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

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

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

Antibodies to native (n) and denatured (d) DNA were studied in 70 patients with primary gout and 40 experimental animals with hyperuricemia. Titres of anti-nDNA in patients with gout considerably exceeded similar indices in donors and were in inverse relationship with the severity of arthritis and markedness of morphological manifestations of renal affection. Anti-nDNA directly correlated with the count of B-lymphocytes in the blood and indirectly with other immunological indices. Anti-dDNA directly correlated with the count of B-cells, reaction of lymphocytes to Kon-A and the titres of antirenal antibodies but were in inverse relationship with the content of uric acid and IgG in the blood serum. Long-term feeding of rats with yeast autolysate with ammonium molybdate and inosine was accompanied by the development of hyperuricemia, an abrupt drop in the level of DNA in the plasma and by a rise in the level of anti-DNA antibodies.
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PMID:[Anti-deoxyribonucleic acid antibodies in podagra]. 267 95

It is shown that the intensity of ammonium genesis, purines biosynthesis and redox processes increases in the organism of chicken with visceral gout. Sodium bicarbonate-correction of the acid-alkaline state of chickens is performed in order to normalize disturbances observed under gout.
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PMID:[Characteristics of nitrogen metabolism in chickens with gout]. 300 41

Several previous studies have demonstrated an increased prevalence of gout in New Zealand Maoris. The aetiology of the hyperuricaemia and its effect on morbidity, apart from gout, are unknown. A survey of 115 Maori men of working age revealed a history of gout in 10 (8%) and asymptomatic hyperuricaemia in 26 (23%). The relationship of hyperuricaemia with obesity was confirmed. Alcohol did not make an obvious contribution to the prevalence of hyperuricaemia. Hypertension was more common and creatinine clearance lower amongst those with gout, but not significantly so. The frequency of hypertension and mean creatinine clearance were similar to that seen in asymptomatic hyperuricaemia and normouricaemia. Urate clearance was lower in the gouty and hyperuricaemic subjects. The normouricaemic Maoris had a reduced fractional urate clearance compared with normal men elsewhere. They also excreted a relatively small proportion of hydrogen as ammonium. Both these features are characteristic of gout, and suggest that the Maoris' susceptibility to hyperuricaemia has a renal mechanism. Obesity is common amongst the Maoris and accentuates their natural tendency to hyperuricaemia.
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PMID:Hyperuricaemia, gout and kidney function in New Zealand Maori men. 648 33

Fifty-nine patients with primary gout were treated with either a combination of colchicine and allopurinol or colchicine alone. Assessments of renal function over 2 years revealed a statistically significant fall of glomerular filtration rate an urine concentrating ability in those receiving only colchicine. The renal function of patients given allopurinol did not change. Treatment with allopurinol resulted ina significant reduction of ammonium excretion, a phenomenon which could not be readily explained. Urate clearance also declined during allopurinol treatment, and the impaired urate clearance associated with gout became more evident. The most important observation was that allopurinol retarded an apparent decline of renal function. Presumably this was achieved through its hypouricaemic effect and implies that the hyperuricaemia of gouty patients is deleterious to the kidneys.
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PMID:Allopurinol treatment and its effect on renal function in gout: a controlled study. 703 23

1. Hyperuricemia is common among the gouty relatives as reported by others (8-11). It is of interest to note that serum urate fluctuates periodically. Hyperuricemia is not necessarily maintained in a steady state throughout the years. Thus a single determination of serum uric acid can be misleading. 2. Development of gout from asymptomatic hyperuricemia is often correlated with the degree of hyperuricemia as observed from population or family studies (12-14). The data presented indicate that unequivocal hyperuricemia is more often accompanied by excessive excretion of uric acid, diminished excretion of ammonia and abnormally high plasma glutamic acid. All are undoubtedly important risk factors for gout. 3. The elevated glutamate could be due to a deficiency of glutamic dehydrogenase, as postulated by Pagliara and Goodman (15). In presence of intracellular accumulation of glutamate in glutamic dehydrogenase deficiency, renal production of ammonium may be reduced due to its inhibitory action on glutaminase 1. As a result of a renal block of ammonia formation, the glutamine in surplus may be diverted for uric acid synthesis. 4. Long-term studies indicate serum urate in most hyperuricemia relatives of gout can be modified by environmental factors, such as diet, weight and changes of life style. When hyperuricemia is under better control, the potential hazard of developing symptomatic gout may be circumvented.
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PMID:The natural history of hyperuricemia among asymptomatic relatives of patients with gout. 742 21

A study of renal function of 51 patients with gout and an equal number of normouricaemic controls revealed significant differences. A relative impairment of the glomerular filtration rate and urine concentrating ability in the gouty subjects could not be wholly explained on the basis of aging or hypertension. Renal dysfunction was generally mild and was not associated with specific clinical characteristics higher levels of uric acid excretion, or hypertriglyceridaemia. Gout patients excreted urine with a significantly lower pH. This was associated with a relatively high excretion of titratable acid and a deficit of ammonium excretion, which was accentuated by ingestion of an acid load. Urate clearance was significantly reduced in gout, even when expressed as a fraction of the glomerular filtration rate.
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PMID:Renal impairment and gout. 743 72

While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
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PMID:[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]. 1264 87

Poisoning by colchicine may occur following ingestion of this alkaloid used for the treatment of acute gouty arthritis. The authors report two fatalities and describe a liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS-MS) triple-quadrupole method for the determination of colchicine in autopsy samples. One milliliter of heart blood, femoral blood, urine, bile, gastric, and vitreous each were extracted with saturated NH4Cl at pH 9.6 and dichloromethane/5% isopropanol. Separation was achieved on a C18-Xterra column with a mobile phase consisting of 2 mM ammonium formate buffer (pH 3)/acetonitrile in a gradient mode. Four product ions of the protonated molecule were monitored. The method was fully validated in whole blood (1 mL) and was linear in the range of 0.5-50 ng/mL (r2>0.99). The limit of detection was 0.1 ng/mL (50 times S/N), and the limit of quantitation was 0.5 ng/mL with RSDs<11.8% intraday (n=6), <18.7% interday (n=18), and accuracy<3% (n=18). Case #1: a 33-year-old nurse committed suicide by the ingestion of 80 colchicine 1-mg tablets. She died 61 h later after resuscitation procedures. Colchicine was found in heart blood at 5.2 ng/mL, femoral blood at 17.4 ng/mL, urine at 19.4 ng/mL, bile at 42.8 ng/mL, gastric at 348 ng/mL, and vitreous at 3 ng/mL. Case #2: a 57-year-old man with gout was found dead at home. Colchicine was found in heart blood at 22.8 ng/mL, femoral blood at 21.9 ng/mL, lung blood at 45.2 ng/mL, urine at 148.5 ng/mL, bile at 1818.5 ng/mL, gastric at 219.8 ng/mL, and vitreous at 0.5 ng/mL. These results were consistent with death. Because of its good sensitivity, this LC-ESI-MS-MS triple-quadrupole method is suitable for the determination of colchicine not only in fatalities but also for pharmacokinetic studies.
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PMID:Liquid chromatography-tandem mass spectrometry for the determination of colchicine in postmortem body fluids. Case report of two fatalities and review of the literature. 1713 57


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