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1.
Journal of the American Society of Nephrology ; 33:550, 2022.
Article in English | EMBASE | ID: covidwho-2125765

ABSTRACT

Background: Sodium glucose cotransporter2 inhibitors (SGLT2i) demonstrate a cardioprotective effect and are associated with slowing or preventing CKD progression in the native kidney. However, there is limited data in the literature about their use after a kidney transplantation. Method(s): This is an observational retrospective study in a cohort of kidney transplant recipients at Washington University in St. Louis, treated with SGLT2i for diabetes mellitus type 2. Data collection was conducted by chart review. Our primary endpoint was to assess the safety and adverse reactions in this cohort. Our secondary endpoints included assessments of change in weight/BMI, blood pressure, serum creatinine and eGFR, LDL, HDL and hemoglobin A1C every 6 months with a follow up to 2 years. Analysis for change of these parameters from baseline (at the time of start of the medication) was conducted using matched paired t test. Result(s): A total of 36 of kidney transplant recipients were included. The average age of patients was 55.5 +/- 10.4 years. 23 of 36 patients (63.9%) were males. The adverse events reported were congestive heart failure 2/36 (5.6%), AKI 2/36 (5.6%), candidiasis 1/36 (2.8%), and urinary tract infection 1/36 (2.8%). Our results also revealed that two patients died unrelated to medication use (1 patient died after COVID infection and 1 patient died due to septic shock from a foot infection). As shown in table 1 there was no significant change from baseline in weight/BMI, blood pressure, serum creatinine and eGFR, LDL, HDL or hemoglobin A1C at 6, 12, 18 and 24 months. Conclusion(s): Our preliminary data shows that SGLT2i are relatively safe in the kidney transplant population. Larger multicenter studies are needed to determine the efficacy of these drugs in improving renal function, decreasing cardiovascular events and survival post-transplant, as seen in non-transplant recipients.

2.
American Journal of Transplantation ; 21(SUPPL 4):609, 2021.
Article in English | EMBASE | ID: covidwho-1494512

ABSTRACT

Purpose: Coronavirus-19 is a novel virus with various clinical presentations ranging from a cold to severe acute respiratory syndrome. However, little is known about it's association with glomerulonephritis. We present a case of COVID-19 in a kidney transplant recipient who developed collapsing Focal segmental glomerulosclerosis (FSGS). Methods: A 49-year-old African American female who had end stage kidney disease secondary to lupus nephritis received a deceased donor kidney transplant. Post-transplant course was complicated with delayed graft function for 12 days. At 4 months after her transplant, she presented to the hospital with malaise, nausea, vomiting, diarrhea and fever of 101 F. Initially treated empirically for urinary tract infection due to pyuria and lack of respiratory symptoms. However because of a persistent fever, Covid-19 PCR test was performed that resulted positive. Results: Chest X ray showed right middle and right lower lobe opacities. She was treated in March 2020 with hydroxychloroquine and we held her mycophenolic acid while continuing tacrolimus and prednisone. Patient was subsequently found to have new onset nephrotic range proteinuria without nephrotic syndrome as well as an AKI with creatinine going to 2. Labs showed negative donor specific antibodies as well as negative DsDNA and normal complement C3 and C4 levels. Urinalysis showed hematuria and proteinuria. Kidney allograft biopsy showed collapsing glomerulopathy with severe podocyte foot process effacement affecting approximately 90-100% of the capillary loop surface area. There was no evidence of cellular or antibody-mediated rejection and c4d was negative. She was treated with plasma exchange and rituximab. Patient was maintained with plasmapheresis every week. Creatinine slowly improved and proteinuria gradually decreased to subnephrotic range as shown in Figure 1. Conclusions: COVID-19 infection may result in a wide range of kidney injuries including collapsing FSGS. COVID-19 may serve as an immunologic trigger for FSGS. The mechanism can be similar to other viral infections such as parvovirus B19, HIV and cytomegalovirus. Large number of cases are needed to examine the best treatment option.

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