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Objective: To evaluate the prevalence and factors associated with the risk of acute kidney injury (AKI) in pediatric patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and multisystem inflammatory syndrome in children (MIS-C).Study Design: We performed a retrospective chart review of 113 patients with SARS-CoV-2 infection with or without MIS-C admitted at Children's Hospital of Michigan (CHM) from March to August 2020. Patient demographic details, laboratory data, imaging studies, echocardiography reports, and treatment data were collected.Results: Of the 92 patients included in the final analysis, 22 (24%) developed AKI with 8/22 (36%) developing stage 3 AKI. The prevalence of AKI was much higher in patients with MIS-C 15/28 (54%) vs. those with acute SARS-CoV-2 infection 7/64 (11%), (p < 0.001). Overall, when compared to patients without AKI, patients with AKI were older in age (11 vs. 6.5 years, p = 0.007), African American (86 vs. 58%, p = 0.028), had MIS-C diagnosis (68 vs. 19%, p < 0.001), required ICU admission (91 vs. 20%, p < 0.001), had cardiac dysfunction (63 vs. 16%, p < 0.001), required inotropic support (59 vs. 6%, p < 0.001) and had a greater elevation in inflammatory markers. In a multivariate analysis, requirement of inotropes [Odds Ratio (OR)−22.8, p < 0.001], African American race (OR-8.8, p = 0.023) and MIS-C diagnosis (OR-5.3, p = 0.013) were the most significant predictors for AKI. All patients had recovery of kidney function, and none required kidney replacement therapy.Conclusion: Children with acute SARS-CoV-2 infection and MIS-C are at risk for AKI, with the risk being significantly greater with MIS-C. The pathogenesis of AKI in acute SARS-CoV-2 infection appears to be a combination of both renal hypo-perfusion and direct renal parenchymal damage whereas in MIS-C, the renal injury appears to be predominantly pre-renal from cardiac dysfunction and capillary leak from a hyperinflammatory state. These factors should be considered by clinicians caring for these children with a special focus on renal protective strategies to aid in recovery and prevent additional injury to this high-risk subgroup.

Steroid-sensitive nephrotic syndrome (SRNS) can cause CKD and necessitate kidney transplant. Here the authors identify FAT1 mutations by homozygosity mapping and whole-exome sequencing in families with SRNS and provide functional mouse and zebrafish evidence that FAT1 is required for normal glomerular and tubular function and that FAT1 mutations can cause SRNS.

Background. Membranous glomerulopathy accounts for 28% of the biopsy-proven systemic lupus erythematosus nephritis in paediatric patients at the time of first biopsy, yet minimal data are available regarding outcomes in this population. Methods. We present a retrospective analysis of 26 paediatric patients with World Health Organization class V lupus nephritis. Patients were subdivided based on renal biopsy findings into the following subclasses: 16 (63%) Va, 2 (9%) Vb, 7 (26%) Vc and 1 (4%) Vd. We evaluated outcomes of renal function and urine protein to creatinine ratio (UPr/UCr). Results. Mean follow-up time was 38.6 (±22) months. Eight patients at presentation had a glomerular filtration rate (GFR) P = 0.002). Twenty-one of the 26 patients had GFR ≥ 90 ml/min/1.73 m2 at last follow-up; the five patients with GFR Conclusions. The initial creatinine in patients with classes Va and Vb lupus nephritis predicted follow-up renal function. We found no correlation with outcome based on therapy with CTX and/or mycophenolate mofetil. [ABSTRACT FROM AUTHOR]