Amantadine-associated delirium in patients with maintenance dialysis: Insomnia-associated recovery and uneven seasonal distribution.

Amantadine hydrochloride is a risky drug for triggering delirium in dialysis patients; however, it is often administered casually. Furthermore, little is known regarding the recovery and prognosis of dialysis patients with amantadine-associated delirium. Data of this retrospective cohort study were collected from a local hospital database for hospitalizations between January 2011 and December 2020. Patients were divided into 2 cohorts: early recovery (recovery within 14 days) and delayed recovery (recovery more than 14 days). The cases were analyzed together with the intermonth temperature using descriptive statistics. A Kaplan-Meier survival curve and binary logistic regression were applied for the analyses of prognoses and factors. A total of 57 patients were included in this study. The most common symptoms were hallucinations (45.61%) and muscle tremors (43.86%). Early recovery was observed in 63.16% of the patients. Only 3.51% of the cases occurred in local summer (June, July, and August). Better prognoses for survival (hazard ratio [HR] = 0.066, 95% confidence interval [95% CI] = 0.021-0.212) and hospitalization costs (7968.42 ± 3438.43 CNY vs 12852.38 ± 9361.13 CNY, P = .031) were observed in patients with early recovery than in those with delayed recovery. In the multivariate logistic regression adjusted by 1:1 propensity score matching, delayed recovery was independently caused by insomnia (P = .022, = 10.119, 95% CI = 1.403-72.990) and avoided in patients with urine volume over 300 mL (P = .029, = 0.018, 95% CI = 0.006-0.621). The increment (per 100 mg) of cumulative dose (P = .190, = 1.588, 95% CI = 0.395-3.172) tended to be a risk of delayed recovery. The area under curve of the receiver operating characteristic curve was 0.867, with a sensitivity of 90.5% and a specificity of 82.4% at the cutoff point (cutoff = 0.432). For amantadine-associated delirium in dialysis patients with uneven seasonal distribution, early recovery with better prognosis should be the aim of treatment by giving priority to the remedy of insomnia.

TRAP1 ameliorates renal tubulointerstitial fibrosis in mice with unilateral ureteral obstruction by protecting renal tubular epithelial cell mitochondria.

Mitochondrial dysfunction causes renal tubular epithelial cell injury and promotes cell apoptosis and renal tubulointerstitial fibrosis (TIF) progression. TNF receptor-associated protein 1 (TRAP1) is a molecular chaperone protein that is localized in mitochondria. It plays an important role in cell apoptosis; however, its functional mechanism in TIF remains unclear. In this study, we observed the effects of TRAP1 in renal tubular epithelial cell mitochondria in mice with unilateral ureteral obstruction and its function in cell apoptosis and TIF. Results show that TRAP1 could protect the mitochondrial structure in renal tubular epithelial cells; maintain the levels of mitochondrial membrane potential, ATP, and mitochondrial DNA copy number; inhibit reactive oxygen species production; stabilize the expression of the mitochondrial inner membrane protein mitofilin; reduce renal tubular epithelial cell apoptosis; and inhibit TIF. These results provide new theoretical foundations for additional understanding of the antifibrotic mechanism of TRAP1 in the kidney.-Chen, J.-F., Wu, Q.-S., Xie, Y.-X., Si, B.-L., Yang, P.-P., Wang, W.-Y., Hua, Q., He, Q. TRAP1 ameliorates renal tubulointerstitial fibrosis in mice with unilateral ureteral obstruction by protecting renal tubular epithelial cell mitochondria.