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

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

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

Malnutrition interacting with infectious and parasitic diseases are the main causes of the appalling mortality in childhood in the tropics. The most important single safeguard against these in infancy is breast feeding and the trend now evident to abandon this is a disaster which demands urgent attention. Reasons for this trend are discussed. Efforts to control infectious diseases, other than smallpox, have had little success and the emergence and spread of dengue haemorrhagic fever in S.E. Asia have added new dimensions to the problem. Malaria is still widely prevalent in the tropics and falciparum malaria, holoendemic in much of Africa, remains a major cause of death with its most serious impact on pregnant women and children. The emergence and spread of drug resistant strains of this parasite in parts of the world is a cause for serious concern. Quartan malaria is also an insidious corruptor of health in childhood and commonly causes the nephrotic syndrome. Neonatal jaundice, often associated with G6PD deficiency, is increasing in frequency in urban areas of Africa and now constitutes a significant hazard to the newborn and requires urgent investigation. These problems in tropical paediatrics indicate the need for urgent reappraisal of our role as a profession in the affairs of the tropical developing world.
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PMID:Aspects of tropical paediatrics. 79 3

A specific relationship between P. malariae and the nephrotic syndrome, originally postulated on epidemiologic evidence, has been substantiated by clinical, pathologic and immunologic observations. It would appear that quartan malaria causes an immune complex nephritis in some individuals that, once established, is sustained by mechanisms not yet fully explained but which may involve an autoimmune process. Evidence to support an immunologic pathogenesis of the renal lesions is provided by the presence of immunoglobulin, complement (C3) and quartan malarial antigen in biopsy specimens studied by immunofluorescence microscopy. In early cases in which some patients respond to treatment, fluorescence is coarsely granular but in late cases in which patients are unresponsive to treatment, fluorescence tends to be diffuse. Renal histology is distinctive and does not conform to any of the categories included in the conventional classification of the nephrotic syndrome in childhood. The basic lesion consists of thickening of glomerular capillary walls, leading to eventual obliteration of capillary lumina, and accompanying mesangial sclerosis leads ultimately to total glomerular sclerosis. A unique feature of electron microscopy is the presence of small lacunae scattered throughout the thickened capillary basement membrane. Histologic grading for severity of lesions shows positive correlation with response to treatment and immunofluorescence appearances. Prognosis is, in general, poor. The large majority of patients do not respond to treatment with prednisolone, azathioprine or cyclophosphamide, and prednisolone administration causes severe hypertension and other serious complications in a high proportion of patients.
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PMID:The quartan malarial nephrotic syndrome. 82 46

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

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

Renal biopsies were performed on 21 of 27 Melanesian patients presenting with significant proteinuria in Vanuatu from 1983 to 1985. All patients had more than 2 g of proteinuria per 24 hours or clinical evidence of the nephrotic syndrome. The average age of the patients who were biopsied was 31 years. Three of the 21 patients had evidence of active malaria at the time of presentation, and all of these patients had Plasmodium falciparum. Renal histopathology revealed that six patients (29%) had amyloidosis and five patients (24%) had mesangiocapillary glomerulonephritis (type 1). Of particular note was the fact that only one patient had membranous glomerulonephropathy and only one patient had minimal change nephrotic syndrome, the two most common lesions reported in nephrotic patients in Europe and the United States. Thus, the spectrum of renal histopathology in patients presenting in Vanuatu with significant proteinuria is very different from that seen in Western Countries.
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PMID:The spectrum of renal histopathology in patients with significant proteinuria in Vanuatu. 349 88

Thirteen cases of amyloidosis are reported from Vanuatu between 1983 and 1985. There appears to be a high incidence of the disease similar to that found in Papua New Guinea. The role of malaria as an aetiological agent is discussed although most cases had a history of past or active tuberculosis. Most patients presented as either nephrotic syndrome or a syndrome of abdominal pain, diarrhoea, weight loss and proteinuria.
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PMID:Amyloidosis in Vanuatu. 361 94

Antibodies with different spectra of reactivity are produced during malarial infections and marked changes in IgG and IgM levels occur. In addition malaria elicits serological changes that are usually associated with connective tissue disease. The excessive anaemia associated with malaria may, in part, be an autoimmune phenomenon. Transient nephritis accompanies many plasmodial infections but chronic malarial nephrotic syndrome is specifically associated with quartan malaria. Malarial infection leads to splenomegaly, the most extreme form of which is idiopathic tropical splenomegaly, which probably represents an aberrant immune response to the infection. Malaria can affect the humoral immune response to unrelated antigens and infectious agents. This may be relevant to the etiology of Burkitt's lymphoma. During pregnancy there is some loss of acquired immunity to P. falciparum and the placenta appears to be an immunologically privileged site for the multiplication of this parasite.
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PMID:Immunopathology of malaria. 421 8


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