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

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

Three types of hypercalciuria are described; their existence and frequent association with calcium urolithiasis in humans are accepted. Various dietary factors such as minerals, electrolytes, fluids, vitamin D, carbohydrates, proteins are discussed with regard to their ability to alter the nature and the degree of calcium excretion following their ingestion. It is emphasised that at present we have only limited knowledge on the chain of events linking calorie intake and the response of the kidney.
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PMID:A survey of calcium urolithiasis in normocalcemic hypercalciuria: possible role of nutrients and diet-mediated factors. 38 96

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

In the literature there is a paucity of references on urolithiasis in children with spinal cord injury. In this paper 28 cases of urolithiasis in 97 children with spinal cord injury are analysed. An attempt is made to evaluate the role of hypercalcemia, hypercalciuria and urinary tract infection in the genesis of these calculi.
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PMID:Urolithiasis in children with spinal cord injury. 43 66

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 causes of, and physiopathological factors underlying the most common metabolic disorders implicated in the formation of renal stones are reviewed. These include hypercalciuria, hyperoxaluria, renal tubular acidosis, cystinuria and disturbances of purine metabolism. Apart from metabolic disorders the risk of stone formation is also influenced by a low inhibitor activity in urine. Though some aspects in the pathogenesis of urolithiasis remain uncertain, the exact knowlege of important aetiological factors of stone formation is the basis of correct treatment and the prevention of recurrence of urinary calculi.
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PMID:[The evaluation of patients with urinary calculi discloses disturbances of metabolism in 75% of all cases (author's transl)]. 47 69

Inborn hypouricemia due to isolated renal tubular defect is a rare disorder. Thus far eight documented families with this condition have been reported. In reviewing the data on these families, hyperuricosuria was found to be a constant associate of the hypouricemia, and hypercalciuria, mainly of the absorptive type, was frequently associated. Urolithiasis appears to be common. The mode of inheritance of this hypouricemia was autosomal, probably recessive. The magnitude of renal urate clearance and the effects on it of probenecid and pyrazinamide suggest the inborn renal hypouricemia to be of two types, due to defective re-secretory tubular urate reabsorption and to total defective tubular urate reabsorption. The question of the renal tubular abnormality for urate transport being the primary defect or secondary to an abnormal metabolite is discussed.
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PMID:Inborn hypouricemia due to isolated renal tubular defect. 47 67

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

Primary hyperparathyroidism is a major cause of calcium urolithiasis and is easily recognised when it is classically manifested. However, subtle presentations of primary hyperparathyroidism may cause confusion with other causes of calcium stone disease or cause diagnostic difficulty. Several pitfalls of parathyroid evaluation and treatment are illustrated by four cases of calcium urolithiasis. Cases 1 and 2 represent ineffective or useless parathyroid surgery rendered for renal hypercalciuria and absorptive hypercalciuria, respectively. Cases 3 and 4 had mild or intermittent hypercalcaemia. The correct diagnosis of primary hyperparathyroidism was made in Case 3 by parathyroid venous sampling and bone densitometry. In Case 4, the thiazide provocative test was used to establish the diagnosis of primary hyperparathyroidism.
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PMID:Pitfalls in parathyroid evaluation in patients with calcium urolithiasis. 50 80


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