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)

The toxicity to broiler chicks of Chaetomium contaminated corn and various chemical forms of oosporein were compared by feeding diets containing 60% Chaetomium contaminated corn (300 micrograms oosporein/g diet), and 300 or 150 micrograms/g of purified oosporein in either the K salt, Na salt, or organic acid form from hatching to 3 weeks of age. The Chaetomium contaminated corn diet caused 100% mortality during the first week of feeding. Necropsies revealed extensive visceral and articular gout, enlarged pale kidneys, dehydration, proventricular enlargement with mucosal necrosis, and a dark green discoloration of the gizzard lining. When the mortality percentages of the two experiments conducted were considered collectively, the K and Na salts of oosporein caused significantly higher mortality than the organic acid form of oosporein. The K salt caused the most severe lesions and the organic acid caused the least severe lesions. No mortality occurred at the 150 micrograms/g K salt or 150 micrograms/g organic acid levels. Relative kidney weights were increased by all forms of oosporein at 300 micrograms/g, but at 150 micrograms/g only the K salt caused an increase in kidney weight. The LD50 values, based on mortality from 1 to 10 days, were 5.77, 5.00, and 4.56 mg/kg for oosporein acid, oosporein Na salt, and oosporein K salt, respectively. These results suggest that the salts of oosporein (particularly the K salt) are more toxic than the organic acid, and the natural occurrence of oosporein in a salt form could contribute to the increased toxicity of the Chaetomium contaminated corn.
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PMID:Comparative toxicity of Chaetomium contaminated corn and various chemical forms of oosporein in broiler chicks. 670 65

Salt poisoning developed in captive sandhill cranes (Grus canadensis) when sea salt was added to normal drinking water to produce a sodium chloride concentration of 1%. Two of 18 cranes died and 2 were euthanatized when moribund. Muscle weakness, paresis, dyspnea, and depression were observed. Brain and serum sodium, serum uric acid, and plasma osmolality values were abnormally high. Lesions were those of visceral gout, renal tubular necrosis, nephrosis, and skeletal muscle necrosis.
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PMID:Iatrogenic salt poisoning in captive sandhill cranes. 732 5

There is a group of inherited cystic nephropathies that are characterized by juvenile onset recessive inheritance (familial juvenile nephronophthisis, FJN) or by adult onset dominant inheritance (medullary cystic disease, MCD) and share similar clinico-pathological presentation to the extent that they are usually grouped together under the term FJN/MCD complex. The main symptoms consist of renal cyst formation in the medulla or the corticomedullary junction and salt wasting. Although earlier reports had suggested that one single gene may be responsible for this pathology, recent reports have shown that the FJN complex itself comprises a genetically heterogeneous group. Here we are presenting two large Cypriot families that segregate autosomal dominant medullary cystic kidney disease (ADMCKD) with hyperuricemia and gout and with very late age of onset (mean 62.2 and 51.5 years). We performed DNA linkage mapping using highly polymorphic microsatellite markers and found linkage to marker locus D1S1595 at 1q21 with a two-point lod score of 6.45 at Theta = 0.00. Analysis of haplotypes and of critical recombinants enabled confinement of the disease locus within an approximately 8 cM region between marker loci D1S498 and D1S2125. FISH mapping with a large P1 clone confirmed the physical localization within 1q21. The two families share the same disease haplotype, thus suggesting their relationship through a common ancestor and the possible existence of a single ADMCKD-causing mutation within these families. To our knowledge this is the first genetic locus identified to cause FJN/MCD pathology of the dominant adult type.
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PMID:Chromosome 1 localization of a gene for autosomal dominant medullary cystic kidney disease. 953 96

The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume. Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin. Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported. Alcohol seems to have dual effects on the blood pressure. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship. This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet. Finally severe alcohol abuse predisposes to acute renal failure and seems to be associated with the general catabolic effects.
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PMID:Alcohol abuse: potential role in electrolyte disturbances and kidney diseases. 987 14

Autosomal dominant familial nephropathies with adult onset, no macroscopic cysts, and progressive deterioration include medullary cystic disease (ADMCKD) as well as other less specific entities. We studied a kindred of Jewish ancestry in which 15 members (both male and female) have suffered from chronic renal failure. The first evidence of renal involvement was observed between 18 and 38 years. It included hypertension followed by progressive renal insufficiency. No polyuria, anemia, gout, hematuria, nor proteinuria were seen. An average of 4.5 years elapsed from diagnosis to end-stage renal disease. Renal pathology at early stages of the disease showed extensive tubulointerstitial fibrosis and global glomerulosclerosis. Linkage analysis was performed at the two known loci of ADMCKD, on Chromosomes 1 and 16. Linkage to the chromosome 16 locus was excluded. However, linkage to the chromosome 1q21 locus of ADMCKD was established with a maximum two-point LOD score of 3.82 to D1S394. The disease interval could be narrowed to about 9 cM/7.4 Mb between D1S1156 and D1S2635. Multiple-point linkage analysis revealed a maximum LOD of 4.21, with a broad peak from markers D1S2858 and D1S2624. This report establishes linkage between a familial nephropathy characterized by hypertension and progressive renal failure to the locus described for ADMCKD, a disease classically associated with macroscopic corticomedullary cysts, salt-losing tubulointerstitial nephropathy, and anemia. This finding broadens the clinical spectrum of ADMCKD positioned on chromosome 1q21 locus.
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PMID:Clinical and genetic characterization of an autosomal dominant nephropathy. 1124 91

To examine whether norepinephrine affects the plasma concentrations and urinary excretion of purine bases and oxypurinol, we orally administered allopurinol (300 mg) to 5 healthy subjects and 9 hours later intravenously administered norepinephrine (12 to 20 microg/kg body weight), which causes a more than 10 mm Hg increase in diastolic pressure for 2 hours. Norepinephrine decreased the urinary excretion of uric acid by 33% (P <.01), oxypurinol by 32% (P <.01), and xanthine by 51% (P <.01), as well as the fractional clearance of uric acid by 32% (P <.01), oxypurinol by 24% (P <.05), and xanthine by 21% (P <.05) when measured 1 to 2 hours after administration. These results indicate that norepinephrine decreases the urinary excretion of uric acid, oxypurinol, and xanthine, probably via hemodynamic change. It is also suggested that the hypouricemic effect of allopurinol may be more potent than that expected in gout patients with enhanced sympathetic tone, such as in salt-sensitive hypertension.
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PMID:Effect of norepinephrine on the urinary excretion of purine bases and oxypurinol. 1158 99

About one-half million adults in the United States experience a renal stone each year, about two hundred thousand of whom are hospitalized; the lifetime incidence of renal stones in men is about ten percent. Risk factors for stone formation include a positive family history, nutritional factors (excessive intake of animal protein, fat, sugar, oxalates, colas, alcohol, caffeine, salt, and vitamin D), nutritional deficiencies (water, magnesium, calcium, potassium, and vitamin B6), lifestyle factors (physical inactivity and problematic pharmaceuticals), and associated disease states (osteoporosis, parathyroid problems, osteoporosis, gout and recurrent urinary tract infections). The chemical makeup of the stone is important since prevention of recurrences varies somewhat depending on the type of stone involved. The outline of preventive steps holds the potential for preventing recurrence in the vast majority of cases.
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PMID:A complementary approach to urolithiasis prevention. 1252 85

Approximately 10 million adults in the United States have experienced the passage of a kidney stone, and up to 5 million have been diagnosed with gout by a physician. Previous reports have suggested that gout increases the risk for the development of kidney stones, but there are no prospective data. We used data from a cohort of 51,529 male health care professionals to examine the independent association between gout and kidney stone disease. In a cross-sectional analysis of gout and kidney stone disease reported on the 1986 baseline questionnaire, the prevalence of kidney stone disease was almost twofold higher in men with history of gout compared to those without (15% vs. 8%). After adjusting for age and body mass index (BMI), a history of gout remained significantly associated with kidney stone disease (OR 1.88; 95% CI 1.68 to 2.11). We then prospectively examined the risk of incident kidney stones in men with and without a confirmed diagnosis of gout after excluding men who reported a history of kidney stone disease or gout on the baseline questionnaire. A confirmed diagnosis of gout increased the multivariate relative risk of incident kidney stones (RR 2.12; 95% CI 1.22 to 3.68). In contrast, a history of kidney stone disease was not associated with increased risk of gout (RR 1.05; 95% CI 0.54 to 2.07). In conclusion, a history of gout independently increases the risk for incident kidney stones in men. Physicians should provide dietary counseling, such as increasing fluid intake and decreasing salt consumption, to subjects with gout in addition to other risk factors, such as family history of kidney stones, in order to decrease the likelihood of stone formation.
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PMID:The association between gout and nephrolithiasis in men: The Health Professionals' Follow-Up Study. 1291 52

Hypertension and hypertension-associated ESRD are epidemic in society. The mechanisms responsible for renal progression in mild to moderate hypertension and those groups most at risk need to be identified. Historic, epidemiologic, clinical, and experimental studies on the pathogenesis of hypertension and hypertension-associated renal disease are reviewed and an overview/hypothesis for the mechanisms involved in renal progression is presented. There is increasing evidence that hypertension may exist in one of two forms/stages. The first stage, most commonly observed in early or borderline hypertension, is characterized by salt-resistance, normal or only slightly decreased GFR, relatively normal or mild renal arteriolosclerosis, and normal renal autoregulation. This group is at minimal risk for renal progression. The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted renal autoregulation, defines a group at highest risk for the development of microalbuminuria, albuminuria, and progressive renal disease. This second stage is more likely to be observed in blacks, in subjects with gout or hyperuricemia, with low level lead intoxication, or with severe obesity/metabolic syndrome. The two major mechanistic pathways for causing impaired autoregulation at mild to moderate elevations in BP appear to be hyperuricemia and/or low nephron number. Understanding the pathogenetic pathways mediating renal progression in hypertensive subjects should help identify those subjects at highest risk and may provide insights into new therapeutic maneuvers to slow or prevent progression.
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PMID:Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link? 1584 66

Autosomal dominant medullary cystic kidney disease type 2 (MCKD2) is a tubulo-in terstitial nephropathy that causes renal salt wasting, hyperuricemia, gout, and end-stage renal failure in the fifth decade of life. This disorder was described to have an age of onset between the age of 20-30 years or even later. Mutations in the Uromodulin (UMOD) gene were published in patients with familial juvenile hyperuricemic nephropathy (FJHN) and MCKD2. Clinical data and blood samples of 16 affected individuals from 11 different kindreds were collected. Mutational analysis of the UMOD gene was performed by exon polymerase chain reaction (PCR) and direct sequencing. We found the heterozygous C744G (Cys248Trp) mutation, which was originally published by our group, in an additional four kindreds from Europe and Turkey. Age of onset ranged from 3 years to 39 years. The phenotype showed a variety of symptoms such as urinary concentration defect, vesicoureteral reflux, urinary tract infections, hyperuricemia, hypertension, proteinuria, and renal hypoplasia. Haplotype analysis showed cosegragation with the phenotype in all eight affected individuals indicating that the C744G mutation may be due to a founder effect. Moreover, we describe a novel T229G (Cys77Gly) mutation in two affecteds of one kindred. Three of the affected individuals were younger than 10 years at the onset of MCKD2/FJHN. Symptoms include recurrent urinary tract infections compatible with the published phenotype of the Umod knockout mouse model. This emphasizes that MCKD2 is not just a disease of the young adult but is also relevant for children.
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PMID:The Uromodulin C744G mutation causes MCKD2 and FJHN in children and adults and may be due to a possible founder effect. 1724 95


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