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

This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.
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PMID:Acute hyperuricemic nephropathy and renal failure after transplantation. 207 15

Diuretics compare well with the large number of other classes of antihypertensive agents now available as first-line treatment in the elderly. Other drugs might be considered for first-line treatment in elderly patients with diabetes, untreated gout, or renal failure, a previous myocardial infarction or multiple ventricular ectopics and for men concerned about potency. A thiazide with a potassium-sparing agent may be preferred in the elderly population. The most telling feature in favor of diuretics is that they comprise the only group of drugs for which a beneficial effect in reducing cardiovascular disease in the elderly has been demonstrated in clinical trials. Although compliance may decline somewhat with age, compliance rates of 80% or more can be expected, even among very elderly patients.
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PMID:Diuretics for elderly patients. 221 86

Blood lead (Pb) and urinary Pb before and after i.v. infusion of 1 g of Na2Ca EDTA were determined (atomic absorption) in 46 control subjects and 91 patients with various stages of renal failure (median serum creatinine 2.5 mg dl-1). Under baseline conditions, patients with renal failure had higher blood Pb levels (112 ng ml-1, range 44-272 vs. 76; 36-187 in controls; P less than 0.001) and lower urinary Pb (16.2 nmol 24 h-1 1.73 m-2, 4.86-66.8 vs. 33; 11-91 in controls; P = 0.001). The increment in urinary Pb after EDTA infusion (mobilizable Pb) was higher (795 nmol 4 days-1 1.73 m-2, range 155-5611 vs. 307; 131-1587 in controls; P = 0.001). In 12 patients with renal failure (13%) mobilizable Pb was above the highest value in controls. Mobilizable urinary Pb correlated (r = 0.68) significantly (P = 0.001) with blood Pb, but only marginally with serum creatinine (r = 0.32; P less than 0.007). Mobilizable Pb was higher in patients with renal failure and a history of smoking or occupational Pb exposure and tended to be higher in patients with alcoholism. Ten of 91 patients had gout; increased mobilizable Pb was present in three of the 10. The data confirm relatively high prevalence of elevated body Pb burden in European patients with chronic renal failure. The question is unresolved whether Pb plays a role in the progression of renal failure.
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PMID:Mobilizable lead in patients with chronic renal failure. 249 82

Exposure to lead results in accumulation in proximal renal tubular lining cells in the form of morphologically discernible inclusion bodies which are lead-protein complexes. Acute nephrotoxicity consists of proximal tubular dysfunction and can be reversed by treatment with chelating agents. Chronic lead nephrotoxicity consists of interstitial fibrosis and progressive nephron loss, azotaemia and renal failure. Potential complications of lead nephropathy include gout and hypertension. Cadmium accumulates in renal tubular lining cells bound to metallothionein, a small protein containing 30% cystine. Metallothionein protects against nephrotoxicity by binding cadmium in a nontoxic form. Renal tubular dysfunction and chronic interstitial fibrosis occur when cadmium levels in the renal cortex exceed the critical concentration of about 200 micrograms/g. Recommendations are made for specific research needs.
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PMID:Mechanisms of lead and cadmium nephrotoxicity. 265 22

The calcium antagonists are effective and safe agents for the treatment of arterial hypertension. They are well tolerated by the patients. In contrast to other types of antihypertensive agents, they cause few metabolic disturbances. They can be combined with diuretics, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors. They can be safely prescribed to patients with hypertension and concomitant diseases such as diabetes mellitus, chronic obstructive lung disease, congestive heart failure, gout, renal failure, peripheral atherosclerotic disease, or Raynaud's phenomenon. Dietary sodium restriction during antihypertensive therapy with calcium antagonists is not required for optimal antihypertensive efficacy. The second generation of calcium antagonists especially the dihydropyridine analogues that have greater potency and vascular selectivity, and a longer duration of action, will optimize the treatment of hypertension. Their antiatherosclerotic, antiplatelet, and "antitrophic" effects in experimental models for atherogenesis and hypertension hold great promise for the future since, so far, there has been no major success in reducing the incidence of coronary death by the treatment of hypertension.
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PMID:Calcium antagonists in hypertension. 265 29

The history of saturnine gout is almost as old as civilization itself. Studies carried out in recent decades explain the development of hyperuricaemia and gout, with the inhibiting effect of lead on the tubular urate transport causing decreased urate excretion. In the case of lead intoxication these effects are often associated with renal failure but may occur without clinical features of lead toxicity and renal damage. The clinical features of saturnine gout are essentially similar to those of primary gout; however, acute attacks tend to occur in the knee more frequently than the first metatarsophalangeal joint. Acute attacks in saturnine gout are frequently polyarticular and tophi rarely develop. The diagnosis of saturnine gout rests on the history of exposure to lead, clinical features of lead toxicity, biochemical confirmation of high serum lead levels and other biochemical abnormalities, and the exclusion of other forms of gout. Treatment consists of excluding the patient from further exposure to lead, the use of chelating agents to remove lead, and control of acute gouty arthritis and hyperuricaemia.
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PMID:Saturnine gout. 266 Oct 30

Oral angiotensin converting enzyme inhibition was introduced eight years ago and is becoming increasingly popular for the treatment of hypertension and congestive heart failure. This treatment causes blood pressure lowering associated with suppression of angiotensin and aldosterone, lack of orthostatic hypotension or metabolic disturbances, redistribution of regional blood flows in favor of vital organs and, in the long term, decreased sympathetic drive and regression of left ventricular hypertrophy. It is effective as monotherapy in more than 50 percent of unselected patients; addition of a diuretic increases the percentage of responders to more than 80 percent. It is the treatment of choice for patients with concurrent diabetes, asthma, gout, depression, or very active life-style. Side effects, observed originally in patients with severe hypertension and renal failure treated with very high doses of captopril, are rare in otherwise healthy hypertensive patients receiving smaller doses of this drug and virtually absent with second-generation angiotensin converting enzyme inhibitors like enalapril.
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PMID:Clinical utility of angiotensin converting enzyme inhibitors in hypertension. 302 82

Urinary excretion of lead (Pb) was measured in the basal state and following the infusion of EDTA (1g of calcium disodium edetate) in healthy German controls and in patients with chronic renal failure with and without gout. When evaluated with Zeeman-compensated atomic absorption spectroscopy using the L'vov platform and urine pretreated with nitric acid and Triton X-100, the control basal Pb excretion (median 28, range 11-19 nmol Pb/24h) and the postinfusion Pb increment (306, range 131-1,587 nmol/4 days/1.73 m2) were considerably lower than most values reported previously in the literature. Elevated Pb body burden was found in 7 of 8 patients who developed gout in the course of renal failure, but only in 2 of 8 patients who had gout prior to development of renal failure; this confirms that appearance of gout in patients with renal failure points to prior Pb exposure. In 7 of 19 nongouty patients with impaired renal function secondary to known renal diseases, urinary Pb excretion was above the 95th percentile of normal. All these patients had occupational Pb exposure. The high prevalence of elevated Pb body burden in patients with renal failure of known cause may not be coincidental and raises the possibility that Pb adversely affects the course of renal disease.
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PMID:Urinary lead excretion in uremic patients. 308 77

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

We measured lead and calcium in multiple bone biopsies from 11 cadavers without known excessive past exposure to lead. Paired iliac crest, transiliac and tibial bone biopsies from these cadavers indicated that in bone biopsy specimens the lead/calcium ratio is more reproducible than the absolute lead concentration. There were no significant differences between the lead/calcium ratios from the iliac crest, transiliac, or tibial specimens. Transiliac bone biopsies from 35 patients (13 patients showing symptoms of slight or moderate degree of renal failure, medical history of gout and/or arterial hypertension and 22 lead workers with chelatable lead in excess of 1000 micrograms) indicated that the lead and the lead/calcium ratio in bone biopsies reflect body lead stores as estimated by the EDT A test (r = 0.87 and 0.83, respectively). Chemical and histological studies of transiliac biopsies previously obtained from 153 dialysis patients (from 8 dialysis centers from Belgium, France and Germany) for studies of aluminum-induced bone disease showed that chronic renal failure and dialysis do not cause accumulation of lead in bone and elevated bone lead does not appear to alter trabecular bone histomorphometry. We found that in 5% of the hemodialysis population studied, bone lead concentrations approximated levels found in active lead workers.
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PMID:Bone lead in dialysis patients. 312 11


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