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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2011  |  Volume : 22  |  Issue : 5  |  Page : 1035-1036
De novo membranous nephropathy after hematopoietic stem cell transplantation


Department of Nephrology, All India Institute of Medical Sciences, Delhi, India

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Date of Web Publication6-Sep-2011
 

How to cite this article:
Gupta A, Lal C, Bhowmik D. De novo membranous nephropathy after hematopoietic stem cell transplantation. Saudi J Kidney Dis Transpl 2011;22:1035-6

How to cite this URL:
Gupta A, Lal C, Bhowmik D. De novo membranous nephropathy after hematopoietic stem cell transplantation. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2020 Jul 12];22:1035-6. Available from: http://www.sjkdt.org/text.asp?2011/22/5/1035/84562
To the Editor,

The emergence of hematopoietic stem cell transplantation (HSCT) for malignant and even benign hematopoietic indications has resulted in the increasing recognition of renal complications following this procedure. Amongst the lesser sought complications is nephrotic syndrome. Case reports describe various pathologic glomerular changes after HSCT, but majority are related to graft-versus-host disease (GVHD). We herein report a relatively unusual presentation of nephrotic syndrome in a setting of post HSCT.

A 26-year-old male, who underwent allogenic HSCT three years back for aplastic anemia, came with progressive swelling all over the body for one month. The patient was not on any immunosuppressive drug for last one year. Investigations revealed normal renal and liver functions. Hemoglobin was 14.4 g/dL, leukocyte count 7,700/mm³, platelet count 235,000/mm³, and proteinuria was 6.8 g/d. There was no evidence of GVHD. Secondary causes of nephrotic syndrome were excluded. A renal biopsy was performed and was suggestive of membranous nephropathy (MN). The patient was started on ramipril 10 mg/d and telmisartan 40 mg/d, and antihypertensives were titrated to keep the blood pressure around 110/70 mmHg. Proteinuria decreased to 1.6 g/d at 2 months and was 560 mg/d at the end of 6 months. He attained complete remission at 18 months.

HSCT-associated renal injury may be related to a combination of factors including chemotherapy, radiation, infection, immunosuppressive agents, ischemia, and GVHD. Case reports in the literature have described variable glomerular histology, comprising mainly MN in almost two-thirds and minimal change disease (MCD) in nearly one-quarter of patients. Review of the literature reveals a close temporal relationship between the development of nephrotic syndrome shortly after cessation of immunosuppression and the diagnosis of chronic GVHD. [1]

Furthermore, there is a debate on entity of post HSCT MN without acute or chronic GVHD. Historically, MN is thought to be a renal manifestation of GVHD. It has been documented that history of acute GVHD is present in 78% and chronic GVHD occurred in 88% cases of MN developing post-allogenic HSCT. [1] Our patient was, however, characterized by the presentation of MN without any history or manifestations of GVHD. Thus, there is a possibility that de novo MN might have occurred in our case. This may result from host-versus-graft reaction. Donor-specific chimeric mesangial cells, tubular cells and endothelial cells have been previously detected in renal biopsies performed in patients who had undergone HSCT. Similarly, the hematopoietic origin of podocytes has been also suggested. Thus, there could be some intra-glomerular chimeric cells leading to alloimmunization and resultant MN. [2]

The treatment of post HSCT MN is with mainly steroids and cyclosporine/cyclophosphamide, aimed at the control of acute manifestations of chronic GVHD. Recently, rituximab is being used in post HSCT MN, suggesting a pathogenic role of CD20-positive cells, possibly as antigen presenting cell. [3] However, our case responded well to a combination of angiotensin converting enzyme inhibitor (ramipril 10 mg/d) and angiotensin receptor blocker (telmisartan 40 mg/d). Fortunately, we did not require any immunosuppressive agent. Earlier, Osugi et al have shown that angiotensin-converting enzyme inhibitors (ACEI) and angiotensin-receptor blockers (ARB) together can be useful in treating even immunosuppressive treatment-resistant nephrotic syndrome after allogenic HSCT. [4]

The patho-physiology behind this case needs further elucidation and clinical studies to confirm whether post HSCT MN is a de novo entity as a manifestation of chimerism or a coincidental phenomenon. Also, the knowledge about pathophysiologic basis of this entity shall help in guiding management issues and preventing irrational use of immunosuppressive agents as a blanket therapy in all such cases.

 
   References Top

1.Brukamp K, Doyle AM, Bloom RD, Bunin N, Tomaszewski JE, Cizman B. Nephrotic syndrome after haematopoietic cell transplantation: do glomerular lesions represent renal graft-versus-host disease? Clin J Am Soc Nephrol 2006;1:685-94.  Back to cited text no. 1
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2.Terrier B, Delmas Y, Hummel A, et al. Post-allogeneic haematopoietic stem cell transplantation membranous nephropathy: clinical presentation, outcome and pathogenic aspects. Nephrol Dial Transplant 2007;22:1369-76.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Vischini G, Cudillo L, Ferrannini M, Di Daniele N, Cerretti R, Arcese W. Rituximab in post allogeneic haematopoietic stem cell transplantation membranous nephropathy: A case report. J Nephrol 2009;22:160-3.  Back to cited text no. 3
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4.Osugi Y, Yamada H, Hosoi G, et al. Treatment with candesartan combined with angiotensinconverting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem cell transplantation. Int J Hematol 2006;83:454-8.  Back to cited text no. 4
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Correspondence Address:
Ankur Gupta
Department of Nephrology, All India Institute of Medical Sciences, Delhi
India
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PMID: 21912044

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