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 enzyme guanine aminohydrolase (guanase) is inhibited by low levels of Pb2+. The inhibition is noncompetitive and the Ki is 3.0 X 10(-6) M. The only other heavy metals that are inhibitory at low concentrations are Ag+, which is 36% more, and Hg2+, which is about 50% less inhibitory than Pb2+. The inhibition of guanase by Pb2+ and Hg2+ is synergistic and the inhibition of the enzyme was readily reversed by EDTA. The relationship of these studies with guanase and to the etiology and treatment of saturnine gout, which appears in humans suffering from lead poisoning, is discussed.
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PMID:Effects of plumbous ion on guanine metabolism. 11 6

Chronic lead nephtropathy, secondary gout (lead-gout) and porphyrinuria may develop after long lasting professional exposure to lead. A printer with giant tophi on his hands and feet excreted a significantly higher amount of lead after infusion of calcium EDTA in comparison with a normal control person. This result indicates an increased mobilization of lead from skeletal deposits. Furthermore, the laboratory findings showed renal insufficency and porphyrinuria up to 1316 mug/l (elevation of total porphyrins with slight or no elevation of delta-amino-levulic acid and porphobilinogene). The clinical triad nephropathy, secondary gout and porphyrinuria seems to be a variant of chronic lead poisoning.
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PMID:[Chronic lead poisoning: Lead gout with giant tophi on the skin, nephrophathy and porphyrinopathy]. 81 45

In this report, we describe the development of renal function impairment in a 33-year-old patient with mesangial IgA nephropathy and a history of recent gout. Increased body lead burden was identified with a positive EDTA mobilization test. The patient was treated with 1 g of edetate disodium calcium weekly for 2 months until normalization of urinary lead excretion. Improvement of renal function and proteinuria were noted. It was even more interesting to find that both immunofluorescence and electron microscopy studies of the second biopsy specimen revealed the loss of previous mesangial immune deposits. Our case demonstrated that lead may be a nonspecifically damaging factor related to the deterioration of renal function in patients with preexisting renal disease. Moreover, the disappearance of mesangial immune deposits after chelation therapy has not been previously documented. The pathogenetic basis of this observation is unknown, and its causal relationship with lead requires further elucidation.
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PMID:Disappearance of immune deposits with EDTA chelation therapy in a case of IgA nephropathy. 129 46

Studies were conducted in 10 healthy Chinese controls, 10 patients with chronic renal failure without gout, 8 patients with gout complicated with chronic renal failure and in 6 patients with chronic renal failure who subsequently developed gout. All the subjects had no history of occupational or accidental lead exposure. Total body lead burden was assessed by 24-hour urine collection measurements over a 72-hour period after intravenous administration of 1 g of calcium disodium EDTA. The postinfusion urinary lead excretion of the healthy controls (90.2, range 57.2-161.5 micrograms/3 days/1.73 m2) was higher than the values recently reported for healthy German controls. Similar to earlier studies, we failed to find elevated urinary lead excretion in patients with chronic renal failure without gout. Nevertheless, the EDTA mobilization test identified 2 patients with occult plumbism in this group of patients. Our study also clearly demonstrated that 4 of 6 patients with renal failure who developed gout de novo had underlying plumbism. The high prevalence of increased lead body burden in patients with chronic renal failure, in particular those associated with gout, indicates that lead may contribute to a significant portion of chronic renal disease in our patients. In addition, our data suggest that chronic low-level environmental lead exposure may subtly affect renal function.
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PMID:Elevated lead burden in Chinese patients without occupational lead exposure. 140

Chronic lead nephropathy has recently been rediscovered. Its usual manifestations are hypertension, gout and renal impairment. Retrospective epidemiological data suggest that prolonged exposure to lead increases the risk of hypertension and nephropathy. An increase in EDTA-induced urinary lead concentration (above 600 micrograms/72 hours), perfectly representative of lead concentration in bone, has been found with a 5 to 12 percent prevalence in chronic renal impairment irrespective of its cause. The origin of lead impregnation and its influence on the course of the renal disease have not yet been elucidated.
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PMID:[Chronic lead nephropathy. Epidemiology and diagnosis]. 153 33

Poultry breeding has economical importance for the people living in Bursa and surrounding villages. Similar to some sporadic disease, gout can also be reason for production loses and death in laying and broiler chickens. Gout cases have been observed in some pens of a big poultry company. In this study 20 healthy control and 40 sick Studler Iso-Brown chickens were used as research materials. Blood were taken from heart by syringe to plastic tubes with EDTA. Plasma were collected and analyzed for total protein, uric acid, bicarbonate, vitamin A, calcium and orotic acid. The blood levels of healthy and sick groups were; total protein % 4.60-5.98 gr, uric acid % 10.19-38.09 mg, bicarbonate 27.37-35.73 mEq/l, vitamin A % 42.20-35.55 mcg, calcium % 8.38-8.25 mg and orotic acid % 1.42-1.97 mg, respectively. Statistical analysis was done by t test. There were statistical importance for total protein, bicarbonate (p less than 0.01) and for uric acid (p less than 0.001) differences. Feeding program analysis was done and a feeding disturbance was determined. Chicken in gout observed pens have fed with chicken developing feed for two weeks earlier. For this case diet was the reason of gout.
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PMID:A biochemical investigation on chicken gout observed in the Marmara region in Turkey. 178 20

Blood lead (Pb) and urinary Pb before and after i.v. infusion of 1 g of Na2Ca EDTA were determined (atomic absorption) in 46 control subjects and 91 patients with various stages of renal failure (median serum creatinine 2.5 mg dl-1). Under baseline conditions, patients with renal failure had higher blood Pb levels (112 ng ml-1, range 44-272 vs. 76; 36-187 in controls; P less than 0.001) and lower urinary Pb (16.2 nmol 24 h-1 1.73 m-2, 4.86-66.8 vs. 33; 11-91 in controls; P = 0.001). The increment in urinary Pb after EDTA infusion (mobilizable Pb) was higher (795 nmol 4 days-1 1.73 m-2, range 155-5611 vs. 307; 131-1587 in controls; P = 0.001). In 12 patients with renal failure (13%) mobilizable Pb was above the highest value in controls. Mobilizable urinary Pb correlated (r = 0.68) significantly (P = 0.001) with blood Pb, but only marginally with serum creatinine (r = 0.32; P less than 0.007). Mobilizable Pb was higher in patients with renal failure and a history of smoking or occupational Pb exposure and tended to be higher in patients with alcoholism. Ten of 91 patients had gout; increased mobilizable Pb was present in three of the 10. The data confirm relatively high prevalence of elevated body Pb burden in European patients with chronic renal failure. The question is unresolved whether Pb plays a role in the progression of renal failure.
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PMID:Mobilizable lead in patients with chronic renal failure. 249 82

Free radical attack upon uric acid (UA) nonenzymatically generates allantoin (ALT), and the presence of ALT in human plasma suggests free radical intervention within the body. To assess this possibility, we determined plasma ALT in patients with chronic renal failure (CRF) and some other diseases by high-performance liquid-chromatography (HPLC). Heparinized blood samples were obtained from 15 healthy controls, CRF patients under conservative management (n = 13) or hemodialysis (HD) treatment (n = 8) and patients with gout (n = 11) or rheumatoid arthritis (RA, n = 13). Although not seen in normal plasma samples, ALT was detected in 63% and 31% of patients receiving HD and conservative treatment, respectively. The plasma ALT level decreased after each HD session. ALT was also detected in 18% and 23% of the patients with gout and RA, respectively. ALT was found to be generated by ultraviolet radiation or by the addition of H2O2 to a normal pool-plasma. Addition of Fe(2+) and H2O2 increased the ALT level to about twice that of only H2O2. Addition of either catalase, desferal, EDTA, DMTU, DMSO or mannitol to the plasma decreased ALT generation. These findings suggest that ALT is generated from UA attacked by free radicals, especially by the hydroxyl radical, and that UA plays a role as an antioxidant in the plasma of patients with CRF and some other diseases.
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PMID:[A new role of uric acid as an antioxidant in human plasma]. 260 55

Urinary excretion of lead (Pb) was measured in the basal state and following the infusion of EDTA (1g of calcium disodium edetate) in healthy German controls and in patients with chronic renal failure with and without gout. When evaluated with Zeeman-compensated atomic absorption spectroscopy using the L'vov platform and urine pretreated with nitric acid and Triton X-100, the control basal Pb excretion (median 28, range 11-19 nmol Pb/24h) and the postinfusion Pb increment (306, range 131-1,587 nmol/4 days/1.73 m2) were considerably lower than most values reported previously in the literature. Elevated Pb body burden was found in 7 of 8 patients who developed gout in the course of renal failure, but only in 2 of 8 patients who had gout prior to development of renal failure; this confirms that appearance of gout in patients with renal failure points to prior Pb exposure. In 7 of 19 nongouty patients with impaired renal function secondary to known renal diseases, urinary Pb excretion was above the 95th percentile of normal. All these patients had occupational Pb exposure. The high prevalence of elevated Pb body burden in patients with renal failure of known cause may not be coincidental and raises the possibility that Pb adversely affects the course of renal disease.
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PMID:Urinary lead excretion in uremic patients. 308 77

Indices of past lead absorption were measured and compared in patients with chronic renal failure from many causes, including some with chronic lead nephropathy. X-ray fluorescence (XRF) yielded finger bone lead concentrations by a new in vivo method. These correlated significantly with excess urinary lead following calcium di-sodium EDTA (ethylenediamine tetra-acetate) and erythrocyte lead concentration. Discriminant function analysis demonstrated that the patients in the study could be separated into two groups without any reference to the EDTA lead excretion test using the following variables, all of which contributed significantly to the discrimination. In order of importance, these were: a childhood history of acute lead poisoning, a history of gout, a family history of gout and detectable XRF finger bone lead. Although the XRF finger bone lead measurement is convenient and non-invasive, its lack of sensitivity (48%) limits its usefulness as a screening test for chronic lead nephropathy.
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PMID:Chronic lead nephropathy in Queensland: alternative methods of diagnosis. 308 47


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