Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distal RTA is characterized by decreased distal renal tubular hydrogen ion secretion, decreased ability to acidify urine, hypercalciuria, hyperphosphaturia, hypocitraturia, and metabolic acidosis. Because of the resulting alterations in urine composition and pH, patients with distal RTA are predisposed to urolithiasis and renal calcification. Diagnosis of distal RTA is important because it is a potentially reversible disorder that, left untreated, may cause nephrocalcinosis, recurrent urolith formation, moderate to severe metabolic acidosis, and renal failure.
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PMID:Canine distal renal tubular acidosis and urolithiasis. 348 13

The syndrome of glomerular immaturity associated with renal tubular acidosis and nephrocalcinosis or urolithiasis is illustrated by a case in which the diagnosis was made before the histological confirmation. Cases of urolithiasis in infants may be associated with this syndrome and attention must be paid to this rare but severe condition.
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PMID:Urinary calculi in association with glomerular immaturity. 360 97

In 78 patients with hypomagnesemia in urolithiasis the clinical course of disease was established in relation to therapy and dynamics of changes of serum magnesium levels. Almost 70% of patients had multiple, bilateral or recurrent nephrolithiasis or nephrocalcinosis. 70% of patients had Ca-oxalate stones or bilateral nephrocalcinosis. In 52% of patients a long-term magnesium supplementation was necessary. Significant progress of nephrolithiasis and nephrocalcinosis was observed in 80% of patients with permanent hypomagnesemia and in 4% of patients with normalization of serum magnesium level. Three of 15 patients with hypomagnesemia and progress of disease were transplanted a kidney and two were treated by hemodialysis. All five patients with renal failure had bilateral nephrocalcinosis, in three of them familiar occurrence of nephrolithiasis and hypomagnesemia was found.
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PMID:Prognosis of urolithiasis and nephrocalcinosis in hypomagnesemia. 393 9

In order to study the mechanism of dystrophic calcification, an anoxic incubation of rat renal cortex in a tissue culture medium was performed in vitro. Calcium and phosphate in the medium were adjusted to 1.6 and 1.2 mM/1 respectively. Calcification occurred in apposition to the inner surface of membranous cellular degradation products and associated with the flocculent densities within the degenerate organelles. The chemical nature of the flocculent density was not determined. In view of the known affinity of calcium for acidic phospholipids, particularly phosphatidyl serine (PS), which lines the inner surface of the plasma membrane, calcification along the inner surface of membrane was thought to be related to the presence of PS. Accumulation of calcium in mitochondria, which is presumably dependent upon residual substrate for energy production, appeared to cause calcification as well. Amorphous calcium phosphate in the form of spheroids, and possibly fine fibrils and granules, also appeared to play a role in calcification by their transformation into apatite. The seemingly simple phenomenon of tissue calcification is complex. Nephrocalcinosis in vitro is remarkably similar to the calcification in acute tubular necrosis in vivo, and is a convenient model with which to study the mechanism of calcification. It is concluded that the cellular degradation products are the initial loci of calcification and have a likely role in urolithiasis.
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PMID:Nephrocalcinosis in vitro. 664 38

Six out of seven patients with primary hyperoxaluria showed various degrees of oxalosis. The radiographic manifestations differ between patients younger than 15 years and those older than 45 years. The mild manifestations in children, only urolithiasis, can be explained by the, as yet, unimpaired renal function. The renal function in the older patients, with extensive pathologic changes like nephrocalcinosis, urolithiasis, soft-tissue calcification, and osseous changes, is very poor. The findings of extensive soft-tissue calcification and the bony changes are not in complete agreement with those in the literature.
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PMID:Radiologic findings in primary hyperoxaluria. 707 78

Magnesium stearate was fed to groups of 20 male and 20 female rats at levels of 0, 5, 10 and 20% in a semisynthetic diet for 3 months. Decreased weight gain was found in males in the 20% group. Urolithiasis was found in 8 males and in 7 females in the same group. Reduced relative liver weight was seen in males in the 10% and in the 20% groups, and an increased amount of iron was found in the livers of the 20% group. Nephrocalcinosis was reduced in females in the 20% group. In this experiment the no-effect-level is estimated to be 5% magnesium stearate in the diet, corresponding to 2500 mg/kg body wt/day.
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PMID:Magnesium stearate given perorally to rats. A short term study. 743 68

Evidence for the suitability of spot urines for selective screening in children was obtained by comparing the 24-hour urinary oxalate excretion with the ratio of urinary oxalate to creatinine [mmol/mol] in spontaneously voided urine samples. Spot urines of 169 healthy children aged 1 day to 13 years were analysed in order to establish reference values for the urinary oxalate/creatinine ratio in relation to age and body surface area. Oxalate was measured by automated ion chromatography. Results showed an inverse relationship between the oxalate/creatinine ratio and age. The highest ratios, 131 +/- 57 mmol/mol (mean +/- 2 SD), were found in infants. At age two years, the ratio was 84 +/- 55, at age five years 56 +/- 35, and for children older than ten years 42 +/- 31. This finding can be explained by the gain of muscle mass and hence increased creatinine production with increasing age. Data for the urinary oxalate/creatinine ratio are presented according to body surface area for the assessment of children with abnormal growth. In 19 urine samples from nine patients with primary hyperoxaluria, the oxalate/creatinine ratio greatly exceeded (286-2022 mmol/mol) the above reference ranges. We therefore propose the determination of the oxalate/creatinine ratio in spot urines for the selective screening for hyperoxaluria in children with nephrocalcinosis or urolithiasis.
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PMID:Determination of oxalate excretion in spot urines of healthy children by ion chromatography. 816 90

Renal tubular acidosis represents a heterogenous group of disorders with various etiologies and mechanisms. The physiopathologic basis of each type of renal tubular acidosis is reviewed, focusing on the laboratory investigations necessary to define the nature of the hyperchloremic renal tubular acidosis. Clinically, the four types of renal tubular acidosis can be associated with complications such as osteomalacia, urolithiasis and failure to thrive. Very often, the chronic administration of alkali results in normal growth and development, and greatly reduces the risk of stone formation or nephrocalcinosis.
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PMID:[Renal tubular acidosis in children]. 839 83

The possibility that dietary fish oil supplementation may benefit patients with hypercalciuric urolithiasis by decreasing calcium excretion and enhancing protective mechanisms has been studied in rats and humans. In experiments on rats in metabolic cages, fish oil inhibited experimental nephrocalcinosis induced by intraperitoneal calcium gluconate. There were no significant changes in urinary biochemistry. In a clinical study on 18 hypercalciuric recurrent stone patients fish oil significantly decreased urinary calcium excretion. This effect was accompanied by decreases in the excretion of magnesium and citrate. Oxalate excretion and urinary fibrinolytic activity were unchanged. Overall, fish oil had a limited impact on the risk profile for recurrent urolithiasis.
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PMID:Does fish oil benefit stone formers? 841 6

Hypercalcaemia is one of the extra-pulmonary symptoms of sarcoidosis. We describe a case of acute and chronic renal failure due to urolithiasis and nephrocalcinosis probably caused by sunlight-induced hypercalcaemia in a patient with undiagnosed sarcoidosis. Attention must be given to excessive sun exposure and vitamin D intake in patients with sarcoidosis.
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PMID:[Nephrocalcinosis and urolithiasis as primary symptoms in Boeck's sarcoidosis]. 864 14


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