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

The management of asymptomatic hyperuricemia is controversial. Reported benefits from treatment prevention of acute gouty arthritis, chronic tophaceous gout, urolithiasis, or gouty nephropathy. A review of experimental and clinical data suggests that the risks of asymptomatic hyperuricemia are small or unknown and the efficacy of long-term treatment in preventing gout or renal disease is unproved. The costs and risks of prolonged drug administration and practical considerations such as patient compliance mitigate against long-term therapy in asymptomatic persons. We offer some recommendations for an expectant approach to the management of asymptomatic hyperuricemia.
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PMID:Asymptomatic hyperuricemia: the case for conservative management. 64 60

Four patients of pure gouty nephropathy are presented. Gout was of over five years duration and asymptomatic nephropathy manifested as non-oliguric acute renal failure. Diseases commonly associated with it like uric acid stones, urinary tract infections, hypertension, diabetes mellitus, hyperlipidemid, obesity and nephrosclerosis were absent. Reduction in serum uric acid level resulted in prompt improvement in renal functions. Early detection and control of hyperuricemia may help in restoration of renal functions.
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PMID:Non-oliguric acute renal failure in gout. 139 13

This paper reports investigations in a young woman with renal disease and six other seemingly healthy young members of a new kindred (four male:two female) with familial juvenile gouty nephropathy (McKusick 16200). The family had previously been known to have a "familial" renal disease, but came to attention through an isolated episode of gout in the propositus when renal function was already impaired. A reduced GFR was found in three of the other six subjects. Hyperuricemia associated with a grossly reduced fractional uric acid clearance (Cur/Ccr x 100) was present in the propositus and five kindred members, three of whom were children. The finding of this abnormality in two subjects with normal GFR suggests that this apparent hallmark of the disease precedes the onset of renal damage. The results confirm the dominant nature of the disorder, and highlight the need to investigate all kindred members of patients with juvenile gout and renal failure. Early recognition is important, since allopurinol therapy in doses adjusted to the reduced renal function may ameliorate the progression of the renal lesion.
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PMID:Familial juvenile gouty nephropathy with renal urate hypoexcretion preceding renal disease. 187 40

Thirty patients with gouty arthritis were studied over 3 years. The diagnosis was established with the help of polarised light microscopy. All the patients were males, with a median age of 45 years. They belonged to the middle or upper socio-economic class and were obese (mean body mass index 29.7). Chronic alcoholism, diabetes mellitus and hypertension were present in one patient each. No patient had symptomatic coronary artery disease. Although 6 patients had a history of renal colic, only one had gouty nephropathy with chronic renal failure. Six patients had a positive family history of gout. The disease involved mostly the joints of the lower extremity and podagra was observed in 70% of patients. Eight patients had tophi at various sites. There were 17 'over producers' and 13 'under excretors' of uric acid. The treatment consisted of patient education, symptomatic control with non steroidal anti-inflammatory drugs and/or colchicine and antihyperuricaemic therapy. The overproducers were treated with allopurinol while the under excretors were treated with [corrected] sulfinpyrazone. In general, there was a good response to therapy as indicated by lowering of serum uric acid and the number of painful episodes per year. The overall profile of the disease appears similar to that seen in the West.
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PMID:Clinical profile, therapeutic approach and outcome of gouty arthritis in northern India. 238 54

Similarity of the morphological picture of gouty nephropathy and primary glomerulonephritides in which purine antagonists turned out to be effective, a positive effect of azathioprine (Az) and 6-mercaptopurine (MP) on purine metabolism, and changes in immunity indices revealed in gout (hyperproduction of immunoglobulins and circulating immune complexes) necessitates the use of antimetabolites in combined therapy of gout patients with proteinuric and latent types of nephropathy. A prolonged use of Az and MP at a daily dose of 50-100 mg often leads to the recovery or improvement of lowered renal function, disappearance of the urinary syndrome, and suppression of hyperuricemia. Uricosuppressors without purine antagonists produce a weaker effect on the course of a renal process, and the treatment of such patients without the use of basic drugs has proved to be utterly ineffective. Strict control over Az and MP therapy makes side-effects of the drugs rare, and they can be easily done away with after reducing a drug dose.
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PMID:[Substantiation and effectiveness of the use of purine antagonists in gouty nephropathy]. 344 85

To the most important prophylactic measures for the prevention of a disturbance of the purine metabolism belong the normalisation of the body-weight, a mixed diet without protein carriers containing much purine, a regular physical activity, a life without hectic conditions as well as without an excess of conflict situations and a moderate taking of alcohol. These recommendations are of particular importance for patients endangered by gout. In patients with hyperuricaemia they form the basic treatment for the prevention of a uric arthritis, a urate nephrolithiasis and a gouty nephropathy. The clinical and paraclinical results of the directives must be continuously tested with regard to the effectiveness. To the comprehensive prophylaxis also belong the preventive measures against an associated disturbance of an associated disturbance of metabolism or concomitant disease. An additional medicamentous therapy is necessary, when the success of the basic therapy is insufficient and there are already organ manifestations of a disturbance of the purine metabolism. The application of antihyperuraemic drugs corresponding to types should be performed by uricostatic drugs, uricosuric drugs and citric acid-citrate mixtures. The approach according to a 3-step-programme is most useful. In the treatment of the concomitant diseases certain preventive measures are to be taken into consideration. The therapy of an acute attack of gout is at present without any essential problems. Patients with disturbances of the purine metabolism need a permanent care by the physician.
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PMID:[Prevention and therapy of disorders of purine metabolism]. 713 86

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

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

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

We report a 29 years old woman with a chronic tophaceous gout, whose disease started at the age of 18. On clinical examination, the blood pressure was elevated. The laboratory assessment showed a serum uric acid of 15 mg/dl, a urinary uric acid of 155 mg/24 h, a creatinine clearance of 59 ml/min/1.73 m2 and a uric acid excretion fraction off 1.3% (normal 7 to 12%). The clinical and laboratory features of this patient suggest the diagnosis of a familial juvenile gouty nephropathy.
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PMID:[Familial gout and nephropathy in a young woman. Report of one case]. 1151 Feb 9


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