Acute kidney injury (AKI) is an important factor affecting the outcome of hospitalized patients under any disease condition. While a lot has been said and studied about pulmonary manifestations of COVID-19 and multisystem inflammatory syndrome in children, this review focuses on its renal manifestations in children with and its complications. For the collection of data, the patient intervention control outcome model was applied to determine all eligible studies. The data was extracted using PubMed/Medline, Embase, and Google Scholar databases using a combination of keywords (AKI, renal failure, kidney disease, children, pediatric, covid-19, SARS COv2). Studies were reviewed after the exclusion of duplicates. The incidence of renal involvement in COVID 19 is up to 10–15%, which is higher than SARS. Both direct and indirect pathogenic mechanisms operate in patients with COVID 19 leading to varied manifestations. While AKI remains the most common manifestation in children admitted to intensive care units, other manifestations like, proteinuria, hematuria, rhabdomyolysis, and thrombotic microangiopathy have also been described in the literature. The children already on immunosuppression due to transplant or immune-mediated renal disorders do not seem to have more severe illness than those without it. The principles of management of AKI in COVID have not been different than other patient groups.

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The exact etiopathogenesis of Kawasaki disease (KD), the most common childhood vasculitis, remains unknown; however, an aberrant immune response, possibly triggered by an infectious or environmental agent in genetically predisposed children, is believed to be the underlying pathogenetic mechanism. Patients with inborn errors of immunity (IEI) are predisposed to infections that trigger immune dysregulation due to an imbalance in various arms of the immune system. KD may develop as a complication in both primary and secondary immunodeficiencies. KD may occur either at disease presentation or have a later onset in IEIs. These include X-linked agammaglobulinemia (XLA), selective IgA deficiency, transient hypogammaglobulinemia of infancy; Wiskott–Aldrich syndrome (WAS), hyper IgE syndrome (HIES); chronic granulomatous disease (CGD), innate and intrinsic immunity defects, and autoinflammatory diseases, including PFAPA. Hitherto, the association between KD and IEI is confined to specific case reports and case series and, thus, requires extensive research for a comprehensive understanding of the underlying pathophysiological mechanisms. IEIs may serve as excellent disease models that would open new insights into the disease pathogenesis of children affected with KD. The current review highlights this critical association between KD and IEI supported by published literature.