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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The pattern of renal disease and its basic principles of management are essentially the same in the tropics as in the temperate environment. Glomerulonephritis and pyelonephritis with concomitant hypertension account for most cases of renal failure. Malaria is now well recognised as a cause of the nephrotic syndrome. Economic and manpower factors dictate a conservative approach to therapy. Maintenance haemodialysis and renal transplantation are not realistic in the present context, having regard to the order of priorities in health care delivery.
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PMID:Nephrology in the tropical setting. 37 Jun 31

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

The frequency of nephrotic syndrome was 0.2% of all medical admission records. A prospective study of 180 nephrotic patients was begun in 1966 and ended in 1976 and the clinical, biochemical and renal histological changes were studied. Unlike other studies of nephrotic syndrome in West and East Africa, in which malaria is believed to play an important aetiological part, this study in Durban was done in a malaria-free area. Most of the patients were between the ages of 12 and 30 years. The aetiology of the nephrotic syndrome was undetermined in 94% of the African patients and in 87% of the Indian patients. The most common histological pattern in both racial groups was proliferative glomerulonephritis, followed by membranous glomerulonephritis. Minimal change on light microscopy was rare. This has important implications from the therapeutic aspect because African patients suffering from nephrotic syndrome will not as a rule respond to steroids or cyclophosphamide therapy. An initial diastolic blood pressure greater than or equal to 110 mm Hg and a low serum complement were more common in proliferative glomerulonephritis. The serum gamma-globulin, though low, was raised compared with the normal serum gamma-globulin, in the white population. A difference in the serum lipoprotein patient between the two races was observed.
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PMID:Nephrotic syndrome in the Africans and Indians of South Africa. A ten-year study. 72 96

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

A study of renal biopsy specimens obtained in Senegal from 24 children and six adults with nephrotic syndrome showed two unusual varieties of nephropathy--namely, an extramembranous glomerulonephritis associated with hypocomplementaemia (four cases), a combination previously described only in systemic lupus erythematosus, and a "tropical nephropathy" (16 cases). The latter, though lacking the diffuse glomerular deposits of immunoglobulin described in quartan malarial nephropathy (Q.M.N.), showed a curious progressive and segmental glomerulosclerosis, characterized by a "flaking" or fibrillary splitting of the glomerular capillary wall, seen in Q.M.N. Serological evidence of malaria was lacking in a third of the childhood cases.
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PMID:"Topical nephropathy" and "tropical extramembranous glomerulonephritis" of unknown aetiology in Senegal. 109 12

Study of urinary waste of chickens with acute Plasmodium gallinaceum malaria indicated that serum proteins of the globulin and albumin classes were passed. Protein extravasation did not begin until globulin-associated serum antigen and its antibody were detected in the blood. Both serum antigen and antibody were found in the wastes for as long as the antigen was present in the blood. Extracts of kidney tissues contained serum proteins that were not present in extracts from normal kidneys, and serum antigen and its antibody were both present. Frozen kidney sections reacted strongly with fluorescein-conjugated antibody to serum antigen, showing diffuse granular immunofluorescence characteristic of immune complex nephritis. Sections from chickens with nephritis induced by injections of malarious plasma also showed deposits of extravasated antigen. The experiments suggested that complexes of serum antigen and antibody served as a permeability factor, or activated other permeability factors and may have caused the glomerulonephritis associated with acute avian malaria. The passing of serum proteins in the urinary wastes after chickens had recovered from acute malaria suggested that persisting damage may have resulted.
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PMID:Pathogenesis of acute avian malaria. IV. Immunologic factors in nephritis of acute Plasmodium gallinaceum infections of chickens. 109 93

The production of Interleukin 6 (IL-6) was studied during experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA) infection. IL-6 is present in the serum of mice with ECM, the highest concentrations being observed in mice with full-blown neurological syndrome. High IL-6 levels were also observed, however, in the absence of pathology in nonlethal malaria infection. These data suggest that IL-6 is produced in large amounts during malaria infection, but does not play a major role in the pathogenesis of ECM. A modulation of IL-6 production in ECM was achieved by in vivo treatment with other anticytokine antibodies: antibodies to interferon (IFN-gamma) or to tumor necrosis factor (TNF) abolished the rise of IL-6, while anti-IL-3 and anti-granulocyte/macrophage colony-stimulating factor antibodies only partially prevented this rise, suggesting that the two cytokines IFN-gamma and TNF are important intermediates in IL-6 production. Passive immunization against IL-6 did not prevent ECM, but significantly reduced serum IgG levels in malaria-infected mice. Thus, by its effects on B cells, IL-6 may be involved in hypergammaglobulinemia and immune-complex diseases, e.g., glomerulonephritis observed during malaria infection.
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PMID:Interleukin 6 production in experimental cerebral malaria: modulation by anticytokine antibodies and possible role in hypergammaglobulinemia. 212 90

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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