Glomerulonephritis associated with endocarditis, deep-seated infections, and shunt nephritis

Endocarditis is a cause of glomerulonephritis. Healthcare interventions (prosthetic valves, indwelling catheters, pacemaker wires) and intravenous drug abuse are presently the most common causes of endocarditis and Staphylococcus aureus is frequently the infecting bacteria. Shunt nephritis is a form of glomerulonephritis associated with infection of ventriculoatrial shunts implanted to relieve hydrocephalus and, typically, are caused by prolonged infections of low-pathogenicity microorganisms. This complication led to the replacement of the technique by ventriculoperitoneal shunts. Deep-seated infections such as chronic abscesses and osteomyelitis can sometimes cause a similar syndrome. In all cases, treatment of the infection is the key strategy. The nature of the glomerulonephritis tends in subacute infection to be a lobular membranoproliferative glomerulonephritis type I pattern associated with low C3 levels. However, an acute post-infectious pattern may also be seen, and a third pattern is focal necrotizing and crescentic glomerulonephritis, which tends to be pauci-immune as seen in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, but usually without positive fluorescence or solid phase assays for ANCA antigens.

Delayed Manifestation of Shunt Nephritis: A Case Report and Review of the Literature

We present an unusual case of shunt nephritis in a 39-year-old male who presented 21 years after placement of a ventriculoperitoneal (VP) shunt. He complained of fevers, headaches, dizziness, and urticarial plaques on arms, trunks, and legs and was found to have anemia, low complement levels, elevated serum creatinine, proteinuria, and new onset microhematuria. Blood and urine cultures were negative. Renal biopsy showed features of acute tubulointerstitial nephritis attributed to vancomycin use. Glomeruli showed increased mesangial hypercellularity and segmental endocapillary proliferation. Immunofluorescence showed focal IgM and C3 staining. Electron microscopy revealed small subendothelial electron-dense deposits. Symptoms and renal insufficiency appeared to improve with antibiotic therapy. He was discharged and readmitted 2 months later with similar presentation. CSF grewPropionibacterium acnesand shunt hardware grew coagulase-negativeStaphylococcus. He completed an intravenous antibiotic course and was discharged. On 1-month follow-up, skin lesions persisted but he was otherwise asymptomatic. Follow-up labs showed significant improvement. We did a brief systematic review of the literature on shunt nephritis and report our findings on 79 individual cases. In this review, we comment on the presentation, lab findings, pathological features, and management of this rare, potentially fatal, but curable disease entity.