ¬ t ®–‰¥â Std (Kt/V) = 1440[0.184 (nPCR-0.17)/Co µÕà «π— ––––– ¢ = 7x1440 [0.184(nPCR-0.17)/Co µÕà  ª— ¥“Àå ––––– ∞

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π‘™ 173 §“à std(Kt/V)  “¡“√∂‡ª√¬’ ∫‡∑¬’ ∫‡ªπì §“à √Õâ ¬≈–¢Õߧ“à ª°µ‰‘ ¥â % ref(Krt/V) = 100[Std(Kt/v)/ref (Krt/v)] ––––– §  ¡°“√ 14 ·≈– 15 „™â‡ªìπ¡“µ√∞“π°“√§”π«≥§à“ std K/V ¢Õß°“√øÕ°‡≈◊Õ¥∑—Èß·∫∫ intermittent ·≈– continuous Õ¬à“߉√°Á¥’ §à“ standard Kt/V ¬—ßµâÕß¡’°“√»÷°…“∂÷ߧ«“¡·¡à𬔠·≈–§«“¡‡°’ˬ«æ—π°—∫ ≈°— …≥–·≈–º≈°“√√°— …“∑“ߧ≈π‘ °‘ ¥«â ¬ «“à ¡§’ «“¡ ¡— æπ— ∏‡å À¡Õ◊ π spK/V À√Õ◊ ‰¡à 8. ¢Õâ ¥¢’ Õß SDHD (µ“√“ß∑Ë’ 3) °“√»°÷ …“¢Õß SDHD ∑ºË’ “à π¡“¡°— ‡ªπì °“√»°÷ …“·∫∫‰¡¡à °’ ≈¡àÿ §«∫§¡ÿ ·≈–¡®’ ”π«πºªŸâ «É ¬‰¡à ¡“° Õ¬“à ߉√°¥Á æ’ ∫¢Õâ ¥À’ ≈“¬ª√–°“√ °“√·ª≈§«“¡À¡“¬¢Õß°“√øÕ°‡≈Õ◊ ¥·∫∫ daily HD æß÷ √–≈°÷ «“à SDHD ¡¢’ Õâ ·µ°µ“à ßÀ≈“¬ª√–°“√®“° LNHD °≈“à «§Õ◊ LNHD „™√â –¬–‡«≈“π“π°«“à ¡“° (7-8 ™¡/§√ßÈ— ) „™â blood ·≈– dialysate flow µ”Ë „π¢≥–∑Ë’ SDHD „™√â –¬–‡«≈“ πÈ— 1.5-2.5 ™¡. ·µà blood flow  ßŸ °“√ §”π«≥§“à spKt/V µÕà °“√øÕ°‡≈Õ◊ ¥ LNHD 1 §√ßÈ— ®–¡§’ “à ¡“°°«“à SDHD ·µ§à “à Std Kt/V ®–„°≈‡â §¬’ ß°π— (√ªŸ ∑Ë’ 7) °“√¢∫—  “√‚¡‡≈°≈ÿ „À≠®à –°√–∑”‰¥¥â °’ «“à „π°≈¡àÿ LNHD º≈¥¢’ Õß daily HD ¡°— Õ¬„àŸ π√ªŸ ¢Õß°“√‡ª≈¬Ë’ π·ª≈ß∑“ߥ“â πº≈‡≈Õ◊ ¥ §≥ÿ ¿“晫’ µ‘ ¿“«–´¥’ ·µ¬à ß— ‰¡¡à °’ “√»°÷ …“∂ß÷ Õµ— √“µ“¬ æ∫«“à °“√øÕ°‡≈Õ◊ ¥·∫∫ LNHD ™«à ¬≈¥√–¥∫— homocysteine, beta2- microglobulin ·≈–¢π“¥¬“ŒÕ√å‚¡π erythropoietin (Epo) ∑’Ë„™â ∑”„Àâ “¡“√∂§«∫§ÿ¡ª√‘¡“≥πÈ”„π √“à ß°“¬‰¥¥â °’ «“à √«¡∑ßÈ— ≈¥√–¥∫— øÕ øÕ√ — ≈ß¡“°®π‰¡µà Õâ ß√∫— ª√–∑“π phosphate binder17  «à π SDHD ¡¢’ Õâ ¥¥’ “â π§«∫§¡ÿ §«“¡¥π— ‚≈Àµ‘  “¡“√∂≈¥®”π«π¬“≈¥§«“¡¥π— ‚≈Àµ‘ ≈߉¥â §“à serum bicarbonate ‡æ¡Ë‘ ¢πÈ÷ ≈¥ª√¡‘ “≥¬“ Epo ·≈–∑”„À§â ≥ÿ ¿“晫’ µ‘ √«¡∑ßÈ—  ¿“«–‚¿™π“°“√¥¢’ πÈ÷ 18-19 µ“√“ß∑’Ë 3 NHD SDHS ¢Õâ ¥¢’ Õß°“√√°— …“¥«â ¬ Daily hemodialysis + ++ + Parameter + Albumin level +++ + Homocysteine level + + Phosphorus level EPO level +++ Blood pressure control + Quality of life

New Frontiers in Dialysis 174 ∏𵑠®‘√ππ— ∑∏å «™—  ‘√‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π‘™ « π— µå  ÿ‡¡∏°ÿ≈ √ªŸ ∑’Ë 7 Standard weekly Kt/V model 9. º≈µÕà  ¿“«–‚¿™π“°“√ ¿“«–∑ÿ‚¿™π“°“√ (malnutrition) ‡ªìπªí≠À“∑’Ëæ∫∫àÕ¬¢≥–°“√øÕ°‡≈◊Õ¥·≈–‡ªìπªí®®—¬∑’Ë  ”§≠— ∑∑’Ë ”„À‡â æ¡‘Ë Õµ— √“µ“¬¢π÷È ‚¥¬‡©≈¬’Ë  “¡“√∂æ∫Õ∫ÿ µ— °‘ “√≥¢å Õß¿“«–∑‚ÿ ¿™π“°“√„πºªŸâ «É ¬ ESRD ‰¥â ∂÷ß√âÕ¬≈– 4020  “‡Àµÿ¢Õß¿“«–∑ÿ‚¿™π“°“√‰¥â·°à Õ“°“√§≈◊Ëπ‰ âÕ“‡®’¬π®“°¿“«–¬Ÿ√’‡¡’¬∑”„Àâ√—∫ ª√–∑“πÕ“À“√‰¥πâ Õâ ¬≈ß ¡§’ «“¡º¥‘ ª°µ¢‘ Õ߇¡µ–∫Õ≈ ‘ ¡¢Õß‚ª√µπ’ ·≈–æ≈ß— ß“π ·≈–°“√øÕ°‡≈Õ◊ ¥ ∑’ˉ¡à‡æ’¬ßæÕ √«¡∑—Èß¡’ ¿“«– inflammation ´÷Ëß√«¡·≈â«®–∑”°“√‡°‘¥Õ—πµ√“¬®“°‚√§À—«„®·≈–À≈Õ¥ ‡≈Õ◊ ¥‡æ¡‘Ë ¢π÷È ®“°°“√»°÷ …“¢Õß The London Daily/Nocturnal Hemodialysis Study ‰¥»â °÷ …“‡ª√¬’ ∫‡∑¬’ ∫º≈ ¢Õß°“√øÕ°‡≈◊Õ¥ 3 «‘∏’ ‰¥â·°à SDHD, LNHD ·≈– Conventional HD „π·ßà¡ÿ¡µà“ßÊ √«¡∂÷ߺ≈¢Õß  ¿“«–‚¿™π“°“√¥â«¬21 æ∫«à“„π°≈ÿà¡ SDHD ·≈– LNHD ¡’§à“ nPNA ‡æ‘Ë¡¢÷Èπ„π¢≥–∑’Ë nPNA ‰¡à ‡ª≈¬Ë’ π·ª≈ß„π°≈¡àÿ §«∫§¡ÿ ·≈–¡§’ “à nPNA µ”Ë ∑ Ë’ ¥ÿ ¥«â ¬ ®“°°“√∫π— ∑°÷ µ“√“ßÕ“À“√æ∫«“à °≈¡àÿ SDHD ¡§’ «“¡Õ¬“°√∫— ª√–∑“πÕ“À“√‡æ¡Ë‘ ¢πÈ÷ ¡§’ “à serum albumin ‡æ¡Ë‘ ¢πÈ÷ ≥ ‡«≈“ 3, 12, 18 ‡¥Õ◊ π À≈ß— ∑”°“√»°÷ …“ „π¢≥–∑°Ë’ ≈¡àÿ LNHD °≈∫— ¡√’ –¥∫— serum albumin ≈¥µ”Ë ≈ß „π‡¥Õ◊ π∑Ë’ 9 „π¢≥–∑°Ë’ ≈¡àÿ §«∫§¡ÿ ¡√’ –¥∫— Õ≈— ∫¡Ÿ π‘ §ß∑√Ë’ –¥∫— cholesterol ·≈– triglyceride ‰¡µà “à ß°π— √–À«“à ß 3 °≈¡àÿ πÈ’ ·µà HDL ¡’ ·π«‚π⡇æ‘Ë¡„π°≈ÿà¡ LNHD ·≈– SDHD ¡«≈°≈â“¡‡π◊ÈÕ·¢π‡æ‘Ë¡¢÷Èπ„π°≈ÿà¡ SDHD ·µà„π°≈ÿà¡ LNHD °≈∫— ¡π’ ”È Àπ°— ≈¥≈ß √«¡∑ßÈ— ¡¡’ «≈°≈“â ¡‡πÕÈ◊ ·¢π≈¥≈߇™πà °π— ‚¥¬ √ªÿ º∑Ÿâ ‰Ë’ ¥√â ∫— °“√øÕ°‡≈Õ◊ ¥·∫∫ daily HD ®–¡ ’ ¿“«–∑“ß‚¿™π“°“√¥¢’ πÈ÷ ¡°’ “√√∫— ª√–∑“πÕ“À“√‰¥‡â æ¡Ë‘ ¢πÈ÷ ®“°‡¥¡‘ √Õâ ¬≈– 10-30 ‚¥¬∑°Ë’ ≈¡àÿ daily HD ®–¡ ’ ¿“«–∑“ß‚¿™π“°“√¥°’ «“à LNHD ·µ∑à ßÈ—  Õß°≈¡àÿ ¥°’ «“à °≈¡àÿ §«∫§¡ÿ °“√»°÷ …“ SDHD „π À√∞— ‡¡√°‘ “‚¥¬ Ting ·≈– §≥–22 „πºªŸâ «É ¬ 42 √“¬∑∑Ë’ ” SDHD π“π 12 ‡¥Õ◊ π 2 ™¡./§√ßÈ— 6§√ßÈ— / ª— ¥“Àå æ∫«“à ∑”„À â ¿“«–‚¿™π“°“√¥¢’ π÷È πÈ”Àπ°— µ«— ‡æ¡‘Ë ¢π÷È (·µ‰à ¡¡à π’ ¬—  ”§≠— ∑“ß ∂µ‘ )‘ ·µ√à –¥∫— albumin,calcium,

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π™‘ 175 alkaline phosphatase, bicarbonate ·≈– parathyroid hormone ‰¡‡à ª≈¬Ë’ π·ª≈ß °“√»°÷ …“ÕπË◊ Ê ∑¡Ë’ °’ “√ ‡ª√¬’ ∫‡∑¬’ ∫§«“¡·µ°µ“à ߢÕß serum albumin ‡¡ÕË◊ ‡ª≈¬Ë’ π°“√√°— …“®“° conventional HD ‰ª‡ªπì SDHD À√Õ◊ LNHD ¥ß—  √ªÿ „πµ“√“ß∑Ë’ 4 ´ßË÷ æ∫«“à √“¬ß“π «à π„À≠¡à §’ “à serum albumin ‡æ¡Ë‘  ßŸ ¢πÈ÷ √«¡∑ßÈ— dry weight ¥â«¬ (µ“√“ß∑’Ë 5) πÈ”Àπ—°∑’ˇæ‘Ë¡π’ÈÕ∏‘∫“¬®“°°“√√—∫ª√–∑“πÕ“À“√√«¡∑—Èß‚ª√µ’π‡æ‘Ë¡¢÷Èπ ∫“ß √“¬ß“π23 °≈∫— æ∫ serum albumin ≈¥≈ß„π°≈¡ÿà LNHD ´ß÷Ë µÕâ ß°“√°“√»°÷ …“µÕà ‡æ¡‘Ë ‡µ¡‘ „πÕ𓧵  “‡Àµÿ ∑’Ë ¿“«–∑“ß‚¿™π“°“√¥’¢÷È𠇪ìπ‡æ√“–°“√‡æ‘Ë¡§«“¡∂’Ë¢Õß°“√øÕ°‡≈◊Õ¥ ∑”„Àâ√–¥—∫¢Õ߇ ’¬„π‡≈◊Õ¥ ·≈–ª√‘¡“≥ “√πÈ”·°«àߢ÷Èπ≈ßπâÕ¬≈ß √–¥—∫ TAC (time-averaged concentration) ¢Õ߬Ÿ‡√’¬≈¥≈ß §à“ µ“√“ß∑Ë’ 4 °“√‡ª≈¬Ë’ π·ª≈ߢÕß√–¥∫— Serum albumin level ‡¡Õ◊Ë ‡ª≈¬Ë’ π°“√√°— …“®“° IHD ¡“‡ªπì SDHD ·≈– NHHD Reference Modality/No. Interval (mon) Albumin (g/dL) Change (%) P of Patients Buoncristiani et al, 1997 SDHD/50 12 3.9 to 4.4 + 12.8 <0.001 Lugon et al 1997 SDHD/5 6 4.0 to 4.3 + 7.5 NS (0.09) Pinciaroli, 1998 SDHD/22 12 3.5 to 4.26 + 21.7 NA Kooistra and Vos, 1999 SDHD/13 6 4.22 to 4.32 + 2.0 NS Woods et al, 1999 SDHD/72 12 3.88 to 4.35 + 12.1 <0.001 OûSullivan et al, 1998 NHHD/5 2 3.63 to 3.68 + 1.3 NS (<0.10) Perrrats et al, 1998 NHHD/12 12 4.12 to 4.14 + 0.4 NS McPhatter et al, 1999 NHHD/9 12 (6 on NHHD) 3.4 to 4.1 + 20.5 NA Cacho et al, 2000 NHHD/5 7.4 (mean) 4.30 to 4.38 + 1.9 NS µ“√“ß∑Ë’ 5 · ¥ß∂ß÷ °“√‡ª≈¬’Ë π·ª≈ߢÕß Ideal dry weight ‡¡Õ◊Ë ‡ª≈¬’Ë π°“√√°— …“®“° IHD ¡“‡ªπì SDHD À√Õ◊ NHDD Reference Modality/No. Interval (mon) Dry Weight (kg) Change P of Patients Buoncristiani et al, 1988 SDHD/12 26.7 (mean) 67 to 71.5 +6.7% NA Lugon et al, 1997 SDHD/5 6 57.7±11 to 59.8±10 +3.6% NA (0.13) Ting et al, 1998 SDHD/18 6 76.7±11 to 59.8±28 +1.7% NS (0.08) Pinciaroli et al, 1998 SDHD/22 12 58 to 57.6 -0.6% NA Traeger et al, 1998 SDHD/4 12 NA +0.5±4.5 kg(range) NA Woods et al, 1999 SDHD/72 24 (median) NA +0.85 kg/6 mon 0.02 Williams et al, 1998 NHHD/5 2 Stable +0.1±2.9 kg (range) NA Pierratos et al, 1998 NHHD/12 12 NA +1.0±3.0 kg NA McPhatter et al, 1999 NHHD/9 3-12 (range) NA +2.0%-3.0% NA

New Frontiers in Dialysis 176 ∏π‘µ ®‘√ππ— ∑å∏«—™  ‘√‘¿“ ™“â ß»‘√‘°ÿ≈™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°≈ÿ std Kt/V  ßŸ ¢πÈ÷ §«“¡º¥‘ ª°µ¢‘ Õß protein metabolism ≈¥≈ß ¿“«–¥ÕÈ◊ µÕà anabolic factors ‡™πà growth hormone, insulin ·≈– insulin-like growth factor (IGF) ≈¥≈ß, ‡æ¡Ë‘ °“√ uptake ¢Õß°≈‚Ÿ § ‚¥¬‰¡„à ™â insulin24  «à π°“√∑” LNHD ¡√’ “¬ß“πæ∫«“à DPI, nPNA ·≈– serum albumin ≈¥≈ߥߗ ∑‰Ë’ ¥°â ≈“à «¡“·≈«â ¢“â ßµπ⠥ߗ ππÈ— „π·ß¢à Õß ¿“«–‚¿™π“°“√·≈–æ∫«“à SDHD ®–¥°’ «“à LNHD 10. °“√§«∫§¡ÿ ª√¡‘ “µ√ “√πÈ”·≈–§«“¡¥π— ‚≈Àµ‘ ‡ªπì ∑∑’Ë √“∫°π— ¥«’ “à ‚√§À«— „®·≈–À≈Õ¥‡≈Õ◊ ¥‡ªπì  “‡Àµ°ÿ “√µ“¬Õπ— ¥∫— Àπß÷Ë ¢ÕߺªŸâ «É ¬ESRD‚¥¬ ‡ªπì  “‡Àµ∂ÿ ß÷ √Õâ ¬≈– 40-50 ®“°°“√√“¬ß“π¢Õߪ√–‡∑» À√∞— ‡¡√°‘ “·≈–·§π“¥“25 ºªâŸ «É ¬‚√§‰µ«“¬¡°— ¡’§«“¡¥—π‚≈À‘µ Ÿß¡“° µâÕß√—∫ª√–∑“π¬“≈¥§«“¡¥—π¡“°°«à“ 1 ™π‘¥ ·¡â«à“®–¡’°“√æ—≤π“‡∑§π‘§ ¢Õß°“√øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ „’ À¡Êà µ≈Õ¥‡«≈“ ·µ°à ‰Á ¡ à “¡“√∂≈¥Õ∫ÿ µ— ‡‘ Àµ°ÿ “√≥·å ≈–Õµ— √“µ“¬π≈’È ß‰¥â ºªŸâ «É ¬ CKD ¬ß— µÕâ ߇º™≠‘ °∫— ¿“«–§«“¡¥π—  ßŸ π”È ‡°π‘ À«— „®ÀÕâ ß≈“à ß´“â ¬‚µ (left ventricular hypertrophy, LVH) ·≈– hyperhomocysteinemia ·≈–¿“«–‡À≈à“π’ÈÕ“®¡’¡“°àÕπ∑’˺ŸâªÉ«¬‡√‘Ë¡∑”°“√∫”∫—¥√—°…“∑¥·∑π‰µ √«¡∑ß—È Õ“®√πÿ ·√ߢπ÷È À≈ß— ‡√¡‘Ë øÕ°‡≈Õ◊ ¥·≈«â ºŸâªÉ«¬∑’Ë∑”°“√øÕ°‡≈◊Õ¥·∫∫‡¥‘¡ (conventional intermittent HD) ®–¡’πÈ”§—Ëß„π√à“ß°“¬ À≈“¬°‘‚≈°√—¡°àÕπ®–∂÷ß«—πøÕ°§√—Èß∂—¥‰ª ´÷Ëß ¿“«–∑’ËπÈ”‡°‘π‡√◊ÈÕ√—ßπ’È®–∑”„À⇰‘¥§«“¡¥—π‚≈À‘µ Ÿß ‡°¥‘ À«— „®‚µ·≈–¡√’ –¥∫— homocysteine „π‡≈Õ◊ ¥‡æ¡Ë‘ ¢πÈ÷ °“√欓¬“¡¥ß÷ π”È ÕÕ°®“°√“à ß°“¬§√ßÈ— ≈–¡“°Ê ®–°àÕ„À⇰‘¥§«“¡¥—π‚≈À‘µµË” °“√øÕ°‡≈◊Õ¥·∫∫∂’Ë¢÷Èπ (daily HD, quotidian HD) ‡™◊ËÕ«à“™à«¬∑”„Àâ  ¿“«–πÈ”§—Ëß„π√à“ß°“¬≈¥≈ß ‡æ√“–°“√‡«âπ√–¬–Àà“ߢÕß°“√øÕ°‡≈◊Õ¥®– —Èπ≈ß º≈µàÕ°≈â“¡‡π◊ÈÕ À«— „®°®Á –≈¥≈ßµ“¡‰ª¥«â ¬ ∑”„À§â «∫§¡ÿ §«“¡¥π— ‰¥ßâ “à ¬¢π÷È ®“°°“√»°÷ …“¢Õß The London Daily/Nocturnal Hemodialysis Study ‰¥â»÷°…“∂÷ߺ≈µàÕ§«“¡¥—π‚≈À‘µ·≈–√–¥—∫ homocysteine „π™à«ß 18 ‡¥◊Õπ ∑∑’Ë ”°“√»°÷ …“æ∫«“à „π°≈¡ÿà SDHD ·≈– LNHD ®–¡√’ –¥∫— §«“¡¥π— ‚≈Àµ‘ ‡©≈¬’Ë °Õà πøÕ°‡≈Õ◊ ¥ (pre dialysis mean arterial blood pressure, MAP) ≈¥≈ß (p<0.04,0.03 µ“¡≈”¥∫— ) „π¢≥–∑°Ë’ ≈¡àÿ ∑øË’ Õ°‡≈Õ◊ ¥«∏‘ ‡’ ¥¡‘ ¡√’ –¥∫— §«“¡¥π— ‚≈Àµ‘ ‰¡‡à ª≈¬Ë’ π·ª≈ß ·≈–°“√‡ª≈¬Ë’ π·ª≈ßπæÈ’ ∫µ≈Õ¥™«à ߇«≈“ 18 ‡¥Õ◊ π∑∑Ë’ ”°“√»°÷ …“ πÕ°®“°π„’È π°≈¡ÿà SDHD ¬ß—  “¡“√∂≈¥®”π«π¬“≈¥§«“¡¥π— ‚≈Àµ‘ ‰¥√â Õâ ¬≈– 50 ‡©≈¬’Ë ·≈«â ≈¥≈ß 8.8 ‡∑“à „π¢≥–∑°Ë’ ≈¡àÿ LNHD ≈¥≈ß 3.3 ‡∑“à ·µ°à ≈¡ÿà §«∫§¡ÿ °≈∫— µÕâ ß√∫— ª√–∑“𬓇æ¡Ë‘ ¢πÈ÷ 1.4 ‡∑“à 26 ºªâŸ «É ¬∫“ß §π “¡“√∂ߥ¬“≈¥§«“¡¥π— ‚≈Àµ‘ ‰¥¥â «â ¬ (√ªŸ ∑Ë’ 8) „π°≈ÿà¡ SDHD ®–¡’πÈ”Àπ—°‡æ‘Ë¡¢÷Èπ√–À«à“ß session πâÕ¬≈ß ¿“¬„π 3 ‡¥◊ÕπÀ≈—ß®“°∑’Ë ‡ª≈¬Ë’ π°“√√°— …“¡“‡ªπì SDHD æ∫«“à ®–¡π’ ”È Àπ°— ‡æ¡Ë‘ ¢πÈ÷ „π·µ≈à – session πÕâ ¬≈ß¡“° „π°≈¡àÿ LNHD ®–¡’°“√‡æ‘Ë¡¢÷Èπ¢ÕßπÈ”Àπ—°‡™àπ°—π∑’ˇ«≈“ 6 ·≈– 15 ‡¥◊Õπ (p<0.05) ·µà„π°≈ÿࡧ«∫§ÿ¡®–‰¡à¡’°“√ ‡ª≈’ˬπ·ª≈ߢÕß°“√‡æ‘Ë¡À√◊Õ≈¥¢ÕßπÈ”Àπ—°√–À«à“ß°“√øÕ°‡≈◊Õ¥·µà≈–§√—Èß æ∫«à“√–¥—∫ serum homocysteine ®– ßŸ °«“à „π°≈¡àÿ §«∫§¡ÿ Õ¬“à ß¡π’ ¬—  ”§≠— °“√µ√«®«¥— extracellular fluid volume (ECFV) ®–¡§’ “à ≈¥≈ß„π°≈¡àÿ SDHD ·µ„à π°≈¡àÿ LNHD ®–‰¡µà “à ß®“°°≈¡àÿ §«∫§¡ÿ °“√‡æ¡Ë‘ §«“¡∂¢Ë’ Õß°“√øÕ° ‡≈Õ◊ ¥®–∑”„Àπâ ”È Àπ°— µ«— ¢ÕߺªŸâ «É ¬‡æ¡Ë‘ ¢πÈ÷ ‰¡¡à “°√–À«“à ß session ‡æ√“–§“à ECFV27 ≈¥≈ß ·≈– ¡— æπ— ∏å

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π‘™ 177 √ªŸ ∑Ë’ 8 ®”π«π¬“≈¥§«“¡¥π— ‚≈Àµ‘ ∑√Ë’ ∫— ª√–∑“π„π°“√»°÷ …“∑ßÈ— 3 «∏‘ ,’ *· ¥ß∂ß÷ π¬—  ”§≠— ∑“ß ∂µ‘ ‘ °∫— °“√∑§Ë’ «“¡¥π— ‚≈Àµ‘ ≈¥≈ߥ«â ¬ ·µ„à π°≈¡àÿ LNHD °≈∫— ¡’ interdialytic weight gain ‡æ¡Ë‘ ¢πÈ÷ Õ“®‡ªπì ‡æ√“–ºªâŸ «É ¬¥¡◊Ë πÈ”‰¥¡â “°¢π÷È ∂ß÷ ·¡«â “à °≈¡ÿà LNHD®–¡π’ È”Àπ°— ‡æ¡‘Ë ¢π÷È ¡“°·µ§à «“¡¥π— ‚≈Àµ‘ ‡©≈¬’Ë °≈∫— ≈¥≈ß ´÷ËßÕ∏‘∫“¬®“°°“√øÕ°‡≈◊Õ¥π“π¢÷Èπ®– “¡“√∂¢®—¥ vasoactive mediator ÕÕ°‰¥â‡æ‘Ë¡¢÷È𠧫“¡¥—π ‚≈Àµ‘ ®ß÷ ≈¥≈ß‚¥¬‰¡¢à πÈ÷ °∫— ª√¡‘ “µ√ “√π”È πÕ°®“°πÈ’ LNHD ‡ªπì °“√„™â blood flow ™“â Ê ∑”„À¡â °’ “√ °√–µÿâπ√–∫∫´‘¡æ“‡∏µ‘§πâÕ¬≈ß ∑”„À⧫“¡¥—π‚≈À‘µ≈¥≈ß¡“‰¥â √“¬ß“πÕ◊Ëπ∑’ˇ§¬¡’ºâŸ√“¬ß“π‡°’Ë¬«°—∫ °“√§«∫§¡ÿ §«“¡¥π— ‚≈Àµ‘ „π°≈¡àÿ SDHD ·≈– LNHD ¥ß— · ¥ß„πµ“√“ß∑Ë’ 6 11. Calcium-phosphorus balance æ∫¿“«–øÕ ‡øµ§—Ë߉¥â∫àÕ¬„πºŸâ∑’Ë∑”°“√øÕ°‡≈◊Õ¥·∫∫‡¥‘¡ 3 §√—Èß/ —ª¥“Àå ·≈–‡ªìπªí®®—¬ ∑πË’ ”¡“ ¿àŸ “«– secondary hyperparathyroidism πÕ°®“°π¿È’ “«–øÕ ‡øµ§ßË— ®–∑”„À√â –¥∫— ·§≈‡´¬’ ¡„π ‡≈Õ◊ ¥≈¥µË”≈ßπÕ°®“°ππ—È °“√„À â “√®∫— øÕ ‡øµ„π√ªŸ ¢Õß·§≈‡´¬’ ¡√«à ¡°∫— °“√„À«â µ‘ –¡π‘ ¥·’ ≈–dialysate ∑¡Ë’ ·’ §≈‡´¬’ ¡ ßŸ ®–∑”„À‡â °¥‘ ¿“«–·§≈‡´¬’ ¡„π‡≈Õ◊ ¥ ßŸ ·≈–‡°¥‘ metastatic calcification ‰¥â ¥ß— ππÈ— °“√ øÕ°‡≈Õ◊ ¥‚¥¬∑«Ë— ‰ª®–æ∫√«à ¡°∫— §«“¡º¥‘ ª°µ¢‘ Õߥ≈ÿ ·§≈‡´¬’ ¡·≈–øÕ øÕ√ — ‰¥∫â Õà ¬ °“√∑¢Ë’ ∫«π°“√ hemodialysis∏√√¡¥“‰¡ à “¡“√∂®–¢®¥— øÕ øÕ√ — ‰¥¡â “°æÕ‡ªπì ‡æ√“– «à π„À≠øà Õ øÕ√ — ®–Õ¬„Ÿà π‡´≈≈å „π™à«ß·√°¢Õß°“√øÕ°‡≈◊Õ¥ √–¥—∫øÕ øÕ√— ®–≈¥µË”≈ß¡“°∑’ˇ«≈“ª√–¡“≥ 120 π“∑’ ‚¥¬®–¢®—¥ øÕ ‡øµ„ππÈ”πÕ°‡´≈≈åÕÕ°‰ª°àÕπ ·≈â«øÕ ‡øµ„π‡´≈≈å®÷߇§≈◊ËÕπÕÕ°¡“ àŸπÕ°‡´≈≈å øÕ ‡øµ®– ÕÕ°‰ª°∫— π”È ¬“ dialysate „π∑ Ë’ ¥ÿ ·≈–¡’ post dialysis rebound ‰¥â ¥ß— ππÈ— ª®í ®¬— ∑‡Ë’ ªπì µ«— °”Àπ¥„π°“√ ¢®—¥øÕ ‡øµ§◊Õ§«“¡‡√Á«„π°“√¢®—¥„π phase ·√° ´÷Ëߢ÷Èπ°—∫√–¥—∫øÕ øÕ√— „π‡≈◊Õ¥·≈–æ◊Èπ∑’˺‘«¢Õß µ«— °√Õß ª®í ®¬— ∑¡Ë’ º’ ≈µÕà °“√¢®¥— øÕ ‡øµ„π√–¬–∑ Ë’ ÕߧÕ◊ °“√‡§≈ÕË◊ 𵫗 ¢Õß phosphate pool ®“°„π ‡´≈≈ å πŸà ”È πÕ°‡´≈≈å (√ªŸ ∑Ë’ 9)

New Frontiers in Dialysis 178 ∏𵑠®√‘ ππ— ∑∏å «™—  √‘ ‘¿“ ™“â ß»‘√‘°ÿ≈™¬— ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ÿ‡¡∏°ÿ≈ µ“√“ß∑’Ë 6 Systolic blood pressure ·≈– Mean blood pressure À≈ß— ‡ª≈¬Ë’ π°“√√°— …“®“° IHD ¡“‡ªπì SDHD ·≈– NHHD Reference Model No. Interval (mon) MAP (mm Hg) SBP (mm Hg) Change P of Patients (mm Hg) Buoncristiani SDHD/12 et al, 1988 26.7 (mean) NA 157±10 to 132±11 -26 NA Buoncristiani SDHD/50 et al, 1997 12 105±20 to 96±15 NA -10 <0.001 Traeger et al, SDHD/4 12 108±8 to 96±5 145±16to 127±7 -18 (SBP) NA (SBP) 1998 -12 (MAP) <0.01(MAP) Ting et al, SDHD/6 6.3 (mean) NA 146±15 to 133±16 -13 <0.04 1998 Kooistra and SDHD/13 6 102±10 to 95±12 141±17 to 131±19 -10 (SBP) -7 (MAP) <0.05 (both) Vos, 1999 Pinciaroli, SDHD/12 12 NA 174 to 141 -33 NA 1999 12 NA Only changes noted -7 (all) 0.02 (all) Woods et al, SDHD/72 -13 (meds) <0.01(meds) 1999 Mohr et al, NHHD/6 NA NA 150 to 120 -30 NA 1999 º≈¢Õß daily HD µàÕ¥ÿ≈·§≈‡´’¬¡·≈–øÕ øÕ√— ¬—߉¡à¡’°“√»÷°…“°—π·æ√àÀ≈“¬π—° º≈°“√ »°÷ …“¢Õß The London Daily/Nocturnal Hemodialysis Study æ∫«“à °“√øÕ°‡≈Õ◊ ¥·∫∫ SDHD ·≈– LNHD ‰¡‰à ¥∑â ”„À√â –¥∫— ·§≈‡´¬’ ¡‡ª≈¬’Ë π·ª≈ß·µ‡à ¡Õ◊Ë ‡∑¬’ ∫°π— ‡Õß„π√–À«“à ß2°≈¡ÿà æ∫«“à √–¥∫— ·§≈‡´¬’ ¡„π°≈¡ÿà LNHD ®–µ”Ë °«“à SDHD Õ¬“à ß¡π’ ¬—  ”§≠— (p = 0.009)  «à π√–¥∫— øÕ øÕ√ — ®–µ”Ë  ¥ÿ „π°≈¡àÿ LNHD ´ßË÷ æ∫«“à µ”Ë °«“à °≈¡àÿ SDHD ∑‡Ë’ «≈“ 18 ‡¥Õ◊ π (3.9 mg/dl „π°≈¡àÿ LNHD ·≈– 5.5 mg/dl „π°≈¡àÿ SDHD) πÕ°®“°π—Èπ°“√„™â phosphate binder °Á≈¥≈ß¡“°„π°≈ÿà¡ LNHD ¥—ßπ—Èπº≈§Ÿ≥¢Õß·§≈‡´’¬¡·≈– øÕ øÕ√ — ®ß÷ µ”Ë ≈ß¡“°∑ Ë’ ¥ÿ „π°≈¡àÿ LNHD §“à serum alkaline phosphatase  ßŸ ¢πÈ÷ ∑ßÈ— „π°≈¡àÿ SDHD ·≈– LNHD ·µ„à π°≈¡àÿ LNHD ®– ßŸ °«“à °“√‡ª≈¬Ë’ π·ª≈ߢÕߧ“à iPTH °‡Á ™πà ‡¥¬’ «°π— °≈“à «§Õ◊ ®– ßŸ ¢πÈ÷ ∑ßÈ— 2 °≈¡àÿ ·µ„à π°≈¡àÿ LNHD ®– ßŸ ¢πÈ÷ ¡“°°«“à ( ßŸ  ¥ÿ 777.4 pg/ml) (‡∑¬’ ∫°∫— SDHD 138.9 pg/ml ·≈–„π °≈ÿࡧ«∫§ÿ¡ 144.6 pg/ml) Yuen ·≈–§≥–29 °Áæ∫°“√‡ª≈’ˬπ·ª≈ߢÕß predialsis serum phosphate concentration ‡™πà °π— °≈“à «§Õ◊ ¡§’ “à ≈¥≈ßÕ¬“à ß¡π’ ¬—  ”§≠— ·µ§à “à iPTH ≈¥≈ß · ¥ß«“à °“√‡æ¡Ë‘ §«“¡∂Ë’ ¢Õß°“√øÕ°‡≈Õ◊ ¥¡º’ ≈≈¥√–¥∫— øÕ øÕ√ — ‰¥¡â “°°«“à °“√‡æ¡‘Ë ‡«≈“ ·µà LNHD ®–≈¥øÕ øÕ√ — ‰¥¡â “°°«“à ‡æ√“–¡°’ “√‡æ¡‘Ë ∑ß—È ‡«≈“·≈–§«“¡∂’Ë °“√∑” SDHD ¬ß— §ßµÕâ ß„™â phosphate binder √«à ¡¥«â ¬ „π¢≥–∑L’Ë NHD Õ“® “¡“√∂À¬ÿ¥°“√„™â phosphate binder ‰¥â √“¬ß“πÕ◊Ëπ∑’ˇ§¬¡’ºŸâ»÷°…“‡°’ˬ«°—∫º≈¢Õß SDHD µàÕ √–¥∫— øÕ øÕ√ — „π‡≈Õ◊ ¥¥ß— „πµ“√“ß∑Ë’ 7 Achinger ·≈–§≥–30 ‰¥»â °÷ …“ºªâŸ «É ¬ 77 §π ∑”°“√øÕ°‡≈Õ◊ ¥

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏π—𥓠µ√–°“√«π‘™ 179 √ªŸ ∑’Ë 9 (A) · ¥ß°“√¢®¥— øÕ ‡øµ√–À«“à ߢ∫«π°“√ hemodialysis ´ßË÷ Õµ— √“°“√¢®¥— ®– ßŸ ∑ Ë’ ¥ÿ „π™«Ë— ‚¡ß·√° ®“°¿“æ· ¥ß°“√¢®¥— øÕ ‡øµµÕà ‡«≈“∑ºË’ “à π‰ª ‡¡ÕË◊ „™â blood flow 300 cc/min, dialysate flow 500 cc/min; (B) · ¥ß°“√¢®¥— øÕ ‡øµ¢≥–øÕ°‡≈Õ◊ ¥ ´ßË÷ ¡’ 2 √–¬– „π√–¬–·√° rate-limiting step §Õ◊ §«“¡‡√«Á ∑øË’ Õ ‡øµ‡§≈ÕË◊ πÕÕ°®“° ECF, √–¬–∑Ë’ 2 §Õ◊ ‡¡ÕË◊ øÕ øÕ√ — ≈¥≈ß∂ß÷ ®¥ÿ µ”Ë  ¥ÿ ·≈– rate- limiting step §Õ◊ Õµ— √“°“√‡§≈ÕË◊ π∑¢Ë’ ÕßøÕ ‡øµ®“°‡πÕÈ◊ ‡¬ÕË◊ ∑°ÿ «π— §√ß—È ≈– 3 ™¡ 6 «π— / ª— ¥“Àå æ∫«“à §“à øÕ ‡øµ≈¥≈ß®“° 6.3 ± 2.578 mg/dl ¡“‡ªπì 4.61 ± 0.6 mg/ dl ≥ ‡«≈“ 6 ‡¥Õ◊ π (p<0.004) §“à iPTH ≈¥≈ß ®“°√Õâ ¬≈– 55 ¡“‡ªπì √Õâ ¬≈– 40 ·≈– “¡“√∂≈¥ª√¡‘ “≥ phosphate binder ‰¥√â Õâ ¬≈– 73 ‡¡ÕË◊ ∑”°“√øÕ°‡≈Õ◊ ¥·∫∫∑°ÿ «π— ®– “¡“√∂∑”𓬠Jdip ‰¥¥â ß— πÈ’ Jdip = N × t × Kdip × Cdip [1 - 0.44(1 - exp[-0.0163×t]) / 7] ––––– 1 ‡¡ÕË◊ n = ®”π«π dialysis/ ª— ¥“Àå T = treatment time Kdip = dialyzer phosphate clearance Cdip = Predialysis concentration [1-0.44 (1-exp[-0.0103×t] „™‡â ª≈¬Ë’ π Cdip ‡ªπì time-averaged concentration ¢≥– dialysis

New Frontiers in Dialysis 180 ∏𵑠®‘√ππ— ∑å∏«—™  √‘ ‘¿“ ™“â ß»√‘ °‘ ≈ÿ ™—¬ ∏π—𥓠µ√–°“√«π™‘ « —πµå  ‡ÿ ¡∏°ÿ≈ µ“√“ß∑Ë’ 7  √ªÿ °“√»°÷ …“¢Õß Daily dialysis µÕà º≈¢Õß·§≈‡´¬’ ¡·≈–øÕ øÕ√ — ∑ºË’ “à π¡“ Author No.of Dialysis modality Prescription/ Phosphorus Other Subjects (duration) control factors Kooistra 13 Daily home hemodialysis 6 time weekly (6 months) Decrease dose of Decreased blood P binder pressure in hypertensive patients Uldall 5 Nocturnal hemodialysis 5-7 nighs/wk, 8 hrs/night, Discontinue P binder Increased dietary (6-16 months) use protein intake Mucsi 7 Nocturnal hemodialysis 6 nights/wk, 8 hrs/night. Discontinue P binder Increased dietary (5 months) use protein intake Lindsay 12 Nocturnal hemodialysis 5-6 nights/wk,6-8 hrs/night, Decreased use of P Improved blood (5-36 months) binder, Decreased pressure control, Ca x P product Improved QOL 11 Short daily hemodialysis 5-6 days/wk. 1.5-2.5 Decreased Ca x P Improved blood hrs/day, (5.36 months) Product pressure control, Improved QOL Mizani 51 Conventional hemodialysis 3 days/wk, 4 hrs/day No change in Decrease iPTH (1 year) phosphorus, continued use of phosphate binders 26 Short daily hemodialysis 6 days/wk, 3 hrs/day Decreased serum Decrease iPTH (1 year) phosphorus, 73% patients discontinue the use of phosphate binder at 12 months ®“° ¡°“√¥—ß°≈à“«  “¡“√∂π”¡“∑”‡ªìπ°√“ø ‡ª√’¬∫‡∑’¬∫ t ·≈– Kdip ‰¥â¥—ß√Ÿª∑’Ë 10 ‡ªπì °“√øÕ°‡≈Õ◊ ¥·∫∫∏√√¡¥“ ·≈–√ªŸ ∑Ë’ 11 ‡ªπì °“√øÕ°‡≈Õ◊ ¥·∫∫ SDHD ·≈– LNHD ®–‡ÀπÁ «“à „π°“√ øÕ°‡≈Õ◊ ¥¥«â ¬«∏‘ ∏’ √√¡¥“∂“â „™‡â «≈“øÕ°‡≈Õ◊ ¥π“π 6.5 ™¡ √«à ¡°∫— dialyzer F80 ®– “¡“√∂¢®¥— øÕ ‡øµ‰¥â 900 mg/«π— ·µ∂à “â „™µâ «— °√Õß„À≠Õà “®„™‡â «≈“≈¥‡À≈Õ◊ 4.5 ™¡ ‡∑“à ππÈ— „π°“√øÕ°‡≈Õ◊ ¥·∫∫ dialy HD (SDHD) Jdip ∂°Ÿ ®”°¥— ‡ªπì 500-800 mg/«π— ·≈–‰¡µà Õâ ß„™â phosphate binder ‡≈¬∂“â ª√∫— „Àâ n PCR Õ¬„àŸ π™«à ß 0.8/1.0 °√¡— /«π— ‡¡ÕË◊ 𔧓à std Kt/V ¡“plot °∫— Jdip ®–‰¥‡â ªπì ‡ πâ ‚§ßâ µ“¡√ªŸ ∑Ë’ 10 æ∫«“à ∂“â std Kt/V = 4.0 ®–∑”„À¡â °’ “√¢®¥— øÕ ‡øµ¡“°¢πÈ÷ ®π‰¡µà Õâ ß„™â phosphate binder ‰¥â

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π‘™ 181 √ªŸ ∑’Ë 10 · ¥ß°“√¢∫— øÕ ‡øµ‡¡ÕË◊ ∑”°“√øÕ°‡≈Õ◊ ¥·∫∫∏√√¡¥“ „πºªâŸ «É ¬∑¡Ë’ §’ “à Kdip 72-225 l/min ·≈–¡§’ “à nPCR 0.8-1.4 g/day √ªŸ ∑Ë’ 11 · ¥ß°“√¢®¥— øÕ ‡øµµÕà «π— ‡¡ÕË◊ ∑”°“√øÕ°‡≈Õ◊ ¥·∫∫ SDHD ·≈– LNHD 12. Model ¢Õß phosphate balance in dialysis therapy Phosphate µà“ß°—∫¬Ÿ‡√’¬ µ√ß∑’Ë√–¥—∫¢ÕßøÕ ‡øµ®–‡ªìπµ—«∫Õ°√–¥—∫§«“¡‡ªìπæ‘… ¥—ßπ—Èπ ®ß÷ µÕâ ß¡§’ «“¡æ¬“¬“¡∑®’Ë –§«∫§¡ÿ √–¥∫— øÕ ‡øµ„ÀÕâ ¬„àŸ π‡°≥±ªå °µ‘ Model

New Frontiers in Dialysis 182 ∏π‘µ ®√‘ ππ— ∑å∏«™—  ‘√¿‘ “ ™“â ß»‘√‘°≈ÿ ™¬— ∏π—𥓠µ√–°“√«π‘™ « π— µå  ÿ‡¡∏°≈ÿ d (CaPO4) dt = Gip-Kdip(TACip)-Ksip×Cip ––––– 1 ‡¡ÕË◊ d (CaPO4) dt ‡ªπì Õµ— √“°“√ – ¡¢Õß CaPO4 „π‡πÕÈ◊ ‡¬ÕË◊ Gip = Õµ— √“°“√º≈µ‘ øÕ ‡øµ·≈–¥¥Ÿ ´¡÷ ®“°°√–‡æ“–Õ“À“√ Kdip(TACip) = Õµ— √“°“√¢®¥— øÕ ‡øµ¢Õßµ«— °√Õß ·≈–§“à time averaged serum concentration ¢≥– dialysis Ksip×Cip = º≈§≥Ÿ ¢Õß°“√¥¥Ÿ ´¡÷ øÕ ‡øµ∑“ߪ“° ®¥ÿ ¡ßàÿ À¡“¬¢Õß°“√øÕ°‡≈Õ◊ ¥ §Õ◊ 欓¬“¡≈¥ d (Ca PO4)/dt „À‡â ªπì »πŸ ¬å ¥ß— ππÈ— 0 = Gip-Kdip(TACip)-Ksip×Cip ––––– 2 „π°√≥’ SDHD ·≈– LNHD ®–ª√–‡¡π‘  ¡°“√ 2 ‚¥¬‰¡„à ™â sorbent therapy ∑”„Àµâ ¥—  ¡°“√ ÕÕ°‡À≈Õ◊ ‡ªπì Kdip(TACip) = Gip ––––– 3  ¡°“√ 3 · ¥ß«“à ∂“â Kdip(TACip) < Gip Õ“®µÕâ ß°“√ sorbent À√Õ◊ ¡©‘ –ππÈ— √–¥∫— øÕ ‡øµ®– §ßË— ‰¥â ·µ∂à “â Kdip(TACip) > Gip ®–¡¿’ “«–æ√Õà ßøÕ ‡øµ Phosphate Profile ¢≥– dialysis æ∫«à“√–¥—∫øÕ ‡øµ®–≈¥≈ß„π™—Ë«‚¡ß·√°·≈–®–‡æ‘Ë¡¢÷Èπ„π™—Ë«‚¡ß∂—¥‰ª¢Õß°“√øÕ°‡≈◊Õ¥ ®“°»°÷ …“¢Õß Desoi ·≈– Uman æ∫«“à Cn = Ct/Co ––––– 4 Co = Predialysis concentration Ct = all sequential intradialysis concentration ·≈«â §”π«≥ time averaged normalized concentration (TACnip) ®“° TAC nip = [fto d (Cnip)/dt]/t ––––– 5 ®“°°“√»°÷ …“π”√Õà ß„πºªâŸ «É ¬ 6 √“¬ ∑”„À‰â ¥§â “à TACnip = 0.64 ·≈–·∑π§“à ‰¥¥â ß— π’È TAC nip = 1-0.44 (1-exp[-0.0163xt]) ––––– 6 ·µ∂à “â ‡ªπì °“√øÕ°‡≈Õ◊ ¥·∫∫ LNHD §«√¡§’ “à StdKt/V = 5.0 ®ß÷ ®– “¡“√∂¢®¥— øÕ ‡øµ‰¥â ¿“æ‚¥¬√«¡ ‡Õߧ«“¡ ¡— æπ— ∏¢å Õß nPCR ·≈–Õµ— √“°“√¢®¥— øÕ ‡øµ¢Õß°“√∑” SDHD ·≈– CNHD ¥ß— · ¥ß„π√ªŸ ∑Ë’ 11 ¥ß— · ¥ß„À‡â ÀπÁ ∂ß÷ °“√¢∫— øÕ ‡øµ¢πÈ÷ °∫— ¢π“¥µ«— °√Õß·≈–ª√¡‘ “≥ nPCR 13. °“√¢∫— Middle molecules ®“°°“√§”π«≥§“à equivalent renal clearance (EKR) ·≈– StdKt/V Gold farm-Rumyantzev ·≈– §≥–31 æ∫«“à Õµ— √“°“√¢®¥— «µ‘ “¡π‘ ∫’ 12 ®–‡æ¡Ë‘ ¢πÈ÷ ¡“°°«“à «∏‘ °’ “√øÕ°‡≈Õ◊ ¥∏√√¡¥“√Õâ ¬≈– 16.1 («¥— ‚¥¬ EKR) ·≈–√Õâ ¬≈– 25.7 («¥— ‚¥¬ Std Kt/V) ·µ∂à “â „™«â ∏‘ ’ LNHD ®–æ∫«“à Õµ— √“°“√¢®¥— ∑ßÈ—  “√‚¡‡≈°≈ÿ

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏ππ— ¥“ µ√–°“√«π™‘ 183 µ“√“ß∑’Ë 8 Std Kt/V Values ¢≥–∑” Conventional HD, Short Daily HD ·≈– Long HD Std Kt/V Conventional Short Daily Long HD Solute HD HD 3.26 (35.8) 2.98 (43.3) Urea 2.40 3.26 (35.8) 2.27 (57.6) 3.67 (45.6) Creatinine 20.8 2.72 (30.8) 4.90 (16.1) Vitamin B12 1.44 1.81 (25.7) Inulin 2.58 3.02 (17.1) B2-Microglobulin 4.22 4.47 (5.9) ‡≈°Á ·≈–‚¡‡≈°≈ÿ „À≠®à –‡æ¡Ë‘ ¢πÈ÷ ¡“° (µ“√“ß∑Ë’ 8)  «à πÕµ— √“°“√¢®¥— β2-microglobulin ‡æ¡Ë‘ ¢πÈ÷ √Õâ ¬≈– 2.5 («¥— ‚¥¬ EKR) ·≈–√Õâ ¬≈– 5.9 («¥— ‚¥¬ std Kt/V) 14. ¿“«–´¥’ ®“°°“√»÷°…“¢Õß Ting ·≈–§≥–æ∫«à“°“√∑” daily HD  “¡“√∂≈¥§«“¡µâÕß°“√¬“ erythropoietin ≈߉¥√â Õâ ¬≈– 45 (®“°‡¥¡‘ 22.1±17.0 × 103 u/WK) ‡À≈Õ◊ 12.6±14.0 ×103 u/WK) (P = 0.0001) À≈ß— °“√»°÷ …“ 12 ‡¥Õ◊ π Õ¬“à ߉√°¥Á §’ “à hematocrit ¡°— ‰¡§à Õà ¬‡ª≈¬Ë’ π·ª≈ß transferrin saturation Õ¬„àŸ π √–¥∫— ª°µ‘  «à π°“√»°÷ …“¢Õß Williams ·≈–§≥–32 æ∫«“à §“à ¥™— π¢’ Õß√–∫∫‚≈Àµ‘ «∑‘ ¬“‰¡‰à ¥·â µ°µ“à ß°π— ‡≈¬√«¡∑ßÈ— ¢π“¥¢ÕߌÕ√‚å ¡π erythropoietin ¥«â ¬ 15. Vascular access ®“°°“√»°÷ …“¢Õß Ting ·≈–§≥–„π°“√»°÷ …“ SDHD π“π 12 ‡¥Õ◊ π æ∫«“à ¡ª’ ≠í À“®“°°“√ „™‡â  πâ 0.94 problem/access-year ´ß÷Ë ‰¡µà “à ß®“°°“√∑”°“√øÕ°‡≈Õ◊ ¥·∫∫∏√√¡¥“ vascular access survival ∑‡Ë’ «≈“ 12, 24, 36 ·≈– 48 ‡¥Õ◊ π §Õ◊ √Õâ ¬≈– 100, 89, 89 ·≈– 80 µ“¡≈”¥∫— 33 16. Hospitalization æ∫«“à °“√øÕ°‡≈Õ◊ ¥·∫∫ SDHD ∑”„ÀÕâ µ— √“Õ¬‚àŸ √ß欓∫“≈≈¥≈ß®“°√Õâ ¬≈– 34.4 ¡“‡ªπì 8.0 «—π/®”π«πºâŸªÉ«¬/ªï  “‡Àµÿ à«π„À≠à¢Õß°“√πÕπ‚√ß欓∫“≈§◊Õ À—«„®«“¬‡≈◊Õ¥§—Ëß  à«πÕ—µ√“µ“¬¢÷Èπ °—∫«à“ºâŸªÉ«¬¡’ªí®®—¬‡ ’ˬߡ“°πâÕ¬‡æ’¬ß„¥ ∂â“¡’ªí®®—¬‡ ’ˬߡ“°®–¡’Õ—µ√“√Õ¥πâÕ¬°«à“ºŸâ∑’Ë¡’ªí®®—¬‡ ’Ë¬ß πÕâ ¬°«“à (√ªŸ ∑Ë’ 12)

New Frontiers in Dialysis 184 ∏π‘µ ®√‘ ππ— ∑å∏«—™  ‘√¿‘ “ ™“â ß»√‘ ‘°≈ÿ ™—¬ ∏ππ— ¥“ µ√–°“√«π™‘ « π— µå  ÿ‡¡∏°≈ÿ √ªŸ ∑Ë’ 12 · ¥ßÕµ— √“√Õ¥™«’ µ‘ „πºªâŸ «É ¬∑∑Ë’ ” SDHD therapy „πºªâŸ «É ¬ 42 √“¬ æ∫«“à ∑ÕË’ µ— √“√Õ¥™«’ µ‘ √Õâ ¬≈– 50 ∑‡Ë’ «≈“ 32 ‡¥Õ◊ π ·≈–√Õâ ¬≈– 33 ∑‡Ë’ «≈“ 6 ªï 17. §≥ÿ ¿“晫’ µ‘ æ∫«“à °“√øÕ°‡≈Õ◊ ¥∂¢’Ë π÷È ∑”„À§â ≥ÿ ¿“晫’ µ‘ ¥¢’ π÷È 34°“√»°÷ …“∑º’Ë “à π¡“ √ªÿ ∂ß÷ °“√‡ª≈¬’Ë π·ª≈ß ¢Õߧ≥ÿ ¿“晫’ µ‘ À≈ß— °“√∑” SDHD ∑‡Ë’ §¬¡√’ “¬ß“π¡“„πÕ¥µ’ ¢Õâ ¥·’ ≈–√“¬≈–‡Õ¬’ ¥¢Õߧ≥ÿ ¿“晫’ µ‘ ∑Ë’ ¥¢’ πÈ÷ ‰¥·â °à Õ“°“√ÕÕà π‡æ≈¬’ À≈ß— °“√øÕ°‡≈Õ◊ ¥, Õ“°“√πÕπ‰¡Àà ≈∫— ´ßË÷ æ∫«“à „π°≈¡àÿ SDHD ®–¡Õ’ “°“√ postdialysis fatigue ≈¥≈ß Pinciaroli √“¬ß“𧫓¡ “¡“√∂∑“߇滠—¡æ—π∏奒¢÷ÈπÀ≈—ß®“°‡ª≈’ˬπ°“√ √°— …“¡“‡ªπì SDHD ·≈–æ∫«“à cognitive function ¥¢’ π÷È ≈¥°“√‡°¥‘ delusion ·≈–hallucination °“√»°÷ …“¢Õß Lacson ·≈–§≥– ·≈–√“¬ß“πÕπ◊Ë Ê æ∫«“à °“√«¥— §≥ÿ ¿“晫’ µ‘ ‡™πà KSQOL, CHEQ score ®–¥¢’ π÷È „π SDHD ·≈– LNHD Õ“°“√µ“à ßÊ ∑‡Ë’ °¥‘ ¢πÈ÷ √–À«“à ß°“√øÕ°‡≈Õ◊ ¥°¥Á ¢’ πÈ÷ ‡™πà cramp §«“¡¥π— ‚≈Àµ‘ µ”Ë ‡«¬’ π»√’ …– ‡ªπì µπâ 18. ¢Õâ ®”°¥— ¢Õß Daily dialysis ¢Õâ ®”°¥— ¢Õß SDHD §Õ◊ °“√µÕâ ߇¥π‘ ∑“ß¡“øÕ°‡≈Õ◊ ¥∂ß÷  ª— ¥“À≈å – 6 §√ßÈ— ´ß÷Ë ∂Õ◊ ‡ªπì §“à „™®â “à ¬ ∑‡’Ë æ¡‘Ë ¡“°¢π÷È 36 ·µ à ”À√∫— º∑Ÿâ ∑’Ë ” long nocturnal HD Õ“®‰¡¡à ª’ ≠í À“¥“â π°“√‡¥π‘ ∑“ß ·µ°à µÁ Õâ ßΩ°ñ °“√øÕ° ‡≈Õ◊ ¥‡Õß∑∫Ë’ “â π (home hemodialysis) Õ¬“à ߉√°¥Á ¡’ º’ æŸâ ∫«“à „πÕ𓧵¡·’ π«‚π¡â ∑ºË’ ªâŸ «É ¬Õ“®Àπ— ¡“ π„® ∑” daily HD ‡æ¡Ë‘ ¢πÈ÷ ‡æ√“–ºªŸâ «É ¬∑‡Ë’ ¥¡‘ øÕ°‡≈Õ◊ ¥®–æ∫¿“«–·∑√°´Õâ π¡“°¢πÈ÷ ¡’ adequacy of HD ‰¡‡à 欒 ßæÕ  √ªÿ ‡Àµºÿ ≈∑µË’ Õâ ß√Õ°“√»°÷ …“‡√ÕË◊ ß daily dialysis ‡æ¡Ë‘ ¥ß— · ¥ß„πµ“√“ß∑Ë’ 9

Whatûs New in Hemodialysis, Daily Hemodialysis? ∏π—𥓠µ√–°“√«π‘™ 185 µ“√“ß∑Ë’ 9 ‡Àµºÿ ≈∑¬Ë’ ß— µÕâ ß»°÷ …“‡√ÕË◊ ß Daily hemodialysis (DHD) µÕà ‡æ¡Ë‘ ‡µ¡‘ Quality of current evidence supporting DHD Major selection bias in present studies Lack of randomized trials Differences in infrastructure required for NHD versus SDHD A randomized trial examining NHD and SDHD is starting Potential adverse effects on nutritional status Potential adverse effect on hemodialysis angioaccess Comparison of adequacy of regimens must be validated 19.  √ªÿ ªí®®ÿ∫—π‰¥â¡’§«“¡ π„®∑’Ë®–∑”°“√øÕ°‡≈◊Õ¥‚¥¬‡æ‘Ë¡§«“¡∂’ËÀ√◊Õ‡«≈“„Àâ¡“°¢÷Èπ‚¥¬¡’¢âÕ¥’ À≈“¬ª√–°“√∑’ˉ¥â°≈à“«¡“ ·µà¬—ß¡’ªí®®—¬À≈“¬ª√–°“√∑’ˬ—ßµâÕß√Õ°“√»÷°…“µàÕ¥—ß∑’Ë √ÿª„πµ“√“ß∑’Ë 9 ´ßË÷ ¬ß— µÕâ ß¡°’ “√»°÷ …“‚¥¬„™â sample size ∑¡Ë’ “°°«“à πÈ’ ·≈–√–¬–‡«≈“π“π¢πÈ÷ ¢Õâ ¥Õ’ ¬“à ß·ππà Õπ¢Õß daily HD §Õ◊ ‡æ¡Ë‘ adequacy of dialysis ·µ°à √–ππÈ— º≈µÕà Õµ— √“°“√µ“¬·≈–Õµ— √“°“√Õ¬√àŸ Õ¥‰¡·à π™à ¥— §ßµÕâ ß Õ“»¬— °“√»°÷ …“µÕà ‰ª„πÕ𓧵 ‡Õ° “√Õ“â ßÕß‘ 1. Laupacis A, Keown P, Puis N, Drueger H, Ferguson B, Wong C, Muerhead N. A study of the quality of life and cost-utility of renal transplantation. Kidney Int 1996; 50:235-42. 2. Kjellstrand C, Evans R, Petersen R, Shideman J, von Hartitzsch B, Buselmeier T. The çunphysiologyé of dialysis: A major cause of dialysis side effectsû. Kidney Int Suppl2 1975; s30-4. 3. Charra B, Calemard E. Cuche M. Laurent G. Control of hypertension and prolonged survival on maintenance hemodialysis. Nephron 1983;33:96-9 4. Pierratos A. Nocturnal hemodialysis: an update on a 5-year experience. Nephrol Dial Transplant 1999;1414:2835- 40. 5. Jaber B. Zimmerman D. Rationale and experience with short daily hemofiltration. Semin Dialysis 2004;17:146- 40. 6. Gotch F, Levin N. Daily dialysis: The long and the short of it. Blood Purif 2003;21:271-81 7. National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health Task Force on Daily Dialysis April 2001:11-2. 8. Lacson E, Diaz-Buxo J. Daily and nocturnal hemodialysis. How do they stack up. Am J Kidney Dis 2001;38:225- 39.

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