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Heat stress (HS) is a growing public health concern as rising global temperatures and occupational hazards expose a significant portion of the world's population to extreme heat. The kidneys are particularly vulnerable to heat-induced injuries, with oxidative stress (OS) playing a central role in their pathogenesis. The process involves heat-induced mitochondrial dysfunction and stimulation of inflammatory pathways. This leads to the production of excessive reactive oxygen species (ROS) that eventually overwhelm the kidney's natural antioxidant defenses. The resultant OS directly damages lipids, proteins, and DNA in renal tubular cells, a condition that is worsened by systemic inflammation and renal hypoxia. Although cells initially activate protective mechanisms involving heat shock proteins (HSPs) to preserve mitochondrial integrity, prolonged heat exposure undermines these defenses, increasing stress and triggering apoptotic pathways. This article focuses on the impact of HS on kidney health and the role of OS in the pathogenesis of heat-induced kidney injuries. Key markers of heat-induced OS, such as lipid peroxidation products (e.g., malondialdehyde [MDA], F₂-isoprostanes, 4-hydroxynonenal [4-HNE], and 8-hydroxy-2'-deoxyguanosine [8-OHdG]) and their effects on hematological indices and inflammatory response are highlighted. Ultimately, clarifying these specific mechanisms is essential to guide the development of early diagnostic tools and targeted treatments. This will help to reduce kidney damage, especially in vulnerable populations. We suggest that strategies such as adequate hydration, educating vulnerable groups on signs of heat strain, wearing light clothing, and heat acclimatization can mitigate the adverse effects of the rising global temperatures on kidney health.