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

Abnormalities in uric acid metabolism are associated with uric acid and calcium oxalate urolithiasis. Clinical stone formation depends on multiple identifiable risk factors that affect uric acid and calcium oxalate solubility. The understanding of urinary pH is critical to direct appropriate treatment of uric acid-related nephrolithiasis. Understanding uric acid metabolism and the pathophysiology of uric acid and calcium oxalate stone formation leads to a rational treatment approach to uric acid and hyperuricosuric calcium oxalate stone disease.
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PMID:Uric acid-related nephrolithiasis. 904 57

Xanthinuria is an uncommon metabolic disorder clinically manifested as urolithiasis. There are two forms of the disease, congenital and iatrogenic. The former was diagnosed in a four-year-old dachshund bitch. The patient was presented with signs of terminal chronic renal failure. Urine was bacteriologically sterile with massive amorphous crystalluria. Bilateral nephrolithiasis was diagnosed at necropsy. The kidneys were shrunken with marked atrophy of the renal cortex and medulla. Infrared spectrometry revealed that the stones comprised 100 per cent xanthine. Later, two of the patient's siblings were examined for urine xanthine content; both showed higher concentrations of xanthine than a control dog. The described case is compared with seven known published cases of congenital xanthinuria.
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PMID:Bilateral xanthine nephrolithiasis in a dog. 923 33

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

Idiopathic calcium nephrolithiasis (ICN) is a frequent disease in Western countries. The physicochemical theory of lithogenesis, which explains stone formation by the precipitation, growth, and crystalline aggregation of lithogenic salts in the urine, has contributed greatly to the understanding of the pathogenesis of calcium urolithiasis. However, several aspects are still unexplained; the co-existence of familial occurrence, primary tubular dysfunctions with ICN, and anomalies in the systemic handling of oxalate and calcium led to the development of a cellular hypothesis of ICN. A number of cellular defects in the handling of ions has been reported that involves both anion and cation transport. These anomalies are probably the expression of a still unknown cellular defect in idiopathic calcium stone formers. We suggested that an anomaly in the cell membrane composition might be responsible for the complex array of cell ion flux abnormalities observed in ICN. Recently, a disorder in the n-6 polyunsaturated fatty acid series has been described; it is characterized by a lower linoleic acid content and a higher arachidonic acid concentration in both plasma and erythrocyte membrane phospholipids of renal calcium stone patients. This anomaly could cause an increased activity of ion carriers; furthermore, it may lead to increased prostaglandin synthesis and to secondary phenomena at the kidney, skeletal, and intestinal level. As a consequence, critical conditions for lithogenesis in the kidney may ensue. The data suggest a common pathogenesis for hypercalciuria and hyperoxaluria. The systemic defect in the phospholipid arachidonic acid level may be both of dietary or genetic origin; experimental data suggest that the increase in delta-6 desaturase activity, the limiting enzyme in the metabolic pathway of polyunsaturated fatty acids, might be relevant to the pathogenesis of lipid abnormalities observed in nephrolithiasis and to the pathogenesis of ICN and its related problems (at the kidney, intestinal, and bone level).
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PMID:Pathogenesis of idiopathic calcium nephrolithiasis: update 1997. 959 25

Dynamic nephroscintigraphy (DSG) was performed in 112 patients aged 14 to 76 years who had undergone 1 to 6 sessions of EL for unilateral or bilateral nephrolithiasis. A total of 254 EL sessions on 119 kidneys were performed. DSG was conducted before EL and at least 12 months after elimination of the stone fragments. The improvement of secretory renal function occurred in 68(57%) patients, aggravation was registered in 17(14.3%), unchanged renal function was in 34(28.6%) patients. Out of 17 cases of aggravation EL was responsible for only 3 of them. The others were due to other factors (progressive chronic pyelonephritis, acute pyelonephritis, hematoma, etc.). The conclusion is made that EL is a low-traumatic treatment of urolithiasis which is a method of choice in making decision on therapeutic policy in urolithiasis.
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PMID:[Kidney function based on dynamic nephroscintigraphic data in the late period after extracorporeal lithotripsy]. 982 46

51 patients with urolithiasis complicated by pyelonephritis in the active phase of inflammation were studied for the condition of local immunity by determining the urine content of secretory immunoglobulin A (SIgA) under conditions of combined treatment with making use of phlogenzyme, a drug of II-generation systemic enzymotherapy (SE). Recordable in this patients population was a marked increase in the urine level of SIgA. Incorporation in a combined treatment of phlogenzyme results in normalizing the status of the urinary system local immunity. Evidence has been obtained on the lack of parallelism in the dynamics between the serum IgA content and urine concentration of SIgA, which fact suggests independence of local immunity. Our theory is that an appreciable increase in the urine level of SIgA in patients with urolithiasis concurrent with pyelonephritis may have an important part to play in the genesis of nephrolithiasis.
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PMID:[The local immunity of the urinary system in patients with recurrent urolithiasis]. 1047 53

It is unclear why men have a higher incidence of calcium oxalate nephrolithiasis than women. This study examined the role of sex hormones on urinary oxalate excretion and kidney stone formation in an experimental model of urolithiasis. Adult male and female Sprague Dawley rats with different sex hormone modulations were given 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposition. The study groups were: intact male and female rats; castrated male and female rats; intact male or female rats with opposite sex hormone implants; and castrated male and female rats with either testosterone or estradiol implants. Overall, a significant negative correlation between urinary oxalate and plasma estradiol/testosterone ratio was found. None of the estradiol-implanted rats, whether male or female, intact or castrated, developed kidney crystal deposits. The three groups of testosterone-implanted rats had a 43 to 88% rate of kidney calcium oxalate crystal deposition. These results indicate that androgens increase and estrogens decrease urinary oxalate excretion, plasma oxalate concentration, and kidney calcium oxalate crystal deposition. These findings may partly explain why nephrolithiasis is a predominantly male disease.
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PMID:Role of sex hormones in experimental calcium oxalate nephrolithiasis. 1054 Dec 67

The purpose of this study was to determine the incidence of nephrolithiasis in radical cystectomy patients treated with either intestinal conduit or continent urinary diversion. The charts from 94 patients who had undergone radical cystectomy with urinary diversion at our institution from 1988 to 1998 were reviewed retrospectively for this study. Charts and radiographs from all patients were examined for renal function and evidence or urinary tract calculi. Two groups were compared: group I patients had undergone diversion with an intestinal conduit, and group II patients had received a continent diversion (primarily involving an Indiana pouch). Conduit diversions were typically done with a freely refluxing anastomosis (Bricker), whereas continent diversions were done with a nonrefluxing ureteral-intestinal anastomosis. Group I consisted of 54 patients who had undergone ileal conduit (50) or colon conduit (4) diversion with a mean follow-up of 2.5 years (range 0.6-7.0 years). Group II consisted of 40 patients who had undergone continent diversion (33 Indiana pouches, 7 orthotopic diversions) with a mean follow-up of 3.1 years (range 0.5-10.5 years). Laboratory studies of serum blood urea nitrogen, creatinine, and CO(2) were similar between the two groups. Six patients in group I developed urolithiasis, all in the upper tract. Stones developed at a mean of 3.1 years after urinary diversion. Three patients required operative intervention, whereas the others were managed expectantly. One patient in group II had an upper tract stone at the time of presentation for his bladder cancer, but no patient developed new upper tract stones during the present study period. Two patients in group II developed pouch calculi at a mean of 5 years after diversion; both required surgical intervention. In our study the risk for upper tract urolithiasis seemed higher in the intestinal conduit group (group I), with 11% of the patients developing stones. In the continent diversion group, no patient developed upper tract stones, although two patients (5%) developed pouch stones. Refluxing urine may contribute to an increased risk for stone formation after urinary diversion, whereas pouch stasis may contribute to stone formation in the continent diversion group.
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PMID:Incidence of urolithiasis in cystectomy patients after intestinal conduit or continent urinary diversion. 1055 49

A set of simple guidelines for metabolic evaluation and medical/dietary management of patients with urolithiasis is presented. The evaluation scheme is based on the documented risk factors in the Nordic area and the results of controlled clinical trials, and takes its basis in the severity of the stone disease in the individual stone patient. The initial evaluation in all patients aims at diagnosing conditions with a definitive metabolic, infectious or anatomical/functional cause of stone formation (MIAF urolithiasis). Patients with MIAF urolithiasis are treated according to the nature of the underlying disease. Having excluded/diagnosed MIAF urolithiasis, patients with idiopathic calcium nephrolithiasis remain, and in this group, which comprises approximately 85% of the total stone population in the Scandinavian region, only those with a complicated stone disease are subjected to additional evaluation, which aims at identifying underlying pathophysiological derangements for which medical therapy has been proven to be effective in controlled clinical trials.
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PMID:Metabolic evaluation and medical management of upper urinary tract stone disease. Guidelines from the Scandinavian Cooperative Group for Urinary Stones. 1063 76

Bacteria or their antigens persisting in the kidneys may induce the classical type of chronic pyelonephritis (CP), which progresses slowly, and may finally result in end-stage renal failure requiring dialysis. Pyelonephrogenic strains enter uro-epithelial and renal epithelial cells--where they accumulate--or may invade the renal interstitium. Promoting factors are obstruction, reflux, urolithiasis, nephrolithiasis, pregnancy, diabetes mellitus, humoral and cellular immunodeficiencies, immunosuppression treatment (e.g. following transplants), autoimmune phenomena (antigenic mimicry). Therapy comprises the treatment of underlying disease, antibiotics as indicated by the resistogram, acidification of urine (L-methionine), i.v. immunoglobulins (IgM, IgG) and oral vaccination with lyophilized uropathogens.
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PMID:[Chronic pyelonephritis. Synopsis of laboratory values and ultrasound lead to diagnosis]. 1090 12


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