Category: Diseases

Pathogenesis of primary hypercalciuria: Primary Hyperparathyroidism

In PHPT, a hypersecretion of PTH from a benign solitary parathyroid adenoma (80%) or multiglandular parathyroid hy- perplasia (15%) produces excessive bone resorption. Under normal circumstances, an increase in circulating ionized calci­um is followed by a rapid decrease in PTH secretion. In PHPT with adenoma, this feedback control is impaired, resulting in hypersecretion of PTH. […]

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Pathogenesis of primary hypercalciuria: Regulators of Calcium Transport in the Nephron

Although the active transcellular reabsorption of calcium in the distal nephron accounts for only about 20% of total reabsorbed calcium, it is the major target for regulation by key factors impli­cated in the development of hypercalciuria. Luminal pH. Using patch-clamp electrophysiological recording of recombinant EcaC1 channels expressed in cultured cells, low extracellular pH directly inhibited […]

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Pathogenesis of primary hypercalciuria: Sarcoidosis

Sarcoidosis is a granuloma-forming disorder characterized by mild to severe hypercalcemia in 10% of patients, with hypercal­ciuria occurring in up to 50% of patients at some time during the course of their disease. For many years, it was believed that hy­percalcemia and/or hypercalciuria resulted from increased sen­sitivity to the biological effects of vitamin D. Subsequently, […]

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Pathogenesis of primary hypercalciuria: Genetic Studies in Human Beings with AH

AHRAC Gene. Prior studies have indicated that the inheritance of AH is compatible with an autosomal dominant trait. Reed et al. identified a locus on chromosome 1q23.3-24 in three kin­dreds with phenotypically well-defined AH. Within this re­gion, they identified a candidate gene, the absorptive hypercal- ciuria-related adenylyl cyclase (AHRAC), on account of its as­sociation with […]

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Pathogenesis of primary hypercalciuria: General Description

Absorptive hypercalciuria (AH) describes a stone-forming con­dition in which the primary defect is presumed to be enhanced intestinal absorption of calcium. The increased absorbed calcium transiently raises serum calcium and suppresses parathyroid function. Hypercalciuria ensues from the increased renal filtered load of calcium, and decreased renal tubular re- absorption of calcium due to parathyroid suppression. […]

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Pathogenesis of primary hypercalciuria

Introduction Hypercalciuria is clinically important since it often accompanies the formation of calcium-containing kidney stones. Among pa­tients with idiopathic calcium oxalate nephrolithiasis, hypercal­ciuria is the main determinant for the formation of calcium phosphate nidus (in the thin loops of Henle of the nephron) that may initiate calcium oxalate crystallization. The correction of hypercalciuria by thiazide […]

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