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)

We have prospectively studied 37 adult patients (15 males, 22 females; age 31 +/- 10.6 years) with previously undiagnosed isolated hematuria in which hypercalciuria or hyperuricosuria was found. Eighteen of them had had episodes of gross hematuria. Isolated hypercalciuria (4.4 to 10.4, X 5.6 +/- 1.9 mg/kg/24 hr) was found in nine patients (Group I), isolated hyperuricosuria (784 to 1500, X 1088 +/- 228 mg/24 hr) in 11 (Group II), and both hypercalciuria (4 to 8, X 4.9 +/- 1 mg/kg/24 hr) and hyperuricosuria (752 to 1476, X 1042 +/- 181 mg/24 hr) in 17 patients (Group III). Thiazide treatment for patients with hypercalciuria and allopurinol for those with hyperuricosuria were administered; calciuria and uricosuria became normal by the first month of therapy in every case. In 22 (59.4%) cases (Responder patients) hematuria resolved completely as soon as calciuria and uricosuria became normal. In the remaining 15 cases (Nonresponder patients) hematuria persisted despite the normal calcium and uric acid excretions. Several disorders that explained hematuria were diagnosed later in most of Nonresponder patients. Responder patients persisted without hematuria on the follow-up; only in three patients a transient relapse of hematuria was seen associated with a sudden increase of calciuria and uricosuria because of treatment withdrawal. There were no differences in age, male/female ratio nor in the basal values of calciuria and uricosuria between Responder and Nonresponder patients. A familial history of urolithiasis was found more frequently in Responder patients (64%) than in Nonresponders (20%) (P less than 0.05). We conclude that hypercalciuria and hyperuricosuria are definable and potentially reversible causes of hematuria in adult patients.
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PMID:Hematuria due to hypercalciuria and hyperuricosuria in adult patients. 281 Oct 59

Between 1981 and 1983, 49 children aged 2 to 15 years were diagnosed as having idiopathic hypercalciuria (IH). They were divided into 3 groups based on their response to dietary manipulation: group I (32/49) had absorptive hypercalciuria; group II (8/49) had renal hypercalciuria and group III (6/49) had sodium-dependent hypercalciuria. Response to diet was more reliable than Pak's test in differentiating between the three groups. A control group (CG) of 45 healthy, age matched children determined baseline levels for all metabolic parameters. At the time of presentation IH children did not differ from the CG in height or weight. Fifty percent of IH children had first degree relatives with urolithiasis. Yet, only 16% of the IH children had urolithiasis, the majority presenting with gross hematuria and urinary tract infections (UTI). With few exceptions the clinical symptoms resolved when urine calcium excretion was controlled. Severe calcium restriction in a few patients produced osteoporosis and delayed bone age although growth velocity was unaffected. Thiazide therapy in a few patients produced some metabolic derangements. The authors conclude that IH in childhood is a benign disease which may present with UTI or hematuria. They further propose a new classification method based on response to dietary manipulation.
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PMID:Idiopathic hypercalciuria in children. Classification, clinical manifestations and outcome. 359 Dec 93

We evaluated the efficacy of selective treatment in 126 patients with recurrent calcium urolithiasis who were chosen on the basis of ability to correct underlying physiochemical disturbances. Patients with hyperparathyroidism underwent an operation. Patients with renal hypercalciuria were treated with thiazide and those with absorptive hypercalciuria were given a low calcium, low oxalate diet with or without thiazide. The only treatment for normocalciuric patients was high fluid intake, which was suggested also to the other groups. A significant individual mean reduction in stone formation was observed in all groups after 5 years of treatment. However, only 48 per cent of the normocalciuric patients were in remission after 5 years of high fluid intake therapy and 45 per cent of those with absorptive hypercalciuria were free of recurrence with diet only. Thiazide treatment seemed to be effective despite the type of hypercalciuria. The effect of the treatment on stone formation was mediated through reduction of risk factors in the urine. Conversely, a high level of risk factors commonly predicted stone recurrence.
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PMID:Five years of experience with selective therapy in recurrent calcium nephrolithiasis. 608 13

Exposure of male weanling Fischer 344 rats to 4.0% terephthalic acid (TPA) in the diet (positive controls) for two weeks (postnatal days 28-42) resulted in a 50% incidence of bladder calculi, aciduria, elevated urinary excretion of calcium (Ca) and magnesium (Mg), and slightly elevated serum levels of Ca and Mg relative to negative controls. Possible mechanisms of TPA-induced urolithiasis were examined by daily oral administration of allopurinol, chlorothiazide, or neutral phosphates, at their recommended therapeutic doses during exposure to dietary 4.0% TPA. An additional group was fed 4.0% TPA and 4.0% sodium bicarbonate in the diet for two weeks. Chlorothiazide or dietary bicarbonate abolished TPA-induced urolithiasis, but allopurinol and neutral phosphates had no effect. Bicarbonate increased water intake above that of positive controls and ameliorated the TPA-induced aciduria. It also increased urinary Mg and TPA above positive control values. Chlorothiazide reduced urinary Ca and TPA levels below those of positive controls. Treatment with chlorothiazide, neutral phosphates or bicarbonate slightly reduced serum Ca below the levels in either positive or negative controls. Drug treatment did not alter TPA-induced elevated serum Mg levels, but bicarbonate reduced serum Mg levels to negative control values. In conclusion, TPA-induced urolithiasis in male weanling rats was abolished by therapeutic agents which reduced urinary Ca and TPA excretion (chlorothiazide), or which enhanced water intake, urinary Mg and TPA excretion, and ameliorated TPA-induced aciduria (dietary bicarbonate). These factors appear to be critical for TPA-induced urolithiasis.
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PMID:Effects of selected therapeutic agents on urolithiasis induced by terephthalic acid in the male weanling Fischer 344 rat. 666 96

The prophylactic effect of hydrochlorothiazide on stone formation was studied in 66 patients with calcium urolithiasis, (49 men and 17 women between 25 and 76 years old, mean 52.2 +/- 11.7 years) due to idiopathic hypercalciuria. Urinary calcium excretion was significantly decreased during treatment when compared to the baseline value. The stone formation rate was also significantly reduced when compared with that before treatment. With regard to side effects, hyperuricemia was observed in 21 patients, hypokalemia in 9 patients, hypotension in 3 patients, and glycosuria in 4 patients. Thiazide treatment was concluded to be effective for preventing the recurrence of calcium stones in patients with idiopathic hypercalciuria. However, this therapy should be used only in conjunction with the careful monitoring of possible adverse reactions.
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PMID:[Thiazide treatment for calcium urolithiasis in patients with idiopathic hypercalciuria]. 807 54

Several clinical and epidemiological studies revealed increased bone turnover and lower bone mass in patients with urolithiasis. Bone mass loss is particularly evident in idiopathic calcium stone formers. However, pathogenetic mechanisms and factors implicated in bone loss in these patients are still unknown. Dietary calcium restriction, increased intake of salt and animal proteins, vitamin D receptor polymorphisms are likely risk factors, while role of inflammatory cytokines, osteopontin and prostaglandin mediated bone resorption is yet to be determined. Regarding treatment and prevention, it has been proven that calcium supplements and high calcium diet with the addition of potassium alkali have an important role in prevention and treatment of both, urolithiasis and osteoporosis. Thiazide diuretics reduce hypercalciuria in renal tubules, and in addition promote osteoblast differentiation. Finally, bisphosphonates, a commonly used drugs in treatment of osteoporosis, show the potential to inhibit calcium stone formation, whereas a possible protective effect of antioxidants in bone loss and renal injurie needs to be investigated further.
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PMID:Urolithiasis and osteoporosis: clinical relevance and therapeutic implications. 2012 Apr 12

Hypercalciuria is the most common metabolic abnormality that causes urolithiasis. The pathogenetic mechanisms responsible for hypercalciuria include enhanced gastrointestinal absorption of calcium, increased bone resorption and/or decreased renal reabsorption of calcium; the main dietary factors promoting hypercalciuria are high dietary sodium intake and protein-rich diet. The authors discuss pathophysiology of hypercalciuria and genetic factors behind 'idiopathic hypercalciuria'. The simplified diagnostic approach to hypercalciuria is outlined herein, and available therapeutic interventions of proven efficacy in idiopathic hypercalciuria are presented as well. Dietary intervention for hypercalciuria should include reduced sodium, protein and oxalate intake. Thiazide diuretics, in conjunction with a low-sodium diet, tend to reduce urinary calcium excretion and ameliorate idiopathic hypercalciuria. Potassium citrate acts as an inhibitor of calcium stone formation in the urinary tract. A low-calcium diet should generally be avoided, as it may increase urinary oxalate excretion and actually promote stone formation. In addition, a low-calcium diet may lead to negative calcium balance in subjects with hypercalciuria, and therefore increases the risk of osteopenia.
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PMID:[Hypercalciuria]. 2175 20