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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes the characterization of proteinuria in Aotus monkeys infected with quartan malaria (Plasmodium brasilianum), using a micro-disc-electrophoresis system. In the post infection urine samples, increases in total proteinuria, albuminuria and gamma-globulinuria were noted a few weeks after peak parasitaemia. Two new proteins also appeared in the urine of malaria infected animals. These findings are discussed with reference to the belief that the Aotus-P. brasilianum system can be a model for human malaria in renal immunopathology.
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PMID:[Proteinuria in quartan malaria-infected Aotus monkeys]. 5 72

Swiss albino mice infected with Plasmodium berghei berghi showed the serum-soluble malarial antigen and antibody on day 10 of infection onward. Immune complex nephritis in these mice developed on the seventh day after inoculation. The infected kidneys revealed the deposition of mouse gamma globulin, mouse beta1C globulin and malaria antigen along the capillary wall of the glomeruli. Proteinuria was detected on seventh day of infection. Serum-soluble malaria antigen in probably responsible for forming the soluble immune complex which causes glomerulonephritis in infected mice.
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PMID:Serum-soluble malarial antigens and immune complex nephritis in Plasmodium berghei berghei infected mice. 5 12

Malaria infection leads to renal involvement. Reversible proteinuria accompanies many plasmodial infections. Chronic malarial nephrotic syndrome is specifically associated with quartan malaria. Acute renal failure is restricted to infections with Plasmodium falciparum. The pathogenesis of renal involvement during malarial infections includes immunological mechanisms. It is now realized that there exist at least two types of immunological processes: acute transient immune-complex glomerulonephritis with reversible proteinuria and chronic immune-complex glomerulonephritis with irreversible nephrotic syndrome.
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PMID:[Renal involvement in malaria (author's transl)]. 13 74

A 50-year-old Swiss male died from strongyloidiasis 8 weeks after renal allotransplantation. Past history revealed malaria at age 20 years, when the patient had stayed in tropical and subtropical areas, as well as pulmonary tuberculosis. Hypertension, erythrocyturia, proteinuria and unexplained episodes of blood eosinophilia were first noticed age 45, and 4 years later dialysis was started. A mild acute rejection crisis was successfully treated 4 weeks after transplantation. 2 weeks later, however, bilateral pneumonia developed. Despite vigorous antibiotic and tuberculostatic therapy the patient died in septic shock. Autopsy revealed strongyloidiasis with adult females, eggs and rhabditiform larvae of Strongloides stercoralis in the small intestine. Numerous filariform larvae were detected in the lungs, in the walls of bronchi and trachea, in the brain, in the walls of arteries, and in lymphnodes. Massive granulomatous inflammatory reaction and extensive pulmonary hemorrhage were the main pathological findings.
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PMID:[Strongyloidiasis following kidney transplantation]. 36 Mar 82

Rat-adapted Plasmodium chabaudi caused a syndrome characterized by hemolytic anemia, splenomegaly, and glomerulonephritis. All rats recovered and appeared normal after 4 weeks despite persistence of proteinuria. Serologic studies on the malarious rats revealed that the infection was associated with a soluble antigen which was present concurrently with antibody in plasma, in material eluted from blood cells, in extracts of kidney tissues, and in the urine. This antigen appeared to be identical with one extracted from P. chabaudi parasites and did not cross-react with antigens of Plasmodium gallinaceum. Tests for the cold-active hemagglutin (CAH) and the globulin associated serum antigen (SA) previously associated with acute malaria, revealed that CAH, but not SA, was present. From these observations it is suggested that soluble complexes of the parasite antigen and its antibody may have been causal in this syndrome.
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PMID:Experimental infection with Plasmodium chabaudi in rats: antigen and antibody associated with anemia and glomerulonephritis of acute infection. 59 39

Mice were infected with 1X 107 Plasmodium berghei Yoelii parasites intraperitoneally. Circulating parasite, malaria antibody and C3 concentrations were measures: parasitaemia and hypocomplementaemia were transient, but the antibody response was persistent. Animals were sacrificed at intervals and their kidneys examined: a glomerulonephritis associates with predominantly mesangial deposits of C3, IgG1, IgM and some IgA always developed after 7 days and persisted for up to 6 mth. Malaria antigen and antibody were demonstrated within the glomeruli. Microscopic haematuria occurred with proteinuria but without marked deterioration in renal function. Strains producing high and low affinity antibody were equally susceptible to the disease. Treatment with glucocorticoid, immunosuppressive, platelet function inhibiting and/or anticoagulant drugs, or indomethacin from the 1st day of infection failed to prevent development of the disease or to lead to its early cure. Eradication of the infection within its first 3 days prevented glomerular deposition of antibody and complement, and infection with a smaller antigen load followed by later treatment also produced subsequent cure.
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PMID:Mouse malaria nephropathy. 79 19

Immune complexes play an important role in the pathogenesis of malaria-associated nephropathies. Two main types of lesion are demonstrable: (a) acute (transient-reversible) lesions typical of falciparum infections in man, with mild clinical symptoms developing a week or two after infection. Renal biopsies at that time show deposits of immunoglobulins, complement, and sometimes antigen. The lesions respond to antimalarials. (b) Chronic (progressive) lesions characteristic of quartan infections in man, developing slowly into a chronic stage with persistent proteinuria and gradually deteriorating renal function and hypertension. Renal biopsies at the onset of the disease show deposits of immunoglobulins, complement, and P. malariae antigens in glomerular capillary walls. Antimalarial therapy has no effect. Recent immunochemical findings confirm that these lesions are of the immune-complex type and are associated with malaria infection. However, several questions remain to be solved.
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PMID:Immunopathology of nephropathies associated with malaria. 108 8

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.
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PMID:Membranous nephropathy: an overview. 120 87

Fifteen (34.8%) of 43 patients of falciparum malaria screened for urinary abnormalities showed significant proteinuria (greater than 150 mg/24 h), haematuria (greater than 1/HPF) and casts, with or without azotaemia. Light microscopic examination of renal biopsy tissue from 12 patients revealed mesangial and endothelial proliferative change in 8, and acute tubular necrosis in one patient. Immunofluorescence showed IgM alone, or IgG and IgM along with C3, in 7 patients within the mesangium or along the capillary walls. Repeat kidney biopsy after 6 wk in 5 patients revealed no residual pathology indicating the reversible nature of the lesions.
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PMID:Immunopathological changes in kidney in Plasmodium falciparum malaria. 218 4

A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cis-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both 'soluble' and high-molecular-weight membrane particles (vacuolar blebs, greater than 10(6) dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular 'histuria' which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.
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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76


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