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)

During the last 2 years we examined 186 patients with secondary and 42 patients with primary chronic pyelonephritis. In most cases the secondary pyelonephritis is the sequel of a urolithiasis, less frequently in congenital renal anomalies, adenomas of the prostatic gland and patients with superposed pyelonephritis in renal lesion on account of metabolic disturbances (diabetes, gout) or abuse of analgetics. The course of the disease as well as the results of the therapy show peculiarities in the two forms of pyelonephritis. Thus, for example, the recidivations are more frequently in the secondary pyelonephritis, in the urine culture other germs appear more frequently, and the disease shows a more rapid course. The bacterial sanation in patients with primary pyelonephritis remains stable in the course of one year, where as in the obstructive pyelonephritis (non-operated cases) in the same period all patients show recidivations. After operative treatment of the obstruction the conservative treatment leads to a bacterial sanation in about 70%. In patients with superposed pyelonephritis at first the basic disease is to be treated, i.e. the metabolic disturbances are to be compensated and at the same time an antibacterial therapy is to be performed.
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PMID:[The pathogenesis of chronic pyelonephritis and its therapeutic consequences]. 55 Jun 11

The management of asymptomatic hyperuricemia is controversial. Reported benefits from treatment prevention of acute gouty arthritis, chronic tophaceous gout, urolithiasis, or gouty nephropathy. A review of experimental and clinical data suggests that the risks of asymptomatic hyperuricemia are small or unknown and the efficacy of long-term treatment in preventing gout or renal disease is unproved. The costs and risks of prolonged drug administration and practical considerations such as patient compliance mitigate against long-term therapy in asymptomatic persons. We offer some recommendations for an expectant approach to the management of asymptomatic hyperuricemia.
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PMID:Asymptomatic hyperuricemia: the case for conservative management. 64 60

We have carried out biochemical and clinical studies on a large family in which xanthinuria, xanthine lithiasis, uric acid lithiasis and/or gout were discovered. The analysis of its pedigree has shown that : a) the mode of transmission of xanthinuria is autosomal recessive; b) the occurence of xanthine urolithiasis is likely to be due to the association of a second genetic disorder.
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PMID:Xanthinuria : study of a large kindred with familial urolithiasis and gout. 86 50

After World War II the incidence of urolithiasis increased consistently among the general population in this country. Nearly 25% of all examined renal calculi contain uric acid, sodium acid urate or ammonium acid urate as constituents. There are two peaks in lifespan of occurring urate stones: in the adolescence and in the age between 40 and 60 years. The following conditions are due to the formation of uric acid-containing stones: 1. Gout and primary hyperuricemia; 2. secondary hyperuricemia; 3. idiopathic cases with normal renal excretion of uric acid and normouricemia, but with a higher degree of acidity of the urine than normal considering the total renal excretion of acid products; 4. iatrogenic hyperuricemia during insufficient uricosuric therapy. Up to more than 30% of all the patients with recurrent formation of oxalate stones show a clear association with hyperuricemia, hyperuricosuria and increased renal excretion of calcium. In the presence of sodium urate a considerable promotion of precipitation of crystals consisting of calcium oxalate from a meta-stable solution may occur (so-called epitaxy). Frequently the existence of uric acid stones is without any symptoms. Modern views with regard to prophylactic procedures, diet, general and specific medical management including surgical intervention are presented.
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PMID:[Urate nephrolithiasis. Cause of consequence?]. 95 52

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

Gout as a multifactorial syndrome can cause the death of chicken. In this study, the lesions formed were studied macro-, and microscopically in 134 gouty chicken. The gross and microscopic changes were found in all kidneys and renal capsules, though the other internal organs were also involved in many cases. Their serosal surfaces were more severely affected than the parenchymal parts. These organs were liver, lungs, heart, spleen and synovial sacs. Uroliths were found in all cases and were formed in ureters. This finding indicated that the gouty lesions were the results of urolithiasis. Physical characteristics and the chemical composition of the stones were studied, and the results confirmed that they were made up by urates of calcium, ammonium cations.
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PMID:Organic distribution and interrelationships of lesions occurring in laying hens suffering from gout and urolithiasis. 178 18

Extreme degrees of hypoxanthine phosphoribosyltransferase (HPRT) deficiency in man are associated with gross sex-linked neurological dysfunction, gout and urinary stones (the Lesch-Nyhan or 'complete HPRT-deficiency' syndrome). The less severe degrees of enzyme deficiency (sex-linked recessive gout and/or urolithiasis or the 'partial HPRT-deficiency' syndrome) may be associated with minor neurological manifestations. Whole body purine synthesis de novo is accelerated in both these groups of patients. A strain of mice with an experimentally produced mutation at the HPRT locus showed some residual 'apparent HPRT activity' in brain, liver, testicular, splenic, kidney and ovarian tissues but not in erythrocyte haemolysates. The mutation removes exons 1 and 2 of the coding region of the gene together with the promotor and about 10 kb of upstream sequence from the gene. It is therefore possible that the observed 'apparent HPRT activity' in these mice is due to the operation of an alternative metabolic pathway. Purine synthesis de novo was markedly accelerated in their brain, testicular, splenic and kidney tissues. It was not accelerated in the liver tissue of male mice hemizygous for the mutation and the degree of acceleration in the female homozygotes only just reached statistical significance at the p = 0.02 level. This observation casts doubt on the importance of modulations in the rate of hepatic purine synthesis de novo as a mechanism for maintaining a steady supply of purines for translocation to other organs.
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PMID:Purine synthesis de novo and salvage in hypoxanthine phosphoribosyltransferase-deficient mice. 209 36

An outbreak of urolithiasis characterized by high mortality and emaciation in a flock of leghorn pullets is reported. The etiology was not ascertained. Other signs were swollen feet associated with articulate gout. Visceral gout, atrophy, or irregular hypertrophy of the kidneys were also observed. Many birds had one or both ureters enlarged with white uroliths. Microscopic lesions were urate granulomas, necrosis and loss of kidney parenchyma associated with tubular dilation, and edematous and fibrotic interstitium.
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PMID:An outbreak of urolithiasis in single-comb white Leghorn pullets. 319 72

Among 196 patients with primary gout examined in hospital or earlier stable or transient hyperuricemia was noted in 160 (81.6%). These patients were entered into the study group. The control group included 36 persons in whom the level of blood uric acid did not exceed normal values. The familial pattern of disease was established in the patients of the study group. Urolithic, proteinuric and hypertensive types of nephropathy as well as chronic renal insufficiency were more frequently observed in hyperuricemia patients. Alongside with severe tubular, interstitial and vascular changes, glomeruli in the form of mesangioproliferative or mesangiocapillary glomerulonephritis were regularly involved in the pathological process. In the rest of the patients vascular lesions were less marked and less frequent, renal glomerular changes reminded the picture of mesangioproliferative glomerulonephritis only; urolithiasis in them took a more favorable course. Thus, a high level of blood uric acid is one of the risk factors of renal affection in gout determining in many ways prognosis of disease.
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PMID:[Hyperuricemia as a risk factor of nephropathy in gout]. 336 19

An echographic study of the kidneys was performed in 24 men with proved gout aged 40 to 50 and a disease duration of 10-20 yrs. On the basis of case history data urolithiasis was noted in 4 patients, whereas by echodiagnosis it was found in 12. Cysts were detected in 6 patients with gout complicated by urolithiasis and in 1 patient without it. Echoroentgenography was shown to be a highly informative method in the diagnosis of urolithiasis and cystic regeneration of the kidneys opening up prospects for earlier treatment of complications in gout.
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PMID:[Echodiagnosis of the kidney lesion in gout]. 353 10


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