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)

Gout rarely develops in nephropathy with advanced renal failure unless other risk factors are present. It has recently been demonstrated that gouty patients with renal failure have greater amounts of mobilizable lead. We have used the EDTA lead mobilization test for 12 gouty patients with renal impairment. Only 7 of these had experienced occupational exposure to lead. 12 patients with nephropathy caused by chronic glomerulonephritis, without a history of gout or lead exposure, were selected as controls. The urinary excretion of lead after the mobilization test was significantly higher in gouty patients. Only in gouty patients was lead excretion directly correlated with the serum creatinine level. Thus, renal failure did not induce any increase in mobilizable lead. Since it is not infrequent in Italy to observe patients with a progressively declining renal function due to chronic interstitial nephritis and with a previous history of gout, we think the EDTA test will be useful to look for lead storage in these patients.
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PMID:Chronic lead accumulation as a possible cause of renal failure in gouty patients. 309 21

A study of the level of beta 2-microglobulin (beta 2-MG) in the blood serum and urine was conducted in 67 patients: 22 with chronic pyelonephritis, 13 with gout with renal lesion, 25 with chronic glomerulonephritis (5 without hyperuricemia, 20 with hyperuricemia) and 7 with amyloidosis accompanied mainly by renal lesion. A raised level of beta 2-microglobulin was found in the patients with chronic pyelonephritis, gout, latent glomerulonephritis with hyperuricemia, and in over half of the cases its raised level was found in the urine. The results obtained indicate a frequent and in some cases predominant involvement of the tubules as well as interstition in the patients with hyperuricemia.
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PMID:[Beta 2-microglobulin in the blood serum and urine of patients with interstitial kidney lesions]. 353 9

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98