HIV infection in injecting drug users.
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Biomedical subjects
Publications and source records attributed to A Durante.
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112 cases of MPGN, whose diagnosis was made on light microscopy, were reviewed. Histological examination showed 66 cases of 'classical' MPGN, 33 of MPGN with a lobular pattern and 13 of MPGN with epithelial crescents. In 11 patients dense intramembranous deposits were observed. On immunofluorescence (95 cases) 62 patients showed deposits of C3 together with immunoglobulins, 20 had a predominant deposition of C3 and in 13 C3 alone was present. At the moment of biopsy 57 patients had nephrotic syndrome, 43 hypertension, 43 impaired renal function and 65 hypocomplementaemia. In 23 cases, one or more episodes of macroscopic haematuria occurred. The actuarial survival was 70% after 10 years and 50% after 20 years from onset. At last observation 25 patients were dead or on haemodialysis, 22 had impaired renal function, 62 had normal renal function and 2 were in complete remission. The histological variety with epithelial crescents had a significantly worse outcome. The presence of dense deposits or of any specific immunofluorescence pattern had no prognostic significance. Nephrotic syndrome, renal function impairment and hypertension indicated a poor prognosis: however, macroscopic hamaturia or hypocomplementaemia did not influence the outcome.
The clinical course of IgA Mesangial Deposits Glomerulonephritis (MDGN) has been investigated in 178 patients for 1 to 32 years (mean 6 years) from the onset of symptoms. Impairment of renal function occurred in 28 patients, 13 of whom required RDT or died in uraemia. Hypertension was observed in 67 patients. The actuarial survival rate at ten years was 91%. A significant correlation was observed between the occurrence of renal failure and the following features: absence of episodes of gross haematuria, early appearance of hypertension, marked proteinuria and sclerosing glomerular lesions. These data suggest that IgA MDGN has generally a very prolonged course, but in a few cases may evolve, sometimes early, to chronic renal failure.
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90 patients, whose renal biopsies showed on light microscopy a pattern of MPGN, have been studied by immunofluorescence. 10 cases showed dense intramembranous deposits. Fluoresceinated antisera against IgG, IgA, IgM, C3, fibrinogen, IgD, IgE, C4, C1q, properdin and C3A were employed. Granular depostis of C3 were observed in all cases; IgG, IgM, properdin, C1q and C4 were found in 2/3 cases; IgA, IgE and C3A were rarely found. The localization of these deposits was parietal and often also mesangial. On the basis of glomerular deposition of C3 with or without immunoglobulins (Ig), we separated the cases into three groups: 1) C3 + Ig (59 cases), 2) predominant C3 (19 cases), 3) isolated C3 (12 cases). Most patients with dense deposits disease were classified in the third group. Deposits of C1q and C4 were found only in the first two groups. The localization of C3 deposits showed a more frequent mesangial extension in the second and third groups. Patients in these 3 groups also had different serum complement profiles. No significant differences in the major clinical features could be found in the 3 groups. Variable immunofluorescence patterns, in agreement with other serological parameters, confirm the heterogeneity of pathogenetic mechanisms in patients with MPGN.
In 205 cases of GN the glomerular deposits of C3, C1q, C4, and C3A and the serum levels of the same complement components at the time of biopsy were studied. Alterations of serum complement profile were found only in acute GN, membranoproliferative GN and lupus nephritis, while glomerular deposition was observed with a different incidence and intensity in all nephropathies. A strict correlation between the intensity of deposits and the degree of hypocomplementaemia was found only in early acute GN and in active lupus nephritis.
Five episodes of acute renal failure due to rifampicin (R-ARF) were observed in four patients and the clinical and histological data were compared with the records of 52 episodes reported in the literature. The bulk of data supports the assumption that the by far most frequent renal injury responsible for R-ARF is acute tubular necrosis produced by a vasomotor mechanism. Nevertheless a few data, above all immunohistological findings, suggest the local presence of allergic process. It may be, that the development of an immunological renal lesion is prevented or blunted by the consequences of vasomotor effects.
Biopsies from 400 patients affected by glomerular diseases, both "primary" and secondary to systemic diseases, have been studied by immunofluorescence. Staining was performed for immunoglobulins fibrogen and C1q, C4, C3 and C3A. C1q, C4 and C3 were positive in a high percentage of cases in focal glomerulosclerosis, membranoproliferative glomerulonephritis, lupus nephritis and essential cryoglobulinaemia glomerulonephritis. C1q and C4 were very rarely present in focal proliferative glomerulonephritis and rheumatoid purpura glomerulonephritis. C3A was found frequently only in acute glomerulonephritis. Results are discussed with reference to their diagnostic value and to information about mechanisms of complement activation.
Drug-induced hypersensitivity nephritis may show several histological and clinical patterns. In most of these microscopic vascular involvement of the kidney seems to be very frequent. On immunofluorescence, deposits of C3 in mesangium and in arterioles were observed in almost all cases, independently of histological features on light microscopy. The pointing out of clinico-histological relationship seems to be the best rational approach to diagnosis of these conditions.
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Explore the source record for details and available documents.