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Hypercalciuria and stones.

J Lemann1, E M Worcester, R W Gray

  • 1Department of Medicine, Medical College of Wisconsin, Milwaukee 53226.

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
|April 1, 1991
PubMed
Summary
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Hypercalciuria, a key risk factor for kidney stones, involves elevated urinary calcium despite normal kidney function. This condition stems from reduced tubular calcium reabsorption, not primarily diet, and may involve bone metabolism and familial factors.

Area of Science:

  • Nephrology
  • Metabolic Bone Disease
  • Calcium Metabolism

Background:

  • Hypercalciuria (excessive urinary calcium) affects ~50% of patients with calcium oxalate/apatite nephrolithiasis.
  • It is a significant risk factor for kidney stone formation.
  • Elevated urinary calcium occurs despite normal glomerular filtration rate and serum calcium levels.

Purpose of the Study:

  • To investigate the underlying mechanisms of hypercalciuria in nephrolithiasis.
  • To differentiate between dietary, absorptive, and renal tubular causes of hypercalciuria.
  • To explore the relationship between hypercalciuria, bone metabolism, and potential familial links.

Main Methods:

  • Analysis of urinary calcium excretion rates in hypercalciuric stone formers versus normal subjects.

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  • Assessment of dietary intake (NaCl, protein, K) and urinary excretion markers (Na, SO4, K).
  • Evaluation of serum phosphate, 1,25-(OH)2-D levels, intestinal calcium absorption, and bone mineral density.

    • Main Results:

    • Hypercalciuria is linked to impaired net tubular calcium reabsorption, not solely dietary factors.
    • Subsets of patients show hypophosphatemia-induced or 1,25-(OH)2-D-independent augmented intestinal calcium absorption.
    • Evidence suggests accelerated calcium turnover, negative calcium balance, reduced bone density, and potential familial predisposition.

    Conclusions:

    • Hypercalciuria in nephrolithiasis results from complex mechanisms involving renal tubular dysfunction and altered intestinal calcium absorption.
    • Dietary factors are not the primary drivers; hormonal and intrinsic cellular mechanisms are implicated.
    • The condition may involve generalized calcium transport abnormalities and has potential familial links.