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)

Proceeding from the results of a study of 139 patients suffering from primary gout with kidney involvement the authors have defined 4 clinicomorphological types of nephropathy which differed both in their course and prognosis. The I proteinuric type was characterized by early signs of stable proteinuria, sometimes with the development of the nephrotic syndrome in which a morphological study revealed mainly glomerular changes. The II urolithic type was characterized by the appearance of renal colics at the onset of nephropathy, frequently with the passage of concrements (a morphological study revealed mainly tubular and stromal lesions). The III hypertensive type was characterized by the appearance of persistent arterial hypertension (a morphological study revealed mainly vascular and interstitial changes). The IV latent type was characterized by the absence of or a transient urinary syndrome (a morphological study showed mainly interstitial changes). The first signs of renal failure in these types of nephropathy developed, on an average, 7, 15, 11 and 12 years later, the 20-year survival was 24, 92, 68 and 100%, respectively.
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PMID:[Course and prognosis of nephropathy in gout]. 376 59

Renal failure as a consequence of manifest lead intoxication (nephropathia saturnina) has almost completely disappeared in the FRG. However, there has been rising concern that increased lead burden, primarily as a result of environmental pollution, may adversely affect blood pressure and renal function even in the absence of extrarenal signs of lead intoxication. Such concern is based on epidemiological studies which demonstrated a relation between blood lead level and blood pressure and on experimental studies which showed that lead activates several pressor mechanisms. Furthermore, increased body lead burden is found in a substantial proportion of patients with renal failure, particularly when concomitant gout is present. Unfortunately, none of the above findings constitute irrefutable evidence and further studies are clearly necessary.
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PMID:[Kidney function in lead burden]. 377 30

Recently, calcium oxalate crystals have been identified in the synovial fluid of patients with arthritis and end-stage renal failure. We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin. Clinical manifestations included podagra, tenosynovitis, olecranon bursitis, and acute and chronic synovitis of the large joints that were associated with chondrocalcinosis or subchondral bone erosions. Diffuse involvement of the hand, with chondrocalcinosis of the finger joints, miliary calcified deposits in the skin, and artery calcifications, was observed in 3 patients. The fourth patient had erosive arthropathy. Oxalosis secondary to end-stage renal failure in patients treated with long-term hemodialysis can present with articular manifestations that resemble those of gout, pseudogout, and apatite deposition disease. Other characteristic features of the synovitis associated with oxalosis secondary to end-stage renal disease were: predominant involvement of the hand, mild inflammatory changes in the synovial fluid and synovium, and poor response to administration of nonsteroidal antiinflammatory agents.
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PMID:Arthropathy and cutaneous calcinosis in hemodialysis oxalosis. 377 44

High dose furosemide is commonly used in renal failure to induce diuresis but rarely employed in cardiac failure. As furosemide elimination depends largely on renal excretion, drug accumulation with attendant side-effects would be expected to occur more commonly with renal failure than with cardiac failure. Response to a combination of thiazide diuretics and lower doses of furosemide is often unpredictable, ineffective and sometimes hazardous. High dose furosemide (greater than or equal to 0.5 g day-1) was administered for at least four weeks in 24 patients with severe cardiac failure refractory to a lower dose and to other conventional therapy. Mean maintenance dose of furosemide was 0.7 g day-1 and the maximum dose of furosemide averaged 1.3 g day-1. A peak dose of 8 g day-1 was used successfully in one patient. Improvement was observed in all patients when dosage was increased to and above 0.5 g day-1. There were no major side-effects although new-onset gout (4) and tinnitus (1) were reported; hypokalaemia was readily controlled with spironolactone or potassium supplements. Average duration of therapy was 12 months with a maximum of 33 months. High dose furosemide is logical and effective therapy (with other measures) for severe cardiac failure and relatively safe when administered cautiously. The maximum safe dose is probably no less than that used in renal failure.
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PMID:High dose furosemide in refractory cardiac failure. 407 5

We have previously described a 14-yr-old boy with hyperuricemia, renal failure, and accelerated purine production resistant in vivo and in vitro to purine analogs. This patient demonstrated normal red cell hypoxanthine-guanine phosphoribosyltransferase (HPRT) heat stability, electrophoresis at high pH, and activity at standard substrate levels. In the present report an abnormal HPRT enzyme was demonstrated by enzyme kinetic study with phosphoribosylpyrophosphate (PRPP) as the variable substrate and inhibitory studies with sodium fluoride. Apparently normal HPRT activity in a patient with hyperuricemia and gout does not exclude a functionally significant HPRT mutation.
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PMID:Hypoxanthine-guanine phosphoribosyltransferase variant associated with accelerated purine synthesis. 435 74

A simple, rapid screening method using alizarin red S stain and ordinary light microscopy to detect microcrystalline or noncrystalline calcium phosphate salts was used on wet drop preparations of synovial fluids. This proved to be helpful in detecting apatite crystal clumps and small calcium pyrophosphate dihydrate (CPPD) crystals missed by polarized light. The staining was positive in 100% of synovial fluids from patients later proven to have apatite and/or CPPD deposition diseases. Apatite and CPPD crystals were commonly found together in the same fluids. In addition, some synovial fluids from patients with osteoarthritis, renal failure dialysis, rheumatoid arthritis, and gout also exhibited positive staining. The correlation of positive alizarin red S staining with radiologic evidence of osteoarthritis suggests that apatite crystals might be related to articular cartilage degeneration in different rheumatic diseases.
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PMID:Alizarin red S staining as a screening test to detect calcium compounds in synovial fluid. 618 60

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 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

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

The CaNa2EDTA lead mobilization test permits identification of lead nephropathy in a variety of situations in which past-exposure is uncertain and acute symptoms of lead poisoning are lacking. In addition to lead workers and moonshiners, lead nephropathy has been identified in gout patients with renal failure and in hypertensives with renal failure. The presence of excessive mobilizable lead in these patients and its absence in control patients with comparable renal dysfunction suggests that unrecognized lead poisoning is sometimes responsible for renal failure in gout and hypertension. Use of the EDTA lead-mobilization test may thus permit prevention and sometimes treatment of renal failure in patients who might otherwise enter the End-Stage Renal-Disease Program. The controversies surrounding interstitial nephritis in lead poisoning, gout and hypertension may in part be explained by the surreptitious role of lead.
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PMID:The role of lead in renal failure. 675 98


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