A Case of Autoimmune Hemolytic Anemia Following COVID-19 Infection Accompanied by Acute Tubulointerstitial Nephritis in a Kidney Transplant Recipient

Abstract

Background

Acute tubular injury is one of the main causes of acute tubular injury (acute kidney injury ) in patients with COVID-19 infection. Autoimmune hemolytic anemia (AIHA) is also one of the autoimmune complications of COVID-19. However, AIHA accompanied by acute tubulointerstitial nephritis (ATIN) caused by SARS-CoV-2 is rarely reported. Here, we report a kidney transplant recipient who underwent graftectomy owing to ATIN accompanied by AIHA, possibly exacerbated by COVID-19 infection.

Case Presentation

A 32-year-old male renal allograft recipient owing to immunoglobulin A nephropathy visited the emergency department owing to dyspnea and general weakness. Three weeks earlier, the patient had been transplanted with deceased-donor kidney with full HLA-A, -B, -DR match, and had been on tacrolimus, prednisolone, and mycophenolate since then. At the time of the visit, laboratory findings revealed hemoglobin of 2.4 g/dL, reticulocyte of 21.7%, total bilirubin of 1.9 mg/dL, direct bilirubin of 0.3 mg/dL, lactate dehydrogenase of 946 U/L, haptoglobin of <10 mg/dL, and severe red cell agglutination on peripheral blood smear, which suggested AIHA. In addition, his SARS-CoV-2 real-time polymerase chain reaction test was positive. During steroid treatment for AIHA, a sudden decrease in urine volume, estimated glomerular filtration rate (from 64.9 to 35.1 mL/min/1.73 m²) and increase of creatinine (from 1.42 to 2.36 mg/dL) indicated renal function deterioration, so steroid was increased to 500 mg. On the third day of renal function deterioration, dialysis was started owing to anuria and fluid retention. On renal biopsy, C4d was absent; however, ATIN with eosinophilic infiltration was observed. On renal ultrasound examination, a severely enlarged kidney with edema was observed. At the same time, the patient had a high fever with increased C-reactive protein and procalcitonin. Graftectomy was performed to prevent secondary infection. The postgraftectomy renal biopsy showed renal parenchymal and hilar inflammatory change, endotheliitis, and lymphocytic infiltration of peripheral nerve fibers. After graftectomy, dialysis was maintained and AIHA had ameliorated.

Conclusion

The patient had to have his allografted kidney removed owing to ATIN possibly caused by COVID-19 infection. Acute kidney injury caused by SARS-CoV-2 can be either by direct viral infection or as consequence of immunological response. The exact immunological mechanism of AIHA secondary to COVID-19 infection remains to be elucidated.