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

The origin of uric acid, metabolic pathways of purine metabolism and the disposition of uric acid in normal man are reviewed. Two thirds of the uric acid is normally excreted through the kidney while one third gains entrance to the gut where it undergoes uricolysis. The pathogenesis of hyperuricemia in primary and secondary gout is discussed. Increased production or decreased excretion of uric acid are the two principal mechanisms of hyperuricemia. The known biochemical defects associated with primary overproduction gout are outlined. Extrarenal uricolysis assumes a greater role when the renal excretion of uric acid is compromised.
Nephron 1975
PMID:Origin and extrarenal elimination of uric acid in man. 112 37

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.
Nephron 1975
PMID:Intrinsic renal disease leading to abnormal urate excretion. 112 38

Serum and 24-hour urinary phosphate levels in primary gout patients and control subjects were measured. About 45% of gouty patients showed mild hypophosphatemia. However, mean 24-hour urinary excretion of phosphate was significantly elevated as compared with that of controls. Gouty patients showed a significantly decreased tubular reabsorption of phosphate and renal phosphate threshold. It seems that tubular phosphate transport in gouty patients is impaired, and this is the major cause of hypophosphatemia.
Nephron 1992
PMID:Decreased renal phosphate threshold in patients with gout. 143 4

This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.
Nephron 1990
PMID:Acute hyperuricemic nephropathy and renal failure after transplantation. 207 15

Two unrelated boys with mild persistent proteinuria and underexcretory-type hyperuricemia of more than 9.0 mg/dl (535 mumols/l) are described. The proteinuria was detected at age 10 and 6 years, respectively. The fractional excretion of uric acid in both was low at 2-3%, when the creatinine clearance was decreased by about 50%. Tissue examination revealed focal interstitial fibrosis in both patients and medullary urate crystals in one patient in whom medullary tissue was obtained on biopsy. An immunofluorescence study was negative for immunoglobulins, complements and fibrin. Treatment of hyperuricemia did not prevent further deterioration of their renal function. One of them underwent a renal transplantation and then his serum uric acid level returned to the normal range. Neither patient had a family history of hyperuricemia, gout or inherited progressive renal disease. Both patients are likely to be sporadic cases of familial nephropathy with gout, an autosomal dominant disease, due to a new mutation. Hyperuricemia due to diminished uric acid clearance may be a risk factor or predictor for the development of progressive renal disease in some subjects.
Nephron 1990
PMID:Underexcretory-type hyperuricemia, disproportionate to the reduced glomerular filtration rate, in two boys with mild proteinuria. 208 6

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.
Nephron 1986
PMID:Urinary lead excretion in uremic patients. 308 77

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.
Nephron 1986
PMID:Chronic lead accumulation as a possible cause of renal failure in gouty patients. 309 21

Histological studies were performed on 3 patients with gout and proteinuria measured at 1.0 g a day or more. Light microscopy revealed diffuse thickening of the glomerular capillary walls accompanied by spike formation and bubble-like appearance as well as tophaceous granuloma in the interstitium, tubular atrophy and benign nephrosclerosis. Immunofluorescence technique showed fine granular deposits of IgG and C3 along the glomerular capillary walls together with the renal tubular epithelial antigen (RTE) in 1 patient. Subepithelial dense deposits were also observed by electron microscopy. These findings suggest that the association of membranous nephropathy should be considered in patients with gout having moderate to severe proteinuria and that RTE may be involved in the pathogenesis of subepithelial deposits in gouty membranous nephropathy.
Nephron 1986
PMID:Gouty kidney associated with membranous nephropathy: participation of renal tubular epithelial antigen. 379 76

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.
Nephron 1983
PMID:Familial nephropathy with hyperuricemia and gout. 685 96

Urate deposits within microtophi were found in 8% of unselected autopsies in Brisbane, Australia. Significant association were demonstrated with (a) a history of gouty arthritis and (b) the existence of nitrogen retention and renal disease of apparently primary, but not gouty, origin. However, in 26% of the patients, a retrospective survey of their medical records did not reveal any causative factor. The possible aetiological importance of the urine flow rate is stressed. The presence of medullary urate deposits at autopsy was most frequently associated with a history of gout or the presence of pre-existing and non-gouty renal disease, although no aetiological factor could be determined in a quarter of the cases.
Nephron 1981
PMID:Urate deposits in the renal medulla. Prevalence and associations. 732 50


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