Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gentamicin was given to rats in the doses and intervals equivalent to those used in the patients. It has been established that the dose of 3 mg/kg/day did not affect the urea and creatinine plasma levels. The doses of 6 and 12 mg/kg/day for 10 consecutive days caused an increase of urea and creatinine plasma levels, proteinuria, erythrocyturia and cylindruria which were statistically significant. These changes were directly dose related and subsided after drug withdrawal.
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PMID:[Studies of the effect of gentamicin on the kidneys of healthy young rats. I. Effect of gentamicin on serum urea and creatinine levels and urinary protein levels in experimental animals]. 264 Jun 96

An international multicentre study of adverse reactions to D-penicillamine was undertaken on 2879 patients exposed to the drug--1491 of them a prospective sample. The majority of patients were being treated for rheumatoid arthritis. Over a period of 18 months, 319 (21%) of patients in the prospective sample developed adverse reactions necessitating drug withdrawal; two thirds of these occurred during the first 3 months of treatment. The most frequently-occurring adverse reactions involved skin (6%), kidneys (4%), gastro-intestinal tract (4%) and haemopoiesis (3%). Adverse effects, considered to be serious by the reporting physician, included fever and leucopenia during the early weeks of treatment and, after some months of drug exposure, proteinuria, myasthenia gravis, dyspnoea and pemphigus. Two patients died, one of fulminating septicaemia and the other was found at autopsy to have had multiple lung abscesses following unexplained anaemia and hemiparesis.
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PMID:European League against Rheumatism study of adverse reactions to D-penicillamine. 293 13

An 87-year-old woman presented with the nephrotic syndrome 12 months after administration of ketoprofen, 100 mg daily for osteoarthritis. Clinical course and laboratory data were consistent with drug-induced nephropathy. Kidney biopsy showed membranous glomerulonephritis. Evolution was favorable with resolution of proteinuria after drug withdrawal and steroid administration. A review of the literature on nephrotic syndrome associated with NSAID reveals membranous glomerulonephritis to be an unusual complication.
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PMID:Reversible membranous glomerulonephritis associated with ketoprofen. 378 72

Three clinical cases of toxic nephropathy in young horses were ascribed to gentamicin toxicity. Criteria for defining gentamicin-induced nephrotoxicosis were a serum urea nitrogen value greater than the pretreatment value or cylindruria, hematuria, and proteinuria in the absence of pyuria and bacteriuria. Recommended doses of gentamicin had been given in all cases. The nephropathy was reversible in 1 case in which the toxicosis was detected early and was treated by volume diuresis and drug withdrawal.
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PMID:Gentamicin toxic nephropathy in horses with disseminated bacterial infection. 706 5

One hundred and one patients with rheumatoid arthritis were followed prospectively to assess the efficacy and toxicity of therapy with D-penicillamine. After a mean total followup of 11.5 months (38 patients have completed 2 years of followup) there was a 70% overall improvement rate with 2 complete remissions. Sixty-one patients developed 84 separate toxic reactions, 36 of which required drug withdrawal. Skin rashes (27/84), proteinuria (15/84), low platelets (14/84), and taste abnormalities (10/84) were the most common side effects of therapy at a mean D-penicillamine dose of 463 mg/day. The majority of toxic reactions (85%) occurred in the first 6 months, but proteinuria and thrombocytopenia were more common in the 6 to 12 month treatment period. Previous gold toxicity was a risk factor for developing D-penicillamine toxicity (10/13). Our observations suggest that D-penicillamine related toxicity is a major problem even at 500 mg/day, but the drug can be used with an increased safety margin after 9 months of continuous therapy.
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PMID:The toxicity pattern of D-penicillamine therapy. A guide to its use in rheumatoid arthritis. 736 66

Patients with rheumatoid arthritis who develop membranous glomerulonephritis associated with gold or penicillamine therapy have been shown to get better when the drugs are discontinued, whereas up to 50% of patients with idiopathic membranous glomerulonephritis develop renal failure. A feature of the lesion in rheumatoid disease is the presence of mesangial immune complex deposits in addition to the basement membrane deposits of classical idiopathic membranous glomerulonephritis. To determine whether the presence of mesangial immune complexes indicates a different renal outcome in membranous glomerulonephritis we studied 3 groups: group A 10 patients with rheumatoid arthritis and drug induced membranous glomerulonephritis with mesangial immune complex deposits, group B 14 patients with idiopathic membranous glomerulonephritis with additional mesangial immune complex deposits and group C 25 patients having classic idiopathic membranous glomerulonephritis with deposits solely in the glomerular basement membrane. After median follow up of 72 months, nephrotic range proteinuria resolved in all cases in group A after drug withdrawal, 93% of group B, but only 60% of group C (groups A + B vs C, X2 = 7.8, p < 0.01). Serum creatinine remains less than 500 mumol/l in all patients in group A, 93% of group B, but only 64% of group C (groups A + B vs C, X2 = 7.6, p < 0.01). Mesangial immune complex deposits were predominantly of the IgM isotype in both the rheumatoid and idiopathic membranous group. The presence of mesangial immune complex deposits suggests either a different pathogenesis or host responsiveness to that found in classic idiopathic membranous glomerulonephritis, and predicts a more favourable renal outcome.
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PMID:Do mesangial immune complex deposits affect the renal prognosis in membranous glomerulonephritis? 805 Feb 6

Angiotensin I converting enzyme inhibition (ACEi) has been shown to lower urinary protein excretion in human renal disease. The mechanism of this antiproteinuric effect is hypothesized to be mediated by changes in renal hemodynamics. However, clinical studies suggest that the effect on renal hemodynamics is fully established immediately after the start of treatment, whereas others show the antiproteinuric effect to reach maximum only after several weeks. To clarify this issue we studied the course of renal hemodynamics, blood pressure and proteinuria during 28 days of ACEi (enalapril 10 mg oid) in nine patients with proteinuria due to non-diabetic renal disease. The effect of ACEi on blood pressure and renal hemodynamics was already maximal within few hours after start of treatment, and remained stable thereafter: MAP was lowered with 8.6 +/- 1.9%, 10.6 +/- 2.1%, 12.8 +/- 2.3% and 12.9 +/- 2.5%, while FF fell 23.0 +/- 2.0%, 17.0 +/- 2.6%, 16.8 +/- 2.8% and 15.9 +/- 4.0% on days 1, 7, 14 and 28 of ACEi, respectively. However, the antiproteinuric effect only gradually reached its maximum on day 28. Urinary protein excretion decreased with 10.9 +/- 6.1%, 32.7 +/- 6.2%, 46.3 +/- 2.5% and 54.0 +/- 2.5% on days 1, 7, 14 and 28 of ACEi, respectively. After drug withdrawal all parameters returned towards baseline. We conclude that a dissociation occurs in the course of the ACEi induced effects on hemodynamics and urinary protein excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation between the course of the hemodynamic and antiproteinuric effects of angiotensin I converting enzyme inhibition. 823 Oct 31

The preponderance of the medical literature supports the concept that modest or moderate dietary salt restriction enhances the blood pressure lowering responses to most antihypertensive medications and may permit either dose reduction or, in a few cases, complete drug withdrawal. Moreover, reduction in salt intake has a permissive action on the antiproteinuric responses of angiotensin converting enzyme inhibitors and nondihydropyridine calcium channel blockers. It does not, however, affect proteinuria in those receiving dihydropyridine calcium channel blockers. The importance of selecting out those individuals who can most benefit from dietary salt modification (the "salt sensitive" groups of hypertensive patients) is important. Prospective randomized clinical studies are needed to assess the correlation between dietary salt intake and renal endpoints, such as time dialysis. This will be particularly important in different demographic groups that may have a greater predisposition to salt sensitivity, such as elderly or obese hypertensives, hypertensives of black or Hispanic descent, and those with non-insulin-dependent diabetes mellitus.
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PMID:Salt intake and reductions in arterial pressure and proteinuria. Is there a direct link? 896 35

The case of an AIDS patient with cytomegalovirus (CMV) retinitis who was treated with cidofovir for 17 consecutive months, without any adverse effect, is presented. In the context of antiretroviral therapy, cidofovir therapeutic regimen was 5 mg/kg of body weight for 2 weeks and 5 mg/kg thereafter every other week. Probenecid, hydration and monitoring for proteinuria were also used to prevent nephrotoxicity. The patient stopped maintenance therapy for CMV retinitis after the permanent rise of CD4+ cells above 100 c/mm3. For more than 10 months after drug withdrawal the patient remains free of retinitis.
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PMID:Lack of reactivation of cytomegalovirus retinitis in an AIDS patient, during and after stopping long-term cidofovir treatment: case report. 1087 23

The nonpeptide AT(1) receptor antagonist candesartan is generated from the prodrug candesartan cilexetil during gastrointestinal absorption. In vitro studies have shown that candesartan acts as an insurmountable, tightly bound antagonist at the AT(1) receptor, producing a dose-dependent reduction in the maximal responses to angiotensin II (AII) and virtually an elimination of the AT(1) receptor-mediated effects of AII at high concentrations. The binding of candesartan to the AT(1) receptor is highly selective, and the drug dissociates slowly from the receptor. Candesartan cilexetil produces the expected changes in the parameters of the renin-angiotensin system. Plasma renin activity and plasma AII concentrations were increased and aldosterone levels decreased following drug application. As a consequence, stimulation of AT(2) receptor-mediated actions of AII, such as growth inhibition and vasodilation, may contribute to the overall effects of the AT(1) antagonist, since the AT(2) receptors are left unopposed by candesartan. The antihypertensive efficacy of candesartan cilexetil has been demonstrated in different animal models of hypertension including 2 kidney-1 clip and 1 kidney-1 clip hypertensive rats and spontaneously hypertensive rats (SHR). Candesartan cilexetil produced a slow onset, long-lasting antihypertensive action at a dose range of 0.1-10 mg/kg with no rebound effect upon drug withdrawal. A growing number of studies indicate that candesartan cilexetil can produce end organ protection in addition to lowering blood pressure. In preclinical studies, candesartan cilexetil caused prevention and regression of left ventricular hypertrophy and cardiac fibrosis, protected the heart against ischemia-reperfusion injury and reduced myocardial damage during myocarditis. In different animal models of renal dysfunction, candesartan cilexetil reduced proteinuria and albuminuria, inhibited histopathological renal changes and controlled the renal expression of TGF-beta1 and collagen types I and III. Finally, in stroke prone SHR, candesartan cilexetil markedly attenuated the incidence of stroke even at low doses, with minimal blood pressure lowering effects, and fully protected against stroke at higher doses.
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PMID:Candesartan cilexetil: development and preclinical studies. 1297 13


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