Anubha Mutneja
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Anubha Mutneja has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
A. Vijayan
Renal Division, Washington University in St Louis, St Louis, Missouri, United States
1 shared publication- Helen Liapis
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri; Renal Pathology, Arkana Laboratories, Little Rock, Arkansas
1 shared publication - L. Nicholas Cossey
Renal Pathology Division, Arkana Laboratories, 10810 Executive Center Dr., Suite 100, Little Rock, AR 72211, United States
1 shared publication L. Saling
Mallinckrodt Institute of Radiology, Washington University in St Louis, St Louis, Missouri, United States
1 shared publicationM. Yano
Mallinckrodt Institute of Radiology, Washington University in St Louis, St Louis, Missouri, United States
1 shared publication- Ying Maggie Chen
Division of Nephrology, Department of Internal Medicine
1 shared publication
Latest Publications
- 1 November 2017
- Published by Elsevier in Transplantation Proceedings
- Vol. 49 (9) , 2007-2010
Financial Impact of Incidental Radiologic Findings During Living Kidney Donor Evaluation
- 1 November 2017
- Published by Elsevier in Transplantation Proceedings
- Vol. 49 (9) , 2007-2010
Financial Impact of Incidental Radiologic Findings During Living Kidney Donor Evaluation
- Open Access
- 10 February 2017
- Published by Springer Nature in BMC Nephrology
- Vol. 18 (1) , 1-5
A rare case of renal thrombotic microangiopathy associated with Castleman’s disease
Castleman’s disease (CD) is an uncommon, heterogeneous lympho-proliferative disorder leading to high circulating levels of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF). Renal involvement has been only described in a limited number of small studies. Herein, we report a rare case of renal thrombotic microangiopathy (TMA) associated with CD and investigate the podocyte expression of VEGF in the renal biopsy prior to initiation of treatment. An 18-year-old male presented with fever, diarrhea, diffuse lymphadenopathy, ascites and acute kidney injury. Laboratory tests for hemolytic uremic syndrome and thrombotic thrombocytopenic purpura were negative. The kidney biopsy showed TMA. An excisional lymph node biopsy was consistent with CD, plasma cell variant. Immunofluorescence staining showed suppressed podocyte VEGF expression. Chemotherapy that inhibits production of inflammatory mediators including IL-6 and VEGF led to complete recovery of renal function. Our case illustrates a rare renal histological feature of CD. IL-6 and VEGF are postulated to suppress glomerular VEGF expression, thereby causing renal TMA. Therapy directed against these inflammatory mediators may have important therapeutic implications.
- 10 February 2017
- Published by Springer Nature in BMC Nephrology
- Vol. 18 (1) , 1-5
Open AccessA rare case of renal thrombotic microangiopathy associated with Castleman’s disease
Castleman’s disease (CD) is an uncommon, heterogeneous lympho-proliferative disorder leading to high circulating levels of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF). Renal involvement has been only described in a limited number of small studies. Herein, we report a rare case of renal thrombotic microangiopathy (TMA) associated with CD and investigate the podocyte expression of VEGF in the renal biopsy prior to initiation of treatment. An 18-year-old male presented with fever, diarrhea, diffuse lymphadenopathy, ascites and acute kidney injury. Laboratory tests for hemolytic uremic syndrome and thrombotic thrombocytopenic purpura were negative. The kidney biopsy showed TMA. An excisional lymph node biopsy was consistent with CD, plasma cell variant. Immunofluorescence staining showed suppressed podocyte VEGF expression. Chemotherapy that inhibits production of inflammatory mediators including IL-6 and VEGF led to complete recovery of renal function. Our case illustrates a rare renal histological feature of CD. IL-6 and VEGF are postulated to suppress glomerular VEGF expression, thereby causing renal TMA. Therapy directed against these inflammatory mediators may have important therapeutic implications.