Acute kidney injury (AKI) is a common and severe complication following renal transplantation, largely driven by ischemia-reperfusion injury (IRI). However, reliable biomarkers for post-transplant AKI remain unavailable. In this study, we analyzed transcriptomic datasets from multiple cohorts to identify robust gene signatures associated with transplant-related AKI. Weighted gene co-expression network and differential expression analyses in the discovery cohort revealed 222 candidate genes altered during early allograft IRI, which were subsequently refined in an integrated training cohort using least absolute shrinkage and selection operator (LASSO) regression and support vector machine-recursive feature elimination (SVM-RFE) to a four-gene signature comprising SOCS3, MYC, TGIF1, and LETM2. This signature showed excellent discriminative performance in the training cohort (10-fold cross-validation AUC = 0.969) and was validated in independent external datasets, including a large cohort (AUC = 0.942). Decision curve analyses indicated potential clinical utility for early AKI identification across a broad threshold-probability range, with favorable performance compared with several established biomarkers such as neutrophil gelatinase-associated lipocalin. Single-cell transcriptomics revealed cell type-specific expression of the four genes across renal compartments. Moreover, their protein levels were elevated at 24 h after IRI in mouse kidneys, and displayed high expression in human AKI biopsies. Additionally, serum protein levels of SOCS3 and LETM2 were elevated in patients with cardiac surgery-associated AKI, whereas TGIF1 and MYC did not reach statistical significance. Collectively, this study identified a four-gene signature with potential utility as an early diagnostic biomarker panel for post-transplant AKI. Further large-scale clinical trials are needed to validate its diagnostic efficacy.

Long non-coding RNAs (lncRNAs) have emerged as critical regulators of kidney homeostasis, and their dysregulation has been implicated in a wide range of kidney diseases including acute kidney injury, chronic kidney disease and renal cell carcinoma, as well as in age-related kidney dysfunction. Increasing evidence indicates that lncRNAs have roles in key cellular processes including inflammation, autophagy, cell proliferation, senescence, apoptosis, mitochondrial dysfunction, angiogenesis, epithelial-mesenchymal transition and interstitial fibrosis. LncRNAs interact with RNA, DNA and protein to regulate gene expression via multiple mechanisms, including RNA modifications, scaffold assembly, chromatin remodelling, transcription and post-transcriptional control. Beyond their non-coding functions, some lncRNAs can be translated into bioactive micropeptides that further modulate cellular activity. Given their tissue-specific expression and high stability in body fluids, lncRNAs hold promise as biomarkers for early detection and monitoring of kidney diseases. Furthermore, lncRNA-based therapies offer novel opportunities to halt disease progression in chronic kidney disease and overcome drug resistance in renal cell carcinoma. Improved understanding of lncRNA-mediated disease mechanisms could therefore lead to improvements in the diagnosis and treatment of kidney pathologies.

The necessity of iodinated contrast agents in radiographic diagnosis comes with an increased risk of kidney injury. The sclerotium of Poria cocos (Schw.) Wolf, a traditional Chinese medicine, exhibits anti-inflammatory and diuretic pharmacological properties. Its extracted polysaccharides demonstrate anti-apoptotic, antioxidant, and anti-inflammatory activities. This study aimed to investigate the effects and potential mechanisms of Poria cocos polysaccharides (PCP) on contrast-induced acute kidney injury (CI-AKI). The purified PCP was characterized using FTIR and monosaccharide analysis. A CI-AKI mouse model was established to evaluate its preventive effects via oral gavage. Mitochondrial structure, function, and biogenesis were assessed by measuring mitochondrial membrane potential (MMP), ROS, ATP, and mitochondrial DNA copy number. Antioxidant capacity and apoptosis levels were evaluated by detecting 8-OHdG, caspase 3/7 activity, cleaved-PARP, MDA, and GSH. Finally, the mechanism of action of PCP was analyzed using qPCR and immunoblotting. The results showed that PCP significantly mitigated CI-AKI by inhibiting contrast-induced apoptosis and oxidative stress in kidney tissue. Furthermore, PCP maintained mitochondrial homeostasis in the kidneys by enhancing mitochondrial biogenesis and antioxidant capacity. These findings were consistent with in vitro data. Notably, PGC-1α was identified as a key factor in the nephroprotective effects of PCP, with its activation attributed to the CaMKK2-AMPK signaling pathway. These findings suggest that PCP offers significant benefits in mitigating CI-AKI by enhancing antioxidant defenses and promoting mitochondrial biogenesis through activation of the CaMKK2/AMPK/PGC-1α signaling pathway in the kidney. Therefore, PCP could be a potential preventive agent for CI-AKI.

The atherogenic index of plasma (AIP) is a lipid-based marker of cardiovascular risk, yet its prognostic value for severe acute kidney injury (AKI) in critically ill patients with cardiovascular disease (CVD) remains uncertain. This retrospective study analyzed 5,872 patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, with external validation in the eICU Collaborative Research Database (eICU-CRD). The primary outcome was stage 3 AKI, and secondary outcomes included renal replacement therapy (RRT) and length of stay. Stage 3 AKI was observed in 20.7% of patients, with the incidence increasing across AIP quartiles (Q1-Q4: 15.9-26.8%), and 5.3% of patients requiring RRT (Q1-Q4: 2.6-10.9%). High AIP was associated with stage 3 AKI (adjusted OR = 1.35; 95% CI: 1.11-1.64), RRT (OR = 1.95; 95% CI: 1.33-2.87), longer hospital LOS (β = 3.58; p < 0.001) and ICU LOS (β = 1.14; p < 0.001). Restricted cubic splines revealed linear associations between AIP and both renal outcomes (stage 3 AKI and RRT). Mediation analysis indicated that stage 3 AKI mediated 12.6% of the association between the AIP and in-hospital mortality. The predictive models achieved AUCs of 0.916 for RRT and 0.727 for stage 3 AKI. These associations with renal outcomes were robust, as confirmed by entropy balancing and external validation in the eICU-CRD. Elevated AIP is a robust, externally validated predictor of stage 3 AKI and RRT, with substantial predictive accuracy for RRT. Furthermore, it appears to influence in-hospital mortality partially through renal injury, warranting confirmation in future prospective studies.

Renal trauma is the most frequent type of genitourinary injury, while unilateral renal agenesis is an uncommon congenital anomaly. When trauma involves a solitary kidney, it raises significant concern due to the risk of compromised overall renal function. We report the case of a 25-year-old male patient presenting with blunt trauma to the right flank following a horse kick. Imaging revealed a Grade III renal injury in a solitary kidney due to contralateral agenesis. The patient was managed conservatively with close monitoring and supportive care, resulting in a favorable clinical and radiological outcome. This case highlights the effectiveness of non-operative management in hemodynamically stable patients, even in the context of a solitary kidney, with careful surveillance to prevent complications.