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

Urate deposits within microtophi were found in 8% of unselected autopsies in Brisbane, Australia. Significant association were demonstrated with (a) a history of gouty arthritis and (b) the existence of nitrogen retention and renal disease of apparently primary, but not gouty, origin. However, in 26% of the patients, a retrospective survey of their medical records did not reveal any causative factor. The possible aetiological importance of the urine flow rate is stressed. The presence of medullary urate deposits at autopsy was most frequently associated with a history of gout or the presence of pre-existing and non-gouty renal disease, although no aetiological factor could be determined in a quarter of the cases.
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PMID:Urate deposits in the renal medulla. Prevalence and associations. 732 50

Information on a familial syndrome of hyperuricemia and renal disease with or without gout was obtained on 33 of 41 blood relatives: Nine had renal disease; abnormalities of the urinary sediments were minimal; serum uric acid levels were elevated in seven and were not measured in two. Hyperuricemia was noted in three additional family members without evidence of renal disease. Goulty arthritis (three patients) did not precede renal disease. One individual had hyperuricosuria. The following erythrocyte purine enzyme levels were normal: adenine phosphoribosyltransferase, hypoxanthine-guanine phosphoribosyltransferase, phosphoribosylpyrophosphate, synthetase, adenosine deaminiase, and purine nucleoside phosphorylase. Renal biopsy specimens showed focal global and segmental sclerosis of glomeruli, occasional hypercellularity, foci of atrophic tubules, chronic interstitial inflammation, and folding and wrinkling of glomerular basement membrane without electron-dense deposits. There were no immunofluorescent abnormalities.
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PMID:Familial hyperuricemia and renal disease. 739 93

Six members of kindred with only one surviving male in three generations, a history of an unusual combination of precocious gout in a girl of nine and rapidly progressive renal disease in young women, have been investigated. Sensitive indicators of the familial defect were the early development of hyperuricemia, an inability to concentrate the urine, and a patchy non-specific interstitial nephritis at biopsy. All these features were disproportionately severe for the young age and sex of affected subjects, and the relatively moderate reduction of GFR in some. Identification of these characteristics enabled the recognition of an early stage of the disease in one young family member whose renal function had previously been normal. The histopathology of the renal lesion in this normotensive teenage girl was similar to that frequently attributed to ageing or hypertension in the archetypal middle-aged gouty male, indicating that neither age nor vascular lesions are necessarily implicated in the latter. Allopurinol has halted further progression of the renal lesion in this young girl over two years. It is thus possible that early diagnosis may benefit the subsequent clinical course and may be important since the number of such families in our experience suggests that precocious familial gout with renal failure is more prevalent than currently recognized.
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PMID:Familial gout and renal failure in young women. 742 92

A report of 20 cases of gout considered to be secondary to chronic renal disease is presented. Studies of renal function and of uric acid metabolism were carried out in 16 patients. The daily production of urate remained within normal limits in the face of progressive renal dysfunction. Renal excretion of uric acid was decreased to a mean of 35.5% of the turnover. The cumulative urinary recovery of intravenously injected 14C-uric acid averaged 32.0%. In 3 patients 14C was successively retrieved in urinary allantoinand urea, in carbon dioxide of expired air, and in faeces. As in normal man, carbon dioxide and ammonia were the principal uricolytic products. The extrarenal excretion of uric acid assumes a greater role in chronic renal disease and eventually becomes the major route of elimination of uric acid. The possibility that gout may be secondary to intrinsic renal disease should be entertained when azotaemia is present.
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PMID:Gout secondary to chronic renal disease: studies on urate metabolism. 743 73

A 36-year-old Chinese man presented with clinical and biochemical features of renal failure. He has had recurrent attacks of acute gouty arthritis since the age of 15 years. Present radiographic features of extensive chronic tophaceous gout included soft tissue masses, calcification, and typical erosions in the hand and feet. The condition of familial juvenile gouty nephropathy is discussed. Awareness of juvenile-onset gouty arthropathy should lead to early investigation, diagnosis and appropriate management. The complication of associated nephropathy may potentially be prevented.
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PMID:Clinics in diagnostic imaging (2). Juvenile gouty arthropathy with associated nephropathy. 757 Jan 44

The prevalence of asymptomatic hyperuricaemia among Polynesian women (Maoris, Cook Islanders, Samoans, Tongans) was high--44%. This hyperuricaemia resulted from a reduced fractional uric acid clearance (FEur: uric acid clearance factored by creatinine clearance x 100--6.7 +/- 1.5%) compared with the FEur in healthy UK women (12.8 +/- 2.9%). This reduction in FEur was not as great as that in young UK women with familial juvenile hyperuricaemic nephropathy (FJHN: 5.1 +/- 1.5%) and was not associated with impaired renal function. The FEur in the normouricaemic Polynesians (9.7 +/- 1.9%) was also lower than that in healthy UK women (12.8 +/- 2.9%). The reduced FEur in these Polynesian women supports the hypothesis that indigenous Pacific races share a similar genetic defect in renal urate handling to that reported as the basis for the susceptibility to hyperuricaemia in Maori men. Neither alcohol nor hypertension contributed to this. This study also confirmed that, compared with their European counterparts, Polynesian women have a high purine intake and a strong tendency to obesity which increases with age. These factors, together with the reduced FEur, put them at added risk for gout. However, the reduction in FEur was not as great as that reported for the normouricaemic or asymptomatic hyperuricaemic Maori male (4.9 +/- 1.5% and 3.9 +/- 1.4%, respectively), confirming the same sex difference in renal urate handling in adult Polynesians as in caucasians.
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PMID:Polynesian women are also at risk for hyperuricaemia and gout because of a genetic defect in renal urate handling. 792 53

Purine metabolism disturbances which may be responsible for urate nephropathy were revealed in 35% of the examinees with arterial hypertension. Gout manifestations occurred in many of the above patients. Purine metabolism disturbances contribute much to progression of renal disorders and arterial hypertension, require early diagnosis and treatment. Urate symptoms may serve a primary diagnostic indication.
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PMID:[Urate nephropathy in patients with arterial hypertension]. 794 Mar 61

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.
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PMID:[Hyperuricemia]. 800 1

Gout is an acute episodic monarthritis or chronic pauci- or polyarticular arthritis. The symptoms of gout are induced by monosodium-urate crystals that are liberated from accumulations in connective tissue structures, primarily cartilage. Deposition of monosodium-urate crystals is caused by hyperuricaemia, which is dealt with in a previous paper. Only a minority of persons with hyperuricaemia develop gout, however. The diagnosis is based on detection of urate crystals in synovial fluid or tophi. Acute gout is treated with antiinflammatory agents, primarily NSAIDs or colchicine. Predisposing diseases and associated conditions such as hypertension, diuretic drugs, overweight and nephropathy should be controlled as well as possible. In patients with recurrent attacks of acute gout or chronic gout, treatment with urate lowering drugs, principally allopurinol, should be given. Treatment with allopurinol should be adjusted according to levels of serum urate and renal function. Serious complications to allopurinol treatment have been described.
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PMID:[Arthritis urica. Clinical picture, diagnosis and treatment]. 800 2

Progressive hereditary nephropathy is described in 6 members of a single family. Renal biopsies, performed in 3 patients, revealed tubular atrophy, interstitial fibrosis, and lymphomonocytic infiltration associated with severe vascular lesions. These features were disproportionately serious when related to age, arterial pressure, and renal function. Similar familial nephropathy has been reported in the literature, generally in association with gout or asymptomatic hyperuricemia. The patients described here had normal blood concentrations of uric acid. It is proposed that the members of the present group of patients are suffering from the same interstitial nephropathy as that described in the literature and that the hyperuricemia found by other investigators is coincidental and does not play a pathogenetic role.
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PMID:Familial interstitial nephropathy without hyperuricemia. 813 42


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