<s>[INST] context: Refer Robbins page no 915By light microscopy the glomeruli either appear normal in the early stages of the disease or exhibit uniform, diffuse thick- ening of the glomerular capillary wall (Fig. 20-12A). By electron microscopy the thickening is seen to be caused by irregular electron dense also deposits containing immune com- plexes between the basement membrane and the overlying epithelial cells, with effacement of podocyte foot processes (Fig. 20-12B and D). Basement membrane material is laid down between these deposits, appearing as irregular spikes protrud- ing from the GBM. These spikes are best seen by silver stains, which color the basement membrane, but not the deposits, black. In time, these spikes thicken to produce domelike protru- sions and eventually close over the immune deposits, burying them within a markedly thickened, irregular membrane. Immunofluorescence microscopy demonstrates that the granu- lar deposits contain both immunoglobulins and complement (Fig. 20-12C). As the disease advances segmental sclerosis may occur; in the course of time glomeruli may become totally sclerosed. The epithelial cells of the proximal tubules contain protein reabsorption droplets, and there may be consider [/INST] question: On electron microscopy in most of the cases characteic slpiiting of GBM with subepithelial deposits in few cases is seen in | options: A: RPGN B: Membranous nephropathy C: FSGS D: Minimal change disease | answer: B </s>