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

Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible. Recent work suggests that allopurinol reduces the incidence of urolithiasis and the urinary excretion of both oxalate and uric acid in patients without intestinal disease. We have assessed the effect of allopurinol, 300 mg daily for 2 weeks, on urine biochemistry in patients with EHO due to small bowel Crohn's disease and/or resections. Compliance with treatment was confirmed by a fall in plasma uric acid in every patient. Allopurinol failed to alter 24 h urinary oxalate excretion or oxalate concentration. There were also no significant changes in the urinary excretion of glycollate (like oxalate, a breakdown product of glyoxylate), citrate, magnesium or calcium, each of which was at the lower end of the normal range before and during treatment with allopurinol. It appears unlikely that allopurinol will prove useful in the prevention of urolithiasis in patients with EHO.
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PMID:Failure of allopurinol to modify urinary composition in enteric hyperoxaluria. 280 58

Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.
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PMID:The treatment of gout and disorders of uric acid metabolism with allopurinol. 592 71

The pathophysiologic consequences of renal function impairment and chronic renal failure among others result from the loss of excretory and regulatory functions of the kidneys. The role of the exchange of cellular hydrogen ions of tubular fluid in the reabsorption of bicarbonate and in the urinary excretion of titratable acid and ammonia (acid-base regulation) is outlined. The effects of decreased glomerular filtration rate on calcium and phosphorus homeostasis are discussed. De novo urolithiasis in these patients is uncommon. However, it is well recognized that they may form matrix stones with calcium oxalate inclusions. Of greater significance is the prophylaxis in those patients, in whom urolithiasis has been the cause of chronic renal failure. In these patients it is of importance to modify the drug dosage or to abandon the prophylaxis when it interferes with the metabolic changes of renal function impairment. Some agents require no modification, others minor or major modifications. Some are even contraindicated. Hazards of stone prophylaxis in chronic renal failure: Acidification - cave metabolic acidosis! Cave RTA! Antibiotic agents - special rules to prevent accumulation. Thiazides - contraindicated! Hypokalemia; hyperuricemia; cave HPT! Triamterene - contraindicated! Acetazolamide (cystinuria) - contraindicated. Spironolactone - contraindicated. Sodium-cellulose-phosphate - Hyperoxaluria, hypomagnesiuria , hyperphosphatemia, cave HPT. Orthophosphate - cave urinary infection, cave poor renal function, cave obstruction. Allopurinol - dose reduction advisable. Brenzbromaron - contraindicated.
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PMID:[Prevention of calculus recurrence in impaired kidney function]. 653 25

29 patients (20 male and 9 female, average age 55 years), suffering from uric acid-urolithiasis were treated with Zyloric-U over a period of 8 to 20 months. Two of them had side effects (cutaneous symptoms). In all other cases the stones were dissolved or diminuated. Chemical analysis demonstrated a significant reduction of serum uric acid as well as a decrease of calcium secretion in the urine. Yet the urine-pH of 5 remained unchanged. In some cases, if the patients excreted gravel and if the level of uric acid was not lowered sufficiently the dose was raised to twice 300 mg. A report of the follow-up of these patients shall be published later.
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PMID:[Long-term treatment and prevention of uric acid urolithiasis with allopurinol]. 680 89

A survey shall be given of the present state of prevention and therapy of urolithiasis as well as of the up to now much restricted possibilities of the chemolitholysis. Particular attention is paid to calcium on account of its participation in the development of oxalate and phosphate calculi which together might be 70--80% of all calculi as well as to the rather limited possibilities of the reduction of the oxalate secretion in the urine. The encouragement of the oxalate lithiasis by increased uric acid in the urine as well as the reduction of the frequency of relapses not only of the concrements of the uric acid but also of the oxalate concrements by the uricostatic Allopurinol (e.g. zyloric) is dealt with.
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PMID:[Current status of prevention and therapy of urinary calculi and peroral chemo-litholysis with special attention to the relationship of increased excretion of uric acid in oxalate lithiasis]. 743 87

APRT deficiency is an enzyme disorder which is inherited as an autosomal recessive trait. The use of adenine in purine metabolism is disturbed and it accumulates in the body, where it is oxidised by xanthine oxidase to poorly insoluble 2, 8-dihydroxyadenine (DHA). The dihydroxyadenine forms stones which cause recurrent urolithiasis, frequent episodes of urinary tract infection or interstitial nephritis, and finally renal insufficiency in some cases. We report a case of APRT deficiency discovered by urine examination. The patient was a 33-year-old man who had never had any episodes of urolithiasis. He was admitted to our hospital because of pseudoarthrosis of his left arm caused by a traffic accident. His urinalysis revealed no proteinuria nor hematuria, but disclosed numerous round brown crystals in the sediment. These crystals had the characteristics of 2, 8-DHA. The enzyme activity of APRT in his blood was completely deficient. He was diagnosed as an APRT* QO homozygote. In addition, diagnostic imaging revealed that his right kidney was poorly hypoplastic and the pelvis of his left kidney was extra-renal. The renal function was slightly disturbed. In Japan 6 cases of 2, 8-DHA urolithiasis associated with hypoplastic kidney had been reported by 1989. Theoretically, the incidence of hypoplastic kidney is around 20% of all 2, 8-DHA urolithiasis cases. We suspect a genetic correlation between hypoplastic kidney and APRT deficiency. This patient was treated with Allopurinol, which inhibits the process of xanthine oxidation, after which crystals were no longer detected in his urine.
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PMID:[A case of adenine phosphoribosyltransferase (APRT) deficiency discovered by urine examination]. 781 52

Uric acid (UA), a waste product of purine metabolism, may be involved in calcium phosphate crystallization and deposition. Rats, which develop nephrocalcinosis on high-fat or magnesium-deficient diets, and patients with idiopathic calcium urolithiasis have hyperproteinuria, especially of nonalbumin protein, and a shift toward elevated serum UA. In rats, an increase in UA precursors and renal UA suggests hypoxemia, which stimulates xanthine oxidase. In patients, a primary increase in renal xanthine oxidase would explain the low urine UA in the presence of an elevated serum concentration. For calcium phosphate deposition (rats) or incorporation into stones (humans) to occur, a crucial factor may be xanthine oxidase-mediated overproduction of free radical species and subsequent tissue damage. Another factor may be whether sufficient UA is synthesized to neutralize these free radicals. Allopurinol use, which inhibits xanthine oxidase and has long been favored for the treatment of idiopathic calcium urolithiasis, may not prevent stones, because it also diminishes the availability of UA. An investigation of the factors that control serum UA homeostasis may be rewarding in research into the etiology of idiopathic calcium urolithiasis.
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PMID:Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study. 1060 15

We report the case of a 65 year old man, with a history of recurrent urolithiasis, who was referred for an acute renal failure. Investigations deny obstructive or glomerular involvement. 2,8-Dihydroxyadeninuria was diagnosed with the help of crystalluria. This rare metabolic disease is due to a deficiency of adenine phosphoribosyltransferase, a purine salvage enzyme. Allopurinol, a low purine diet and high fluid intake made possible the nearly entire regression of renal failure.
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PMID:[Acute renal failure and 2,8-dihydroxyadeninuria]. 1558 40

Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is a genetic disease of purine metabolism resulting in uric acid overproduction. Allopurinol, which inhibits the enzyme xanthine oxidase and reduces uric acid synthesis, is widely used for the treatment of gout and uric acid overproduction. The aim of the study was to analyze the long-term efficacy and safety of allopurinol in patients with HPRT deficiency. Nineteen patients (13 with Lesch-Nyhan syndrome and 6 with partial HPRT deficiency) were treated with allopurinol (mean dose, 6.4 mg/kg body weight per day; range, 3.7-9.7 mg/kg body weight per day) and followed up for at least 12 months (mean follow-up, 7.6 years). The efficacy of allopurinol was evaluated by serial measurement of purine metabolic parameters and renal function as well as by clinical manifestations. Safety was assessed by recording adverse events. Treatment with allopurinol normalized serum urate level in all patients and resulted in a mean reduction in serum urate of 47%. Allopurinol treatment was associated with a mean 74% reduction in urinary uric acid-to-creatinine ratio. In contrast, allopurinol treatment increased mean hypoxanthine and xanthine urinary excretion rates 5.4- and 9.5-fold, respectively, compared with baseline levels. The decrease in uric acid excretion in complete and partial HPRT-deficient patients was not accompanied by a stoichiometric substitution of hypoxanthine and xanthine excretion rates. Allopurinol-related biochemical changes were similar in patients with either complete or partial HPRT deficiency. Renal function remained stable or improved with treatment. Three patients had urolithiasis during allopurinol treatment. In 2 patients, xanthine stones were documented and they required allopurinol dose adjustments aimed at reducing excessive oxypurine excretion rates. No allopurinol hypersensitivity reactions occurred. Neurologic manifestations were not influenced by allopurinol therapy. In conclusion, allopurinol is efficacious and generally safe for the treatment of uric acid overproduction in patients with HPRT deficiencies. Xanthine lithiasis, developing as a consequence of allopurinol therapy, should be preventable by adjustment of allopurinol dose.
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PMID:Efficacy and safety of allopurinol in patients with hypoxanthine-guanine phosphoribosyltransferase deficiency. 1769 59

We have studied 36 patients with HPRT deficiency, 25 with Lesch-Nyhan syndrome and 11 with partial HPRT deficiency (grades 1 to 3). Patients diagnosed with HPRT deficiency have increased 50% since 2000. The most relevant recent advances have been made in molecular diagnosis. Nevertheless, enzyme determinations are still essential for the diagnosis of HPRT deficiency. Therapy for the neurological manifestations of HPRT deficiency has not advanced. Allopurinol remains the drug of choice to diminish uric acid overproduction, but the optimal allopurinol dose must be established in each patient to prevent xanthine or uric acid urolithiasis, a process aided by sequential determination of urinary oxypurines and uric acid.
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PMID:The diagnosis of HPRT deficiency in the 21st century. 1860 May 5


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