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

Metabolic disorders are the most frequent risk factor for the development of urolithiasis. They are manigenic substances or deficiency of inhibitors of crystalgenic substances or deficiency of inhibitors of crystallization and aggregation. The authors use for their diagnosis a modification of Pak's procedure. It involves examination of 24-hour urine with the patient on a low-calcium diet, supplemented by urine examination on fasting and after a 1000 mg calcium load. The procedure includes also examination of serum and bacteriological examination of urine. A total of 93% of patients with calcium lithiasis had a metabolic disorder, 42% suffered from idiopathic hypercalciuria, 32% from hyperuricosuria, 19% from hyperoxaluria, 15% from magnesium deficiency and 38% from hypocitraturia. On the other hand, patients with uric acid lithiasis had a detectable metabolic disorder only in 62%. Active detection of metabolic disorders is essential for the introduction of effective, specific metaphylaxis of urolithiasis.
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PMID:[Detection of metabolic disorders as a cause of urolithiasis in clinical practice]. 272 Jul 28

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.
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PMID:Effects of magnesium deficiency on intratubular calcium oxalate formation and crystalluria in hyperoxaluric rats. 706 46

One hundred fifty-five recurrent noninfectious calcium oxalate stone formers were evaluated in an effort to assess the importance of magnesium excretion on calcium oxalate stone formation. All patients evaluated had normal urinary magnesium excretion, and any elevation of the calcium/magnesium ratio was related to the presence of hypercalciuria. The findings indicate that magnesium deficiency does not appear to be a significant cause of calcium oxalate urolithiasis. If magnesium supplement is of value in some patients, it is likely related to its inhibitory effect on calcium oxalate crystallization.
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PMID:Magnesium excretion and calcium oxalate urolithiasis. 714 7