SUMMARY
Three cases of post‐partum acute renal failure are described, the clinical and pathological features of which are identical to those previously reported. Renal failure accompanied by micro‐angiopathic hremolytic anæmia occurred after a non‐specific prodromal illness early in the puerperium. The features of the disease closely resemble those of thrombotic thrombocytopenic purpura and the hæmolytic uræmic syndrome of children and adults. The similarity of the hæmatological and histological features to their counterparts in the generalized Shwartzman reaction (GSR) is striking. Pregnancy predisposes humans to the GSR, a modification of which may play a part in the pathogenesis of this disease. The prognosis in the cases described and those previously reported is bad because of the irreversible nature of the renal and other pathological changes. Heparin therapy may be of value if given early but clinical recognition of the condition may not occur soon enough.
Mesangial IgA depostiiton was detected by routine fluorescent microscopy of 19 cases of glomerulonephritis. Twelve patients had a variable degree of diffuse mesangial proliferative glomerulonephritis. The heterogeneous histological findings in the other seven patients show that mesangial IgA deposition alone does not have diagnostic specificity. However, when interpretation of the mesangial IgA deposition is complemented by clinical and histological information, a group of patients with the characteristic combined features can be distinguished.
Summary: The nephrotic syndrome in Papua New Guinea: aetiological, pathological and immunological findings. K. C. Powell, R. Meadows, R. Anders, C. C. Draper and C. Lauer, Aust. N.Z. J. Med., 1977, 7, pp. 243–252.
Studies were carried out on 34 patients with the nephrotic syndrome within Papua New Guinea to determine the aetiology, with special reference to the role of P. malariae. Biopsies were taken and examined by light microscopy, with a few additionally examined for immunofluorescence. Sera were studied for titre of malarial antibody, presence of select viral antibodies, Australia Antigen, immunoglobulins IgA, IgG and IgM, and for the third component of complement (C3). The selectivity of proteinuria was examined by a method using IgG and transferrin. Control subjects were used when appropriate.
Histological findings showed a wide range of changes with the Minimal Lesion type being very uncommon. Proliferative lesions accounted for 24 of the 34. Focal lesions were uncommon, in contrast to findings of an earlier publication concerning New Guinea patients. Immunofluorescence studies on nine showed the presence of complement, IgG, IgM or IgE, findings accepted as consistent with the concept of immune complex disease.
The serum results showed a low level of total IgG, a low IgG specific for P. malariae, a normal level of IgM specific for P. malariae and a raised total IgM. These serological findings, along with the histological findings, are strongly against P. malariae being a common cause of the nephrotic syndrome.
The viral findings excluded type B hepatitis virus and some arboviruses, as causing the nephrotic syndrome. The ASOT titres were usually normal and the VDRL readings all non‐reactive. Leptospira! infections were excluded as a cause. The cause(s) of the nephrotic syndrome in Papua New Guinea remains obscure.
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