Chapter 47 - Acute Glomerulonephritis

Abstract

Glomerular disease can cause acute renal failure but typically accounts for fewer than 10% of all cases. The most common cause is a rapidly progressive glomerulonephritis resulting from granulomatous polyangiitis (GPA, Wegener granulomatosis), microscopic polyangiitis (MPA), anti–glomerular basement membrane (GBM) disease or, less often, diffuse proliferative lupus nephritis, immunoglobulin A nephropathy, or poststreptococcal glomerulonephritis. Acute renal failure also complicates mixed cryoglobulinemia, mesangiocapillary glomerulonephritis, membranous nephropathy, hemolytic uremic syndrome–thrombotic thrombocytopenic purpura, and scleroderma. Early detection of the rapidly progressive glomerulonephritis as the cause of acute renal failure is critical to commence specific and aggressive treatment that greatly improves patient and renal outcomes. Clinical manifestations of rapidly progressive glomerulonephritis include a prodrome of fever, malaise, arthralgia, and microscopic hematuria, but macroscopic hematuria, proteinuria, and oliguria are also common. Depending on the clinical features, a number of diagnostic assays can support the working hypothesis: antineutrophil cytoplasmic antibodies (ANCA), and anti–double-stranded DNA antibodies, anti–GBM antibodies, antistreptolysin O and anti–DNase B antibodies, rheumatoid factor, cryoglobulins, serologic hepatitis C markers, antiphospholipid antibodies, and complement levels. Chest radiography, computed tomography scans, and abdominal ultrasound are also useful. Renal biopsy demonstrates the activity and reversibility of the glomerular lesion, and crescents with epithelial cells and inflammatory cell infiltrate Bowman's space. Immune deposits are present as few or no (“pauci-immune”) linear or granular patterns. Urgent treatment options include high-dose corticosteroids, cyclophosphamide, and plasma exchange.