What solid organ transplant healthcare providers should know about renin-angiotensin-aldosterone system inhibitors and COVID-19.

The data on the outcomes of solid organ transplant recipients who have contracted coronavirus disease 2019 (COVID-19) are still emerging. Kidney transplant recipients are commonly prescribed renin-angiotensin-aldosterone system (AAS) inhibitors given the prevalence of hypertension, diabetes, and cardiovascular disease. As the angiotensin-converting enzyme 2 (ACE2) facilitates the entry of coronaviruses into target cells, there have been hypotheses that preexisting use of renin-angiotensin-aldosterone system (RAAS) inhibitors may increase the risk of developing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Given the common use of RAAS inhibitors among solid organ transplant recipients, we sought to review the RAAS cascade, the mechanism of SARS-CoV-2 entry, and pertinent data related to the effect of RAAS inhibitors on ACE2 to guide management of solid organ transplant recipients during the COVID-19 pandemic. At present, there is no clear evidence to support the discontinuation of RAAS inhibitors in solid organ transplant recipients during the COVID-19 pandemic.

Longitudinal changes in kidney function following heart transplantation: Stanford experience.

Many heart transplant recipients experience declining kidney function following transplantation. We aimed to quantify change in kidney function in heart transplant recipients stratified by pre-transplant kidney function. A total of 230 adult heart transplant recipients between May 1, 2008, and December 31, 2014, were evaluated for up to 5 years post-transplant (median 1 year). Using 19 398 total estimated glomerular filtration rate (eGFR) assessments, we evaluated trends in eGFR in recipients with normal/near-normal (eGFR ≥45 mL/min/1.73 m2 ) vs impaired (eGFR <45 mL/min/1.73 m2 ) kidney function and the likelihood of reaching an eGFR of 20 mL/min/1.73 m2 after heart transplant. Baseline characteristics were similar. Immediately following heart transplant, the impaired pre-transplant kidney function group showed a mean eGFR gain of 9.5 mL/min/1.73 m2 (n = 193) vs a mean decline of 4.9 mL/min/1.73 m2 (n = 37) in the normal/near-normal group. Subsequent rates of eGFR decline were 2.2 mL/min/1.73 m2 /y vs 2.9 mL/min/1.73 m2 /y, respectively. The probability of reaching an eGFR of 20 mL/min/1.73 m2 or less at 1, 5, and 10 years following heart transplant was 1%, 4%, and 30% in the impaired group, and <1%, <1%, and 10% in the normal/near-normal group. Estimates of expected recovery in kidney function and its decline over time will help inform decision making about kidney care after heart transplantation.