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)

A 39 year old man with 4 of the 5 cardinal features of the Laurence-Moon-Biedl syndrome (LMBS) had proteinuria and moderate renal failure. Excretory urography showed small cysts communicating with the dilated calyceal system. Renal biopsy showed diffuse mesangial sclerosis and cellular proliferation. Excretory urograms in 22 of 24 reported patients demonstrated similar findings. Review of renal pathology reports on 16 patients revealed either chronic glomerulonephritis or severe tubulo-interstitial disease with cysts or both in 8 of 9 who died from uremia and 2 of 7 who died from other causes. The abnormalities seen on excretory urography occur more frequently than 2 of the cardinal features, and as uremia is often the cause of death for these patients, renal disease should be considered a cardinal feature of LMBS.
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PMID:Renal disease-a sixth cardinal feature of the Laurence-Moon-Biedl syndrome. 729 73

A laboratory model of renal osteodystrophy was developed in rats by a single injection of glycopeptide isolated from renal cortical tissues of rats according to the method used by Shibata et al. to induce glomerulonephritis. Approximately 60-70 days after injection, severe proteinuria appeared and continued for at least 170 days at a rate of more than 1 g/day. Morphological changes in the kidney were typical of chronic glomerulonephritis. The plasma calcium concentration was lowered transiently by the 96th day after injection, but was restored to the normal range thereafter. Plasma parathyroid hormone levels, however, continued to rise in parallel with the degree of proteinuria. Marked secondary hyperparathyroidism was induced which led to severe bone atrophy. Histological examinations showed a marked increase of resorbing cavities, with a quantitatively larger number of osteoclasts in cortical bone tissues compared with the control animals. No spontaneous remission was observed. It is emphasized that all of the biochemical and morphological changes reported here were induced by a single injection of homologous renal glycopeptide, and they were highly reproducible.
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PMID:Osseous changes and abnormalities of mineral metabolism in rats with glycopeptide-induced nephritis. 737 53

Sera from 22 children with acute poststreptococcal glomerulonephritis were examined for circulating immune complexes (CIC) during the acute phase of the disease and six to eight months following its onset. CIC were found in 10 of 22 (45%) children during the acute phase and in 4 of 19 (21%) during follow-up. No correlation was found between the presence of CIC during the acute phase and disease severity as measured by several clinical and laboratory parameters. There was, however, a positive correlation between the presence of CIC in serum and the duration of proteinuria following disease onset. The possible role of CIC in the induction of chronic glomerulonephritis following acute poststreptococcal glomerulonephritis is discussed.
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PMID:Circulating immune complexes in children with acute poststreptococcal glomerulonephritis. 739 65

Follow-up of 7 patients with nephritically active mesangiocapillary chronic glomerulonephritis which received for 22 months combined therapy with prednisone (60 mg), chlorambucil (0.2 mg/kg), curantyl (400 mg), heparin or fenilin has found a significant lowering of proteinuria, hypercreatinemia, a rise in osmotic concentration. A complete remission was achieved in 2 patients, partial in 3 patients, a progression occurred after 8 years in one.
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PMID:[The therapy of mesangiocapillary glomerulonephritis]. 748 19

Sandimmun (ciclosporin A) treatment of chronic glomerulonephritis with nephrotic syndrome in a dose 2.5-5 mg/kg for 6-10 months relieved nephrotic syndrome in 2 and resulted in clinical improvement in other 2 of 4 patients treated. In 3 cases the patients failed previous therapy with high-dose corticosteroids and cytostatics. The drug reduced proteinuria, elevated serum levels of albumin and total protein, had low nephrotoxicity.
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PMID:[The treatment of nephrotic-type chronic glomerulonephritis with Sandimmun (cyclosporin A)]. 748 20

The paper treats of the mechanisms of antiaggregant and vasoactive effect of curantyl (C) in chronic glomerulonephritis (ChGN). As many as 85 ChGN C-treated patients were examined; positive treatment effect was seen in 35.5%, negative one in 12.9% of the patients; no effect in 25.8%. It has been ascertained that in some instances prognostically unfavourable forms of ChGN do respond to C treatment. Efficacy of C therapy is predictable from the baseline 24 h proteinuria and decrease in urinary excretion of products of fibrinogen/fibrin degradation during the first week of treatment.
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PMID:[The efficacy of kurantil and its effect on thrombocytic hemostasis in patients with chronic glomerulonephritis]. 760 56

The paper provides evidence and results of using new therapeutical treatment of glomerulonephritis, such as pulse-therapy with cyclophosphane, therapy with angiotension-converting enzyme (ACE) inhibitors or that with antihyperlipidemic agents. Based on much experience with pulse-therapy with cyclophosphane (over 100 patients with chronic glomerulonephritis (CGN) and lupus nephritis), it is concluded that this method is highly effective. Treating 57 patients with ACE inhibitors has shown that in CGN these drugs should be used only when taking into account their antihypertensive effect and capacity of lowering intraglomerular hypertension, as evidenced by the renal functional reserve, and diminishing proteinuria. The long-term (7-12 month) antihyperlipidemic therapy (diet and lovastatin) in 20 patients with CGN accompanied by the nephrotic syndrome caused a significant reduction in the concentration of serum cholesterol and proteinuria, a significant increase in serum albumin levels; remission of the nephrotic syndrome occurred in 9 patients; but better effects were observed in non-inflammatory nephropathies, such as membranous nephropathy, focal segmental glomerulosclerosis, and nephrosclerosis.
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PMID:[New approaches to the treatment of nephritis]. 762 87

Time course of 187 pregnancies was followed up in 103 females with chronic renal diseases (CRD), 76 females with essential hypertension (EH) and 14 posteclampsia females. Three variants of arterial pressure (AP) and 5 types of proteinuria changes were recognized in CRD and EH patients. The pattern of these changes was compared to that in posteclampsia patients, the eclampsia being an absolute criterium of late toxicosis. It is shown that neither elevated AP and proteinuria nor their absolute values can serve reliable signs of late gestosis in CRD and EH patients. Only the trend in these parameters is significant. CRD and EH females with late gestosis exhibit rapidly growing proteinuria in line with the onset or exacerbation of EH. Retrospective analysis of the pregnancies has confirmed association of late gestosis in 15% of EH and 7% of chronic glomerulonephritis patients. These estimates are lower than commonly accepted. Early diagnosis of late gestosis in pregnant females with CRD and EH requires not only regular AP registration, but also dynamic, in some cases hourly, evaluation of proteinuria.
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PMID:[The dynamic importance of proteinuria and arterial pressure for detecting late toxicosis in pregnant women with chronic kidney diseases and hypertension]. 763 70

Recently there has been a renewed interest in the possibility that lipoprotein(a)--Lp(a)--may be important in the pathogenesis of thrombosis-related disease. In nephrotic syndrome, hyperlipidemia is a common finding, and thrombosis is a major complication. With this regard, if Lp(a) levels increase concomitantly with low-density lipoprotein and/or very-low-density lipoprotein levels in nephrotic syndrome, this may be considered a thrombogenic factor. To probe this possibility and to corroborate the relationship between Lp(a) and fibrinolytic profiles, we measured the Lp(a) levels in patients with nephrotic syndrome (n = 43), in patients with chronic glomerulonephritis with less proteinuria than in nephrotic syndrome (n = 28), and in healthy controls (n = 50) and observed the relation between Lp(a) levels and tissue-type plasminogen activator (t-PA) activity, euglobulin fibrinolytic activity, and t-PA antigen. The Lp(a) levels were significantly higher in the patients with nephrotic syndrome as compared with both patients with chronic glomerulonephritis and healthy controls (p < 0.001). There was a direct correlation with serum cholesterol level (r = 0.780; p = 0.0001), triglyceride level (r = 0.445; p = 0.0001), and urine protein level (r = 0.675; p = 0.0001) and a reverse correlation with serum albumin levels (r = 0.566; p = 0.0001). The Lp(a) levels showed a reverse correlation with t-pA activity (r = 0.627; p = 0.0001), total fibrinolytic activity in euglobulin fraction (r = 0.458; p = 0.0001), and t-PA activity divided by the t-PA antigen (r = 0.567; p = 0.0001), but no correlation with t-PA antigen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein(a) levels and fibrinolytic activity in patients with nephrotic syndrome. 874 69

Endogenous nitric oxide (EDRF) plays an important role in the regulation of systemic and renal blood pressure by an alteration of vascular tone. To assess the effect of L-arginine (160 mumol/min i.v. for 3 hours), the precursor of EDRF, on blood pressure, protein-excretion and renal function (GFR = glomerular filtration rate, RPF = renal plasma flow) we performed a prospective, double blind, placebo controlled study. 18 patients with chronic glomerulonephritis (51.3 +/- 11.5 years), renal insufficiency (GFR < 65 ml/min) and hypertension were investigated for changes in GFR and RPF by continuous inulin- and PAH-clearances and for changes in permselectivity by determination of protein-excretion. L-arginine infusion results in a reduction of proteinuria (p < 0.05, t-test). There is no significant effect on renal hemodynamics and mean arterial pressure (MAP). Comparing the excretion of the endogenous proteins, only albuminuria is decreased significantly (p < 0.01), whereas IgG-excretion is reduced slightly (p < 0.05). This can be considered as an indicator of a special influence on the mesangial cells or the basement membrane of the glomerulum itself by EDRF. In conclusion L-arginine reduces protein-excretion without significant alterations in renal hemodynamics and so might prevent a decline in renal failure.
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PMID:Does L-arginine alter proteinuria and renal hemodynamics in patients with chronic glomerulonephritis and hypertension? 778 Dec 5


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