Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 2564 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
CASE REPORT Table of Contents   
Year : 2008  |  Volume : 19  |  Issue : 5  |  Page : 793-795
De Novo Collapsing Glomerulopathy in a Renal Allograft Recipient


1 Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr. H L Trivedi Institute of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad, Gujarat, India
2 Department of Nephrology and Clinical Transplantation, Dr. H L Trivedi Institute of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad, Gujarat, India

Click here for correspondence address and email
 

   Abstract 

Collapsing glomerulopathy (CG), characterized histologically by segmental/global glomerular capillary collapse, podocyte hypertrophy and hypercellularity and tubulo-interstitial injury; is characterized clinically by massive proteinuria and rapid progressive renal failure. CG is known to recur in renal allograft and rarely de novo. We report de novo CG 3 years post­transplant in a patient who received renal allograft from haplo-identical type donor.

How to cite this article:
Kanodia K V, Vanikar A V, Patel R D, Shah P R, Nagpal M, Firoz A, Falodia J, Kasat P, Trivedi H L. De Novo Collapsing Glomerulopathy in a Renal Allograft Recipient. Saudi J Kidney Dis Transpl 2008;19:793-5

How to cite this URL:
Kanodia K V, Vanikar A V, Patel R D, Shah P R, Nagpal M, Firoz A, Falodia J, Kasat P, Trivedi H L. De Novo Collapsing Glomerulopathy in a Renal Allograft Recipient. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Sep 20];19:793-5. Available from: http://www.sjkdt.org/text.asp?2008/19/5/793/42462

   Introduction Top


Collapsing glomerulopathy (CG) is characte­rized histologically by segmental/global glomerular capillary collapse, podocyte hypertrophy and hypercellularity, and tubulo-interstitial in­jury. It is characterized clinically by massive proteinuria and rapid progressive renal failure. CG is regarded as a distinctive variant of focal segmental glomerulosclerosis (FSGS). [1] CG is known to recur in renal allograft and rarely de novo. [2]

A morphologically similar lesion has been described in human immuno deficiency virus (HIV) associated nephrotic syndrome. [3] The pathogenesis of CG is unknown.

We report de novo CG 3 years post-transplant in a patient who received renal allograft from haploidentical donor.


   Case Report Top


A 28-year-old man underwent renal trans­plantation for hypertension induced end-stage renal disease in our institute on 26 th February 2003, with haploidentical kidney from his mother. He maintained creatinine around 1.6 mg/dL till April 2006 when a gradual rise in s. creatinine to 3.12 mg/dL was noticed over 4 months. He was maintained on standard triple drug immunosuppression of prednisolone 10 mg/day, azathiporine 100 mg/day, and cyclos­porine 2 mg/kg/day.

The laboratory investigations at time of biop­sy revealed urine albumin: 100 mg/day, 24­hour urinary protein: 3.27 gm, urine microscopy: 4–5 pus cells and 5-6 RBCs/ high power field, hemoglobin: 14.2 gm/dL, total WBC count: 8,200/mm 3 , and blood urea- 121 mg/dL. Hepa­titis HBs Ag was positive, and HIV, Hepatitis C Virus antibodies were non-reactive.

Renal biopsy adequate revealed 9 glomeruli, two medium caliber arteries, few small caliber arteries, and surrounding tubules. There was visceral cell hyperplasia with collapsed capil­lary tufts in 40 % of glomeruli and microcystic changes in tubules, [Figure 1],[Figure 2]. The remai­ning glomeruli revealed uniform mild mesan­gial matrix accentuation with segmental hyper­cellularity. Capillary lumina were fairly open and lined by mildly thickened membranes. Bowman capsule was thickened and revealed periglomerular fibrosis around one glomerulus. Tubules were moderately degenerated. Inters­titium was moderately prominent for focal fibrosis and mononuclear cellular infiltration (in 30 % of parenchyma). Small caliber arteries revealed segmental subintimal hyalinosis. No endothelialitis was observed. Immunofluore­scence studies were negative for all immune deposits including C4d. Therefore, the patient was diag-nosed as a case of de novo CG, and currently is on the waiting list for deceased donor transplantation program.


   Discussion Top


Our patient with de novo CG presented at 41 months post-transplant with marked proteinu­ria and rapidly progressive allograft impair­ment. Hyaline arteriolosclerosis and interstitial fibrosis could be attributed to chronic cyclos­porine toxicity. Arterial and arteriolar narrow­wing besides glomerular collapse may be attri­buted to ischemia with cyclosporine toxicity. Meehan et al reported five HIV negative patients with de novo CG at 6–25 months post­transplant. [4] Immunofluorescence study in these cases revealed segmental mesangial deposits of IgM and C3. Electron microscopy illus­trated podocyte microvillous changes and seg­mental effacement of foot processes. However, we did not observe any immune deposits.

We conclude that De novo CG can occur rarely in a renal allograft with presentation of rapidly progressive graft failure. The patho­genesis of CG is not known. This report may encourage researchers for finding out its cause in order to improve graft survival.

 
   References Top

1.Detwiler RK, Falk R, Hogan S, Jennette JC. Collapsing glomerulopathy: A clinically and pathologically distinct variant of focal seg­mental glomerulosclerosis. Kidney Int 1994; 45:1416-24.  Back to cited text no. 1    
2.Detwiler RK, Falk R, Hogan S, Jennette JC. Collapsing glomerulopathy in renal transplant patients: Recurrence and de novo occurrence. JAm Soc Nephrol 1996;7:1331A.  Back to cited text no. 2    
3.D'Agati VV, Suh JI, Carbon L, Cheng JT, Appel G. Pathology of HIV associated nephro­pathy: a detailed morphologic and comparative study. Kidney Int 1989;35(6):1358-70.  Back to cited text no. 3    
4.Meehan SM, Pascual M, William W, Tolkoff, Rubin N. De novo collapsing glomerulopathy in renal allograft. Transplantation 1998;65(9): 1192-7.  Back to cited text no. 4    

Top
Correspondence Address:
K V Kanodia
Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr. H L Trivedi Institute of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad-380016, Gujarat
India
Login to access the Email id


PMID: 18711298

Rights and Permissions


    Figures

  [Figure 1], [Figure 2]

This article has been cited by
1 Collapsing glomerulopathy in renal allograft biopsies: A study of nine cases
Gupta, R. and Sharma, A. and Agarwal, S.K. and Dinda, A.K.
Indian Journal of Nephrology. 2011; 21(1): 10-13
[Pubmed]



 

Top
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
    Introduction
    Case Report
    Discussion
    References
    Article Figures
 

 Article Access Statistics
    Viewed2423    
    Printed70    
    Emailed0    
    PDF Downloaded387    
    Comments [Add]    
    Cited by others 1    

Recommend this journal