Aug 1, 1967

Studies of the mechanism by which chronic metabolic acidosis augments urinary calcium excretion in man

The Journal of Clinical Investigation
J LemannE J Lennon

Abstract

We carried out clearance studies in nine healthy adults and four patients with hypoparathyroidism before and after inducing stable metabolic acidosis with either NH(4)Cl or acetazolamide. Clearances were repeated in seven normal subjects and three of the patients 3 days after stopping these agents.During acidosis in the normal subjects, serum ultrafilterable calcium concentration rose significantly, but inulin clearance fell to a greater extent, so that the calculated filtered load of calcium fell significantly. Despite this, urinary calcium excretion rose. Urinary calcium excretion remained elevated in the recovery studies when the serum ultrafilterable calcium concentration and filtered load of calcium had returned to control levels. Evidence is presented indicating that the increased calcium excretion which occurred during acidosis and recovery clearances was not due to natriuresis or to increased excretion of complexing anions. The comparable results in the four patients with hypoparathyroidism, two of whom also had hypothyroidism, suggest that the capacity to alter secretion rates of parathyroid hormone, thyrocalcitonin or both is not a critical determinant of the augmented rates of calcium excretion during acidosis.We con...Continue Reading

  • References11
  • Citations114

Citations

Mentioned in this Paper

PTH protein, human
Calcium [EPC]
Calcium
Recombinant parathyroid hormone
Parathyroid Hormone [EPC]
Acetazolamide
Allanson Pantzar McLeod Syndrome
Kidney
Tubular Cells
PTH gene

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