Urate stones

The low solubility of uric acid has unfortunate consequences since at higher than normal concentrations it can crystallise in the body. For example, when the urine is unusually acid, calcium urate stones can form in the kidney and bladder. High levels of uric acid in the blood can result in the formation of urate crystals in the joints, which causes a very painful condition, since it results in inflammation in these joints. Gout is unlikely to develop if the urate concentration remains low (<0.4 mmol/L) but any factor that increases the rate of production or decreases that of elimination by the... 

Alkalinization of urine Hematuria, renal colic, costovertebral pain, and formation of urate stones associated with use in gouty patients may be prevented by alkalization of urine and liberal fluid intake monitor acid-base balance. 

Uric acid is minimally water-soluble and most cases of gout arise from inadequate excretion by the kidneys (souric acid and precipitation of urate stones In the kidneys and extremities. 

The adverse effect of formation of urate stones in the kidney can be reduced by adequate hydration and alkalinization of the urine. 

Uricosurics, such as probenecid or benz-bromarone (100 mg/day), promote renal excretion of uric acid. They saturate the organic acid transport system in the proximal renal tubules, making it unavailable for urate reabsorption. When underdosed, they inhibit only the acid secretory system, which has a smaller transport capacity. Urate elimination is then inhibited and a gout attack is possible. In patients with urate stones in the urinary tract, uricosurics are contraindicated. 

Noncalcareous stones occur most commonly in the presence of urea-splitting organisms which create conditions in which magnesium ammonium phosphate (struvite) stones form. Urate stones form when urine is vmusually acid (pH < 5.5). 

Uric acid stones account for about 10% of all kidney stones in the United States. Most kidney stones consist of calcium phosphate or calcium oxalate. The risk for developing urate stones increases with increased levels of plasma urate and with... 

Ascorbic acid 4 g/day increases uric acid clearance in volunteers (23), although it does not reduce protein-bound uric acid in blood. Ascorbic acid 4-12 g/day causes acidification of the urine, which can cause precipitation of urate and cystine and consequently formation of urate stones or cystinuria. Ascorbic acid is excreted largely as oxalate, and hyperoxaluria results when large doses are... 

Pyrazinamide should be used with extreme caution in patients with a history of gout, especially in elderly people, in whom urinary urate stones can cause renal insufficiency. 

Some investigators believe that urate may potentiate calcium stone formation, although this perception is not universally accepted. However, hyperuricosuria is common in calcium stone-forming patients, and treatment with allopurinol, thereby decreasing urate synthesis, reduces the rate of stone recurrence. Allopurinol treatment is therefore recommended for hyperuricosuric patients with calcium stone disease. The formation and management of pure urate stones are discussed in Chapter 24. 

Renal disease is a eommon complication of hyperuricaemia. Several types of renal disease have been identified. The most comnutn is urate nephropathy which is caused by the deposition of urate crystals in renal tissue or the urinary tract to form urate stones. This mtiy be associated with chronic hyperuricaemia. Acute renal failure can be cau.sed by the rapid precipitation of uric acid crystals w hich commonly occurs during treatment of patients with leukaemias and lymphomas. In the acute tumour lysis syndrome (p. 129), nucleic acids are released as a result of tumour cell breakdown and arc rapidly metabolized to uric acid. 

An additional observation, hinting indirectly at the parallelism between uric acid and calcium in urine, is the high coincidence of uric acid and calcium crystalluria in the group of recurrent stone formers that has been measured in 16 (oxalate and urate) stone patients and in 11 controls during our long-term study. Twenty-eight percent of all urine samples collected in male stone patients and thirty-one percent of those collected in female patients contained both calcium and uric acid crystals. 

Increased uric acid in serum as a result of animal protein overconsumption and alcohol abuse is frequent nowadays. Concentrations above 6,5 mg uric acid/100 ml serum can lead to the deposition of uric acid or its salts in tissues, which in turn can lead to gout. Up to 40% of the patients suffering from gout also have uric acid nephrolithiasis. Without showing the symptoms of gout, however, uric acid stones as well as urate stones can form when the solubility product is exceeded either because of extreme uricosuria and/or because of an unfavorable urinary pH. About 20% of all urinary stones are totally or partially composed of uric acid or urate. 

Lonsdale [87, 88] has reviewed the epidemiology of urinary lithiasis and concludes that bladder stones have become rare in adult man. The bladder stones Lonsdale found were urate stones and were believed to result from faulty diet. Bladder stones, composed of urate and oxalates, are seen in young people, rarely in the West, but commonly in India, Turkey, and Thailand. In contrast, kidney stones are a relatively frequent ailment in the West (200,000 new cases a year in the United States). Kidney stones are usually made of calcium oxalate, calcium phosphate, or MgNH4 phosphates. The incidence seems to be highest among those with sedentary professions, and renal lithiasis is said to constitute an occupational hazard among airplane pilots. 

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