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

Gout rarely develops in nephropathy with advanced renal failure unless other risk factors are present. It has recently been demonstrated that gouty patients with renal failure have greater amounts of mobilizable lead. We have used the EDTA lead mobilization test for 12 gouty patients with renal impairment. Only 7 of these had experienced occupational exposure to lead. 12 patients with nephropathy caused by chronic glomerulonephritis, without a history of gout or lead exposure, were selected as controls. The urinary excretion of lead after the mobilization test was significantly higher in gouty patients. Only in gouty patients was lead excretion directly correlated with the serum creatinine level. Thus, renal failure did not induce any increase in mobilizable lead. Since it is not infrequent in Italy to observe patients with a progressively declining renal function due to chronic interstitial nephritis and with a previous history of gout, we think the EDTA test will be useful to look for lead storage in these patients.
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PMID:Chronic lead accumulation as a possible cause of renal failure in gouty patients. 309 21

The 6 day calcium EDTA lead excretion test was performed on German and Australian subjects with normal and impaired renal function, some of whom had gout, in order to determine if the pattern of results differed between the two countries. The German subjects lived around Heidelberg in an industrialized area where chronic lead nephropathy had not hitherto been thought to exist, while the Australian subjects were all from the State of Queensland where chronic lead nephropathy from the ingestion of lead paint during childhood continues to contribute to morbidity and mortality. Apart from the subjects with normal renal function, the German subjects consistently excreted less lead than the Queensland subjects and a strikingly consistent pattern was found: in both countries, subjects with a history of lead exposure, whether gouty or not, had greater EDTA lead excess values than subjects with gout but no lead exposure, these subjects in turn having greater EDTA lead excess values than subjects with neither gout nor lead exposure. In each country, the highest median EDTA lead excess occurred not in the group with gout and lead exposure, but in the group without gout and with lead exposure.
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PMID:Patterns of lead excretion in patients with gout and chronic renal failure--a comparative German and Australian study. 312 Mar 9

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

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256

Similarity of the morphological picture of gouty nephropathy and primary glomerulonephritides in which purine antagonists turned out to be effective, a positive effect of azathioprine (Az) and 6-mercaptopurine (MP) on purine metabolism, and changes in immunity indices revealed in gout (hyperproduction of immunoglobulins and circulating immune complexes) necessitates the use of antimetabolites in combined therapy of gout patients with proteinuric and latent types of nephropathy. A prolonged use of Az and MP at a daily dose of 50-100 mg often leads to the recovery or improvement of lowered renal function, disappearance of the urinary syndrome, and suppression of hyperuricemia. Uricosuppressors without purine antagonists produce a weaker effect on the course of a renal process, and the treatment of such patients without the use of basic drugs has proved to be utterly ineffective. Strict control over Az and MP therapy makes side-effects of the drugs rare, and they can be easily done away with after reducing a drug dose.
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PMID:[Substantiation and effectiveness of the use of purine antagonists in gouty nephropathy]. 344 85

Gout is a clinical syndrome encompassing a group of metabolic diseases that are all characterized by abnormal uric acid metabolism. In its fullest form, gout is defined by: an increase in the serum urate concentration; characteristic, recurrent, acute arthritic attacks, with monosodium urate monohydrate crystals demonstrable in synovial fluid leukocytes; tophi, usually in and around joints of the extremities, composed of monosodium urate monohydrate deposits; renal disease, often accompanied by hypertension with glomerular, tubular, interstitial, and vascular involvement; and uric acid nephrolithiasis. Any combination of these manifestations may occur, although tophi and urate nephropathy rarely antedate gouty arthritis.
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PMID:Hyperuricemia and gout. 351 32

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.
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PMID:Lead intoxication. 354 May 17

Human purin metabolism is summarized briefly and the terms primary and secondary gout are defined. Asymptomatic hyperuricemia as a risk factor for gout, urate nephropathy and ischemic heart disease is discussed. Treatment modalities of hyperuricemia are presented.
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PMID:[Hyperuricemia: explain, ignore or treat?]. 372 11

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

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


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