Although the lungs are major targets for COVID-19 invasion, other organs—such as the kidneys—are also affected. However, the renal complications of COVID-19 are not yet well explored. This study aimed to identify the incidence of acute kidney injury (AKI) in patients with COVID-19 and to evaluate its impact on patient outcomes. This retrospective study included 704 patients with COVID-19 who were hospitalized at two hospitals in Daegu, Korea from February 19 to March 31, 2020. AKI was defined according to the serum creatinine criteria in the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. The final date of follow-up was May 1, 2020. Of the 704 patients, 28 (4.0%) developed AKI. Of the 28 patients with AKI, 15 (53.6%) were found to have AKI stage 1, 3 (10.7%) had AKI stage 2, and 10 (35.7%) had AKI stage 3. Among these patients, 12 (42.9%) recovered from AKI. In the patients with AKI, the rates of admission to intensive care unit (ICU), administration of mechanical ventilator (MV), and in-hospital mortality were significantly higher than in patients without AKI. Multivariable analysis revealed that old age (Hazard ratio [HR] = 4.668, 95% confidence interval [CI] = 1.250–17.430, p = 0.022), high neutrophil-to-lymphocyte ratio (HR = 1.167, 95% CI = 1.078–1.264, p < 0.001), elevated creatinine kinase (HR = 1.002, 95% CI = 1.001–1.004, p = 0.007), and severe AKI (HR = 12.199, 95% CI = 4.235–35.141, p < 0.001) were independent risk factors for in-hospital mortality. The Kaplan-Meier curves showed that the cumulative survival rate was lowest in the AKI stage 3 group (p < 0.001). In conclusion, the incidence of AKI in patients with COVID-19 was 4.0%. Severe AKI was associated with in-hospital death.

The problem of organ shortage is an important issue in kidney transplantation, but the effect of kidney donation on AKI is unclear. The aim of this study was to investigate the impact of acute kidney injury (AKI) on post-transplant clinical outcomes for deceased donor kidney transplantation (DDKT) using standard criteria donors (SCDs) versus expanded criteria donors (ECDs). Five-hundred nine KT recipients receiving kidneys from 386 deceased donors (DDs) were included from three transplant centers. Recipients were classified into the SCD-KT or ECD-KT group according to corresponding DDs and both groups were divided into the AKI-KT or non-AKI-KT subgroups according to AKI in donor. We compared the clinical outcomes among those four groups and investigated the interaction between AKI in donors and ECD on allograft outcome. The incidence of delayed allograft function was higher when the donors had AKI within SCD-KT and ECD-KT groups. In allograft biopsies within 3 months, chronic change was more significant in the AKI-ECD-KT subgroup than in the non-AKI-ECD-KT subgroup, but it did not differ between AKI-SCD-KT and non-AKI-SCD-KT group. AKI-ECD-KT showed higher risk for death-censored allograft failure than the other three groups and a significant interaction was observed between AKI in donors and ECD on the allograft outcome. The presence of AKI in ECDs significantly impacted the long-term allograft outcomes of kidney transplant recipients, but it did not in SCDs.

Studies report beneficial effects of 3-hydroxybutyrate (3-OHB) on the treatment of type 2 diabetes and obesity, but the effects of 3-OHB on diabetic nephropathy have not been elucidated. This study was designed to investigate the efficacy and mechanism of 3-OHB against progression of diabetic nephropathy (DN). Mice (db/db) were fed normal chow, high-fat, or ketogenic diets (KD) containing precursors of 3-OHB. Hyperglycemia was determined based on random glucose level (≥250 mg/dL). Fasting blood glucose and body weights were measured once a week. Twenty four-hour urine albumin to creatinine ratio was determined 5 weeks after the differential diet. Energy expenditure was measured 9 weeks after the differential diet. Body weights were significantly lower in the KD group than those in other groups, but no significant differences in fasting blood glucose levels among three groups were observed. Urine albumin to creatinine ratio and serum blood urea nitrogen (BUN) to creatinine ratio in the KD group were significantly lower than in other groups. Histologic and quantitative analysis of mesangial area suggested that KD delayed the progression of DN phenotype in db/db mice. Metabolic cage analysis also revealed that KD increased energy expenditure in db/db mice. In vitro studies with proximal tubular cells revealed that 3-OHB stimulated autophagic flux. 3-OHB increased LC3 I to LC3 II ratio, phosphorylation of AMPK, beclin, p62 degradation, and NRF2 expression. Moreover, we found that 3-OHB attenuated high glucose-induced reactive oxygen species (ROS) levels in proximal tubular cells. In vivo study also confirmed increased LC3 and decreased ROS levels in the kidney of KD mice. In summary, this study shows in both in vivo and in vitro models that 3-OHB delays the progression of DN by augmenting autophagy and inhibiting oxidative stress.

Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary and progressive renal disease. By the age of 65 years, 45% to 70% of patients with ADPKD reach end-stage renal disease (ESRD). Although there are various treatments for this condition, no standard therapy exists to delay the progression of ADPKD. Hence, understanding the factors that affect disease progression may be helpful for the treatment of ADPKD. The medical records of 288 patients with ADPKD at Keimyung University Dongsan Medical Center between January 1989 and August 2018 were analyzed retrospectively. Furthermore, we inspected the risk factors involved in the progression of ADPKD and the kidney survival rates of patients using the Cox proportional hazards model and Kaplan–Meier survival analysis. The mean age at the time of diagnosis was 43.1 ± 14.1 years, and there were 146 males (50.7%). In total, 197 patients (68.4%) had hypertension and 11 patients (3.8%) had cerebral aneurysm. Stroke occurred in 35 patients (12.1%), including 11 cases of cerebral hemorrhage and 24 cases of cerebral infarction. Twenty-eight patients (9.7%) died during the follow-up period (117.1 ± 102.1 months). Infection (42.9%) was the most common cause of mortality, followed by sudden cardiac death (25.0%). Overall, 132 patients (45.8%) progressed to ESRD and 104 patients (36.1%) required renal replacement therapy (RRT). The mean duration from diagnosis to RRT was 110.8 ± 93.9 months. Age at diagnosis after 30 years (odd’s ratio [OR], 2.737; 95% confidence interval [CI], 1.320–5.675; P = .007), baseline serum creatinine levels (OR, 1.326; 95% CI, 1.259–1.396; P < .001), and cyst infection (OR, 2.065; 95% CI, 1.242–3.433; P = .005) were the independent risk factors for kidney failure in multivariable analysis. To delay the advance of ADPKD to ESRD, early diagnosis and close observation for the onset of cyst infection are crucial.

Key Points: As a biomarker, urinary metabolites could bridge the gap between genetic abnormalities and phenotypes of diseases. We found that levels of betaine, choline, fumarate, citrate, and glucose were significantly correlated with kidney function and could predict kidney outcomes, providing prognostic biomarkers in CKD. Background: Because CKD is caused by genetic and environmental factors, biomarker development through metabolomic analysis, which reflects gene-derived downstream effects and host adaptation to the environment, is warranted. Methods: We measured the metabolites in urine samples collected from 789 patients at the time of kidney biopsy and from urine samples from 147 healthy participants using nuclear magnetic resonance. The composite outcome was defined as a 30% decline in eGFR, doubling of serum creatinine levels, or end-stage kidney disease. Results: Among the 28 candidate metabolites, we identified seven metabolites showing (1) good discrimination between healthy controls and patients with stage 1 CKD and (2) a consistent change in pattern from controls to patients with advanced-stage CKD. Among the seven metabolites, betaine, choline, glucose, fumarate, and citrate showed significant associations with the composite outcome after adjustment for age, sex, eGFR, the urine protein–creatinine ratio, and diabetes. Furthermore, adding choline, glucose, or fumarate to traditional biomarkers, including eGFR and proteinuria, significantly improved the ability of the net reclassification improvement (P < 0.05) and integrated discrimination improvement (P < 0.05) to predict the composite outcome. Conclusion: Urinary metabolites, including betaine, choline, fumarate, citrate, and glucose, were found to be significant predictors of the progression of CKD. As a signature of kidney injury–related metabolites, it would be warranted to monitor to predict the renal outcome.

We investigated if clinical outcomes after kidney transplantation (KT) from deceased donors (DDs) with high Kidney Donor Profile Index (KDPI) can be different according to the age of KT recipients (KTRs). Six-hundred fifty-seven KTRs from 526 DDs were included from four transplant centers. We divided KTRs into elderly-KTR and young-KTR groups based on age 60 and each group was subdivided into high- or low-KDPI subgroup based on KDPI score of 65%. We compared short-term and long-term clinical outcomes among those four subgroups (low KDPI-young KTR, low KDPI-elderly-KTR, high KDPI-young-KTR, high KDPI-elderly-KTR). In short-term outcomes including acute rejection, BK virus and CMV infection, there was no significant difference among the four subgroups. In the long-term outcomes, the development of cardiovascular disease was higher in the high KDPI-elderly-KTR group than the other groups. In comparison of allograft survival rate, the high KDPI-young KTR subgroup showed highest risk for allograft failure and there was significant interaction between high-KDPI donors and young-KTR on allograft survival rate (P = 0.002). However, there was no significant difference in comparison of the patient survival rate. In conclusion, clinical impact of high-KDPI in DDs on post-transplant allograft survival may be less significant in elderly-KTR than in young-KTR.