Aim Data published on COVID-19 in the Filipino population, particularly those with end stage kidney disease (ESKD) are still lacking. Methods We performed a retrospective, observational study of 68 ESKD patients admitted with COVID-19 infection at a tertiary hospital in Metro Manila, Philippines from April 1, 2020 to July 31, 2020. We compared the clinical features, baseline laboratory data, treatment strategies and short-term outcomes between those who survived and those who died. We also determined the risk factors associated with mortality from COVID-19. Results Mean age was 54.5 years old, 66% were male. All patients admitted were on maintenance hemodialysis (HD). The most common presenting symptoms were dyspnea (57%), fever (47%) and cough (38%). There was an equal number of patients on high flow nasal cannula (17.7%) and invasive mechanical ventilation (17.7%). ICU admission was required in 17.7% of the cohort. In-hospital death occurred in 25% of the patients. Admission PaO 2 /FiO 2 (PF) ratios (162 ± 134 versus 356 ± 181; p=0.0009) were lower, and procalcitonin (6.07 ± 10.5ng/mL versus 0.73 ± 3.61 ng/mL; p=0.02), lactate dehydrogenase (396 ± 274U/L versus 282 ± 148 U/L; p=0.03), and white blood cell counts (10 ± 7.3 x 10 9 /L versus 6.3 ± 4.2 x 10 9 /L; p= 0.0039) were significantly higher among those who died compared to those who survived. After adjusting for confounders, only low PF ratio (HR 1.01 for every unit decrease, 95% CI 1–1.01) and need for ventilation (HR 6.45, 95% CI 1.16–35.97) conferred a significant risk for in-hospital mortality. Conclusion Short-term, in-hospital mortality is high among patients on chronic hemodialysis admitted for COVID-19 infection. They present similarly with the general population. Low PF ratio on admission and need for ventilation are independent risk factors for in-hospital mortality.

>BACKGROUND AND AIMS The COVID-19 pandemic has brought to the forefront a wide spectrum of renal injuries that included glomerulopathies, some of which were recently highlighted in various case reports. These consist of focal and segmental glomerulosclerosis (FSGS) and minimal change disease (MCD).1 These changes were found among seemingly vulnerable populations such as the African American and Caucasian ethnicities with paucity of reports among other races. We present two cases of biopsy-confirmed MCD secondary to COVID-19 infection among adult Filipino patients. METHODS Case Report RESULTS: Case 1 A 40-year-old Filipino female with a history of right total mastectomy 2 years prior for a low-grade phyllodes tumor and no other medical comorbidities was admitted due to stillbirth. She was noted to have bipedal edema with a positive COVID-19 RT-PCR swab. Further workup revealed a serum creatinine 1.04 mg/dL, urine RBC 1/HPF and a 24-h urine protein of 9.22 g with hypoalbuminemia and dyslipidemia. Serologic workup was noted to be negative. She was started on Losartan, Atorvastatin, and Furosemide. A kidney biopsy was performed which demonstrated unremarkable light microscopy and immunofluorescence and widespread podocyte-foot process effacement. These biopsy findings were interpreted to be consistent with minimal change disease. She was started on Prednisone at 1 mg/kg/day with continuation of both Losartan and Atorvastatin. Six weeks after, the patient achieved complete remission with resolution of both hypoalbuminemia and dyslipidemia. She also reports no further recurrence of edema. Case 2 A 61-year-old Filipino male with a history of type 2 diabetes mellitus, hypertension, dyslipidemia and mild COVID-19 infection 4 months prior now presented with diarrhea. A routine COVID-19 RT-PCR swab revealed a re-infection. Physical examination noted bipedal edema. Further workup demonstrated a serum creatinine 3.39 mg/dL, urine RBC 2/HPF and urine ACR 2.6 g/g. Serologic tests were negative. He was diagnosed with Nephrotic Syndrome and underwent kidney biopsy. Findings showed an unremarkable light microscopy and immunofluorescence with widespread podocyte-foot process effacement. These findings were found to be consistent with minimal change disease and acute tubular injury. He was started on Prednisone (1 mg/kg/day), Losartan, Furosemide and Atorvastatin. Eight weeks later, the patient achieved complete remission with resolution of edema. CONCLUSION It is currently suspected that APOL1 risk variants found in reported cases of COVID-19-associated glomerulopathies are underlying toxic gain-of-function mutations that drive kidney disease.2 It is interesting to note that APOL1 renal risk variants are found exclusively in African-derived chromosomes and are rarely found among European or Asian chromosomes.3 Even though an APOL1 genotyping was not performed, our case reports provide the first examples of MCD among individuals without a high-risk genotype (APOL1) by epidemiology and enlarge the literature on MCD in COVID-19. We posit that there may be other underlying predispositions or mechanisms that may be driving glomerulopathy formation among COVID-19 patients aside from their inherent APOL 1 risk. Both of our patients were started on steroid therapy with a tapering regimen and achieved complete remission on subsequent follow-up. Existing reports suggest that most cases of COVID-19-associated MCD will often achieve resolution of AKI and proteinuria with steroid therapy, even in those with high-risk APOL1 genotype, emphasizing the need for an accurate histologic classification.4