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

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

FActors predisposing to renal stone formation have been studied in 309 patients. Dehydration before diagnosis of urolithiasis was due in 12% of the cases to frequent diarrhea and in 36% to bad working conditions. Daily fluid intake was less than 1 liter in 25% of the patients before stone formation and was persistently low in 11% after stone discovery. 41% of the patients drank irregularly over the day, before stone formation, and 11% continued to do so after its detection. Immobilization was present in the patient's history in over 20% of the cases. Normocalcemic hypercalciuria was found in 26% of the patients. 24% of the patients drank water with a calcium concentration of 100--500 mg/l before the lithiasis was diagnosed; 21% continued to do so after stone discovery or paradoxically even drank harder water than before stone detection.
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PMID:High fluid-low calcium intake: not all renal stone formers adhere to this simple treatment. 42 10

The clinical peculiarities, and the etiological and pathogenetic factors of urolithiasis in 296 patients suffering from spontaneous stone elimination were studied. It was established that 209 patients eliminated stones consisting of uric acid, sodium salts and ammonium salts. Moderate hypocalcemia and hyperphosphatemia and also hyperuricemia and hyperuricuria were present. There were 39 'eliminators' of calcium stones. Their blood calcium content was higher, hypercalciuria, inorganic phosphorus and normal uric acid, were noted. Compound stones were present in 48 observations. When carrying out additional biochemical tests in 57 patients with calcium and compound stones, primary hyperparathyroidism was diagnosed in 34 observations; and parathyroidectomy was successfully performed.
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PMID:On the pathogenesis of stone formation in stone-eliminating patients. 42 6

Eighty patients with proved calcium urolithiasis participated in an outpatient study designed to define the most likely metabolic problem related to the cause of the stone disease. Diagnostic categories included absorptive hypercalciuria (33 patients), renal leak hypercalciuria (20 patients), hypomagnesiumuria (27 patients), hyperuricemia and hyperuricuria (16 patients), hyperoxaluria (15 patients), normal stone-former (4 patients), renal tubular acidosis (2 patients) and suspicion of hyperparathyroidism (7 patients). Of the 80 patients 40 had more than 1 defect. Patients with a high suspicion of hyperparathyroidism were excluded from the study. Based on these criteria treatment plans incorporating medications, diet or both were instituted. Of 21 patients observed for greater than 2 years 90 per cent have shown no new stone disease.
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PMID:Outpatient evaluation of patients with calcium urolithiasis. 43 49

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

In three groups--patients with recurrent calcium urolithiasis (RCU), patients with primary hyperparathyroidism (pHPT), and healthy controls--citrate was measured enzymatically in 24 and in 2-hr urine after an overnight fast. Citrate excretion per 24 hr was significantly lower in RCU than in age and sex matched controls, whereas there was no significant difference in citrate excretion in urines from the 2-hr morning collection. In pHPT citrate was also lower than in controls and fell within the range of RCU of comparable age. Both categories of urines (24 and 2hr) have in common the characteristic that the actual citrate concentration is lower by 50 per cent in RCU and pHPT than in controls, mainly as a result of the higher urine volume. Correction of citrate for creatinine does not disclose further differences among the populations studied but conversely hampers exact interpretation of urinary citrate in the absence of strict separation of individuals according to sex and age. From these data we conclude that (i) a low excretion and concentration of urinary citrate is detectable in calcium lithiasis and may contribute to a deficiency in inhibitory activity against nucleating processes in stone-forming urine; and (ii) the differences in urinary citrate elicited in samples of 24 and 2-hr morning urine are of unknown origin and merit further investigations.
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PMID:Citrate in daily and fasting urine: results of controls, patients with recurrent idiopathic calcium urolithiasis, and primary hyperparathyroidism. 44 79

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

An X-ray diffraction analysis of kidney stones from the bivalved mollusc Macrocallista nimbosa has revealed the calculi composition to be amorhpous calcium phosphate. The use of this animal for the study of urolithiasis is suggested because of the spatial and temporal ubiquity of its renal calculi.
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PMID:Analysis of renal calculi from a marine mollusc (Marcocallista nimbosa). Implications for the study of urolithiasis. 46 17

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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