Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 40 days of treatment with Cyclosporine A (CSA) on plasma and urine free amino acids were investigated in sham-operated (C) and partially nephrectomized (Pnx) female Fischer 344 rats. High Dose CSA (30 mg/kg/day ip) was associated with reduced weight gain, increased plasma urea nitrogen, and hypoproteinemia in C and Pnx animals. These animals also demonstrated increased plasma levels of alanine, markedly reduced levels of tryptophan, and an increase in urinary excretion of methylhistidines. C but not Pnx animals also showed a significant increase in plasma serine and a decrease in plasma taurine. CSA treatment of group C resulted in a progressive aminoaciduria involving substrates of the neutral and acidic renal amino acid transport systems; however, the renal excretion of taurine and beta-alanine by these animals was markedly reduced as compared to vehicle treated controls. High dose CSA exacerbated aminoaciduria in Pnx animals, but in this group, the excretion of beta amino acids was also increased. Our findings demonstrate that chronic CSA toxicity in rodents with normal renal function is characterized by increased muscle protein catabolism, significant reductions in plasma tryptophan, and an apparent decrease in whole body taurine pools. With the exception of the taurine abnormalities. CSA treatment had similar effects on Pnx animals; however, in this group, CSA-induced pathological changes were superimposed on the changes due to renal insufficiency per se. CSA toxicity as identified by the parameters investigated in this study was no more severe in Pnx animals with moderate chronic renal insufficiency than in controls with intact renal function.
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PMID:Free amino acids during chronic cyclosporine A toxicity in intact and partially nephrectomized rats. 188 71

Hypoproteinaemia, proteinuria and edema are the main features of Nephrotic syndrome (NS) and are the result of greater permeability of glomerular basal membrane for proteins. It is difficult to predict course of disease and outcome. During 1989-1998 year 18 children were followed up, 9 boys and 9 girls, at the age of 2 to 14 years and diagnosis of NS. Therapy with pronison was initiated in all children according to the protocol of ISKDC. Children were then divided in two groups, depending on success of therapy. In the first group (13 patients, 72.22%) were the patients that had remission, and the second group consisted of 5 patients that did not have remission. In the first group relapses occurred in 7 patients (53.84%), because of side effect of pronison therapy was discontinued in 3 patients. Those 3 patients along with 5 patients from second group were then turned to immuno-suppressive therapy. One patient responded well to cyclophosphamide, rest of them with regular follow up. Two years latter two of them had relapse but responded well on pronisone therapy in the full dose. Biopsies that were done showed that 2 had minimal changes, 2 had focal segmental sclerosis and one membranous proliferative glomerulonephritis. One patient developed chronic renal insufficiency. We conclude that our experience shows that if there is not favorable effect of corticosteroid therapy cyclosporine A is the first choice in NS, without regarding of the patho-hystological findings.
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PMID:[Remission of nephrotic syndrome in children treated with corticosteroids and other immunosuppressive therapy]. 1075 59