The Outcome of COVID-19 Infection on Kidney Transplantation Recipients in Southern Saudi Arabia: Single-Center Experience.

BACKGROUND: To report the incidence, risk factors, and outcome of severe COVID-19 disease in kidney transplant recipients attending a Saudi hospital at a single center in the Kingdom of Saudi Arabia. METHODS: A retrospective chart-based cohort study involving all kidney transplant recipients tested for COVID-19 in the Armed Forces Hospital Southern Region, KSA. RESULTS: Of 532 kidney transplant recipients who reported to the center, from March 2020 to June 2022, 180 were tested for COVID-19. Of these recipients, 31 (17%) tested positive. Among the 31 positive recipients, 11 were treated at home, 15 were admitted to the noncritical isolation ward, and 5 were admitted to the intensive care unit (ICU). Older age (P = .0001), higher body mass index (P = .0001), and history of hypertension (P = .0023) were more frequent in the COVID-19-positive recipients. Admission to the ICU was more frequent in older recipients (P = .0322) with a history of ischemic heart disease (P = .06) and higher creatinine baseline (P = .08) presenting with dyspnea (P = .0174), and acute allograft dysfunction (P = .002). In the ICU group, 4 (80%) patients required hemodialysis, and 4 (80%) died. CONCLUSIONS: Kidney transplant recipients with COVID-19 could have a higher risk for developing acute kidney injury, dialysis, and mortality than the general population. ICU admission and renal replacement therapy were more evident in older recipients with a history of ischemic heart disease, presenting with shortness of breath (P = .017) and a higher serum creatinine baseline. Acute allograft dysfunction was the independent predictor of mortality among patients admitted to the ICU.

Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome as a Presentation of Coronavirus Disease 2019.

The novel coronavirus disease 2019 (COVID-19) has led to a global pandemic. While acute respiratory failure has been the predominant concern, there have been reports of other end-organ damage such as renal failure. We report a case of an elderly woman who presented with BRASH syndrome, a constellation of bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia (BRASH), which was likely triggered by COVID-19.

Plc1p is required for proper chromatin structure and activity of the kinetochore in Saccharomyces cerevisiae by facilitating recruitment of the RSC complex.

High-fidelity chromosome segregation during mitosis requires kinetochores, protein complexes that assemble on centromeric DNA and mediate chromosome attachment to spindle microtubules. In budding yeast, phosphoinositide-specific phospholipase C (Plc1p encoded by PLC1 gene) is important for function of kinetochores. Deletion of PLC1 results in alterations in chromatin structure of centromeres, reduced binding of microtubules to minichromosomes, and a higher frequency of chromosome loss. The mechanism of Plc1p's involvement in kinetochore activity was not initially obvious; however, a testable hypothesis emerged with the discovery of the role of inositol polyphosphates (InsPs), produced by a Plc1p-dependent pathway, in the regulation of chromatin-remodeling complexes. In addition, the remodels structure of chromatin (RSC) chromatin-remodeling complex was found to associate with kinetochores and to affect centromeric chromatin structure. We report here that Plc1p and InsPs are required for recruitment of the RSC complex to kinetochores, which is important for establishing proper chromatin structure of centromeres and centromere proximal regions. Mutations in PLC1 and components of the RSC complex exhibit strong genetic interactions and display synthetic growth defect, altered nuclear morphology, and higher frequency of minichromosome loss. The results thus provide a mechanistic explanation for the previously elusive role of Plc1p and InsPs in kinetochore function.