New-onset pediatric nephrotic syndrome following Pfizer-BioNTech SARS-CoV-2 vaccination: a case report and literature review.

Various new vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been rapidly developed. The new onset and recurrence of nephrotic syndrome triggered by some vaccines have been documented and several adult cases of minimal change nephrotic syndrome newly developing after SARS-CoV-2 vaccination have been reported. However, no reports of pediatric cases have been published. Indications for SARS-CoV-2 vaccines have been expanded to those as young as 12 years old and vaccination of children has just started in Japan. We encountered a 15-year-old boy without underlying disease who newly developed nephrotic syndrome after SARS-CoV-2 vaccination with BNT162b2 (Pfizer-BioNTech). He developed eyelid edema 4 days after vaccination and peripheral edema of the lower extremities a further 4 days later. Twenty-one days after vaccination, 60 mg of oral daily prednisolone was started. He achieved complete remission in 12 days without complications such as hypertension or acute kidney injury. We clinicians should be aware of the possibility of nephrotic syndrome developing after SARS-CoV-2 vaccination, not only in adults, but also in children.

Childhood Nephrotic Syndrome Complicated by Catastrophic Multiple Arterial Thrombosis Requiring Bilateral Above-Knee Amputation.

Background: Thromboembolic events are rare but critical complications in childhood nephrotic syndrome. The veins are more commonly affected, while arterial thrombosis is extremely rare but often life-threatening. Herein, we describe the clinical course of a 10-years-old girl with catastrophic multiple arterial thrombosis at the primary onset of nephrotic syndrome who underwent bilateral above-knee amputation. Case diagnosis/treatment: A previous healthy 10-years-old girl contracted the influenza B virus. Five days later, she suddenly developed severe ischemia in both legs. Physical examination showed eyelid and leg edema, and laboratory tests revealed hypoalbuminemia and acute kidney injury. After undergoing contrast-enhanced computed tomography, the patient was diagnosed with multiple arterial thrombosis (including the bilateral iliac arteries) due to nephrotic syndrome. Despite the performance of surgical thrombectomies, fasciotomy, and systematic heparinization, she required bilateral above-knee amputation. The patient achieved spontaneous remission of nephrotic syndrome, and her renal function fully recovered. There were no findings suggestive of secondary nephrotic syndrome and antiphospholipid syndrome. Her protein C and protein S concentrations were slightly decreased at admission. However, whole-exome sequencing revealed a thrombotic risk variant (T630I) in the PROS1 gene encoding protein S. This missense variant is often reported in patients with thrombosis or protein S deficiency, and may result in a thrombotic predisposition in some situations, such as nephrotic syndrome. Conclusions: Arterial thrombosis is a rare complication; however, it must be considered, especially in patients with new-onset nephrotic syndrome. Early recognition is important for early intervention and prevention of serious sequelae.

Influenza A(H3N2) virus exhibiting reduced susceptibility to baloxavir due to a polymerase acidic subunit I38T substitution detected from a hospitalised child without prior baloxavir treatment, Japan, January 2019.

In January 2019, two influenza A(H3N2) viruses carrying an I38T substitution in the polymerase acidic subunit (PA), which confers reduced susceptibility to baloxavir, were detected from epidemiologically unrelated hospitalised children in Japan. The viruses exhibited reduced susceptibility to baloxavir but were susceptible to neuraminidase inhibitors. Only one of the two children had been treated with baloxavir. An epidemiological analysis suggests possible transmission of the PA I38T mutant A(H3N2) virus among humans.