Abstract: PO1411
Renal-Limited Lupus Nephritis Misdiagnosed as Advanced CKD: Addressing the Need for Increasing Renal Biopsies in the Community Setting
Session Information
- Glomerular Diseases: Fibrosis and Extracellular Matrix
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix
Authors
- Chauhan, Rajeev, Renal Associates LLC., Columbus, Georgia, United States
- Kalia, Megha, Augusta University, Augusta, Georgia, United States
- Hazim, Katrina, Augusta University, Augusta, Georgia, United States
Introduction
“Full-house” nephropathy is characteristic of lupus nephritis, but may be seen in patients without other evidence of SLE. Patient was presumed to have acute renal failure prior to renal biopsy and was placed on dialysis for chronic management of ESRD. Despite no extrarenal or clinical manifestations of SLE, renal biopsy revealed histopathology consistent with lupus nephritis.
Case Description
A 61-year old African American female presented to an outside hospital with complaints of mild abdominal pain, nausea, emesis, and diarrhea. Family history was positive for autoimmune disorders, including SLE and Sjogren’s Syndrome. Initial lab work revealed creatinine 8.1 mg/dL, eGFR 7 mL/min, BUN 117 mg/dL, proteinuria, and hyperkalemia with potassium 5.2. Renal biopsy revealed collapsing glomerulopathy with “full-house” immune complex deposition without active glomerular lesions commonly seen with lupus nephritis. Evaluation was positive for anti-nuclear antibody (ANA), but anti-double stranded DNA (anti-dsDNA), serum immunofixation (IFE), hepatitis screen and HIV screen were negative. She was treated for lupus nephritis with a three-day course of Solu-medrol and continued on home peritoneal dialysis and oral prednisone. Renal function recovered with creatinine of 0.64 mg/dL and eGFR 116 mL/min/ leading to discontinuation of dialysis.
Discussion
Renal biopsy revealed collapsing glomerulopathy with “full-house” immune complex deposition without active glomerular lesions. Lupus nephritis is an immune mediated glomerulonephritis with characteristic histological pattern including “full house immunofluorescence” with glomerular deposits that stain for IgG with co-deposits of IgA, IgM, C3 and C1q. “Full-house” immune complex deposits are commonly seen in lupus nephritis, but are not pathognomonic. Nine adult cases of limited renal disease in absence of other evidence of SLE have been reported. Although there are no guidelines on treatment of lupus-like nephritis, all reported patients were treated with regimens of immunosuppressive agents and steroids. To date our patient has not developed additional manifestations of SLE and her renal function remains normal without signs of injury. We advocate for a lower threshold for performing renal biopsies as they can provide valuable information regarding disease diagnosis and treatment.