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Renal osteodystrophy in chronic renal failure.

L Tammy Ho1, Stuart M Sprague

  • 1Division of Nephrology, Evanston Northwestern Healthcare, Northwestern University Feinberg School of Medicine, Evanston, IL 60201, USA.

Seminars in Nephrology
|November 14, 2002
PubMed
Summary

Bone disease is common in chronic kidney disease. Management shifts towards low-turnover adynamic bone disease, raising concerns about current treatments for renal osteodystrophy.

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Area of Science:

  • Nephrology
  • Endocrinology
  • Bone Metabolism

Background:

  • Bone disease, or renal osteodystrophy, is a common complication of chronic renal failure (CRF).
  • Current understanding of renal osteodystrophy is largely derived from studies of patients undergoing dialysis.
  • The classic lesion in dialysis patients is high-turnover osteitis fibrosa, driven by secondary hyperparathyroidism due to hypocalcemia, hyperphosphatemia, and calcitriol deficiency.

Purpose of the Study:

  • To review the evaluation and management of renal osteodystrophy in chronic renal failure.
  • To discuss the changing patterns of bone lesions, including the rise of adynamic bone disease.
  • To evaluate current treatment strategies for non-dialysis patients with kidney disease.

Main Methods:

  • Review of existing literature on renal osteodystrophy in dialysis and non-dialysis populations.
  • Analysis of factors contributing to high-turnover (osteitis fibrosa) and low-turnover (adynamic bone disease) lesions.
  • Discussion of the roles of calcium, phosphate, calcitriol, and vitamin D analogs in bone disease management.

Main Results:

  • Osteitis fibrosa is the traditional high-turnover lesion in dialysis patients, linked to hypocalcemia, hyperphosphatemia, and calcitriol deficiency.
  • Adynamic bone disease, a low-turnover lesion, is increasingly observed in both dialysis and non-dialysis patients.
  • Aggressive use of calcium-based phosphate binders and calcitriol may contribute to the shift towards adynamic bone disease and extraskeletal calcifications.

Conclusions:

  • Treatment of non-dialysis kidney disease focuses on correcting hypocalcemia and hyperphosphatemia, and suppressing parathyroid hormone with calcitriol.
  • The increasing incidence of adynamic bone disease and extraskeletal calcifications raises concerns about the safety and efficacy of current management approaches.
  • Further research is needed to optimize the treatment of renal osteodystrophy and mitigate associated risks in chronic kidney disease patients.

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