To understand the histology of glomerulonephritis, we need to revisit the basic

structure of the normal kidney (see fig 1). Inflammatory, proliferative, and fibrotic
changes may affect specific cells of the kidney differently or may result in more
global changes with particular patterns resulting in a spectrum of clinical
presentations. In table 1, we have attempted to summarise the complex
nomenclature that surrounds glomerulonephritis by naming each disease,
describing its common renal clinical presentation and explaining its underlying
histological lesion. In table 2 we have focused purely on clinical aspects which
may aid rapid diagnosis. Renal biopsies are vital both in defining a diagnosis,
and also in offering prognostic information by differentiating acute reversible
damage from chronically scarred non-viable kidney which does not justify the
risks of potentially toxic therapy. Although current treatments are, at best, crude,
with greater understanding of pathological events we hope to design more
specific therapy both to limit acute damage, and to prevent progression to
chronic scarring with its inevitable decline in renal function.