The widely used Modification of Diet in Renal Disease (MDRD) formula adapts a 1.212 multiplier for individuals who are identified as African Americans (AAs) or Blacks, which leads to a higher GFR estimation. As it stands, AAs have a lower prevalence of chronic kidney disease (CKD) but higher incidence of end-stage renal disease (ESRD) compared with Whites. Many hypotheses have been postulated to explain this paradox, but the imprecision of the GFR estimation with race-adaptation could be contributory. We performed a single-center, longitudinal, retrospective study on a cohort of outpatient AA patients using the MDRD and MDRD_{race removed} and CKD-EPI and CKD-EPI_{race removed} and their progression to CKD G5 (eGFR <15 ml/min/1.73 m²). 327 patients were analyzed. Median follow-up was 88.1 months (interquartile range, 34.4–129.1). When race was removed from MDRD, 39.9% of patients in CKD G1/2 were reclassified to CKD G3a, 72.6% of patients in CKD G3a would be reclassified to CKD G3b, and 54.1% and 36.4% of patients would be reclassified from CKD 3b to CKD G4 and CKD G4 to CKD G5, respectively . Comparing the CKD-EPI formula against the MDRD in our cohort, we found that 8.2%, 18.8%, and 11.4% of patients were reclassified from CKD G1/2 to CKD G3a, CKD G3a to G3b, and CKD G3b to CKD G4 respectively. Overall median time to progression to CKD G5 was 137.4 (131.9–142.8) months in patients who were not reclassified and 133.6 (127.6–139.6) months for patients who were reclassified by MDRD_{race removed} . Concerns of inequitable access to healthcare have elicited calls to review race-corrected eGFR equations. A substantial number of individuals would have their CKD stage reclassified should have the MDRD_{race removed} equation be adopted en masse on an AA-only population. The discrepancy is highest at the 45–59 and >60 ml/min/1.72 min² ranges. This will have tremendous impact on our center’s approach to pharmacological dosing, referral system, best practices, and outcome surveillance. Comprehensive review of the current “race-corrected” eGFR will require a multifaceted approach and adjunctive use of noncreatinine-based approach.

The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCε is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCε expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCε expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCε to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCε, ethanol-induced changes in PKCε expression, the regulation of ethanol-induced PKCε activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCε-RACKε translocation in the presence of ethanol, and the existing literature on the role of PKCε in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.

Background. The SARS-CoV-2 virus caused the global COVID-19 pandemic, with waxing and waning course. This study was conducted to compare outcomes in the first two waves, in mechanically ventilated patients. Methods. This retrospective observational study included all mechanically ventilated COVID-19 patients above 18 years of age, between March 2020 and January 2021. Patients were grouped into first wave from March 2020 to July 2020, and second wave from August 2020 to January 2021. Outcome measures were mortality, the development of acute kidney injury (AKI), and need for renal replacement therapy (RRT). Univariate and multivariate cox regression analysis were used to delineate risk factors for the outcome measures. Results. A total of 426 patients, 285 in the first wave and 185 in the second wave, were included. The incidence of AKI was significantly lower in the second wave (72% vs. 63%; ). There was no significant difference in mortality (70% vs. 63%; ) and need for RRT (36% vs. 30%; ). Risk factors for mortality were increasing age and AKI in both waves, and chronic kidney disease (CKD) (adj. HR 1.7; 95% CI 1.02–2.68; ) in the second wave. Risk factors for AKI were CKD in both the waves, while it was diabetes (adj. HR 1.4; 95% CI 1.02–1.95; ) and increasing age in the first wave. Remdesivir (adj. HR 0.5; 95% CI 0.3–0.7; ) decreased the risk of AKI, and convalescent plasma (adj. HR 0.5; 95% CI 0.3–0.9; ) decreased the risk of mortality in the first wave, however, such benefit was not observed in the second wave. Conclusions. Our study shows a decrease in the incidence of AKI in critically ill patients, however, the reason for this decrease is still unknown. Studies comparing the waves of the pandemic would not only help in understanding disease evolution but also to develop tailored management strategies.

Acute kidney injury due to urinary tract obstruction invariably suggests lower urinary tract obstruction or bilateral ureteric obstruction since obstruction of a single kidney while the contralateral kidney is normal and not obstructed would not cause a perceptible rise in creatinine. Assuming a total body volume of 42 L, 70 kg male that generates approximately 1400 mg of creatinine daily (20 mg/kg/day) who has complete urinary tract obstruction would experience a 3.33 mg/dL per day increase in serum creatinine. Thus, for an individual who had prior normal renal function and who presents with a creatinine of 30 mg/dL, one could surmise that the obstructive pathology had lasted at least 10 days. However, the rise in serum creatinine is a poor marker of renal injury and subsequent prognosis. Urinary tract obstruction leading to AKI can be due to a variety of causes, and its management is tailored to the underlying etiology. This case series describes the varied clinical course of four patients at our center who experienced AKI from atypical causes of obstructive uropathy. Current and future diagnostic modalities and caveats in the treatment of this disease entity are also discussed.

Background: An increased incidence of thrombotic complications in patients with coronavirus disease 2019 (COVID-19) has been reported. Severe acute kidney injury (AKI) is one of the major clinical manifestations of COVID-19 with the need for renal replacement therapy. It was observed that hemodialysis (HD) accesses tended to thrombose more often in the COVID-19 population than in non-COVID-19 patients. We hypothesize that the hypercoagulable state of COVID-19 is associated with higher incidence of access clotting. Method: In this retrospective single-centered study at Kings County Hospital in New York City, 1,075 patients with COVID-19 were screened, and 174 patients who received HD from January 3, 2021 to May 15, 2020 were enrolled to examine the risk factors of dialysis access clotting in patients with COVID-19. Results: Of the 174 patients, 109 (63%) were COVID-19 positive. 39 (22.6%) patients had dialysis access clotting at least once during their hospitalization, and they had significantly higher body mass index (BMI) (p = 0.001), higher rates of COVID-19 (p = 0.015), AKI (p < 0.001), higher platelet counts (p = 0.029), higher lactate dehydrogenase levels (p = 0.009), and lower albumin levels (p = 0.001) than those without access malfunctions. Low albumin levels (p = 0.008), AKI (p = 0.008), and high BMI (p = 0.018) were risk factors associated with HD access clotting among COVID-19 patients. Conclusion: Patients with COVID-19 who receive HD for AKI with high BMI are at a higher risk of clotting their HD access.