86 40 歲男性愛滋病患在追蹤過程中發現腎臟的功能惡化。二十四小時尿蛋白高達 10 克。血清學檢查並 未發現 C 或 B 型肝炎病毒抗體。腎臟生檢展現腎絲球足細胞（visceral podocytes）增殖及局部腎絲球 塌陷。下列疾病中那一個最符合其臨床及病理表現？
(A)Focal segmental glomerulosclerosis
(B)Diffuse crescentic glomerulonephritis
(C)Membranoproliferative glomerulonephritis
(D)Minimal change nephropathy

Example: pt that is HIV “+”, pitting edema – therefore look at urine and note that is greater than 3.5 grams over 24 hrs. Has fatty casts in urine and has HTN.   Do bx, and already know what you are gonna see b/c it the  MCC nephrotic syndrome in AIDs pt.   On bx, some of the glomeruli are abnormal and others are normal, but only a part of the glomerulus is messed up.  Therefore, it is focal segmental.  B/c the renal bx with EM and immunofluorence did NOT show deposits, therefore it’s glomerulosclerosis. So, this is called focal segmental glomerulosclerosis.  This is the MC lesion in AIDs pts and IVDA’s.  Next to rapidly progressive crecentric glomerulonephritis, this is the next worse glomerular dz.  

Example: adult with pitting edema, over 3.5 gram per 24 yrs, fatty casts.  Do a bx and see not many ‘dots’ therefore not a proliferative dz. However  the BM is thicker. Dx?  Diffuse membranous glomerulonephritis = MCC nephrotic syndrome in adults.  This is subepithelial deposit.  Epimembranous spikes – spike like lesion on the outside of GBM seen with silver stain = diffuse membranous glomerulonephritis (only one that looks like that). Many things can cause this (drugs, cancer, nothing, infections); some the drugs include NSAIDs, Hep B, captopril (king of treatment of diabetic nephropathy and heart failure), malaria, syphilis, colon cancer (immune complex is anti-CEA Ab’s). Eventually leads to renal failure and can die unless you get a renal transplant

Type I and II Membranoproliferative Glomerulonephritis (ends in “-itis” therefore it is type III HPY – immune complex!)

1.  Type I has a relationship with Hep C – how do you remember? Membranous = Hep B (also remember the vasculitis – Polyarteritis Nodosa), Membranoproliferative = Hep C (also remember cryoglobinemia). So, type I is a subendothelial deposit that produces nephrotic syndrome.  

2.  Type II is less common, and has an Auto Ab against C3, called C3 nephritic factor.  It causes C3 convertase to become overactive and is constantly breaking complement down.  So, the lowest complement levels you will see is in type II glomerular nephritis – this is called dense deposit dz b/c the entire BM an immune complex.

tram tracks  – mesangial cell (structural component of the glomerular capillary) – the mesangial cell is extending itself between the BM and the endothelial cell, making it look like a tram track; so, it’s a mesangial process btwn the BM and endothelial cell – tram track Membranoproliferative dz

Glomerulus surrounded by proliferating cells that are parietal cells b/c not in the glomerulus, and has crescent shape, hence the name crescentic glomerular nephritis. This is the WORST glomerular nephritis to have b/c in 3 months; pts will go into acute renal failure and die unless pt is on dialysis.  Many dz’s have a crescentic glomerulonephritis, but the only one I need to know is Goodpastures; this is a NEPHRITIC dz; this dz has crescentic glomerulonephritis on bx (therefore a BAD dx).