Search

To identify the demographic, clinical, and pathologic features and the prognosis of renal disease in a series of patients with infectious or postinfectious proliferative glomerulonephritis (GN), data were collected from records of 76 adult patients admitted from 1976 to 1993 to 2 neighboring suburban hospital nephrology units, whose catchment population consists of patients living in a suburban borough of Paris with a below-average socioeconomic status. Thirty-four patients (45%) were alcoholics, diabetics, or intravenous illicit-drug users. Sixty-six patients presented with acute nephritic and/or nephrotic syndrome. Acute renal failure was present in 56 (76%) and required dialysis in 14. The diagnostic workup comprised at least 1 renal biopsy in each case. The patient's background, site of infection, clinical course, laboratory variables, and, when available, bacteriologic findings were analyzed in each case to interpret the evolution of the disease. Initial renal biopsy disclosed endocapillary GN in 44 patients, crescentic GN in 26, and membranoproliferative GN in 6. Ten patients had endocarditis. Staphylococci and Gram-negative strains, not streptococci, were the most common bacteria identified. The origin of sepsis was mainly the oropharynx (21), the skin (19) and the lung (14); 19 cases involved multiple sites of infection. Eight patients died (11%), and 20 (26%) recovered renal function, but GN followed a chronic course in 38 (50%), rapidly requiring maintenance dialysis in 6. Poor prognostic factors included age over 50 years, purpura, endocarditis, and glomerular extracapillary proliferation. Twenty-six patients underwent repeat renal biopsy 1 month to 11 years after the initial presentation. The main finding, irrespective of the interval since the first biopsy, was that ongoing or new iatrogenic infection acquired during hospitalization was almost invariably acquired during hospitalization was almost invariably associated with developing glomerular proliferative changes. This study shows that infectious proliferative GN remains common, but that its epidemiology has changed from what was observed until 2 decades ago. The responsible bacteria, when identified, now comprise a majority of staphylococci and Gram-negative strains, in contrast to the streptococci which predominated 3 decades ago. Infectious GN affects with increasing frequency patients with an underlying condition responsible for immunosuppression, especially alcoholism, even in the absence of cirrhosis. Destructive glomerular proliferation persists, especially but not exclusively until infection has been eradicated, and despite rescue treatment with corticosteroids and/or cytostatic drugs. Thus, the prognosis is poor, and infectious GN often ends in renal death. Infection continues in this decade to represent a frequent and probably often overlooked cause of end-stage renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Glomerulonephritis may complicate infections due to various microorganisms. These microorganisms are bacterial, fungal, viral or parasitic. Considerable clinical and experimental evidence has accumulated to indicate that glomerular injury is due to in situ immune complex deposition. In France, renal lesions are more often due to focal skin infection and sinus or visceral abscesses, with or without endocarditis, rather than to pharyngeal streptococcal infection. Staphylococcal infections are a frequent cause, especially in intravenous illicit drug users. Recovery requires suppression of the infective agent. However, in severe forms, after initial acute glomerular damage the evolution may be characterized by the development of chronic glomerulonephritis.

A rapidly progressive glomerulonephritis with definitive anuria was observed after solvent inhalation in two young women, aged 22 and 17 years. In both cases the renal biopsy specimen showed diffuse epithelial crescents in all glomeruli, with linear deposits of IgG along the glomerular basement membrane (GBM). High circulating anti-GBM antibody levels were found in sera by indirect immunofluorescence and radioimmunoassay. No anti-alveolar basement membrane antibodies were detectable by immunofluorescent microscopy in one patient. It is suggested that the solvent inhalation resulted in a chemical alteration of the alveolar basement membrane giving rise to anti-basement membrane antibodies, some of which may have cross-reacted with the GBM and initiated the glomerulonephritis.

Most glomerulopathies are immunologically-mediated. Their pathogenesis is now better understood. The role of cell-mediated immunity has recently been envisaged. The role of circulating antibodies now seems to be more important than that of circulating immune complexes. Antibodies may recognize structural or "planted" antigens in the kidney, the latter being non-renal molecules that may bind renal structures for non-immune reasons. The linear or granular pattern observed at immunofluorescence depends upon the regular or irregular distribution of the antigen. In susceptible individuals, various toxins (heavy metals such as mercury or gold, drugs with an SH group, non-steroidal anti-inflammatory agents) may induce an immune glomerulopathy. It has recently been shown that Brown-Norway rats exposed to one of the above-mentioned agents develop anti-self class II T lymphocytes that are responsible for a polyclonal activation of B cells. Among the various autoantibodies that are produced, some have a nephritogenic potential. Other drugs are responsible for glomerular lesions due to a direct toxic effect of the compound. Doxorubicin induces a nephrotic syndrome in the rabbit, while mitomycin induces a haemolytic uraemic syndrome in humans. Finally, drug addiction often leads to glomerulosclerosis.

A girl aged 17 developed a nephrotic syndrome with renal insufficiency after narcotic abuse. Renal biopsy showed a diffuse glomerulonephritis with crescents and dense deposits within the glomerular basement membrane; glomerular C3 deposits were present without immunoglobulin. The serum complement profile was typical of activation via the alternative pathway, and tests for C3 nephritic factor were strongly positive. Terminal renal failure occurred within 6 months and required chronic hemodialysis. It is likely that the narcotics used or their contaminants were responsible for the renal damage, presumably by activating the complement system via the alternative pathway.

Macroscopic haematuria is common in IgA nephropathy, but its significance and influence on prognosis remains uncertain. We compared the clinical and pathological features of 11 adult patients with primary IgA nephropathy who had had a renal biopsy during or shortly after a bleeding episode. Six patients developed transient acute renal failure (ARF) (group 1) and five did not (group 2). Patients of group 1 had a higher percentage of tubular red-blood-cell (RBC) casts (<0.05) and of glomerular crescents (<0.001). However, crescents were focal and involved less than 50% of glomeruli. Acute tubular necrosis was only present in patients of group 1, and ARF was attributed to the acute tubular changes rather than to the glomerular lesions. Despite a prolonged duration of ARF (mean: 38 days), further outcome did not differ in patients of both groups. We suggest that acute tubular damage and/or tubular obstruction by RBC casts should be considered in any patient who develops ARF soon after a haematuric episode. [ABSTRACT FROM PUBLISHER]