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)

Nine patients who developed proteinuria while on Tiopronin (a D-Penicillamine-like drug) have been studied. Nephrotic syndrome was observed in six cases. Immunologic analysis revealed a high frequency of ANA positivity and RF seronegativity by the time nephropathy appeared. Six patients were biopsied. Immunofluorescence, electron and light microscopy studies showed: glomerulonephritis with segmental deposits in the mesangium and along the capillary walls in one patient, mesangioprolipherative glomerulonephritis in one case and stage 1 membranous glomerulonephritis in four cases. Immunogenetic typing disclosed a strong association with B35-Cw4 class I antigens.
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PMID:Tiopronin-nephropathy: clinical, pathological, immunological and immunogenetic characteristics. 351 96

This is a report of a round table organized during the second meeting of Clinical Pharmacology held in Giens (France) in September 1985. At the beginning of the meeting, the clinical aspects of drug-induced nephrotoxicity were reviewed. Thus we tried to precise the real interest of the studies of proteinuria, urinary cytology, enzymuria and fractional clearances of lithium or magnesium. The most interesting part of our discussions was to know the point of view of men working in drugs companies when a renal abnormality is found during a clinical trial of a drug and when previous experimental studies did not find any renal adverse effects of the drug. It was suggested in a such situation to do particular studies. Methods generally used to study renal physiology as autoradiography micropuncture, microinjection had to be performed to localize the action of the drug along the nephron. It was also discussed of the use of isolated perfused kidney as a tool in drug disposition and the use of renal cells culture. A better understanding of the mechanisms of direct renal toxicity of drugs was obtained from the results of experimental models. It is not so easy, at the present time, to know the mechanisms of immunological drug-induced nephrotoxicity. It seems necessary to develop new experimental models. The results obtained in animals with Cl2Hg or D. Penicillamine or gold salts afford to suspect some mechanisms for these types of nephropathies. This aspect of drug induced nephropathy is more complex because there is a large interindividual variation in susceptibility to these drugs.
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PMID:[Detection of drug-induced nephrotoxicity]. 374 40

Recently Brewer et al. reported the possibility of an oral zinc therapy in Wilson's Disease. We treated a 19 years old patient with decompensated liver cirrhosis due to Wilson's disease with zinc-sulphate. D-Penicillamine had to be withdrawn since proteinuria occurred under treatment. After the discontinuation of D-Penicillamine an increase of serum copper almost up to normal range was observed; concomitantly urinary copper elimination decreased. Under oral zinc sulphate therapy (145 mg/day) a drop of serum copper level was achieved and liver function improved: serum albumin, gamma globulins and prothrombin time reached normal values. The patient did not complain any side effects during oral zinc sulphate therapy. Oral zinc therapy in Wilson's Disease may be regarded as an alternative to D-Penicillamine treatment when this drug has to be discontinued because of side effects.
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PMID:[Oral zinc in Wilson disease--an alternative to D-penicillamine]. 406 Jul 99

One hundred and ninety-one patients treated with gold and penicillamine over a seven-year period were reviewed retrospectively for the occurrence of haematuria. Over this period 10% had shown haematuria, and in over half of these an identifiable cause was found. In the remaining patients, a clear relationship with their treatment seemed likely in only two. Penicillamine therapy was discontinued in all patients with unexplained haematuria, but two patients have continued to show haematuria. Gold therapy has been continued in the presence of haematuria without ill effect. There has been no deterioration in renal function in those patients who have continued to show unexplained haematuria and at no time was proteinuria an accompanying feature.
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PMID:Haematuria occurring during antirheumatoid therapy. 669 73

Penicillamine treatment of rheumatoid arthritis was compared with gold and other remittive agents by reviewing the literature and studying the patients in our penicillamine clinic with respect to their previous responses to chrysotherapy. Penicillamine compares well with other remittive agents with respect to efficacy and toxicity. Prior chrysotherapy does not determine or predict the subsequent efficacy of penicillamine . Patients who reacted adversely to gold tended to react adversely to penicillamine; proteinuria and rash tended to recur.
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PMID:Penicillamine and other remittive agents in rheumatoid arthritis: comparisons and interaction. 672 26

Long-term-treatment of rheumatoid arthritis (RA) with D-Penicillamine (DPA) is well established. In several controlled clinical studies, DPA-therapy has been shown to be effective, even in lower dosage (450--600 mg/day) than used in first years after introduction of this drug. As the dosage has been reduced there was a marked decrease in unwanted drug effects. Nevertheless proteinuria, agranulocytosis and LED-like syndromes remain serious side-effects. Therefore a close supervision of patients under DPA is still necessary. The limitations for DPA-treatment are age, disease activity and LED-like symptoms. RA-patients with renal insufficiency, penicillin-allergy, hematopoietic dysfunction, cancer and chronic infections should never be treated with DPA.
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PMID:[Current status of D-penicillamine therapy in chronic polyarthritis]. 728 6


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