Kidney implications of SARS-CoV2 infection in children

Abstract

Research indicates that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection can impact every organ, and the effects can range from asymptomatic to severe disease. Since it was first discovered in December 2019, our understanding has grown about its impact on kidney disease. In general, children have less severe disease than adults, and this tendency appears to extend to special pediatric kidney populations (e.g., chronic kidney disease and immunosuppressed patients with solid organ transplants or nephrotic syndrome). However, in a fraction of infected children, SARS-CoV2 causes an array of kidney manifestations, ranging from acute kidney injury to thrombotic microangiopathy, with potential implications for increased risk of morbidity and mortality. Additional considerations surround the propensity for clotting extracorporeal circuits in children with SARS-CoV2 infection that are receiving kidney replacement therapy. This review provides an update on our current understanding of SARS-CoV2 for pediatric nephrologists and highlights knowledge gaps to be addressed by future research during this ongoing pandemic, particularly the social disparities magnified during this period.

Keywords: Acute kidney injury; COVID-19; Chronic kidney disease; Dialysis; Epidemiology; Glomerular diseases; Pediatric nephrology; SARS-CoV2; Transplant.

Fig. 1

Timeline of key developments in the coronavirus-associated disease 2019 (COVID-19) pandemic, December 2019–May 2021. Top of timeline demonstrates key milestones of the COVID-19 pandemic cases and deaths worldwide as of May 2021. Bottom of timeline demonstrates key milestones in therapeutics for COVID-19 (yellow) and vaccine development based on emergency use authorization by the World Health Organization (WHO) (green). Emergency listing by the WHO is key to facilitating vaccine approval and uptake particularly in low- and middle-income countries and a requirement for vaccines to be included in the COVAX initiative [–93]

Fig. 2

Mechanism of SARS-CoV2 infection and potential therapeutic targets. SAR-CoV2 virion enters cells expressing the angiotensin-converting enzyme 2 (ACE2) receptor. The viral spike protein bears significant homology to ACE2, and the interaction with the receptor initiates a process, facilitated by the host transmembrane-bound serine protease 2 (TMPRSS2), resulting in virus to cell membrane fusion, endocytosis, and release of viral RNA-capsid into the cytoplasm. The RNA undergoes RNA-dependent RNA replication followed by translation, virion assembly, and virion release. Potential therapeutic targets are listed with example agents/therapies [2, 94]