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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The different subgroups of hypercalciuria cannot be separated clearly by the Pak calcium-load test. To improve the diagnosis and therapy we examined all relevant parameters of calcium metabolism in 32 patients with calcium urolithiasis and hypercalciuria (> 6.25 mmol/day). We also conducted bone mineral density measurements as well as the Pak calcium-load test. In most cases the pathophysiological constellations which Pak takes as the basis for his classification of hypercalciuria could not be shown. To date, diagnostics only insufficiently explains the genesis of hypercalciuria (except pHPT). As a consequence, a therapeutic problem arises: a low-calcium diet should not be generally recommended, since some patients may develop osteopenia. From our investigation the following diagnostic and therapeutic conclusions can be drawn: (1) Hypercalciuria in primary hyperparathyroidism should be treated by surgical removal of the adenoma. (2) The parathormone-independent osteogenic form should be treated with thiazides. (3) Hypercalciuria with increased 1.25-dihydroxyvitamin D should be treated by low-calcium diet.
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PMID:[Studies of calcium metabolism in patients with hypercalciuria]. 899 31

Crystallization by itself is not harmful as long as the crystals are not retained in the kidneys and are allowed to pass freely down the renal tubules to be excreted in the urine. A number of theories have been proposed, and studies performed, to determine the mechanisms involved in crystal retention within the kidneys. It has been suggested that urinary transit through the nephron is too fast for crystals to grow large enough to be retained. Thus, free particle mechanism alone cannot lead to stone formation, and there must be a mechanism for crystal fixation within the kidneys. Animal model studies suggest that crystal retention is possible through both the free- and fixed-particle mechanisms. Crystal-cell interaction leads to pathological changes which promote crystal attachment to either epithelial cells or their basement membrane. Alternatively, crystals aggregate and produce large enough particles to block the tubules particularly at sites, where urinary flow is affected because of changes in the luminal diameter of the tubule. Crystal deposits plugging the openings of the ducts of Bellini may be the result of such a phenomenon. Intratubular crystals translocating to renal interstitium may produce osteogenic changes in the epithelial or endothelial cells resulting in the formation of the Randall's plaques. Thus, fixation appears to be either through the formation of Randall's plugs, crystal plugs clogging the openings of the ducts of Bellini or sub-epithelial crystal deposits, and the Randall's plaques.
Urolithiasis 2017 Feb
PMID:Histological aspects of the "fixed-particle" model of stone formation: animal studies. 2789 91