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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To differentiate between extrarenal and renal causes of hyperuricaemia and gout, clearances of urate and creatinine were monitored for 3 1/2 days in fifty-two individuals (seven with a history of gout) with no gross impairment of renal function (creatinine clearance 52-137 ml/min). Dietary purine intake was kept constant. Monophasic circadian fluctuations of fractional urate excretion (= urate clearance over creatinine clearance) were observed with peak values in the afternoon, about 50% higher than during the night. Circadian fluctuations of urinary flow rate were almost identical. However, enhancement of urinary flow rate due to water diuresis had no effect on urate clearance. Despite wide variation of plasma urate concentrations among different individuals (+/- 30% SD), daily urate excretion varied little (+/- 4% SD) and did not correlate with plasma urate (r = 0.03). Thus extrarenal factors appear not to account for the occurrence of hyperuricaemia in these patients. In contrast, a clearcut negative correlation was apparent between plasma urate concentration and fractional urate clearance (r = 0.72), which could fully account for the variations of plasma urate concentration. To elucidate further the mechanism responsible for antiuricosuria in hyperuricaemic patients, the effects of the uricosuric agents benzbromarone and probenecid were tested. A clearcut correlation was apparent between control fractional urate excretion and uricosuric effect of both benzbromarone and probenecid (r = 0.83 and 0.88, respectively), suggesting that anti-uricosuria was due to defective secretion. In an additional series, the uricosuric effect of probenecid was tested in ten patients with renal insufficiency. In these patients the uricosuric effect was clearly blunted, indicating that urate reabsorption is reduced in renal insufficiency.
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PMID:Renal handling of urate in healthy man in hyperuricaemia and renal insufficiency: circadian fluctuation, effect of water diuresis and of uricosuric agents. 677 56

Gout may be a primary or a secondary disorder. In both types of gout, overproduction or underexcretion of uric acid, or a combination of these abnormalities, may be the underlying mechanism. Controversy exists over the need for treatment of asymptomatic hyperuricemia. Treatment of tophi requires use of both uricosurics and allopurinol. A xanthine oxidase inhibitor is the drug of choice for patients with uric acid stones and for those with renal insufficiency.
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PMID:Hyperuricemia and gout: an update. 689 39

Although chronic tophaceous gout has become increasingly uncommon, hyperuricemia and acute gout are still common clinical entities. Most patients with hyperuricemia are under-excreters, and many of these cases are drug induced. Since longstanding asymptomatic hyperuricemia does not appear to cause progressive renal insufficiency, and uric acid renal stones are uncommon in underexcreters, these patients generally require no treatment. The minority of patients who overproduce uric acid are at increased risk for urolithiasis, and therapy should be decided on an individual basis. Acute gout is best treated with colchicine or indomethacin. The newer non-steroidal anti-inflammatory drugs (ie, ibuprofen, sulindac) may prove to be equally effective and are associated with fewer gastrointestinal side effects. Prophylaxis should be undertaken in patients with recurrent gout or documented uric acid urolithiasis. Although uricosuric drugs appear to be less toxic than allopurinol, they should not be used in patients who overproduce uric acid or in patients who have a history of urolithiasis or renal insufficiency. The allopurinol hypersensitivity syndrome is being reported with increased frequency and may be fatal.
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PMID:Hyperuricemia and gout. 704

Inulin clearance was measured in 624 patients with gout, and para-aminohippuric acid (PAH) clearance in 359; Group I consisted of 397 patients with uncomplicated gout; Group II, 191 patients with hypertension and/or ischemic heart disease; and Group III, 36 patients with chronic renal disease. Mean inulin clearance was normal in Group I, slightly depressed in Group II and more markedly decreased in Group III. There was some reduction in PAH clearance in all groups, but not in the very young patients with no complications. A disproportionate reduction in PAH clearance was noted in Groups II and III, particularly in the older patients with longer duration of gout. Uncomplicated gout, except in rare cases of fulminating gout, does not lead to decreased renal hemodynamics. An increased incidence of tophi correlates with decreased renal function, but incidence of renal calculi does not. Renal insufficiency when seen in patients with gout usually correlates with coexistence of hypertension, ischemic heart disease, or primary preexistent renal insufficiency.
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PMID:Impaired renal function gout: its association with hypertensive vascular disease and intrinsic renal disease. 705 27

The Authors have analyzed the complex problems of the possible binding between uric acid and plasma proteins using two methods consisting of serum ultrafiltration at 22 degrees C or electrophoresis on different supports with successive specific coloration of the free and bound uric acid. The percentage of free and bound uric acid was established in serum from normal subjects, patients with primary gout, patients with renal insufficiency treated by dialysis and subjects with type IV dyslipidemia. The Authors discuss the results obtained as regards the possible role played by urate-plasma proteins binding in the interpretation of a genetic defect present in gouty patients involving a diminished uric acid binding capacity of plasma proteins.
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PMID:[Study of the binding between uric acid and plasma proteins (author's transl)]. 745 62

Our attention was initially called to 2 young Japanese sisters with gout and renal insufficiency, which led to an investigation of members of their family with similar conditions. One sister, a 26-year-old woman who had suffered from polyuria since infancy, suffered from gout and renal insufficiency. Her younger sister also had a history of polyuria, hyperuricemia, and moderately reduced renal function. Their urinary uric acid levels were reduced but purine enzyme activities in the erythrocytes were normal. A renal biopsy specimen from the younger sister showed severe interstitial fibrosis with tubular atrophy. An investigation of the family revealed an autosomal dominant transmission pattern. We believe these are new familial cases of juvenile gouty nephropathy found in a Japanese family.
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PMID:Newly discovered familial juvenile gouty nephropathy in a Japanese family. 747 27

The content of urea in a tear is close to that in the blood both in health and uremia. This fact permitted development of a new method of laboratory diagnosis of uremia from the content of urea in a tear. The method may be used to diagnose uremia in renal diseases and various endogenous poisonings with clinical manifestations of renal insufficiency. A method for the diagnosis of hyperuricemia from the content of uric acid in a tear has been developed. The method was used for the diagnosis of gout and hyperuricemia in renal diseases. The suggested methods are reliable and available for common clinical biochemical laboratories. Biochemical analysis of a tear is much simpler, rapid, and atraumatic than analysis of the blood collected from the vein.
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PMID:[Diagnostic value of tear analysis in uremia, uricemia and cholesterolemia]. 789 98

Hyperuricemia and gout have been associated with cyclosporine A (CyA) therapy in transplant recipients. We describe 4 patients who developed severe tophaceous gout after renal transplantation. All of the patients received CyA, prednisone, and diuretic therapy. Three had episodes of allograft rejection. No patient had the diagnosis of gout before transplantation. All developed tophi within 5 years of the first attack of gout. Management of these patients has been difficult due to renal insufficiency, drug interactions and toxicity. Clinicians should be aware that tophaceous gout can occur rapidly in CyA treated transplant recipients.
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PMID:Tophaceous gout in patients with renal transplants treated with cyclosporine A. 801 55

Lead intoxication in human beings has been documented since the second century B.C. Renal disease, hypertension, and gout have all been linked to lead by strong circumstantial evidence. Both acute and chronic nephropathy can occur as a result of lead poisoning. Acute renal failure develops following acute lead intoxication and is often associated with gastrointestinal, neurologic, and hematologic disorders. Both blood and urinary laboratory abnormalities are associated with acute intoxication and are often diagnostic. Chronic lead nephropathy, a chronic tubulointerstitial nephritis on biopsy, occurs in the setting of long-term lead exposure and is often associated with hypertension and gout. Diagnosis of chronic lead nephropathy is more difficult since the laboratory abnormalities seen with acute lead intoxication are not present with chronic lead exposure. The typical clinical picture and the exclusion of other causes of renal disease allow the diagnosis of chronic lead nephropathy to be made. Evaluation of lead stores by either the calcium disodium edetate (EDTA) mobilization test or K-x-ray fluorescence are helpful in clinching the diagnosis. Treatment with EDTA lead mobilization is effective for acute lead poisoning while avoidance of further lead exposure prevents recurrence of lead intoxication. Treatment of chronic lead nephropathy with EDTA lead mobilization is useful if renal failure is modest; however, EDTA mobilization is of no benefit in patients with more severe renal insufficiency.
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PMID:Lead and the kidney: nephropathy, hypertension, and gout. 890 77

The risk for renal insufficiency by uric acid precipitation in medulla of kidney correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. The patients with gout or hyperuricemia have sometimes acidic urine and increased uric acid excretion. Accordingly, these patients frequently accompany by renal insufficiency. Improvement of hyperuricosuria, increasing of urine volume, and alkalinization of urine to pH6 6.5, are effective for the prevention from renal insufficiency. Acute renal failure related to hyperuricemia, can also occured secondary to cell lysis. Tumor lysis syndrome is a critical illness characterized by massive tumor cell death leading to severe hyperuricemia, hyperphosphatemia, hypocalcemia, and acute renal failure after starting chemotherapy to cancers, especially lymphoproliferative malignancies. Administration of allopurinol 500-600 mg and adequate hydration and alkalinization of urine are advocated to prevent acute renal failure. Intensive care with hemodialysis is often required to treat renal failure, because renal failure is reversible in most cases.
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PMID:[Hyperuricemia and the kidney]. 897 5


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