This article provides a thorough overview of the biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI) and acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical applications. This review also highlights the links between renal injury and the pathophysiological mechanisms underlying AKI and AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and the cellular senescence of renal cells. Key signaling pathways, such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The renin–angiotensin–aldosterone system (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating the oxidative stress and cellular changes that promote fibrosis. The clinical evidence suggests that RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

This article provides a thorough overview of biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI), acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical application. The pathophysiological mechanisms underlying AKI, AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses, with the impact on renal injury. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and cellular senescence of renal cell. Key signaling pathways, such as Wnt/β-Catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The Renin-Angiotensin-Aldosterone System (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating oxidative stress and cellular changes that promote fibrosis. Clinical evidence suggests RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

Immune checkpoint inhibitors (ICIs) are widely used in cancer therapy but can cause adverse events, including acute kidney injury (AKI). The incidence of ICI-associated AKI (ICI-AKI) varies across studies, and while steroids may aid in kidney recovery, their full effects require further investigation. Additionally, the risk of recurrent AKI with ICI rechallenge remains uncertain. This study assesses the incidence of ICI-AKI, evaluates steroid efficacy, and examines the risk of recurrent AKI after ICI-AKI. A comprehensive search of PubMed, Embase, and the Cochrane Library was conducted through May 2024. Outcomes included the incidence of ICI-AKI, kidney recovery after steroid therapy, and the risk of recurrent AKI with ICI rechallenge. A random-control model was used for analysis. This analysis included 16 studies involving 10,726 participants. The pooled incidence of ICI-AKI after following up for one year was 1.4% (95% CI 1.0-2.1%), with the incidence rate being 4.3 per 100 patient-years (95% CI 2.3-6.3 per 100 patient-years). ICI-AKI patients treated with steroid were more likely to achieve kidney recovery (OR 1.82, 95% CI 1.17-2.83, P = 0.008). No additional benefit was found from combining intravenous and oral steroids (OR 0.928, P = 0.863). The incidence of recurrent AKI after ICI-AKI was 18.0% (95% CI 13.2-23.9%). A substantial incidence of ICI-AKI of those receiving ICI was identified. Steroid treatment promotes kidney recovery, but adding intravenous steroids offers no additional benefit. There is an elevated risk of recurrent AKI with ICI rechallenge, underscoring the need for careful monitoring of kidney function.