Late pericarditis in patients on maintenance haemodialysis.
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Biomedical subjects
Publications and source records attributed to S C Dash.
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Two patients presented with the nephrotic syndrome complicating non-specific aorto-arteritis (Takayasu's arteritis). Histologically both had renal amyloidosis. On investigation there was no evidence of chronic infection or any immuno-inflammatory disease known to be associated with amyloidosis. These cases raise the possibility of a significant association between aorto-arteritis of the Takayasu type and systemic amyloidosis.
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Analysis of 80 cases of SLE with renal involvement revealed the following. Angiitis involving arterioles and interlobular arteries was observed in 17 out of 42 cases with diffuse proliferative lupus GN. This was not observed in other types of lupus GN. Out of 17 cases of angiitis, 7 were complicated by thrombosis. Irregular deposits of immunoglobulins and complement were demonstrated in the vessel walls and in luminal thrombi and suggested an immune-complex origin. Fibrinogen was also demonstrable frequently. The vascular lesions were associated with severe glomerular and tubulointerstitial injury and a poor prognosis. A relatively favorable outcome was observed in SLE without renal angiitis.
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36 consecutive patients whose biopsies showed significant extracapillary proliferation in the face of rapidly declining renal function were reviewed between 1967 and 1979. About 30% of the patients belonged to the pediatric age group with a male:female ratio of 2.5:1. Oliguria/anuria, hematuria, and progressive renal insufficiency were present in all cases. There was evidence of 9 cases being poststreptococcal, 2 SLE, 1 Henoch-Schönlein purpura, 2 possibly viral and 1 staphylococcal. Histologically, 29 cases had more than 60% crescents, 5 between 50 and 60% and 2 cases a little less than 50%. 28 cases were fatal in less than 10 months. 2 were lost of follow-up. 6 survivors with reversal of renal functions had 3 common factors to note, namely an antecedent disease, less crescents both in number and size, accompanied by fewer interstitial changes and early treatment. Rebiopsy in 2 survivors showed regression of histologic severity.
Ten out of 66 cases of glomerulonephritis (GN) with variable crescent formation appeared to be of post-streptococcal origin. Immunofluorescent studies of biopsies from 42 of the patients showed findings suggestive of immune complex glomerular injury in 86% whilst there was no evidence of immunologic or nonimmunologic injury in the remainder. Anti-GBM GN was not demonstrable, although it can not be certain that there were no cases amongst the patients whose biopsies were not examined by immunofluorescence. Conservative measures were adequate for the treatment of cases with less than 50% crescents. In the others, with greater than or equal to 50% crescents, appreciable improvement was observed with anticoagulation, immunosuppression and dialysis. The mortality was 30% in cases with 50-80% and 65% in cases with greater than 80% crescents. No appreciable difference in survival was observed between post-streptococcal and idiopathic cases. The single most important factor in prognosis, regardless of etiology, appeared to be the extent of crescent formation. Tubulo-interstitial damage was contributory. Necrotizing angiitis, present in 4 cases, affected the course adversely.
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