This review aims to provide a comprehensive overview of the pathophysiological processes involved in early kidney injury and to evaluate the role of established and emerging biomarkers in facilitating earlier diagnosis, risk stratification, and clinical decision-making, particularly within urological practice. Specifically, the review: (i) outlines the key mechanisms underlying the development of early kidney injury; (ii) examines the current evidence supporting established and novel biomarkers of kidney injury and renal dysfunction; (iii) evaluates their diagnostic, prognostic, and clinical relevance in urology; and (iv) explores existing challenges, future directions, and the potential incorporation of biomarker-guided approaches into precision medicine strategies for kidney injury management. This review examines the underlying mechanisms of early kidney injury, including ischemia, hypoxia, oxidative stress, and the differential contributions of tubular and glomerular damage. Particular attention is given to clinical contexts relevant to urology, such as surgical interventions and obstructive uropathy, where timely detection is essential for preventing irreversible damage. Current and emerging biomarkers are discussed within a pathophysiological framework to provide a more integrated understanding of kidney injury. Tubular injury markers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18), are highlighted for their ability to detect injury at an earlier stage than traditional measures. In addition, cell cycle arrest biomarkers such as TIMP-2 and IGFBP7 offer predictive value by identifying patients at risk before significant functional decline occurs. The review further explores novel and experimental approaches, including microRNAs, urinary exosomes, and metabolomics-based markers, which may enhance early diagnosis and support precision medicine strategies. Importantly, the clinical relevance of these biomarkers is examined in specific urological settings, including postoperative AKI, contrast-induced injury, obstructive uropathy, and kidney injury associated with renal cell carcinoma. The novelty of this review lies in its integration of mechanistic insights, biomarker biology, and disease-specific urological applications within a single translational framework. Unlike previous reviews that focus primarily on individual biomarkers or general AKI populations, this work emphasizes the relationship between specific injury pathways and biomarker responses, while highlighting emerging precision medicine approaches and their potential role in urological patient care.

Background: Many deaths during heat waves stem not only from body overheating but also from heat stress, which can intensify pre-existing medical conditions, leading to fatal outcomes. Aim: This study aimed to investigate whether the intensity of pathological changes in the heart muscle and lung tissue of albino rats exposed to hyperthermia correlates with different water temperatures (WT) and to determine whether the histological structure of the myocardium and lungs varies. Methods: A sample of 21 albino rats was exposed to water temperatures of 37°C, 41°C, and 44°C. Temperature readings were recorded before immersion, immediately after immersion, at the point of reaching hyperthermia, at 20 minutes, and at the time of death. Tissue samples were collected from the dissected rats, fixed in 10% buffered formalin at room temperature, embedded in paraffin, sectioned into 4–5 μm slices, and stained using the hematoxylin-eosin method. Results: The severity of myocardial histopathological alterations increased with both higher temperatures and longer exposure durations WT. However, the progression of morphological alterations in cardiomyocytes was not markedly significant, likely due to the brief exposure time, which limited the visualization of subcellular alterations in Hematoxylin and Eosin staining-stained tissue. All lung samples from the seven rats exposed to the highest temperatures displayed bronchiolitis and acute bronchitis, along with early bronchopneumonia. Conclusion: While some organs exhibit greater tolerance to heat stroke than other organs, most organs show similar alterations characterized by capillary dilation, vascular pathway disruption, and extravasation. The extent of pathological changes in myocardial and lung tissue intensified with higher temperatures and longer exposure durations to elevated WT. However, the progression of morphological alterations in cardiomyocytes did not demonstrate marked significance, likely because of the brief exposure period. This short duration may limit the detection of subcellular changes when using hematoxylin-eosin staining.