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Query: UMLS:C0392525 (nephrolithiasis)
 2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of nephrolithiasis depends mainly on the type of stone present. Uric acid calculi can be dissolved by oral medication producing alkalinization of the urine. Cystin stones can only rarely be dissolved by oral administration of D-penicillamine. The best and least expensive prophylaxis is a high and constant fluid intake of 600 ml every 4 hours. This way the pathologically increased cystin excretion can be kept soluble. Calcium containing calculi and so-called "infection stones" need surgical intervention. Because of the high recurrence rate of renal stones every indication for an operative procedure has to be considered very carefully. For lasting results elimination of urinary obstruction is necessary. The treatment of choice of patients with staghorn calculus disease is surgical, even in the solitary kidney and in geriatric patients. As recent advances in the operative treatment of nephrolithiasis coagulum pyelolithotomy, intraoperative pyeloscopy, hypothermia and "bench surgery" (extra-corporeal renal surgery) are reviewed. Attempts to dissolve renal calculi by percutaneous nephrostomy as well as extraction of pelvic stones by the same procedure are mentioned. Finally, the importance of postoperative prophylaxis and the progress made in the medical treatment of calcium stones are pointed out.
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PMID:[Recent advances in the treatment of nephrolithiasis (author's transl)]. 4 17

Under the term "non-calcium nephrolithiasis", three types of renal stone formation are considered. (1) Infected nephrolithiasis, which is due to bacteriological ureolysis. Its treatment includes lowering of oversaturation by antibiotics, urease inhibition and/or acidification of the urine; lowering of crystallization by eradicating concomitant infections caused by non-ureolytic organisms; prevention of crystal adherence by exogenous glycosaminoglycans, and prevention of bacterial adherence by glycolipids. (2) Uric acid lithiasis is defined on physico-chemical and physiopathological grounds. Medical treatment consists of increasing water intake, reducing puric acid intake, alkalinizing the urine inhibiting xanthine-oxidase. (3) Cystinuria is described as a nephrolithogenic proximal tubulopathy. Medical treatment includes reduction of urinary cystine concentration by a strong increase of water intake; reduction of urinary cystine excretion by diet and increase of cystine solubility by urinary alkalinization or administration of some thiol compounds.
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PMID:[Physiopathology, etiology and medical treatment of non-calcium lithiasis]. 178 96

Since 1962 our group has performed four studies on uric acid values in blood donors in southern Germany (Bavaria). Uric acid levels in men have increased over the years, from 4.86 mg/dl in 1962 to 6.00 mg/dl in 1971, 5.60 mg/dl in 1984, and 5.90 mg/dl in 1989. Levels in women have increased slightly, from 4.05 mg/dl in 1962 to 4.35 mg/dl in 1971, 4.10 mg/dl in 1984, and 4.16 mg/dl in 1989. Women aged 51 to 60 years had significantly higher uric acid levels than those in the fourth decade. In women treated with oral contraceptives uric acid levels were significantly lower than in other women of the same age. Hypouricemia (uric acid levels less than or equal to 2.0 mg/dl) was observed in three women, none of whom had a history of medication. Hyperuricemia exists when uric acid levels are greater than or equal to 6.5 mg/dl. In 1989 2.6% of the female blood donors and 28.6% of the males were hyperuricemic, with an increased risk of gout, nephrolithiasis, and nephropathy.
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PMID:Uric acid levels in southern Germany in 1989. A comparison with studies from 1962, 1971, and 1984. 229 Mar 9

Hyperuricosuria is a frequent finding in patients with recurrent calcium nephrolithiasis (RCN) that has been related to purine overingestion . The influence of diet and the renal handling of uric acid were investigated in patients with RCN to assess the pathogenic mechanism of excessive urate excretion. Among 50 patients with recurrent nephrolithiasis 42 formed renal stones containing calcium and 9 of these 42 patients demonstrated concomitant asymptomatic hyperuricosuria while on a self-selected diet. Ingestion of a purine-free diet normalized the uric acid excretion in 4 of these 9 patients. The other 5 patients showed persistent hyperuricosuria while on a purine-free diet. In order to assess a possible dysfunction in the renal handling of uric acid, pharmacological tests were undertaken in these 9 patients. Pyrazinamide administration almost completely suppressed urate excretion, excluding a presecretory reabsorption defect. Urate excretion in response to probenecid administration was decreased in 4 patients and increased in 1. This finding is in accordance with a postsecretory reabsorption defect in the former and an augmented tubular secretion of urate in the latter. This study proves that both dietary factors and tubular transport defects are involved in patients with recurrent calcium nephrolithiasis and hyperuricosuria.
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PMID:Renal handling of uric acid in patients with recurrent calcium nephrolithiasis and hyperuricosuria. 672 86

Urate nephrolithiasis with epistaxis and bleeding around foot pads was diagnosed in ranch mink. Investigation of affected, unaffected-related, and unaffected-unrelated mink did not disclose the cause of these problems but did eliminate inherited bleeding disorders as a cause of the bleeding. All affected mink were males, had been sired by related sires, and were affected in the 1st year of life. Elimination of affected mink and their parents from the breeding stock eliminated the condition from the herd. The findings were consistent with an inherited defect in uric acid metabolism or excretion.
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PMID:Urate nephrolithiasis in ranch mink. 706 99

The first episode of nephrolithiasis provides an opportunity to advise patients about measures for preventing future stones. Low fluid intake and excessive intake of protein, salt and oxalate are important modifiable risk factors for kidney stones. Calcium restriction is not useful and may potentiate osteoporosis. Diseases such as hyperparathyroidism, sarcoidosis and renal tubular acidosis should be considered in patients with nephrolithiasis. A 24-hour urine collection with measurement of the important analytes is usually reserved for use in patients with recurrent stone formation. In these patients, the major urinary risk factors include hypercalciuria, hyperoxaluria, hypocitraturia and hyperuricosuria. Effective preventive and treatment measures include thiazide therapy to lower the urinary calcium level, citrate supplementation to increase the urinary citrate level and, sometimes, allopurinol therapy to lower uric acid excretion. Uric acid stones are most often treated with citrate supplementation. Data now support the cost-effectiveness of evaluation and treatment of patients with recurrent stones.
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PMID:Prevention of recurrent nephrolithiasis. 1059 18

The trend in uric acid stone formation appears to be on the rise again throughout much of the world. This is thought secondary to diet, body habitus, and social reasons. Uric acid stone disease has a rich and fascinating medical history and probably is the oldest known stone disease. Uric acid stone disease is strongly linked to the purine metabolic pathway, and its treatment is primarily medical. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. Surgical intervention with uric acid stone disease represents a failure of medical therapy and a whole host of modern, minimally invasive methods are available for treating patients with this disease. Finally, uric acid nephrolithiasis is associated with a variety of inborn errors of metabolism based on mutations of key enzymes in the purine metabolic pathways. This review of uric acid stone formation will start with historical consideration, review basic biochemistry, and physiology and then focus upon specific clinical scenarios. The discussions will be heavily referenced for those interested in greater details.
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PMID:Uric acid stone disease. 1295 51

Gout is a chronic metabolic disease caused by a disorder of the purine metabolism leading to hyperuricaemia. It is determined by the deposition of monosodium urate crystals in joints and other tissues which causes an acute inflammatory response and can induce a permanent tissue damage which defines the urate chronic joint disease which is characterised by the appearance of ulceration of the joint cartilage, marginal osteophytosis, geodic and erosive lesions and chronic inflammation of synovial membrane. Gout and hyperuricaemia usually occur after the age of 30 years and more frequently in men. Hyperuricaemia is the result of an increased production of uric acid or its hypoexcretion by the kidneys, or both. In the pathogenesis of gout and hyperuricaemia are involved genetic and environmental factors; further, different pathologic condition such as glycogenosis, renal insufficiency, use of some drugs, are associated with gout. Treatment of acute gout includes colchicine, nonsteroidal anti-inflammatory drugs and glucocorticoids, whereas in the intercritical periods colchicine is effective for preventive purposes. Urate-lowering therapy with xanthine-oxidase inhibitors or uricosuric agents is indicate only in patients with more than two gout crisis per year, tophaceous deposits, uric acid nephrolithiasis, and interstitial renal disease, as asymptomatic hyperuricaemia does not requires any treatment but can be controlled with preventive dietetic measures and changes in lifestyle.
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PMID:Pathogenesis, clinical findings and management of acute and chronic gout. 1721 86

The prevalence of urolithiasis has been increasing for the past few decades in industrialized nations. Uric acid calculi account for a significant percentage of urinary stones. Certain risk factors may be involved in the pathogenesis of uric acid nephrolithiasis, including hyperuricosuria, low urinary volume, and persistently low urinary pH. Patients with medical conditions that promote profound hyperuricosuria are at high risk of developing uric acid calculi. These conditions include chronic diarrheal states; myeloproliferative disorders; insulin resistance, including diabetes mellitus; and monogenic metabolic disorders, such as Lesch-Nyhan syndrome. Computed tomography can provide a definitive diagnosis. Except in cases in which there is severe obstruction, progressive azotemia, serious infection, or unremitting pain, the initial treatment of patients with uric acid nephrolithiasis should be medical dissolution therapy because this approach is successful in the majority of cases. A thorough review of the epidemiology and pathophysiology of uric acid nephrolithiasis is crucial for the diagnosis, treatment, and prevention of stones in patients with this condition.
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PMID:Uric Acid nephrolithiasis: recent progress and future directions. 1739 68

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.
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PMID:Gout: an update. 1869


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