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

The authors observed 10 patients from 4 families with hereditarily determined gout and detected some specific features in its course. The familial disease was sex-unrelated, its first signs manifested themselves early acquiring a subsequent severe course; purine metabolic derangement was of a metabolic type, a urolithic form of nephropathy was seldom observed. A morphological picture was characterized by a glomerular lesion looking like focal segmental mesangiocapillary or mesangioproliferative glomerulonephritis with noticeable changes in the tubules, stroma and vessels causing early renal insufficiency. Pathogenetic therapy with uricodepressants made it possible to improve the course of nephropathy. The authors described a pedigree of 3 generations of a family in which gout developed in its 10 out of 17 members, in 6 with chronic renal insufficiency.
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PMID:[Familial gout]. 396 78

The role of the renal papillae in the pathogenesis of pyelonephritis and reflux nephropathy was studied by endoscopy and histology in adult autopsy kidneys. Compound papillae with a concave area cribrosa of the "reflux type" were found in greater frequency in adults than in children. Acute purulent inflammation in the renal parenchyma or coarse pyelonephritic scars were seen almost always overlying "refluxing" papillae or overlying papillae altered by papillary necrosis, obstructive atrophy and other changes of papillary shape. Intrapapillary tubular obstruction in early analgesic nephropathy, gout, myeloma and medullary cystic disease is an other factor favouring bacterial infection to occur. Without an underlying renal papillary damage renal injury attributable to urinary infection seems to be rare.
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PMID:[Significance of kidney papillae in the pathogenesis of pyelonephritis and reflux nephropathy]. 405 18

A familial predisposed diffuse nephropathy is described in three adult patients--brothers, combined with hearing abatement--receiver type--in two of them. Typical gout was also found in them, that is difficult to associate with the azotemia. It was admitted that it concerns the Alport syndrome in adults, developing with certain peculiarities, advanced patient age, disturbances of purine metabolism, moderately selective proteinuria of glomercultubular type and chromosome aberration--thresomia of F chromosome.
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PMID:[Hereditary nephritis with bearing loss of the receiver type (Alport's syndrome) with a description of 2 cases]. 446 73

A family is described many of whose members suffered from renal insufficiency, hypertension, gout, and hyperuricaemia in conjunction. Adequate information was obtained on 72 subjects from five generations. In 17, one or more of the above mentioned abnormalities was or had been present. The hereditary distribution suggested an autosomal dominant disease entity. The renal disease was characterized by an early loss of urinary concentrating power, minimal proteinuria, and death at a relatively early age dominating the clinical picture. The histological picture in three biopsies and one necropsy showed predominant tubular atrophy and interstitial fibrosis, with striking tubular basement membrane thickening. It is suggested that these patients suffered from a hereditary degenerative renal disease. The question whether hyperuricaemia was primary or secondary in these cases is discussed.
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PMID:An unusual form of renal disease associated with gout and hypertension. 555 22

Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.
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PMID:The treatment of gout and disorders of uric acid metabolism with allopurinol. 592 71

Since the initial description, in 1958, of gouty arthritis occurring in association with SCA, more than 12 cases have been reported. The high proportion of women and the relatively young ages are noteworthy. Since 1968, studies of patients with SCA have shown a high prevalence of hyperuricemia, beginning during childhood. The initial event in the development of hyperuricemia presumably is increased synthesis of nucleic acids occurring as part of the erythropoietic response to hemolysis. Catabolism of the nucleic acids generates urate. Increased production of UA normally is compensated for by increased urinary excretion of UA. This response occurs in patients with SCA, but during the third decade of life hyperuricosuria can be reduced, probably by damage to the renal tubules caused by infarction and hypoxia resulting from sickling. Impairment of the compensatory renal response leads to more severe and sustained hyperuricemia, and gouty arthritis may then develop. A number of questions about hyperuricemia and gout in SCA remain unanswered. The prevalence of gout among patients with SCA, both in general and in relation to age and sex, has not been determined. The relationships between specific aspects of SCA and of hyperuricemia and gout need to be determined. These include any effect of sickle cell crises on SUA and attacks of gout, and correlation of abnormalities in renal handling of urate with other indices of tubular function and with the pathologic anatomy of the kidney. Finally, it is important to learn whether hyperuricemia and hyperuricosuria contribute to the renal manifestations of SCA; if so, allopurinol might be useful in the prevention and treatment of the renal disease.
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PMID:Gout and hyperuricemia associated with sickle-cell anemia. 634 53

Ten patients with gout, hypertension, and mild to moderate renal insufficiency were studied for possible lead nephropathy by measuring stimulated urinary lead excretion. Seven had a history of lead exposure, 5 from illegal alcohol and 2 from industrial sources. Occult lead was assessed by 24 h urine collection measurements over a 72 h period after intramuscular administration of calcium disodium EDTA. Two patients with a history of lead exposure excreted 707 and 687 micrograms Pb/72 h, respectively, and a 3rd excreted 506 micrograms Pb/72 h. The remainder had a normal response, with mean urinary lead excretion of 251 +/- 42 micrograms Pb/72 h. Since we were unable to demonstrate that lead was important to the pathogenesis of the renal we were unable to demonstrate that lead was important to the pathogenesis of the renal failure in 7 patients despite a positive history of lead exposure in 2, we suggest that factors other than lead may be the cause of renal failure in most patients with gout and renal disease.
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PMID:Occult lead intoxication in patients with gout and kidney disease. 643 39

A patient with lead nephropathy and gout was treated with three months of edetic acid chelation. The therapy resulted in normalization of a previously abnormal result of edetic acid lead mobilization test. Nevertheless, progressive renal insufficiency occurred. At autopsy, an increased bone lead content was documented, suggesting that the edetic acid lead mobilization test may underestimate total body lead stores and that chelation therapy may not be effective in reversing advanced lead nephropathy. Alternatively, a longer period of therapy may be necessary to remove lead stores. More studies are needed to determine the relationship between the results of the edetic acid test and bone lead stores. Methods other than the edetic acid lead mobilization test should be considered to monitor the adequacy of treatment in lead nephropathy.
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PMID:Failure of chelation therapy in lead nephropathy. 643 41

Two patients had onset of juvenile gouty arthritis at ages 16 and 1 1/2 years, respectively. Both had mild renal insufficiency, with creatinine clearances of 46 and 54 mL/min/1.73 sq m, respectively. Their presenting hyperuricemia (13.8 and 11 mg/dL, respectively) was out of proportion to the degree of renal insufficiency. Clinical and laboratory studies did not suggest an inborn error of purine metabolism, glycogen storage disease type I, or any myeloproliferative disorder. Neither patient had a family history of gout or inherited renal disease. Although juvenile gouty arthritis is rare, it must be considered in the differential diagnosis of episodic arthritis in children, especially if renal impairment, even mild, is present.
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PMID:Juvenile gouty arthritis. Two cases associated with mild renal insufficiency. 647 56

A month old infant had gout and renal failure caused by hypoxanthine guanine phosphoribosyl transferase (HGPRTase) deficiency. Investigations showed a high uric acid value, crystal nephropathy on ultrasound, and uric acid deposition on renal biopsy. The HGPRTase value was low in red cells and fibroblasts.
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PMID:Hypoxanthine guanine phosphoribosyl transferase deficiency presenting with gout and renal failure in infancy. 663 35


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