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

Bile salts are formed from cholesterol and conjugated in the liver, excreted via the biliary system into the duodenum, reabsorbed in the ileum, stored temporarily in the hepatic bile salt pool, and reexcreted into the biliary system. This normal enterohepatic circulation of bile salts is both efficient and rapid. Interruption of the enterohepatic circulation of bile salts may cause cholesterol cholelithiasis or oxalate urolithiasis. Clinical and radiologic features of pediatric patients with gallstones and urolithiasis secondary to abnormalities of the ileum are reported. The pathophysiology of lithiasis due to interruption of the enterohepatic circulation of bile salts is discussed. This enteric cause is included in the differential diagnosis of cholelithiasis and urolithiasis in infants and children.
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PMID:John Caffey Award: lithiasis due to interruption of the enterohepatic circulation of bile salts. 11 96

Both urate and oxalate are organic acids of considerable clinical interest, owing to their limited solubility. Calcium oxalate is the most frequent constituent of renal calculi and occasionally precipitates in body fluids. Urate precipitations are common in the kidney and in various other tissues. In this paper, a short outline of the present knowledge of renal handling of these substances will be followed by some conclusions as to the possible relevance of this knowledge for the understanding of urolithiasis and intrarenal precipitation. Direct (micropuncture) data are available for urate in the rat (1, 6, 7, 10, 21, 23, 28, 36, 42), rabbit (35), dog (34) and cebus monkey (33) and in the rat only for oxalate (11, 15, 20).
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PMID:Renal handling of urate and oxalate: possible implications for urolithiasis. 11 10

Urinary calculi composed of calcium oxalate were produced in male hooded Wistar rats fed a vitamin B6 deficient diet over 16 weeks. This basic diet was modified by doubling the phosphate content or loading with vitamin C or D3 in three treatment groups. The number of rats developing oxalate stones was not altered by the addition of vitamin D3 or phosphate, but there was a significant increase in total weight of stone formed and histological evidence of extensive renal damage in rats on the high vitamin D3 diet. The addition of vitamin C to the vitamin B6 deficient rats resulted in a reduction in the number of rats with uroliths and a fall in urinary oxalate excretion, while similarly loaded vitamin B6 supplemented controls were free of oxalate calculi. It is concluded that the oxalate urolithiasis induced by vitamin B6 deficiency was exacerbated by added vitamin D3 and reduced by vitamin C.
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PMID:Experimental oxalate urolith formation in rats. 23 24

The calciuric response to an oral glucose load (100 g) was determined in 16 patients with calcium oxalate urolithiasis (seven with renal hypercalciuria and nine with absorptive hypercalciuria) and seven normal subjects. The rates of renal calcium excretion increased significantly after glucose ingestion in all three groups. The calciuric response in patients with absorptive hypercalciuria and intestinal hyperabsorption of calcium was indistinguishable from that of normal subjects. However, the calcium excretions were significantly higher during 1 hr preceding and 3 hr after glucose ingestion in patients with renal hypercalciuria (with presumed "renal leak" of calcium) than in normal subjects. The increment in the calcium excretion rate was also higher in patients with renal hyperacalciuria, particularly during the 2nd hour of glucose ingestion. The results provide a further support for the concept of different etiologies of renal and absorptive hypercalciurias.
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PMID:An exaggerated augmentation of renal calcium excretion after oral glucose ingestion in patients with renal hypercalciuria. 34 35

Kinetics of growth and dissolution of calcium oxalate monohydrate were examined in the presence of small concentrations of methylene blue. The data presented show moderate retardation in growth and dissolution rates. It was also found that methylene blue decreased the decalcification rate of calcium oxalate renal calculi. The implications of these findings in the treatment of urolithiasis are discussed.
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PMID:Methylene blue as an inhibitor of stone formation. 35 13

Enteric hyperoxaluria and oxalate urolithiasis in patients with ileal resection seem to be caused by intestinal hyperabsorption of oxalate. The mechanism responsible for hyperabsorption of oxalate is not known. Intestinal transport of oxalic acid was therefore examined by an in vitro technique in rat intestine. Oxalic acid was absorbed by a mechanism of simple passive diffusion. The rate of absorption decreased from the colon to the duodenum (colon greater than ileum greater than jejunum greater than duodenum). Bile acids enhanced oxalic acid absorption in the large and small intestine and increased extracellular space; calcium, however, markedly decreased mucosal-serosal transport of oxalic acid. Cholestyramine known to reduce oxalate excretion in hyperuxaluria associated with ileal resection did not directly affect absorption of oxalic acid, but decreased the enhanced absorption of oxalic acid induced by bile acids. The results suggest that the beneficial therapeutic effect of cholestyramine in hyperuxaluria is rather mediated by its bile acid binding activity than by direct binding of oxalic acid.
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PMID:Intestinal oxalate absorption. I. Absorption in vitro. 41 86

The biochemical findings in urine from 62 male and 20 female consecutive patients with renal stone disease were studied in relation to the size of concrements and the estimated rate of stone formation. There appeared to be good agreement between urine composition and stone history. Biochemical grouping of the patients resulted in different distributions in the different groups of stone-formers. The quotients calcium/magnesium (k1) and calcium X oxalate/magnesium X creatinine (k3) appeared to reflect the severity of stone disease and seemed to provide a rational approach to the evaluation of patients with urolithiasis.
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PMID:Relationship between the severity of renal stone disease and urine composition. 44 8

Many variables are known to be associated with the formation of calcium oxalate urolithiasis but none is essential for the initiation or growth of stones. It is likely that the predisposition to stone formation is related to multiple factors. We herein describe still another metabolic state that seems to predispose to calcium oxalate stone disease, namely heterozygosity for cystinuria. Cystine screening tests were done on 24-hour urine specimens obtained from 126 patients in whom recurrent calcium oxalate stones form and 84 controls and quantitative amino acid determinations were done on all positive specimens. Of those studied 17 of 126 stone patients and 1 of 84 controls were heterozygous cystinurics. A test of the differences between the relative frequencies of cystinuria heterozygotes in the 2 groups with Fisher's exact test revealed them to be highly significant (p less than 0.001). Our study indicates that carrier status for 1 of the cystinuria genes predisposes to calcium oxalate stone formation but, like other factors related to urolithiasis, it is not a necessary cause of stone disease.
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PMID:Heterozygous cystinuria and calcium oxalate urolithiasis. 45 88

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.
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PMID:Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease. 48 60

The safety and effectiveness of sodium cellulose phosphate (SCP) in the treatment of calcium urolithiasis of absorptive hypercalciuria was explored. Eighteen patients with absorptive hypercalciuria with intestinal hyperabsorption of calcium, normal or suppressed parathyroid function, and active stone disease received 10 to 15 Gm SCP daily (2.5 to 5 Gm with meals) and 2 to 3 Gm magnesium gluconate daily (1 to 1.5 Gm twice daily orally separately from SCP) for eight to 54 months, while maintained on a moderate calcium and oxalate restriction. During treatment, serum calcium, immunoreactive parathyroid hormone, and urinary cyclic AMP remained within the normal range. Serum alkaline phosphatase and bone density (measured by photon absorptiometry) did not change significantly or remained within normal limits. Serum concentrations of magnesium, copper, zinc, and iron and blood hematocrit were not significantly altered by therapy. However, urinary calcium returned toward normal, and incidence of renal stone formation markedly decreased. The results suggest that SCP is a safe and an effective drug for absorptive hypercalciuria.
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PMID:Clinical pharmacology of sodium cellulose phosphate. 48 64


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