Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The CaNa2EDTA lead mobilization test permits identification of lead nephropathy in a variety of situations in which past-exposure is uncertain and acute symptoms of lead poisoning are lacking. In addition to lead workers and moonshiners, lead nephropathy has been identified in gout patients with renal failure and in hypertensives with renal failure. The presence of excessive mobilizable lead in these patients and its absence in control patients with comparable renal dysfunction suggests that unrecognized lead poisoning is sometimes responsible for renal failure in gout and hypertension. Use of the EDTA lead-mobilization test may thus permit prevention and sometimes treatment of renal failure in patients who might otherwise enter the End-Stage Renal-Disease Program. The controversies surrounding interstitial nephritis in lead poisoning, gout and hypertension may in part be explained by the surreptitious role of lead.
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PMID:The role of lead in renal failure. 675 98

Chronic interstitial nephropathy with disproportionate hyperuricemia (serum uric acid 10.5-14.8 mg/dl [625-880 mumol/l] at a GFR of 40 ml/min/1.73 m2) was observed in 2 girls and their mother who suffered from gout since the age of 20 years. Urinary excretion of uric acid was normal. Renal biopsies in the 3 patients showed focal tubulointerstitial nephropathy. Absolute values of GFR remained stable in the 2 pediatric patients over a period of 10 years, whereas the older patient required dialysis at the age of 34 years. We speculate that this family suffers from a primary interstitial nephropathy which is accompanied by a subtle defect in tubular excretion of urate. A few similar observations have been reported in literature which suggests that dominantly inherited interstitial nephropathy with hyperuricemia and gout represents a distinct entity.
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PMID:Familial nephropathy with hyperuricemia and gout. 685 96

The quadriceps tendon and patellar ligament rupture rarely, even when under great stress or trauma, but can rupture spontaneously in patients with chronic diseases such as gout, rheumatoid arthritis and renal disease. Several factors probably combine to weaken the tendon, including an impoverished local vascular supply, repeated microtrauma and secondary hypoparathyroidism with osteodystrophy. In the three cases reported here, one of which was bilateral, the patients were being treated for chronic renal disease; surgical repair of the tendons led to sound healing and a return to normal function of the joints.
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PMID:Spontaneous rupture of the quadriceps tendon and patellar ligament during treatment for chronic renal failure. 686 Oct 63

Three adult patients with unilateral renal agenesis/total dysplasia (= aplasia) and with an early chronic renal failure are presented. One patient had renal agenesis without ureter bud and ureteric ostium on one side, and reflux pyelonephritis on the other; one had small compact total renal dysplasia (= aplasia) on one side, while chronic uric acid nephropathy (chronic renal disease as a cause of gout) was diagnosed on the other; the third patient had a total large multicystic dysplasia on one side, and on the other a segmental large multicystic dysplasia. Radiological steps and radiodiagnostic criteria are discussed and the combination of urogenital and extraurogenital anomalies is referred to.
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PMID:Chronic renal failure due to unilateral renal agenesis and total renal dysplasia (= aplasia). Report of three cases. 687 81

Intraosseous calcification in association with gouty arthritis was observed in six patients and a single cadaver. This finding, which is usually associated with chronic tophaceous gout, extensive articular destruction, and severe renal disease, is usually seen in the hands, wrists, and feet. It may be associated with additional calcific deposits in the adjacent soft tissues. Although the radiographic appearance of the calcification simulates that of an enchondroma or bone infarct, the abnormality seems related to intraosseous penetration of calcified urate deposits.
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PMID:Intraosseous calcifications in tophaceous gout. 697 85

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

Accepted causes (acute insults) and risk factors for the development of acute renal failure were defined, quantitatively assessed, and tested for statistical significance in 143 patients with acute tubular necrosis. Sixty-two percent of patients had more than one acute insult, and 48 percent had more than one suspected risk factor. Hypotension, excessive aminoglycoside exposure, pigmenturia, and dehydration were identified as highly significant acute insults, while it was concluded that sepsis and administration of radiocontrast material could not be incriminated as causes of acute tubular necrosis. An additive interaction between acute insults was demonstrated, and the severity of acute renal failure was related to the number and severity of acute insults. Patients with oliguric renal failure had more severe acute insults than patients with nonoliguric renal failure. Preexisting renal disease and chronic hypertension were significant risk factors, the latter only when hypotension had been one of the acute insults. An age of more than 59 years, gout and/or chronic hyperuricemia, diabetes, and long-term diuretic administration were not found to be significant risk factors.
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PMID:Acute renal failure. Multivariate analysis of causes and risk factors. 711 78

Although the incidence of gout, renal stones, or both is increased in patients with hyperuricemia, there is no evidence that long-term therapy offers any substantial long-term benefits. Recent data also suggest that no clear relationship exists between hyperuricemia and the development of interstitial nephritis (so-called urate nephropathy). Finally, the relationship between elevations in the serum concentration of uric acid and the risk of developing cardiovascular disease remains undefined. It is recommended that, in a patient with asymptomatic hyperuricemia, a conservative approach be taken and hypouricemic therapy not be instituted as a matter of routine.
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PMID:Management of asymptomatic hyperuricemia. 728 15

This report describes a family with the rare combination of tophaceous gout and renal failure. We emphasise that asymptomatic hyperuricemia may be associated with significant renal disease and suggest that in addition to tubular atrophy and interstitial fibrosis, both obstructive glomerular and tubular lesions and also vascular lesions are important in the pathogenesis of urate nephropathy. We recommend that potentially affected family members should be actively sought and treated at an early age in the hope of preventing the development of renal failure.
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PMID:Familial urate nephropathy. 729 76

Gout is principally a disease of middle-aged men. There has been a lot of discussion over the cause of the renal lesion, whether it is age, hypertension or crystal induced, as single factors or in combination. We have recently been able to study renal biopsies from three related young women with an hereditary gout, and another girl with 2,8-dihydroxyadenine crystal nephropathy. All were normotensive. These findings were compared with the findings of a crystal-induced nephropathy in pigs. In the renal biopsies many stages of acute and chronic nephritis were found which were similar to the crystal nephropathy in pigs. We concluded that the cause of the original lesion in the women was crystal deposition in the tubules, that crystals were not necessary to keep a non-specific nephritis active and that age and hypertension need not be contributory factors.
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PMID:Uric acid crystal-induced nephropathy: evidence for a specific renal lesion in a gouty family. 731 May 74


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