Acute kidney injury (AKI) is increasing in prevalence and causes a global health burden. AKI is associated with significant mortality and can subsequently develop into chronic kidney disease (CKD). The kidney is one of the most energy-demanding organs in the human body and has a role in active solute transport, maintenance of electrochemical gradients, and regulation of fluid balance. Renal proximal tubular cells (PTCs) are the primary segment to reabsorb and secrete various solutes and take part in AKI initiation. Mitochondria, which are enriched in PTCs, are the main source of adenosine triphosphate (ATP) in cells as generated through oxidative phosphorylation. Mitochondrial dysfunction may result in reactive oxygen species (ROS) production, impaired biogenesis, oxidative stress multiplication, and ultimately leading to cell death. Even though mitochondrial damage and malfunction have been observed in both human kidney disease and animal models of AKI and CKD, the mechanism of mitochondrial signaling in PTC for AKI-to-CKD transition remains unknown. We review the recent findings of the development of AKI-to-CKD transition with a focus on mitochondrial disorders in PTCs. We propose that mitochondrial signaling is a key mechanism of the progression of AKI to CKD and potential targeting for treatment.

Chronic kidney disease (CKD), as a worldwide threat to public health, is a key determinant of poor health outcomes, but the severity of the problem is probably not fully appreciated

Background: Serum uric acid (UA) in end-stage kidney disease (ESKD) patients serves as a critical indicator for nutrition and inflammation, showing a U-shaped association with all-cause mortality. Methods: Our study assessed UA’s survival predictive value in 2615 ESKD patients, stratified by the Charlson Comorbidity Index (CCI) into groups of <4 (n = 1107) and ≥4 (n = 1508). Results: Cox regression revealed distinct patterns. For ESKD patients with CCI < 4, UA levels > 8.6 mg/dL were a mortality risk factor (HR: 1.61, 95% CI: 1.01–2.38) compared to 7.1–7.7 mg/dL. Conversely, in patients with CCI ≥ 4, UA levels < 5.8 mg/dL were a mortality risk factor (HR: 1.53, 95% CI: 1.20–1.95) compared to >8.6 mg/dL. Conclusions: Higher serum UA in ESKD patients with high comorbidities (CCI ≥ 4) is not a risk factor. Low UA should be prevented across all ESKD patients. A personalized approach using CCI and corresponding serum UA levels offers a key reference for managing UA in hemodialysis patients.