Titlebook: Atlas of Renal Pathology; R. A. Risdon,D. R. Turner Book 1980 Springer Science+Business Media Dordrecht 1980 pathology

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4.5 Doses to Patients in Diagnostics,llary cell proliferation, capsular crescent formation, leukocyte infiltration, deposition of fibrin and its derivatives (seen ultrastructurally as deposits of varying electron density) in the mesangium and the widened sub-endothelial space, and swelling of endothelial cells.

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Interstitial Nephritis,stitium (oedema and/or fibrosis, often with inflammatory cell infiltration) and the tubules (tubular atrophy and loss). These lesions may result from direct damage to tubules or interstitium, orfrom vascular insufficiency. Sometimes a combination of factors is involved and frequently the exact mechanisms are obscure.

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,Diffuse Membranous Glomerulonephritis and ‘Minimal Change’ Disease,lution of the glomerular lesion and have shown that, as the lesion progresses, spike-like extensions of the glomerular basement membrane protrude between the deposits like the teeth of a comb (Figure 11.4). The formation of more basement membrane material continues until eventually the deposits are surrounded.