COVID-19 and Severe Rhabdomyolysis Causing Acute Kidney Injury and Life-Threatening Hyperkalemia in a Pediatric Patient: a Case Report.

Though initially believed to primarily be a respiratory pathogen, the SARS-CoV-2 virus has manifested as a virus that has the potential to affect multiple organ systems causing a wide variety of disease and symptomatology. Children have been largely spared in comparison to adult morbidity and mortality; however, acute pediatric illness secondary to COVID-19 infection has become both more common and more serious. Here, we present a teenager with acute COVID-19 who presented to the hospital with profound weakness and oliguria and was discovered to have severe rhabdomyolysis causing life-threatening hyperkalemia and acute kidney injury. He required treatment with emergent renal replacement therapy in the intensive care unit. His initial CK was 584,886 U/L. Creatinine was 14.1 mg/dL and potassium was 9.9 mmol/L. He was successfully treated with CRRT and was discharged on hospital day 13 with normal kidney function on follow-up. Rhabdomyolysis and acute kidney injury are increasingly recognized as complications of acute SARS-CoV-2 infection and require vigilance given the potentially fatal complications and long-standing morbidity associated with these conditions.

Reduced versican cleavage due to Adamts9 haploinsufficiency is associated with cardiac and aortic anomalies.

Here, we demonstrate that ADAMTS9, a highly conserved versican-degrading protease, is required for correct cardiovascular development and adult homeostasis. Analysis of Adamts9(+/LacZ) adult mice revealed anomalies in the aortic wall, valvulosinus and valve leaflets. Abnormal myocardial projections and 'spongy' myocardium consistent with non-compaction of the left ventricle were also found in Adamts9(+/LacZ) mice. During development, Adamts9 was expressed in derivatives of the Secondary Heart Field, vascular smooth muscle cells in the arterial wall, mesenchymal cells of the valves, and non-myocardial cells of the ventricles, but expression also continued in the adult heart and ascending aorta. Thus, the adult cardiovascular anomalies found in Adamts9(+/LacZ) hearts could result from subtle developmental alterations in extracellular matrix remodeling or defects in adult homeostasis. The valvular and aortic anomalies of Adamts9(+/LacZ) hearts were associated with accumulation of versican and a decrease in cleaved versican relative to WT littermates. These data suggest a potentially important role for ADAMTS9 cleavage of versican, or other, as yet undefined substrates in development and allostasis of cardiovascular extracellular matrix. In addition, these studies identify ADAMTS9 as a potential candidate gene for congenital cardiac anomalies. Mouse models of ADAMTS9 deficiency may be useful to study myxomatous valve degeneration.