The aim of this study was to estimate the incidence of COVID-19 disease in the French national population of dialysis patients, their course of illness and to identify the risk factors associated with mortality. Our study included all patients on dialysis recorded in the French REIN Registry in April 2020. Clinical characteristics at last follow-up and the evolution of COVID-19 illness severity over time were recorded for diagnosed cases (either suspicious clinical symptoms, characteristic signs on the chest scan or a positive reverse transcription polymerase chain reaction) for SARS-CoV-2. A total of 1,621 infected patients were reported on the REIN registry from March 16th, 2020 to May 4th, 2020. Of these, 344 died. The prevalence of COVID-19 patients varied from less than 1% to 10% between regions. The probability of being a case was higher in males, patients with diabetes, those in need of assistance for transfer or treated at a self-care unit. Dialysis at home was associated with a lower probability of being infected as was being a smoker, a former smoker, having an active malignancy, or peripheral vascular disease. Mortality in diagnosed cases (21%) was associated with the same causes as in the general population. Higher age, hypoalbuminemia and the presence of an ischemic heart disease were statistically independently associated with a higher risk of death. Being treated at a selfcare unit was associated with a lower risk. Thus, our study showed a relatively low frequency of COVID-19 among dialysis patients contrary to what might have been assumed.
FSGS is a common glomerular disorder that has a high propensity for recurrence after kidney transplant. The pathophysiology of FSGS is unknown, but podocytes seem to be the target of one or several circulating factors that lead to cytoskeleton reorganization and proteinuria. Research on podocytes has identified B7-1 as an important factor in podocyte biology and a new therapeutic target in renal disease. Indeed, in four patients with recurrent FSGS after transplant, treatment with the B7-1 blocker abatacept was associated with proteinuria remission. Here, we prospectively treated nine patients with recurrent FSGS after transplant using either abatacept or belatacept, a B7-1 blocker with higher affinity, and did not induce proteinuria remission. Furthermore, we did not detect B7-1 expression by immunofluorescence in podocytes of biopsy specimens from these or other kidney grafts or podocytes of native kidney biopsy specimens. In conclusion, B7-1 blockade did not induce FSGS remission after transplant in our study.
We report the occurrence of chronic kidney disease after living-related kidney transplant involving monozygotic twin brothers of Afro-Caribbean origin who were both heterozygous for the G1 and G2 APOL1 kidney disease risk alleles. A 21 year-old black man with endstage kidney disease of unknown aetiology received a kidney from his monozygotic twin brother (confirmed by microsatellite analysis). Thirty months after transplantation, the patient presented proteinuria and decreased eGFR with typical focal segmental glomerulosclerosis lesions on the graft biopsy. He received steroid therapy, but progressed to kidney failure 5 years later. The twin brother displayed normal kidney function without proteinuria at the time of transplant; however, 7 years later, he exhibited decreased estimated GFR (40 ml/min/1.73m) and proteinuria (2.5 g/day). APOL1 genotyping of revealed that both donor and recipient were heterozygous for the G1 and G2 alleles. This unique case is in stark contrast to expectations for identical twin transplantation and suggests a role for APOL1 polymorphisms in both the donor and recipient.
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