Abstract: TH-PO207

Cytomegalovirus-Associated Collapsing Glomerulopathy and Tubulointerstitial Nephritis in an African American Patient with T-Cell Lymphoma

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Hernandez- Montalvo, Edgar, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Giusti, Sixto G., Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Fogo, Agnes B., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Paueksakon, Paisit, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Velez, Juan Carlos Q., Ochsner Clinic Foundation, New Orleans, Louisiana, United States
Background

Collapsing glomerulopathy (CG) may occur in association with human immunodeficiency virus (HIV) and parvovirus B19 (PVB19) infections. However, published reports of CG associated with cytomegalovirus (CMV) infection are sparse.

Methods

We describe a case of a 69 year-old African American woman with T-cell lymphoma who presented with 1-week history of fever, anorexia and delirium. She was on chemotherapy with alemtuzumab. On arrival, blood pressure was 110/64 mmHg, temperature 38.0 oC. Physical examination was remarkable for 2+ pitting leg edema. She was pancytopenic with serum creatinine 2.6 mg/dL. Urinalysis revealed 3+ protein and 3+ blood without red blood cell (RBC) casts or dysmorphic RBCs. The urine protein-to-creatinine ratio was 24.8 g/g. Anti-nuclear, hepatitis C, HIV and PVB19 antibodies, polymerase chain reaction (PCR) for HIV RNA, complement levels, hepatitis B antigen and antibodies were all negative or normal. Acute CMV infection was subsequently diagnosed upon detection of serum CMV DNA PCR of 3,450,814 copies/mL. Renal ultrasound revealed normal sized kidneys with hyperechoic parenchymal echotexture. Her kidney function deteriorated and hemodialysis was initiated on hospital day 10. A kidney biopsy was performed. The biopsy showed 10-20% interstitial fibrosis, tubular dilatation, acute tubular injury and multifocal lymphocytic interstitial infiltrates with positive tubular CMV immunostaining. Glomeruli (2 out of 3) showed collapse of the glomerular tuft, overlying visceral epithelial cell hyperplasia and diffuse foot process effacement without immune complexes, characteristic of CG. Despite treatment with valgancyclovir, the patient progressed to require permanent hemodialysis.

Conclusion

Although CMV immunostaining was negative in glomeruli, we suspect that the glomerular lesion was induced by the viral infection. The patient described herein, as well as those described in the only 3 published cases of CMV-associated CG in the literature, are individuals of African descent. Therefore, we speculate that an interaction between CMV and apolipoprotein L1 risk alleles could trigger cases of CMV-associated CG.