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- Transplant kidney with proteinuria
| 以下是引用清静无为在2009-7-7 16:46:00的发言：
nephrin、podocin、CD2AP（CD2相关蛋白）等是构成肾小球足突间裂孔隔膜（Slide Diaphragm，SD）核心蛋白，共同组成SD复合体，对于维持足细胞正常结构及肾小球屏障的完整功能起关键作用，主要见于肾病综合症、大量蛋白尿的实验研究。考虑到nephrin、podocin属于足细胞特异性蛋白（但在神经组织也可表达），因此建议做免疫组化染色试试。此外，还有一种最特异的足细胞标志蛋白podocalyxin（只存在于足细胞）。 我也很想知道结果。 |
| 以下是引用老者在2009-7-19 21:22:00的发言：
患者移植前肾脏病是什么？ 考虑细胞型FSGS。免疫荧光是什么？ |
移植前肾脏病 is polycystic kidney disease. The proteinuria developed suddenly right after switched from one drug to the other (I cannot remember what the drugs were). I did not perform immunofluorescence stains on transplant kidney.
Thank you very much for your taking part in discussion and comment.
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I wonder if there are any immunohistochemical markers to separate true crescent from pseudocrescent. I have tried some markers, such as cytokeratin 7, cytokeratin 20, EMA, high molecular weight cytokeratin, and WT-1. They are useless. Hale's colloid iron stain is not helpful either.
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本帖最后由 于 2009-06-19 22:51:00 编辑
This patient's primary kidney disease is polycystic kidney disease.
- Nadasdy T, Allen C, Zand MS. Zonal distribution of glomerular
collapse in renal allografts: possible role of vascular changes. Hum Pathol. 2002 Apr; 33(4):437-41.
- Meehan SM, Pascual M, Williams
WW, Tolkoff-Rubin N, Delmonico FL, Cosimi AB, Colvin RB. De novo
collapsing glomerulopathy in renal allografts. Transplantation. 1998 May
15; 65(9):1192-7.
Crescentic glomerulonephritis was my initial diagnosis. I immediately called the nephrologist. The nephrologist expressed serious doubt about my diagnosis because the patient had 13 grams of urine protein per 24 hour, but only mild elevation of creatinine. I realized these were pseudocrescents. My final diagnosis is collapsing glomerulopathy.
The morphologic hallmark is the cellular lesion (collapsing glomerular capillaries with hypertrophic and hyperplasticpodocytes). This type of pattern of renal injury is seen in native kidney and allograft kidney. Clinically, patients often have nephrotic syndrome and rapidly progressive renal failure. When it occurs in the allograft kidney, the proteinuria may not be as severe as in the native kidney, even absent, but it has a rapidly progressive course toward allograft loss. The pathogenesis of CG is unclear. The following is the references.
