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)

During nephrotoxic nephritis in the rat, an increased urinary excretion of glucosyl-galactosyl hydroxylysine and of galactosyl-hydroxylysine has been observed in the autologous phase of the disease. This due mainly to an elevation of the polypeptide-bound fraction of these hydroxylysyl glucosides with a molecular weight over 1,000 daltons. The levels of both urinary hydroxylysyl glucosides were correlated with proteinuria. Their increased excretion appears to originate in the lysed glomerular basement membrane. At the same stage of nephrotoxic nephritis, an increased glucosyl transferase activity could be demonstrated in the isolated glomeruli, correlated with albuminuria, attesting a higher turn-over of the disaccharide units of the glomerular basement membrane.
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PMID:Excretion and synthesis of basement membrane disaccharide units in Masugi nephritis. 52 79

Isolated glomerulonephritis with mesangial IgA deposits was the most common single finding encountered in a large biopsy series in an Australian community and was found in 50 patients, 18% of those presenting for the investigation of primary glomerular disease. A uniform histopathological picture of mesangial enlargement, with or without focal and segmental features was present. A tendency to progression was suggested by the frequent presence of glomerulosclerosis, interstitial scarring and vascular hyalinization. Because of the uniform histological immunofluorescence and ultrastructural appearances, the term IgA nephropathy has been used for this condition. The clinical picture, however, was heterogenous. Presenting symptoms included macroscopic hematuria (34%), proteinuria (32%) acute nephritis (10%), nephrotic syndrome (6%), malignant hypertension (8%), acute renal failure (6%) and chronic renal failure (4%). There was a striking correlation of increased blood pressure and decreased renal function with increasing age. While the period of follow-up was too short to assess individual patient data, a gradual and progressive decrease in renal function over several decades is suspected in patients with this condition.
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PMID:IgA nephropathy: a syndrome of uniform morphology, diverse clinical features and uncertain prognosis. 58 77

D-penicillamine treatment of 50 patients with rheumatoid arthritis with negative ANF tests, was followed by means of protein disk electrophoresis of the urine. In the beginning the urine proteins were analysed every 4 weeks, later at intervals of 3 to 6 months. A glomerular proteinuria, caused by an immune-complex nephritis, can be recognized very early by this method. A glomerular proteinuria was the reason for discontinuing the treatment in 10 of the 50 patients (8 seropositive, 2 seronegative), drug fever occurred in one case with seropositive arthritis. Protein disk-elektrophoresis of the urine is an appropriate method to recognise renal damage earlier than with any other known routine method.
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PMID:[Control of penicillamine therapy in patients with chronic polyarthritis through urine disc electrophoresis]. 59 10

In tests conducted with 165 mongrel sexually mature and immature rats it is shown that azathioprine used in nephrotoxic nephritic improves the general condition, reduces the edema of subcutaneous cellular tissues, as well as the intensity of proteinuria and helps retaining its selective type, lessens the degree of hypo- and dpsproteinemia and, especially, of hyper-beta-lipoproteinemia; in the kidneys the pathomorphological changes characteristic of nephritis become less marked. Azathioprine does not influence the process of acido-and ammoniogeness in the tubuloar system of the nephron, nor does it modify diuresis. The effect of azathioprine is most spectacular in the acive phase of developing nephritis. In rattlings with nephritis theaction af azathioprine in regard to a number of factors (proteins, beta-lipoproteids, gamma-globulins of the blood) is somewhat stronger than in the sexually mature rats.
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PMID:[Experimental study of azathioprine in nephrotoxic nephritis in rats]. 65 69

A case of meningococcal meningitis is described in which 10 days later there developed the histological lesions of acute exsudative proliferative glomerular nephritis without proteinuria, hematuria, hypertension or salt and water retention. The relationship between structural and functional changes in the kidney in glomerular nephritis is discussed in the light of these findings.
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PMID:Post meningococcal acute glomerular nephritis. 66 26

The effects of indomethacin and lysine acetylsalicylate (L-ASA) were compared in rats in which autologous nephrotoxic serum nephritis had been induced. The aim of this study was to offer support to the hypothesis that indomethacin might reduce proteinuria through increased synthesis of glomerular basement membrane by the podocytes. Both drugs were injected intraperitoneally at the dosage of 4 mg/kg body weight daily during a 6-day period into 40 rats rendered nephritic by rabbit nephrotoxic serum injection. Rats treated with indomethacin showed a marked decrease of proteinuria (tested by the 3% sulfosalicylic aicd method) and a clear ultrastructural picture of hyperplasia and hypertrophy of podocytes. Rats given L-ASA showed only a slight correction of proteinuria and less specific ultrastructural modification. These observations suggest that indomethacin decreases proteinuria in nephritic rats not only through its anti-inflammatory activity, but possible also by a peculiar mechanism, namely an increase in podocytic basement membrane synthesis.
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PMID:Indomethacin and lysine acetylsalicylate in rats with autologous nephrotoxic serum nephritis. Biochemical and morphological studies. 74 Jan 8

Degradation and synthesis of the collagen portion (CLP) of the glomerular basement membrane (GBM) in glomeruli of rats with nephrotoxic nephritis (NTN) were determined in vivo and in vitro. Degradation of CLP in rats with NTN was only increased during the first 24 h after induction of NTN. After 24 h, the half-life of CLP in NTN rats (16.9 days) was not significantly different from that in the controls 15.6 days). The loss of CLP during the first 24 h is accompanied by an increased synthesis, measured in vivo and in vitro. The increased synthesis, however, does not seem to be sufficiently high to result in accumulation of CLP-like material in NTN. Since degradation and synthesis of CLP was not altered during the later phase of NTN, it is unlikely that chronic proteinuria is the result of an ongoing abnormal turnover of CLP.
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PMID:Synthesis and degradation of glomerular basement membrane in rats with nephrotoxic nephritis. 74 Jan 13

The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.
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PMID:The role of polymorphonuclear leucocytes in the autologous phase of nephrotoxic nephritis. 76 16

Association of membranous glomerulonephropathy with crescentic glomerulonephritis is apparently extremely rare. We report three patients who had this combination. One patient had biopsy-proven membranous glomerulonephropathy thirteen months prior to sudden and rapid decline in renal function necessitating hemodialysis. A repeat renal biopsy showed a superimposed crescentic nephritis and antiglomerular (GBM) antibodies were demonstrable in the serum. A second patient had proteinuria of unknown duration and then developed renal failure. Renal biopsy showed crescentic nephritis with a fine granular glomerular immunofluorescence for IgG typical of membranous glomerulonephropathy. Anti-GBM antibodies were present in this patient's serum. The third patient presented with acute renal failure of moderate severity. A renal biopsy revealed crescentic nephritis, granular deposits of immunoglobulins, and epimembranous electron-dense deposits typical of membranous glomerulonephropathy. Although his creatinine clearance improved spontaneously, nephrotic syndrome has persisted and a repeat renal biopsy showed a progression of the membranous glomerulonephropathy with the disappearance of the crescentic lesions. The reason for this peculiar association of membranous glomerulonephropathy and crescentic glomerulonephritis is unclear. It is possible that deposition of immune-complexes along glomerular basement membrane may render the glomerulus more susceptible to additional injury from a variety of other agents. Alternatively, depostis formed in one disease could initiate release of normal or altered basement membrane material and lead to formation of anti-GBM antibodies and subsequent development.
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PMID:Association of crescentic glomerulonephritis with membranous glomerulonephropathy: a report of three cases. 78 51

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.
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PMID:Defibrination with ancrod in nephrotoxic nephritis in rabbits. 79 57


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