Kanodia K V, Vanikar A V, Nigam L K, Patel R D, Suthar K S, Patel H V, Trivedi H L
Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, G. R. Doshi and K. M. Mehta Institute of Kidney Diseases and Research Centre, Dr. H. L. Trivedi Institute of Transplantation Sciences, Civil Hospital Campus, Asarwa, Ahmedabad, Gujarat, India.
Department of Regenerative Medicine and Cell Therapy, G. R. Doshi and K. M. Mehta Institute of Kidney Diseases and Research Centre, Dr. H. L. Trivedi Institute of Transplantation Sciences, Civil Hospital Campus, Asarwa, Ahmedabad, Gujarat, India.
Indian J Nephrol. 2017 Sep-Oct;27(5):342-346. doi: 10.4103/ijn.IJN_287_16.
Collapsing glomerulopathy (CG) is a well-recognized distinct morphological pattern of proliferative parenchymal injury leading to rapid graft failure. We conducted a single-center retrospective study to evaluate the prevalence, clinicopathological features, and prognosis of CG in renal transplant recepient. We analyzed 2518 renal allograft biopsies performed from 2007 to 2015 and correlated their clinicopathological features. The prevalence of CG was 0.83% (21 out of 2518) of allograft biopsies with a higher prevalence of 1.4% during the period from 2012 to 2015. Out of 21 patients, 18 (85.71%) patients had undergone live donor and 3 (14.28%) patients had undergone deceased donor renal transplant. Hypertension was observed in 3 (14.28%) patients. The mean duration of diagnosis for CG was 1.85 ± 1.91 years. Urinalysis revealed microhematuria in 5 (23.8%) patients. The mean 24 h urinary protein excretion was 4.77 ± 5.3 g and serum creatinine was 2.12 ± 1.5 mg/dl. The predominant native kidney diseases in recipients were chronic glomerulonephritis of unknown etiology in 12 (57.14%) patients and hypertensive nephropathy in 3 (14.28%) patients. CG was associated with rejection in 9 (42.85%), calcineurin-inhibitor toxicity in 2 (9.5%), and BK virus nephropathy in 1 patient. All patients received standard triple immunosuppression. Eleven (52.38%) patients developed graft failure over a mean period of 2.2 ± 1.7 years and 6 (28.57%) patients recovered with stable graft function. CG can coexist with viral infection, drug toxicity, rejection, microvascular injury, etc. CG usually presents with moderate to severe proteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients.
塌陷性肾小球病（CG）是一种公认的独特的增殖性实质损伤形态学模式，可导致移植肾迅速失功。我们进行了一项单中心回顾性研究，以评估肾移植受者中CG的患病率、临床病理特征及预后。我们分析了2007年至2015年期间进行的2518例移植肾活检，并将其临床病理特征进行关联分析。CG在所有移植肾活检中的患病率为0.83%（2518例中有21例），在2012年至2015年期间患病率较高，为1.4%。21例患者中，18例（85.71%）接受了活体供肾移植，3例（14.28%）接受了尸体供肾移植。3例（14.28%）患者出现高血压。CG的平均诊断时间为1.85±1.91年。尿液分析显示5例（23.8%）患者有镜下血尿。24小时尿蛋白排泄平均为4.77±5.3g，血清肌酐为2.12±1.5mg/dl。受者中主要的原发病为病因不明的慢性肾小球肾炎12例（57.14%），高血压肾病3例（14.28%）。9例（42.85%）CG与排斥反应相关，2例（9.5%）与钙调神经磷酸酶抑制剂毒性相关，1例与BK病毒肾病相关。所有患者均接受标准的三联免疫抑制治疗。11例（52.38%）患者在平均2.2±1.7年的时间内发生移植肾失功，6例（28.57%）患者移植肾功能稳定恢复。CG可与病毒感染、药物毒性、排斥反应、微血管损伤等并存。CG通常表现为中度至重度蛋白尿，在大多数患者中可能导致移植肾功能迅速减退及随后的移植肾失功。
