Chronic kidney disease (CKD) requires assessment of both glomerular filtration and kidney damage, particularly albuminuria, for diagnosis, risk stratification, and longitudinal care. Point-of-care testing (POCT) can shorten turnaround time and improve access when conventional laboratory testing is unavailable or would delay a clinical pathway. This narrative review summarizes established and emerging POCT approaches for kidney assessment in CKD, with emphasis on creatinine/eGFR and urine albumin-to-creatinine ratio (UACR), and distinguishes analytical validity from workflow utility and patient-level clinical utility. Evidence is strongest for rapid creatinine measurement in selected workflows, especially pre-imaging assessment and decentralized screening, while quantitative/semiquantitative UACR POCT can support CKD detection when abnormal results are appropriately confirmed. Cystatin C microfluidic systems remain investigational, and kidney injury/stress or molecular biomarkers such as NGAL, KIM-1, L-FABP, [TIMP-2]·[IGFBP7], extracellular vesicles, and microRNAs should be regarded primarily as a research horizon rather than direct measures of GFR. Important implementation requirements include assay-specific validation, calibration traceability, quality assurance, recognition of biological and analytical interference, and confirmation of results near major clinical decision thresholds. Evidence that POCT improves long-term CKD outcomes, safety, adherence, or cost-effectiveness remains limited. Future studies should prioritize prospective clinical utility, implementation, cost-effectiveness, home-use validation, and patient-centered outcomes.

Acute kidney injury (AKI) remains a serious clinical condition associated with high rates of morbidity and mortality, while effective pharmacological treatment options remain limited. This systematic review and meta-analysis examined the effects of linagliptin in experimental models of AKI. The protocol was prospectively registered in PROSPERO (CRD420261399729), and the review was reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. PubMed, Scopus, Embase via Ovid, and Web of Science were searched from inception through 25 May 2026 to identify controlled in vivo studies evaluating linagliptin in mammalian AKI models. Pooled effect estimates were calculated using random-effects models, and methodological quality was assessed with the SYRCLE risk-of-bias tool. Six studies met the eligibility criteria. Compared with control treatment, linagliptin treatment resulted in significant reductions in serum creatinine, the primary outcome (mean difference [MD] = −1.17 mg/dL, 95% confidence interval −1.94 to −0.39; p = 0.0031; I² = 94.41%), and blood urea nitrogen (MD = −79.33 mg/dL, 95% CI: −130.38 to −28.27; p = 0.0023; I² = 99.15%). Changes in cystatin C, kidney injury molecule-1, inflammatory mediators, oxidative-stress indices, and apoptosis-related markers were also reported. However, the considerable heterogeneity indicated substantial variation among studies. Because only six studies were available and most potential subgroups contained one or two studies, reliable subgroup analyses by AKI induction model, animal species, linagliptin dose, or treatment duration could not be performed. Five studies had an unclear overall risk of bias, and publication bias could not be assessed. Therefore, the pooled estimates should be considered exploratory average associations across heterogeneous experimental models rather than uniform treatment effects. Additional rigorously designed preclinical studies are required to determine the reproducibility and translational relevance of these findings.

Acute kidney injury (AKI) is a major global health challenge associated with substantial morbidity, mortality, and progression to chronic kidney disease. Increasing evidence indicates that oxidative stress, mitochondrial dysfunction, inflammatory signaling, regulated cell death, and maladaptive tissue repair play central roles in AKI pathogenesis, yet effective disease-modifying pharmacological therapies remain unavailable. This narrative review critically evaluated current evidence regarding the pharmacological characteristics, molecular mechanisms, and translational potential of alpha-mangostin (AM), the principal prenylated xanthone isolated from the pericarp of Garcinia mangostana L., through a comprehensive synthesis of experimental and mechanistic studies. Available preclinical evidence consistently demonstrates that AM improves renal function and attenuates histopathological injury, particularly in cisplatin-induced nephrotoxicity and glycerol-induced rhabdomyolysis models. These renoprotective effects are primarily associated with suppression of oxidative stress, activation of the Nrf2/HO-1 antioxidant pathway, inhibition of NF-κB-mediated inflammatory signaling, preservation of mitochondrial function, and attenuation of apoptosis. Several emerging pathways may also contribute to AM-mediated renoprotective effects; however, current evidence remains indirect, and their roles require validation in kidney-specific models. Clinical translation remains limited by poor oral bioavailability, insufficient pharmacokinetic data, lack of standardized formulations, and the absence of human clinical trials. Overall, current evidence suggests that AM has preliminary renoprotective potential in experimental AKI models. However, the limited number of available studies, predominance of cisplatin-induced nephrotoxicity models, insufficient pharmacokinetic and safety data, and absence of human clinical studies preclude conclusions regarding its clinical efficacy or translational readiness. Further validation in diverse and clinically relevant AKI models is required before clinical investigation can be considered.