Kidney allograft infarction associated with transplant renal artery stenosis in a COVID-19 kidney transplant recipient.

Kidney allograft infarction is rare, but an urgent condition that requires prompt intervention to avoid allograft loss. Renal artery thrombosis is the leading cause of infarction. Apart from traditional risk factors for thrombosis, emerging SARS-CoV-2 predisposes patients to thrombotic diseases both in arterial and venous vasculatures. We report a case of kidney transplant recipient with known transplant renal artery stenosis (TRAS) status post angioplasty with severe COVID-19, complicated by oliguric acute kidney injury requiring continuous renal replacement therapy (CRRT). She did not have a history of thromboembolic disease. The hospital course was complicated by new-onset atrial and ventricular fibrillation and cardiac arrest requiring multiple rounds of cardiopulmonary resuscitation. She had no signs of renal recovery, and an abdominal CT scan showed evidence of allograft infarcts. She underwent an allograft nephrectomy. Pathology revealed diffuse thrombotic microangiopathy involving glomeruli, arterioles, and arteries associated with diffuse cortical infarction with negative SARS-CoV-2 immunostain and in situ hybridization. This is the first case of kidney allograft infarct with a history of TRAS in a COVID-19 patient. Underlying TRAS and COVID-19-associated thrombosis in this patient are unique and likely play a key role in allograft infarction from arterial thrombosis. Recognizing risk factors and early therapy for allograft infarction may improve transplant outcomes.

Hyponatremia: A possible immuno-neuroendocrine interface with COVID-19 in a kidney transplant recipient.

There is fast-emerging, cumulative clinical data on coronavirus disease 2019 (COVID-19) in kidney transplant recipients. Although respiratory tract symptoms are often the initial presentation among kidney transplant recipients who contract COVID-19, other clinical features which may indicate underlying SARS-CoV-2-related inflammation, such as gastrointestinal symptoms, are not uncommon. Hyponatremia can develop and may reflect underlying inflammation. Interferon-6 is an important pro-inflammatory cytokine involved in the pathogenesis of severe COVID-19 complications and may play a role in the inappropriately higher secretion of antidiuretic hormone leading to hyponatremia. This pathway is the so-called immuno-neuroendocrine interface. Hyponatremia in COVID-19 has been reported in a few case series of non-kidney transplant patients and only one reported kidney transplant recipient. However, the clinical course and prognostic value of hyponatremia in this population are not described in detail. We report a kidney transplant recipient who was infected with COVID-19 and exhibited severe hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion. Hyponatremia is one of the clinical presentations of COVID-19, although less common, and may occur more frequently in kidney transplant recipients. Thus, the possible underlying immuno-neuroendocrine relationship related to the inflammatory process of COVID-19 leading to hyponatremia and its prognostic value are reviewed.