Glomerulonephritis associated with Staphylococcus aureus infection.

Renal lesions commonly seen in SBE include localized infarcts, abscesses, therapy-related interstitial nephritis, and glomerulonephritis ( 1-2). The incidence of glomerulonephritis associated with SBEhas not been determined. The most commonorganisms leading to SBEare the streptococcus viridans group and coagulase-negative staphylococci, including Staphylococcus (Staph.) epidermidis ( 1). The renal manifestations are microscopic hematuria, which is occasionally macroscopic. Proteinuria may be detected in urine, but nephrotic syndromeis unusual. The extent of renal failure is frequently mild, but uremia was reported to be present in 5 to 10% of patients with SBE (2). In addition, non-specific evidence of inflammation, rheumatoid factor, cryoglobulinemia, and circulating immunecomplexes are present. Depression of complement levels is typical but not always present. On histopathological examination, focal and segmental (occasionally diffuse) glomerular changes with fibrinoid necrosis or intracapillary thrombosis are seen in the acute stages (2). In addition, polymorphonuclearneutrophils or nuclear debris are present. Adhesions to Bowman'scapsule or cellular crescents are often seen. In the late stages, segmentally sclerotic glomerulonephritis with or without fibrocellular crescents is present. It is usually situated at the periphery of one or several lobules. Adhesions between the sclerotic lesion and Bowman's capsule or cellular crescents are also seen. This segmentally sclerotic region is thought to represent a later lesion resulting from healing of the necrotic lesion (2). IgG, IgM, and C3 depositions in the mesangial regions and the glomerular capillaries are demonstrated by immunofluorescence study, and dense mesangial and subendothelial deposits are revealed by electron microscopy. The frequency of acute bacterial endocarditis is increasing, particularly in intravenous drug abusers (3). Many causal organisms have been implicated, but the most commonis Staph. aureus (3). Symptoms of severe infection and signs of cardiac involvement always precede the renal symptoms. The renal manifestations are microscopichematuria, whichis occasionally macroscopic, and proteinuria. Oliguria is sometimes present at the onset of renal involvement. The extent of the renal failure is frequently mild, but occasionally acute renal failure with a rapid deterioration in renal function is seen. Hypertension is unusual. Serological examination demonstrates non-specific evidence of inflammation, rheumatoid factor, cryoglobulinemia, and circulating immune complexes are present. Complement levels are decreased during the acute phase of this disease. Histopathological examination commonlyreveals diffuse exudative proliferation with or without crescents, an expression which is similar to poststreptococcal acute glomerulonephritis (2). Polymorphonuclear neutrophils or mononuclearcells are present. IgG and C3 deposits along the capillary walls or in the mesangial regions are demonstrated on immunofluorescence study. Electron-dense subepithelial and intramembranous deposits are most commonly seen on electron microscopy, and subendothelial and mesangial deposits also occur. Although infection of V-A or V-P shunts seems to be relatively common, the subsequent development of glomerulonephritis may occur in less than 5%of infected patients (1). The causal organism is Staph. epidermidis in approximately 70% of shunt nephritis and Staph. aureus in 20%(1). The renal manifestations that appear following symptomsof infection and signs of increasing intracranial pressure are microscopic hematuria, and occasionally macroscopic hematuria. Proteinuria is variable, but is sufficient to result in a nephrotic syndrome. There is non-specific evidence of inflammation in most patients, and in some cases, rheumatoid factor and cryoglobulinemia are detected. Complement studies indicate reduced C3, C4 and Clq levels. The most common glomerular lesion is type I mesangiocapillary glomerulonephritis, in some cases with crescent formation (2). On immunofluorescence microscopy, depositions of IgMand C3 in capillary walls are usually revealed. Ultrastructural examination commonlyshows subendothelial electron-dense deposits. Recently, we reported glomerulonephritis in association with methicillin-resistant Staph. aureus (MRSA)infection as a new type of staphylococcal infection-associated glomerulonephritis (4-7). The renal manifestations appeared within 10 weeks after MRSAinfection. The most commonrenal manifestation was rapidly progressive glomerulonephritis (RPGN) with nephrotic syndrome in about 60%of patients. Henoch-Schonlein