Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General prophylaxis of renal stone formation consists of 1. high fluid intake and 2. modest consumption of protein-rich foods. Specific prophylactic measures are based on pathophysiologic mechanisms of stone formation. In infection-induced renal stones, combined treatment with culture specific antibiotics and complete stone removal is of utmost importance. In all cases where stone fragments cannot be removed completely and/or partial obstruction remains, long-term antibiotics in combination with urine acidification by methionine (urine pH 5.6 to 6.2) are most appropriate. Prophylaxis of uric acid stones primarily consists of reducing purine intake and alkalizing the urine by potassium citrate. Only if this regimen failed or gout occurred, allopurinol should be administered. In patients with cystine stones, urine volume should be increased to greater than 3000 ml/die. Alkalizing the urine to a pH greater than 7.5 rises cystine solubility, whereas cystine excretion may be reduced by a diet low in sodium and/or low in methionine/cysteine. Thiols form mixed thiol-cysteine disulfides that are many times more soluble than cystine in urine; because of their high rate of adverse side-effects, however, these compounds are of lowest priority in the treatment of cystine stones. There is no convincing evidence for the efficacy of high dose ascorbic acid treatment in cystinuria.
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PMID:[Preventive measures in stones due to infection, uric acid and cystine]. 173 1

Significant alterations in the structure and functions of the kidney are caused by a number of metabolic disturbances and deficiencies of physiological substances. These include intercapillary glomerulosclerosis, gout, hypercalcemia, hereditary cystinuria, potassium depletion, pyrophosphates deficiency, vitamin D deficiency and liver disorders. Some of these metabolic disorders are secondary to drug ingestion.
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PMID:Renal disease secondary to metabolic disorders or physiological deficiency states. 604 89

Homozygous cystinuria was ascertained in 110 individuals (44 men) from 78 families because of symptoms in the propositi. The most common renal symptoms were calculi which occurred in 91% of the propositi and in 52% of affected family members. One-third of patients had urinary tract infections. There was a high rate of renal morbidity at an early age; 16 patients had undergone nephrectomy at a mean age of 25 years (range, 12-40 years). Two-thirds of subjects had type I cystinuria on family testing--the same ratio as that reported in a previous study of cases detected by newborn screening in the same population--which eliminates genetic type as a risk factor for stone formation. On the basis of all data, a 62% probability of stone formation by the age of 25 years in patients with cystinuria was estimated. The patients were shorter than Australian controls, and an association between gout and cystinuria was found in adult men.
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PMID:Homozygous cystinuria in New South Wales. A study of 110 individuals with cystinuria ascertained by methods other than neonatal screening. 648 95

While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
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PMID:[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]. 1264 87