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

Stone formation was investigated in 162 male and female Sprague-Dawley rats (96 males and 66 females) following a portacaval shunt and in 58 sham-operated rats which served as controls (31 males and 27 females). 70.8% male and only 7.5% female shunted rats developed urolithiasis. All stones of sufficient size were analyzed. The majority of stones in shunt-operated rats were made of potassium hydrogen urate (23/41), 10 rats had struvite stones without urinary tract infection, the remaining 8 rats had composite stones. Analysis of all stone-bearing control animals revealed struvite stones (6/6). Postoperatively, the rats developed polyuria, elevated potassium and uric acid excretion (all sex dependent). Urinary pH levels did not change significantly. Organ changes (atrophy of the liver, the testes and ovaries, hypertrophy of the kidney and the adrenal glands) were significant and differed according to sex. The role of sex hormones and prostaglandins is discussed.
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PMID:Sex-dependent urolithiasis in the portacaval shunt rat. Part I. 846 Apr 52

Hyperuricosuria (HU), defined as a urinary acid excretion higher than 95 percent of normal values, is an important lithogenic factor, accounting for about 5-20% of recurrent hematuria in childhood. We prospectively studied 30 children (15 male, 15 female; aged 3 to 13 years old) with previously undiagnosed isolated hematuria and HU for 6 to 36 months. The family history of nephrolithiasis was positive in 40%. Idiopathic hypercalciuria (IH), UCa > 4 mg/kg/day, was not found initially, but was diagnosed after 6 to 24 months in 20% of the patients. The following treatments were utilized: restricted purine diet (13%), allopurinol (4%) and potassium citrate (1%). No specific treatment was given to 82% of the patients. Therapy normalized uricosuria with resolution of hematuria over 6-12 months. Thirteen percent and 6% of untreated patients developed urolithiasis after 6 and 12 months respectively. The data suggest that HU, like IH, is associated with hematuria. Furthermore, recognition of this association may prevent unnecessary, and in some cases, invasive diagnostic manoeuvres.
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PMID:Hematuria due to hyperuricosuria in children: 36-month follow-up. 940 12

The case study presented here illustrates the diagnosis and management of calcium oxalate urolithiasis in a Bichon Frise, a breed at increased risk for this type of stone. If the Bichon Frise had persistent hypercalcemia, we would have evaluated serum concentrations of ionized calcium, parathyroid hormone, and vitamin D to identify an underlying cause. Because his urine was alkaline, additional potassium citrate was not provided. Likewise, as a fortified diet was fed to him, vitamin B6 therapy was not considered. This case study illustrates the benefits of radiographic evaluation immediately following surgery and during follow-up examinations. If we had postponed radiographs until the patient developed clinical signs, additional surgical procedures may have been required.
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PMID:Canine calcium oxalate urolithiasis. Case-based applications of therapeutic principles. 1002 55

Cystine urolithiasis is the only clinical expression of cystinuria, an autosomal recessive genetic defect of the transepithelial transport of cystine and other dibasic amino acids in the kidney. Stones form due to the increased excretion of cystine, which is poorly soluble at normal urine pH. Cystine stones are often resistant to extracorporeal shock wave lithotripsy, so that percutaneous surgery or ureteroscopy are the preferred techniques of stone extraction. Medical preventative treatment is based on high diuresis (>/=1.5 l/m(2) per day) well distributed throughout the day and night, and urine alkalinization up to pH 7.5 by means of sodium bicarbonate and/or potassium citrate. When these basal measures are ineffective at preventing stone recurrence or dissolving pre-existing stones, sulfhydryl agents such as D-penicillamine or tiopronin, which form highly soluble mixed disulfides with cystine moieties, are to be added to urine dilution and alkalinization, especially when cystine excretion is in excess of 750 mg/day (3 mmol/day). Frequent clinical and ultrasound follow-up is needed to encourage patient compliance and assess efficacy and tolerance of treatment.
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PMID:Treatment of cystinuria. 1104 3

Apart from a minority with urolithiasis, the majority of children diagnosed with idiopathic hypercalciuria present with macro- or microhematuria, abdominal or back pain, or voiding symptoms. With dietary and pharmacological interventions, most such children become asymptomatic and are lost to follow-up, hence their long-term outcome is unclear. In the present study, we evaluated the status of 14 males and 19 females aged 8-17 years (mean 11.9 years, median 11.2 years) 4-11 years (mean 6.9 years, median 6.5 years) after the initial diagnosis of idiopathic hypercalciuria not associated with urolithiasis. A questionnaire was answered and two random urine samples provided 3-4 weeks apart were analyzed for calcium (Ca), sodium (Na), potassium (K), and creatinine (Cr). Urine Ca/Cr ratio > or =20.21 (mg/mg) was defined as hypercalciuria. At the time of the study none were under follow-up, although 7 children were still exhibiting voiding symptoms. No child developed clinical urolithiasis. Based on the first urine specimen, 16 of the 33 (48.4%) were hypercalciuric. Their 2nd urinalysis showed persistent hypercalciuria in 8 and normocalciuria in 8. Urine Na/K ratio (mEq/mEq) decreased in the latter 8 from 5.08+/-2.67 to 3.03+/-2.23 (P<0.05). Of the 17 initially normocalciuric children, 5 did not submit a 2nd specimen, 11 remained normocalciuric, and 1 became hypercalciuric with an increase in urine Na/K ratio. Twenty-three children (all 8 persistently and 9 intermittently hypercalciuric plus 6 normocalciuric) were studied by ultrasonography. Only in 1 asymptomatic persistently hypercalciuric child was a single small renal calcification noted. Introduction of a low-Na/high-K diet in 7 persistently hypercalciuric children resulted in a decrease in UNa/K ratio from 7.34+/-2.15 to 4.14+/-3.09 (P<0.01) and UCa/Cr ratio from 0.25+/-0.04 to 0.13+/-0.03 (P<0.01). We conclude that even though over time most hypercalciuric children become asymptomatic, many remain hypercalciuric. Further follow-up is required to ascertain whether these children are at risk of developing kidney stones. If they are at risk then long-term compliance with a low-Na/high-K diet might be beneficial, as it can normalize calciuria in the majority of these children.
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PMID:Idiopathic hypercalciuria of childhood: 4- to 11-year outcome. 1097 18

Biochemical tests by 12 metabolic blood and urine indices reflecting the condition of renal function and metabolism of urolithogenic substances were made in the course of 1-6 year follow-up of 35 and 79 patients (46 females and 68 males aged 18-65 years) with recurrence-free and recurrent urolithiasis, respectively. The risk of recurrence for uric acid urolithiasis in serum concentration of urea 5.67 +/- 0.14 mmol/l and creatinine 0.090 +/- 0.008 mmol/l, in hyperuricemia and hyperuricuria was associated with elevation of renal excretion of total calcium to 5.88 +/- 0.49 mmol/day and ratio of daily renal excretion of sodium to renal daily excretion of potassium to 3.28 +/- 0.08; for calcium-oxalate lithiasis--with a rise in serum concentration of uric acid to 0.310 +/- 0.042 mmol/l and sodium to 114 +/- 0.8 mmol/l in hypercalciuria and hyperuricuria.
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PMID:[Recurrence-free and recurrent urolithiasis: metabolic differences]. 1115 Jan 60

We report a case of urolithiasis associated with short bowel syndrome. A 56-year-old woman was admitted to our hospital for asymptomatic bilateral renal stones. She had received extensive resection of small intestine due to strangulating obstructive ileus 7 years ago (residual intestine, only 20 cm). Subsequently, she was in a state of short bowel syndrome. Plain film of kidney, uteter, bladder and computed tomography revealed bilateral renal stones (right 4 mm, left 10 mm). The left renal stone was successfully treated by extracorporeal shock wave lithotripsy. Since the right renal stone was small, no treatment was performed. The stone fragments were composed of calcium oxalate and calcium phosphate, and excessive urinary excretion of oxalate (103.8 mg/day) was observed. In this patient, urolithiasis was diagnosed to be due to enteric hyperoxaluria caused by short bowel syndrome. To prevent the recurrence of stone formation, she was treated with oral administration of calcium lactate, sodium/potassium citrate and magnesium oxide. We review the Japanese literatures on urolithiasis with short bowel syndrome.
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PMID:[A case of urolithiasis associated with short bowel syndrome]. 1263 4

This paper deals of kidney stones, hard concretions that grow within the urinary tract, 71.5% of which have calcium contents. A high rate of recurrences underscores the importance of medical prevention with a variety of conservative (increased fluid intake and dietary modifications) and drug therapy (potassium citrate, potassium magnesium citrate, thiazides, allopurinol). In single stone formers and mild recurrent diseases, the conservative therapy may alone be effective and should be maintained in more severe recurrent disease, together with drug treatment. In particular, in idiopathic calcium oxalate nephrolithiasis, the importance of sodium restriction in the diet, that should reduce calcium excretion, has been recently shown, limiting the old assumption of the value of dietary calcium restriction; in fact normal or higher calcium intake, binding oxalate in the intestinal tract, seems to confer protection against stone formation. The urologic approach to urolithiasis has changed with the introduction of extracorporeal shock wave lithotripsy (ESWL), a technique that allows a relatively noninvasive removal of stones. Nevertheless ESWL does not change the propensity of recurrence of stone formers, and the importance of medical prevention remains paramount in the management of renal stone disease.
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PMID:[Etiopathogenesis and clinical aspects of nephrolithiasis--at present]. 1267 82

Cystinuria is an autosomal recessive disorder with an estimated incidence of 1 case in 7000 live births, that results in elevated urinary excretion of cystine and dibasic aminoacids: ornithine, lysine and arginine. Discussed by Sir Archibald Edward Garrod, in 1908, as one of the four first known inborn errors of metabolism, it is characterized by a defect in transport of cystine and dibasic aminoacids, that affects their reabsortion in both renal tubule and gastrointestinal tract. To date, according to the recent molecular findings, two genes have been identified as responsible for this disease: SLC3A1 and SLC7A9. A more accurate pheno/genotyping identification of cystinuric patients will allow to improve prophilaxis and therapy for this illness. Cystinuria only causes recurrent urolithiasis (about 1-2 / of renal calculi in adults) and its associated complications as clinical feature because of poor cystine solubility at low pH. An accurate control over prohylaxis (based on high water intake and potassium citrate treatment, on first line, and tiol-derivatives treatment, on second line) must be taken in patients -like homozygous type I- with high lithiasis risk. However, approximately one half of patients under prophylaxis control will develop recurrent lithiasis; in this case, only urology or surgical approaches would be possible. 474 Updated knowledge about biochemical, genetic, clinical, diagnosis, prevention, treatment and prognosis aspects of this, relatively unusual, disease has been reviewed in this article.
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PMID:[Cystinuria update: clinical, biochemical and genetic aspects]. 1284 5

The objective of the study was to update the evaluation and treatment of idiopathic urolithiasis in children in Western society. A secondary goal was to evaluate patients' compliance with high fluid intake. Over 2 years we prospectively studied children referred to us for idiopathic urolithiasis confirmed radiographically, excluding those with secondary disorders. A metabolic urinalysis, which included calcium, citrate, uric acid, oxalate, cystine, and creatinine, was ordered in all patients. Hypercalciuric patients were first treated with a low-sodium (Na)/high-potassium (K) diet and if hypercalciuria persisted, thiazides or potassium citrate was added. Follow-up ultrasound scans were scheduled every 10-12 months. Urine specific gravity (SG) measured during clinic visits was used to assess compliance with high fluid intake. A survey was sent to pediatric urologists and nephrologists to establish a recommended maximal SG value. Thirty healthy school-aged children served as controls. There were 45 children (24 males, 21 females) aged 10.4+/-2.0 years (median 11.0) studied. Stones were retrieved and analyzed in 28 showing calcium composition in all. Urine chemistry analysis was incomplete in 3, and in the others showed hypercalciuria in 33 (78.6%), hypocitraturia in 1 (2.4%), and normal values in 8 (19.0%). Treatment of 33 hypercalciuric patients consisted of diet alone in 13, potassium citrate in 17, thiazides in 2, and potassium citrate and thiazide in 1. All 33 achieved normocalciuria, apart from 2 who remained mildly hypercalciuric on diet alone. The 12 normocalciuric children were treated by diet modification alone. Follow-up ultrasonography showed no new stones in 36 of 39 patients. In 3, new stone formation was associated with recurrence of hypercalciuria after the potassium citrate dose was lowered or discontinued. Upon their first clinic visit, the urine SG of stone formers (1.021+/-0.007) was significantly higher than the maximum SG recommended by 18 physicians of 1.010+/-0.003 ( P<0.001), and not different from the SG in the control group (1.018+/-0.007). Urine SG at follow-up visits was unchanged in stone formers. We therefore propose a step-wise approach in evaluating children with idiopathic urolithiasis in Western society, in which first only urine calcium is studied. Only if urine calcium is normal, should other chemistries be studied. In many hypercalciuric children, low-Na/high-K diet alone is effective, while in most others the addition of potassium citrate is well tolerated, normalizes calciuria, and protects against new stone formation. Children rarely comply with the recommendation of high fluid intake.
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PMID:Evaluation and treatment of pediatric idiopathic urolithiasis-revisited. 1501 63


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