TREATMENT OF RENAL OSTEODYSTROPHY IN PATIENTS WITH TERMINAL CHRONIC FAILURE TREATED WITH CHRONIC HEMODIALIZATION
Abstract
Renal osteodystrophy (ROD) presents a mineral-bone disorder as a consequence of mineral imbalance and bone metabolism that often occurs in patients with terminal chronic renal failure. Changes in uremic patients are manifested by ostalgias, phosphocalcemic pseudogout, muscle pain, frequent calcifications in soft tissues, calcifying phenomena, osteoporosis, osteitisfibrosis, amyloidosis, metabolic acidosis, which are frequent occurrences in patients with End-stage renal failure (ESRD) (Jürgen Floege, Richard F. et al.). The most important factors in the occurrence of ROD are: reduced elimination of urinary phosphorus with hyperphosphaturia, with increased concentration of phosphate in the blood (hyperphosphatemia), vitamin D deficiency, hypocalcemia and increased parathyroid hormone (PTH). (Gutierrez O, Isakova T, Rhee E, et. al.). Objectives of ROD treatment in patients with terminal chronic renal failure CTRF treated with chronic hemodialysis (HD) are: maintaining blood calcium and phosphorus levels as close to normal as possible, prevention of the development of hyperplasia and secretion of parathyroid hormone (PTH), prevention of extraskeletal calcium deposition and preventing the accumulation of aluminum and iron that can adversely affect the skeleton. Recently, the latest instructions of the foundation of K/DOQI (Kidney Disease Outcomes Quality Initiative) suggest 1,2 gr protein /kg body weight for patients with HD. More than 90% of patients on dialysis use phosphate binders (calcium carbonate, calcium acetate) to reduce the amount of phosphorus absorbed to reach normal levels of serum phosphorus from 3.5-4.5 mg / dl.
PURPOSE: the paper aimed to document and verify the prevalence of ROD submission in patients with ESRD treated with chronic HD bicarbonate, with duration of HD treatment over 72 months and frequency three times a week from 4.5 hours randomized by gender, mean age, and nationality.
MATERIAL AND METHODS: In the time-perspective study (cross-section) a total of 87 patients were involved (of which 42 (48%) with average age-55,00-10.00 old were female, while 45 (52%) were male with average age 12.00 years of 57.00) with ESRD treated with chronic HD with duration of HD treatment over 72 months and frequency three times a week from 4.5 hours with bicarbonate dialysis, with chronic HD over 96 months. To all patients were examined concentrations of calcium, phosphorus, magnesium, alkaline phosphatase and parathyroid hormone (PTH). In patients who were noticed symptoms of ROD we also did radiological examination of the skeleton.
STATISTICAL PROCESSING: from basic statistical methods were used: arithmetic mean value and standard deviation X ± SD. Comparative statistics of examined parameters was analyzed with the so-called Studentov test ‘t’. Statistical significance of differences between groups of patients was analyzed with the so-called “Anonova Two-Factor” test with statistical value for p less than 5%, respectively p <0.0005.
CONCLUSION: Treatment of ROD should be started in the early stages of chronic renal failure in order to prevent later complications. The disease should be treated with medications of calcium, vitamin D, PTH, phosphorus, dietary supplements and dyalysate solutions with the right amount of calcium depending on the disease. Since ESRD is an irreversible disease (in the absence of kidney transplantation), the duration of therapy should be long-term to prevent further complications of ROD.
Keywords: renal osteodystrophy (ROD), Enda Stage Renal Disease (ESRD), hemodialysis (HD).
References
Aubin JE. Advances in the osteoblast lineage. Biochem Cell Biol. 1998; 76(6):899-910.
Barsić, Neven; Cala, Kresimir, et al. “Brown tumor--a rare manifestation of renal osteodystrophy and severe secondary hyperparathyroidism: case report”. Acta Clinica Croatica. (September 2010). 49 (3): 299–304.
Brandenburg VM, Floege J. Adynamic bone disease-bone and beyond. NDT Plus. 2008 Jun; 1(3):135-47. [PMC free article]
Coyne DW, Grieff M, Ahya S, Giles K, Norwood K, Slatopolsky E: Differential effects of acute administration of 19-nor-1,25-dihydroxy-vitamin D2 and 1,25-dihydroxy-vitamin D3 on serum calcium and phosphorus in hemodialysis patients. Am J Kidney Dis 2002; 40: 1283–1288.
Cozzolino M, Ureña-Torres P, Vervloet MG, et al. "Is chronic kidney disease-mineral bone disorder (CKD-MBD) really a syndrome?". Nephrology, Dialysis, Transplantation. (October 2014). 29(10): 1815–1840.
Cozzolino M, Ureña-Torres P, Vervloet MG, et al. "Is chronic kidney disease-mineral bone disorder (CKD-MBD) really a syndrome?". Nephrology, Dialysis, Transplantation. (October 2014). 29(10): 1815–1840.
Elder G. Pathophysiology and recent advances in the management of renal osteodystrophy. J
Bone Miner Res. 2002 Dec;17(12):2094-105.
Eriksen EF. Normal and pathological remodeling of human trabecular bone: three-dimensional reconstruction of the remodeling sequence in normal and in metabolic bone disease. Endocr Rev. 1986 Nov; 7(4):379-408.
Follis RHJ, Jackson DA: Renal osteomalacia and osteitis fibrosa in adults. Johns Hopkins Med J 1943; 72:232.
Gotch FA, Kotanko P, et. al. Method of Determining a Phosphorus Binder Dosage for a Dialysis Patient. Google Patents; 2009
Gutierrez O, Isakova T, Rhee E, et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease, in J Am Soc Nephrol, vol. 16, n. 7, luglio 2005, pp. 2205-15,
Gutierrez O, Isakova T, Rhee E, et.al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease, in J Am Soc Nephrol, vol. 16, n. 7, luglio 2005, pp. 2205-15.
Ho LT, Sprague SM. Renal osteodystrophy in chronic renal failure. Semin Nephrol. 2002 Nov; 22(6): 488-93.
Hruska KA, Teitelbaum SL. Renal osteodystrophy. N Engl J Med. 1995 Jul 20; 333(3):166-74.
Jürgen Floege, Richard F. et al. Comprehensive Clinical Nephrology, 4ª ed., Elsevier, 2010, pp. 969.
Khosla S. Minireview: the OPG/RANKL/RANK system. Endocrinology. 2001 Dec; 142 (12): 5050-5.
Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. & “KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-Mineral and Bone Disorder (CKD-MBD)” (PDF). Kidney International Supplement. 76 (113): S1–130. August 2009.
London GM. “Bone-vascular axis in chronic kidney disease: a reality?”. Clinical Journal of the American Society of Nephrology. (February 2009). 4 (2): 254–257.
London GM. “Bone-vascular axis in chronic kidney disease: a reality?”. Clinical Journal of the American Society of Nephrology. February-2009. 4 (2): 250–280.
Lui S, Chu H. “Studies in calcium and phosphorus metabolism with special reference to pathogenesis and effects of dihydrotachysterol (A.T.10) and iron”. Medicine. 1983, 22: 103–107.
Martin KJ, Gonzalez EA, et al. Therapy of secondary hyperparathyroidism with 19-nor-1alpha, 25-dihydroxyvitamin D2. Am J Kidney Dis 1998; 32(2 Suppl 2):61–66.
Moe S, Drueke T, Cunningham J, et. al.: Definition, evaluation, and classification of renal osteodystrophy: A position statement from kidney disease: Improving Global Outcomes (KDIGO). Kidney Int 69:1945–1953, 2006.
Moe S, Drüeke T, Cunningham J, et al. “Definition, evaluation, and classification of renal osteodystrophy: a position statement from kidney disease: Improving Global Outcomes (KDIGO)”. Kidney International.June-2006, 69 (11): 1945–53.
Moody WE, Edwards NC, et al. Arterial disease in chronic kidney disease. Heart. 2013 Mar; 99(6):365-72.
Pappenheimer AM: Effect of an experimental reduction of kidney substance upon parathyroid glands and skeletal tissue. J Exp Med 1936; 64: 965.
Piraino B, Chen T, et al. Fractures and vertebral bone mineral density in patients with renal osteodystrophy. Clin Nephrol. 1988 Aug; 30(2):57-62.
Slatopolsky E, Gonzalez E, Martin K. Pathogenesis and treatment of renal osteodystrophy. Blood Purif. 2003; 21(4-5):318-26.
Sugimoto T, Ritter C, Morrissey J, et al. Effects of high concentrations of glucose on PTH secretion in parathyroid cells. Kidney Int. 1990 Jun; 37(6):1522-7.
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