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

Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.
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PMID:Intrinsic renal disease leading to abnormal urate excretion. 112 38

This review of 65 black-black patients with gout, in contrast to tan or tinted, is presented to emphasize the universal nature of the disease, irrespective of race or geographic region. One case of a female who delivered a living child 4 yr after her initial attack of gout is reported. No case of gout secondary to chronic renal disease, or to a blood dyscrasia, including sickle cell disease, was discovered. Except for the race, aberrant sex distribution and low incidence of urate stones, this series is not unlike a series of white gout patients.
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PMID:Gouty arthritis in the black race. 112 98

Renal function studies were performed in 524 gouty subjects, including follow-up studies at intervals up to 12 years in 112 of them. In 49 subjects, the glomerular filtration rate was less than 70 ml/min and Curate:glomerular filtration rate ratio tended to rise as the glomerular filtration rate decreased, reflecting a relatively stable urate excretion over varying filtered urate loads. The increment in Tsurate:glomerular filtration rate was small with spontaneous Purate between 7 and 9 mg/100 ml. It was modest with Purate up to 10 mg/100 ml. The increment in Tsurate:glomerular filtration rate became much higher beyond Purate of 10 mg/100 ml. Urinary urate levels above 800 mug/min, designated as excess urate excretion, occurred more commonly in subjects with Purate above 9 mg/100 ml, and with better preserved renal function. Tophi were more frequently observed in subjects with low glomerular filtration rate and proteinuria; but incidence of urolithiasis seemed to be less affected by a decrease in the glomerular filtration rate. Hyperuricemia alone had no deleterious effect on renal function as evidenced by follow-up studies over periods up to 12 years. Deterioration of renal function was largely associated with aging, renal vascular disease, renal calculi with pyelonephritis or independently occurring nephropathy. In only very few instances was diminished renal function ascribable to gout alone.
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PMID:Renal function in gout. IV. An analysis of 524 gouty subjects including long-term follow-up studies. 120 33

Our data demonstrate that adequate control of uric acid production and serum acid concentration in primary gout arrests further deterioration of renal function and in some instances permits subsequent improvement in renal hemodynamic function even when renal impairment is clearly established. In considering the nature of the lesions of urate nephropathy, our study suggests that control of serum uric acid with drug therapy before renal involvement is apparent might prevent or significantly delay the morbidity and mortality of this complication of primary gout.
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PMID:The influence of allopurinol on renal function in gout. 120 Nov 33

Gout may be associated with renal disease in two situations: (i) when the abnormal urate metabolism is the primary phenomenon and renal disease occurs secondary to this; or (ii) when the intrinsic renal disease is primary, and results in secondary abnormalities of renal function. Kidney damage secondary to gout is associated with urate deposits either in the intersitium as microtophi or as uric acid crystals within tubules, and vascular disease and infection are superimposed. Hyperuricaemia is a frequent sequel to parenchymal renal disease, but gouty arthritis develops only when the hyperuricaemia is unusually severe. Urate metabolism alters when renal excretion of urate is reduced. The management of these problems is discussed.
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PMID:Gout, uric acid and renal disease. 127 25

Administration of uricostatics within the scope of radiotherapeutic treatment is indicated in all cases of manifest primary gout; in cases of latent primary gout, uricostatics should be given especially after administration of high integral doses or in case of large tumors with distinct radiation sensitivity. The decision depends on the renal function, as an increased output of substances to be eliminated by urine may induce an attack of gout in cases of latent gout, or, otherwise, may cause renal lesions followed by acute uric acid nephropathy.
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PMID:[Uric acid balance in radiotherapy]. 127 79

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

Lead may exert toxic effects on several organ systems, but those in the kidney are the most insidious. Acute lead nephropathy is characterized by proximal tubular dysfunction with the development of a Fanconi-type syndrome, alterations in mitochondrial structure and the development of cytosolic and nuclear inclusion bodies. Intracellular lead is associated with specific high affinity proteins and can also bind to metallothionein. Chronic lead nephropathy is irreversible and is typically accompanied by interstitial fibrosis, both hyperplasia and atrophy of the tubules, glomerulonephritis and, ultimately, renal failure. In addition, lead produces renal neoplasms in experimental animals. Chronic lead exposure is also implicated in the development of saturnine gout and hypertension. The metal interacts with renal membranes and enzymes and disrupts energy production, calcium metabolism, glucose homeostasis, ion transport processes and the renin-angiotensin system. This review summarizes the biochemical effects of lead on the kidney to understand the mechanisms of lead-induced nephropathy and other associated disorders.
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PMID:Lead nephrotoxicity and associated disorders: biochemical mechanisms. 131 92

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

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


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