The spectrum of bone disease in 200 chronic hemodialysis patients

a correlation between clinical, biochemical and histological findings

Authors

  • Maria Eugênia Leite Duarte Universidade Federal Fluminense
  • Ana Lúcia Passos Peixoto Universidade Federal Fluminense
  • Andréa da Silva Pacheco Universidade Federal Fluminense
  • Angela Vieira Peixoto Universidade Federal Fluminense
  • Rodrigo Dezerto Rodriguez Universidade Federal Fluminense
  • Jocemir Ronaldo Lugon Universidade Federal Fluminense
  • Elisa Albuquerque Sampaio da Cruz Universidade Federal Fluminense

Keywords:

Renal osteodystrophy, Chronic renal failure, Hemodialysis, Aluminum intoxication, Bone metabolism

Abstract

INTRODUCTION: Renal osteodystrophy includes the complete range of mineral metabolism disorders that affect the skeleton in patients with chronic renal failure. PATIENTS AND METHODS: 200 patients with end-stage renal disease and on dialysis were investigated regarding the clinical, biochemical and histological findings of bone disease. RESULTS: The spectrum of renal osteodystrophy consisted mainly of high turnover bone lesions (74.5%), including osteitis fibrosa in 57.5%. Patients with mild bone disease were on dialysis for shorter periods of time and were mostly asymptomatic. Patients with aluminum-related bone disease (16.5%) had the greatest aluminum exposure, either orally or parenterally, and together with patients with high turnover mixed disease, were the most symptomatic. Although on a non-regular basis, the vast majority of the patients (82.5%) had been receiving vitamin D. The incidence of adynamic bone disease was high (n=8) among parathyroidectomized patients (n=12). Significantly higher serum levels of alkaline phosphatase were observed in osteitis fibrosa. CONCLUSIONS: The use of calcitriol and phosphate-binding agents on a non-regular basis seems to be the reason for the apparent reduced response to the treatment of secondary hyperparathyroidism. Alkaline phosphatase has been shown to be a fair marker for bone turnover in patients with osteitis fibrosa. The severity of the clinical manifestations of bone disease correlates with the histological features of bone lesion and to the time spent on dialysis.

Downloads

Download data is not yet available.

Author Biographies

Maria Eugênia Leite Duarte, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Ana Lúcia Passos Peixoto, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Andréa da Silva Pacheco, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Angela Vieira Peixoto, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Rodrigo Dezerto Rodriguez, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Jocemir Ronaldo Lugon, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

Elisa Albuquerque Sampaio da Cruz, Universidade Federal Fluminense

Universidade Federal Fluminense, Department of Pathology and Department of Internal Medicine, Niterói, Brazil

References

Goodman WG, Coburn JW, Ramirez JA, Slatopolsky E, Salusky IB. Renal osteodystrophy in adults and children. In: Favus DM, editor. Primer on the metabolic bone diseases and disorders of mineral metabolism. New York: Raven Press 1996;341-60.

Hruska KA, Teitelbaum SL. Renal osteodystrophy. N Engl J Med 1995;333:166-74.

Goodman WG, Duarte MEL. Aluminum: effects on bone and role in the pathogenesis of renal osteodystrophy. Miner Electrolyte Metab 1991;17:221-32.

Coburn JW, Norris KC, Nebeker HG. Osteomalacia and bone disease arising from aluminum. Semin Nephrol 1986;6:68-89.

Sherrard DJ, Ott SM, Maloney NA, Andress DI, Coburn JW. Renal osteodystrophy. Semin Nephrol 1986;6:56-67.

Llach F, Felsenfeld AJ, Coleman MD, Pederson JA. Prevalence of various types of bone disease in dialysis patients. In: Robinson RR, editor. Proceedings of the ninth international congress of nephrology. New York: Springer-Verlag 1984;1375-82.

Sherrard DJ, Hercz G, Pei Y, et al. The spectrum of bone disease in end-stage renal failure: an evolving disorder. Kidney Int 1993;43:436-42.

Pei Y, Hercz G, Greenwood C, et al. Risk factors for renal osteodystrophy: a multivariant analysis. J Bone Miner Res 1995;10:149-56.

Salusky IB. Bone and mineral metabolism in childhood end-stage renal disease. Pediatr Clin North Am 1995;42:1531-50.

Villanueva AR, Mehr LA. Modifications of the Goldner and Gomori one-step trichrome stains for plastic-embedded thin sections of bone. Am J Medical Technology 1977;43:536-8.

Andress DI, Maloney NA, Coburn JW, Endress DB, Sherrard DJ. Osteomalacia and aplastic bone disease in aluminum-related osteodystrophy. J Clin Endocrinol Metabol 1987;65:11-6.

Maloney NA, Ott AS, Alfrey AC, Miller NI, Coburn JW, Sherrard DJ. Histological quantitation of aluminum in iliac bone from patients with renal failure. J Lab Clin Med 1982;99:206-16.

Serrano S, Marińoso ML, Torres A, et al. Osteoblastic proliferation in bone biopsies from patients with end-stage chronic renal failure. J Bone Min Res 1997;121:91-9.

Alfrey AC, Hegg A, Craswell P. Metabolism and toxicity of aluminum in renal failure. Am J Clin Nutr 1980;33:1509-16.

Hodsman AB, Sherrard DJ, Alfrey AC, et al. Bone aluminum and histomorphometric features of renal osteodystrophy. J Clin Endocrinol Metab 1982;54:539-46.

Parsons V, Davies C, Goode C, Ogg C, Siddiqui J. Aluminum in bone from patients with renal failure. Br Med J 1975;iv:273-5.

Sebert JL, Marie A, Gueris J, et al. Assessment of the aluminum overload and of its possible toxicity in asymptomatic uremic patients: evidence for a depressive effect on bone formation. Bone 1985;6:373-5.

Salusky IB, Foley J, Nelson P, Goodman WG. Aluminum accumulation during treatment with aluminum hydroxide and dialysis in children and young adults with chronic renal disease. N Engl J Med 1991;324:527-31.

Sedman AB, Miller NL, Warady BA, Lum GM, Alfrey AC. Aluminum loading in children with chronic renal failure. Kidney Int 1984;26:201-4.

Winney RJ, Cowie JF, Robson JS. The role of plasma aluminum in the detection and prevention of aluminum toxicity. Kidney Int 1986;29:S91-5.

Ihle B, Buchanan M, Stevens B, et al. Aluminum associated bone disease: clinico-pathologic correlation. Am J Kidney Dis 1982;2:255-63.

Pierides AM, Edwards WG Jr, Cullu, US Jr, McCall JT, Ellis HA. Hemodialysis encephalopathy with osteomalacic fractures and muscle weakness. Kidney Int 1980;18:115-24.

Blumenthal NC, Posner AS. In vitro model of aluminum-induced osteomalacia: inhibition of hydroxyapatite formation and growth. Calcif Tissue Int 1984;36:439-41.

Parfitt AM. The localization of aluminum in bone: implications for the mechanism of fixation and for the pathogenesis of aluminum-related bone disease. Int J Artif Organs 1988;11:79-90.

Baker LR, Muir JW, Sharman VL. Controlled trial of calcitriol in hemodialysis patients. Clin Nephrol 1986;26:185-91.

Berl T, Berns AS, Huffer WE. 1,25-Dihydroxycholecalciferol effects in chronic dialysis: a double-blind controlled study. Ann Intern Med 1978;88:774-80.

Ott SM, Maloney NA, Coburn JW, Alfrey AC, Sherrard DJ. The prevalence of bone aluminum deposition in renal osteodystrophy and its relation to the response to calcitriol therapy. N Engl J Med 1982;307:709-13.

Fukagawa M, Kitaoka M, Kaname S. Suppression of parathyroid gland hyperplasia by 1,25(OH)2D3 pulse therapy. N Engl J Med 1990;315:421-2.

Martin KJ, Bullal HS, Domoto DT, Blalock S, Weindel M. Pulse oral calcitriol for the treatment of hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis: preliminary observations. Am J Kidney Dis 1992;19:540-5.

Coburn JW, Slatopolsky E. Vitamin D, parathyroid hormone, and the renal osteodystrophies. In: Brenner B, Rector F, editors. The Kidney. 4th ed. Philadelphia: WB Saunders 1990;2076-89.

Ott SM, Andress DL, Nebeker HG. Changes in bone histology after treatment with desferrioxamine. Kidney Int 1986;29:S108-13.

Neonakis E, Wheeler MH, Krishnan H, Coles GA, Davies F, Woodhead JS. Results of surgical treatment of renal hyperparathyroidism. Arch Surg 1995;130:643-8.

Llach F. Parathyroidectomy in chronic renal failure: indications, surgical approach, and the use of calcitriol. Kidney Int 1990; 38:S29.

Hruska KA, Teiltelbaum SL, Kopelman R. The predictability of the histological features of uremic bone disease by non-invasive techniques. Metab Bone Dis Rel Res 1978;1:39

Llach F, Felsenfeld AJ, Coleman MD, Keveney JJ Jr, Pederson JA, Medlock TR. The natural course of dialysis osteomalacia. Kidney Int 1986;29:S74-9.

Downloads

Published

1998-09-09

How to Cite

1.
Duarte MEL, Peixoto ALP, Pacheco A da S, Peixoto AV, Rodriguez RD, Lugon JR, Cruz EAS da. The spectrum of bone disease in 200 chronic hemodialysis patients: a correlation between clinical, biochemical and histological findings. Sao Paulo Med J [Internet]. 1998 Sep. 9 [cited 2025 Mar. 9];116(5):1790-7. Available from: https://periodicosapm.emnuvens.com.br/spmj/article/view/2368

Issue

Section

Original Article