169 Collapsing Glomerulopathy In Renal Allografts: A ...

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Nov 2, 2012 - Collapsing glomerulopathy (CG) can be seen in native and, rarely, allograft kidneys. It is characterized by collapsing glomerular capillaries with ...
Surgical Pathology (Gastrointestinal, Genitourinary, Liver, Pancreas, Renal, Bone & Soft Tissue, Cardiovascular)/Friday Session 2, November 2, 2012 

169 Collapsing Glomerulopathy In Renal Allografts: A Prognostic Pattern Indicative of Accelerated Allograft Loss Umer Sheikh, MD, MBBS1, Awais Zaka, MD2, Muhammad Zulfiqar, Hong Qu, MD3 1 Detroit, MI, 2University of Buffalo (Sisters of Charity Hospital), 3St John Hospital & Medical Center, Detroit

Category: Surgical Pathology

©American Society for Clinical Pathology

 

 

Am J Clin Pathol 2012;138:A169

 

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Collapsing glomerulopathy (CG) can be seen in native and, rarely, allograft kidneys. It is characterized by collapsing glomerular capillaries with hypertrophic and hyperplastic podocytes. It usually occurs idiopathically or rarely as a secondary process associated with HIV infection, drugs, vascular and autoimmune diseases, malignancy, and genetic disorders. We identified 7 cases of de novo CG between 2005 and 2012. The patients were 28 to 69 years old and sought care 1 to 16 years after transplantation. Serum creatinine levels ranged from 1.60 to 7.00 mg/dL. Two patients had nephrotic-range proteinuria (3.0-4.2 g/d), whereas all others had only modest or insignificant proteinuria. All patients and donors were negative for the HIV. Renal biopsies showed diffuse or focal, global or segmental GBM collapse with cellular lesions in a few glomeruli. Two cases showed diffuse interstitial neutrophilic infiltrates, whereas all of them exhibited lymphoplasmacytic infiltrates. Immunoflouresecne showed nonspecific IgM and C3 in sclerotic areas. EM showed total effacement of podocytic foot processes with microvillous transformation. Immunohistochemical stains were negative for C4d in peritubular capillaries (highly suggestive of acute antibody-mediated rejection) and polyoma BK nephritis. All cases of CG demonstrate moderate to severe chronicity in interstitial, tubular, and vascular compartments on diagnosis. The morphologic pattern of CG in renal allografts cannot be defined by the mere presence of collapsing glomeruli. Instead, CG represents a pattern of glomerular injury that may morphologically mimic crescent formation. The pattern of CG in allografts is not always associated with severe proteinuria. Progressive allograft dysfunction occurred during an average of 1 to 9 months after diagnosis, culminating in return to dialysis in all patients. These findings emphasize the prognostic significance of CG in renal allografts and may not represent the same disease process as in native kidneys.