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Summary: Background: There is an enormous knowledge gap on management strategies, clinical outcomes, and follow-up after kidney transplantation (KT) in recipients that have recovered from coronavirus disease (COVID-19). Methods: We conducted a multi-center, retrospective analysis in 23 Indian transplant centres between June 26, 2020 to December 1, 2021 on KT recipients who recovered after COVID-19 infections. We analyzed clinical and biopsy-confirmed acute rejection (AR) incidence and used cox-proportional modeling to estimate multivariate-adjusted hazard ratios (HR) for predictors of AR. We also performed competing risk analysis. Additional outcome measures included graft loss, all-cause mortality, waiting time from a positive real-time polymerase test (RT-PCR) to KT, laboratory parameters, and quality of life in follow-up. Findings: Among 372 KT which included 38(10·21%) ABO-incompatible, 12(3·22%) sensitized, 64(17·20%) coexisting donors with COVID-19 history and 20 (5·37%) recipients with residual radiographic abnormalities, the incidence of AR was 34 (9·1%) with 1(0·26%) death censored graft loss, and 4(1·07%) all-cause mortality over a median (interquartile range) follow-up of 241 (106–350) days. In our cox hazard proportional analysis, absence of oxygen requirement during COVID-19 compared to oxygen need [HR = 0·14(0·03–0·59); p-value = 0·0071], and use of thymoglobulin use compared to other induction strategies [HR = 0·17(0·03–0.95); p-value = 0·044] had a lower risk for AR. Degree of Human leukocyte antigen (HLA) DR mismatch had the highest risk of AR [HR = 10.2(1·74–65·83); p-value = 0·011]. With competing risk analysis, with death as a competing event, HLA DR mismatch, and oxygen requirement continued to be associated with AR. Age, gender, obesity, inflammatory markers, dialysis vintage, steroid use, sensitization and ABO-incompatibility have not been associated with a higher risk of AR. The median duration between COVID-19 real time polymerase test negativity to transplant was 88(40–145) days (overall), and ranged from 88(40–137), 65(42–120), 110(49–190), and 127(64–161) days in World Health Organization ordinal scale ≤ 3, 4, 5, and 6–7, respectively. There was no difference in quality of life, tacrolimus levels, blood counts, and mean serum creatinine assessed in patients with a past COVID-19 infection independent of severity. Interpretation: Our findings support that the outcomes of KT after COVID-19 recovery are excellent with absence of COVID-19 sequelae during follow-up. Additionally, there does not seem to be a need for changes in the induction/immunosuppression regimen based on the severity of COVID-19. Funding: Sanofi

The triad of hemolytic anemia, pancytopenia, and thrombosis makes paroxysmal nocturnal hemoglobinuria (PNH) a truly unique clinical syndrome. Intravascular hemolysis in PNH can lead to a severe hemolytic episode with massive hemoglobinuria which can cause acute kidney injury (AKI) probably from acute tubular necrosis (ATN). A 15 -year-old girl was admitted with history of fever, diarrhea, vomiting followed by decreased urine output since 3 days. Urinalysis showed nil protein, no red blood cells (RBCs) on microscopy. Plasma hemoglobin level, total leukocyte count, platelet count, and serum creatinine were 6.5 gm/dl, 6440/μl, 205 000/μl, and 3.1 mg/dl, respectively. She received 3 units of packed red blood cells and the patient was discharged with normal renal function test with a diagnosis of acute gastroenteritis with recovered AKI. After 8 months she again had fever, vomiting, nausea with decreased urine output since 3 days. Laboratory investigations showed hemoglobin - 5.5 gm/dl, total leukocyte count - 1550/ μl, platelet count - 165000/μl, and serum creatinine - 4.89 mg/dl. Serum LDH level was 2188 U/l. She was managed conservatively with steroids, antibiotics and she recovered her kidney functions to normal in a week. Presentation of repeated AKI with hemolytic anemia in a short span after fever led us to perform flow cytometric analysis of peripheral blood granulocytes which revealed the presence of PNH clone. PNH may present with renal disease and anemia only even without classical history of hematuria or venous thrombosis. Thus it needs high index of suspicion as early diagnosis and treatment will help in preventing repeated episodes of AKI and thus chronic kidney disease.