Acute Kidney Injury in a COVID-19 Lung Transplant Recipient

Dear Editor,

A 63-year-old man was referred to our hospital for extracorporeal membrane oxygenation (ECMO) following a severe COVID-19 infection 4 months back. He was put on V-V ECMO and continued on the same for a month. He was evaluated and found to have extensive pulmonary fibrosis. He was considered for a lung transplantation and after appropriate medical evaluation and repeated negative severe acute respiratory syndrome coronavirus 2 (SARS-COV 2) reverse real-time polymerase chain reaction tests, he underwent a deceased donor transplantation 2 months back. He had no comorbidities, and pretransplant evaluation did not reveal any significant cardiac, liver or renal abnormalities. His creatine phosphokinase (CPK) at the time of transplantation was checked and was found to be normal. The posttransplant course was uneventful and he was off ventilatory support from the 14^th posttransplant day. Posttransplant serum creatinine was 0.8 mg/dl, and his urinalysis did not reveal any abnormality. His initial tacrolimus levels were on the lower side (8.7 ng/ml), and accordingly, his tacrolimus dose was increased. The repeat level was 11.9 ng/ml (target 12–15 ng/ml in first 6 months) 6 weeks’ posttransplantation, his urine output started to decrease and his creatinine started to rise. A nephrology consultation was sought and evaluation revealed the presence of new-onset proteinuria. There was no evidence of urinary tract infection. Because of worsening renal functions (serum creatinine – 2.1 mg/dl and blood urea – 210 mg/dl) and reducing urine output, he was advised dialysis. He did not appear to be dehydrated, and his inferior vena cava diameter was 1.8 cm and not collapsible. The high urea was considered because of his steroids (20 mg/day and protein-rich parenteral nutrition. A provisional diagnosis of acute tubular necrosis (ATN) with the underlying glomerular disease was considered. As there was no improvement in his renal functions, he underwent a renal biopsy.

His histopathological examination of the biopsy showed normal viable glomeruli with scattered tubules with denuded lining. There was no interstitial inflammation and tubular atrophy [Figure 1a]. Some tubules showed casts which stained positive for myoglobin [Figure 1b]. The electron microscopy showed podocyte loss (>30%) and significant subendothelial basement membrane rarefaction [Figure 1c]. No new therapy was advised as he was on triple immunosuppression, which was felt to be appropriate for the glomerular pathology. After another 2 weeks of dialysis, he made slow renal recovery. He was discharged off dialysis after another week. His predischarge creatinine was 0.8 mg/dl.

Figure 1: Histopathological examination of the biopsy show features of acute tubular necrosis (a). Myoglobin tubular casts were noted in immunohistochemistry (b). Electron microscopy revealed podocyte injury with significant basement rarefaction (c)

Acute kidney injury (AKI) is common post lung transplantation.^[1] It is anticipated that the incidence of AKI will be a major concern in severe COVID-19-infected patients who undergo lung transplantation as SARS-COV-2 infection has a propensity to involve kidneys.^[2] AKI, in our case, appears to be multifactorial. Our patient had underlying ATN, which we believe was because of the hemodynamic instability secondary to an emergency transplant in a critically sick individual. What was unusual in our case was the co-existence of myoglobin casts and the electron microscopic evidence of basement membrane pathology. Rhabdomyolysis is known to happen in patients with COVID-19 infection^[3] and occasionally in patients on ECMO. As the CPK in the patient was consistently normal from the time of transplantation, it is speculated that the myoglobin casts depict past injury secondary to COVID-19 infection. The third component was the evidence of glomerular injury, which cannot be explained by ATN. Recent evidence also suggests that glomerular disease develops 4–6 weeks following COVID-19 infection.^[4,5] The glomerular involvement in our patient is also a sequelae of COVID-19 infection pretransplant. The most common finding in COVID-19-induced glomerular disease is focal segmental glomerulosclerosis (FSGS).^[6] Our patient had podocytopathy, but the pathology was not consistent with FSGS. We believe the biopsy manifestations of underlying glomerular involvement seem to have been modified by posttransplant immunosuppression. Our case highlights unique pathomechanisms of AKI in a COVID-19 lung transplant recipient.

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