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Many of us were drawn to the field of nephrology after experiencing the thrill of successfully treating an acutely ill patient with rapidly progressive glomerulonephritis (RPGN). The urgent need to recognize and institute aggressive treatment for these relatively rare cases remains of paramount importance, both to optimize patient survival and to reduce the likelihood of dialysis dependence. The characteristic crescentic renal histologic changes in RPGN can result from 3 different pathogenic mechanisms: deposition of immune-complexes, production of anti-glomerular basement membrane (GBM) antibodies or pauci-immune (vasculitic) processes that often include anti-neutrophil cytoplasmic antibodies (ANCA). Commonly used regimens to treat RPGN employ high-dose steroids and cytotoxic agents, with further protocols based on specific pathogenesis and extent and severity of organ involvement. This may include the use of plasmapheresis or plasma exchange to remove circulating antiGBM antibodies or treat ANCA-associated vasculitis when it presents with advanced nephropathy or pulmonary hemorrhage. However, no single or common biologic pathway has yet been identified across the 3 processes that produce crescentic glomerular disease and rapid loss of kidney function. This gap complicates the treatment of patients and limits our understanding of disease pathogenesis. RPGN being an uncommon disorder, appropriate biosamples to assist in identifying common versus independent pathways are frequently lacking. In this issue of the American Journal of Nephrology, Wang et al. [1] performed weighted gene correlation network analysis (WGCNA) [2] aimed at identifying clusters (or modules) of highly correlated genes in patients with

Have We Made “Rapid Progress” Understanding the Pathogenesis in Rapidly Progressive Glomerulonephritis?