LAUSR

A 29-year-old South Asian male presented with fever, myalgia and lower limb swelling of 3 days duration. Four weeks prior to presentation, he had been diagnosed with COVID19 infection and was treated symptomatically in the community isolation facility. He was diagnosed to have nephrotic syndrome with proteinuria of 8.71 g/24 h and serum albumin of 22 g/L. He also had acute kidney injury with peak serum creatinine of 145 μmol/L, estimated glomerular filtration rate (eGFR) of 65 mL/min per 1.73 m2. Urinalysis revealed few dysmorphic red blood cells and presence of white blood cells. Antinuclear antibody, anti-double stranded DNA, antineutrophil cytoplasmic antibodies were negative. Hepatitis B, Hepatitis C and HIV screens were negative and ultrasound imaging showed normal kidneys. Kidney biopsy showed 28 glomeruli with diffusely thickened capillary walls. Some glomeruli displayed segmental increases in mesangial cells amid expanded mesangial matrix. Masson-silver stains showed tiny fuchsinophilic subepithelial deposits and fine vacuolization of tangentially sectioned portions of the glomerular basement membranes (Fig. 1). Immunofluorescence showed 3 + finely granular staining for IgG along glomerular capillary walls, with focal weak segmental staining for anti-phospholipase A2 receptor (PLA2R) regarded as of uncertain significance (Fig. 2). Electron microscopy revealed thickened glomerular basement membranes and subepithelial electron dense deposits. There was severe effacement of podocyte foot processes. Tubular epithelial cells displayed organelles of varying sizes, as well as few electron-dense particles measuring between 90 and 100 nm, which were considered suspicious, but did not display spikes and were hence not diagnostic of virions. Subsequently, serum PLA2R antibody returned positive at a titer of 139.51 RU/mL. Workup for other causes of secondary membranous nephropathy was unrevealing. Due to increasing COVID-19 infections at that time, immunosuppressive treatment was delayed. He was started on an angiotensin-converting-enzyme inhibitor which was titrated to the highest tolerated dose. The serum PLA2R antibody titer decreased to 106.32 RU/mL after 3 months. The patient declined further trending of PLA2R antibody titer. After 8 months, the patient remained nephrotic with urine protein/creatinine ratio of 8.9 g/g, serum albumin of 23 g/L and serum creatinine of 129 μmol/L, eGFR 65 mL/ min per 1.73 m2. Clinical progress and laboratory results are shown in Table 1. Treatment options were rediscussed and immunosuppressive therapy was commenced with oral Cyclophosphamide at a dose of 2 mg/kg, together with Prednisolone 0.5 mg/kg. The patient declined checking of PLA2R antibody titer at the time of initiating immunosuppressive therapy. Two months after starting immunosuppressive treatment, the patient showed partial clinical response. He was asymptomatic and serum creatinine improved to 100 μmol/L with eGFR 88 mL/min per 1.73 m2. Serum albumin increased to 29 g/L and urine protein/creatinine ratio improved to 4.9 g/g. He subsequently returned to his home country for further follow-up. * Weiwen Guo [email protected]