Abstract: SA-PO139
Spontaneous Remission of Membranous Nephropathy in Hematopoietic Stem Cell Transplantation Patients
Session Information
- Onconephrology: Clinical and Research Advances - II
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Brauer Ornelas, Claudia Michelle, Memorial Sloan Kettering Cancer Center, New York, New York, United States
- Glezerman, Ilya, Memorial Sloan Kettering Cancer Center, New York, New York, United States
- Seshan, Surya V., Weill Cornell Medicine, New York, New York, United States
- Salvatore, Steven, Weill Cornell Medicine, New York, New York, United States
Introduction
Secondary membranous nephropathy (MN) is a known complication of hematopoietic stem cell transplantation (HSCT) and is considered a form of the graft versus host disease (GVHD). It usually presents 2 months after discontinuation of GVHD immunosuppression prophylaxis. Patients with secondary MN are treated with immunosuppression. We present two cases of spontaneous remission of the MN in HSCT patients.
Case Description
Case 1.
54-year-old male with history of diffuse large B-Cell lymphoma and HSCT (day +1007) presented with edema. Patient had a history of skin GVHD. He completed the course of tacrolimus for GVHD prophylaxis. Patient developed lower extremity swelling over one month. The vital signs and exam were unremarkable except to lower extremity edema. Serum creatinine was 1.1 (0.6-1.3) mg/dl, urinary protein to creatinine ratio (UPCR) was 9.2. Phospholipase A2 receptor (PLA2R) antibody was negative. Patient was started on an ACE inhibitor and a diuretic and underwent a kidney biopsy. Biopsy revealed diffuse membranous nephropathy with negative PLA2R staining. Proteinuria gradually improved and UPCR was 0.1 approximately 33 months after the kidney biopsy.
Case 2.
71-year-old male with history of Crohn’s disease, myelodysplastic syndrome and HSCT (day+649) presents to renal clinic with edema. Patient was on tacrolimus taper with currently undetectable trough level for GVHD prophylaxis. The vital signs and physical exam were unremarkable except for lower extremity edema. Serum creatinine level was 1.0 mg/dL, UPC was 5.75. Anti PLA2R antibody was negative. Patient underwent a kidney biopsy which revealed diffuse membranous nephropathy with negative PLA2R staining. Patient was managed conservatively. Patient's proteinuria gradually improved and UPC was 0.8 approximately 21 months after the biopsy.
Discussion
In secondary MN associated with HSCT the treatment is geared to address presumed underlying GVHD. Our experience illustrates that conservative management may be an option in selective cases. It is also possible that our patients had PLA2R negative MN. This also highlights the need for wider access to other markers of MN to distinguish between PLA2R negative primary MN such as Thrombospondin type-1 domain-containing 7A and secondary forms of MN for example Protocadherin 7 recently linked to GVHD associated MN.