Renal dysfunction in general overheating (literature review)

Abstract

Over the past 30 years, climate change has taken one of the leading places among the ten main causes of death due to natural disasters. Rising temperatures have been shown to increase emergency department admissions for a wide range of kidney diseases, including acute kidney injury (AKI), chronic kidney disease, kidney stones, and urinary tract infections. The occupational effect of heat stress is also associated with AKI, which can quickly progress to acute kidney failure with high mortality. The basis of the pathogenetic mechanisms of heat-induced AKI is a decrease in the circulating blood volume and electrolyte disturbances due to increased perspiration. Water evaporation from the surface of the skin contributes to dehydration with an increase in serum osmolarity. In response to this, vasopressin is activated, the specific gravity of urine increases, and the amount of urine decreases. The glomerular filtration rate progressively decreases. Hypokalemia develops, which changes to hyperkalemia within 12 hours. Tubular endothelium is damaged, which leads to microthrombosis of afferent and efferent renal arteries, the development of an inflammatory response, and exhaustion of the renal interstitium. Possible rhabdomyolysis and myoglobinemia with subsequent tubular obstruction worsen existing kidney damage. According to the leading mechanism of damage, there are two types of acute heat damage to the kidneys: classical rhabdomyolysis and acute interstitial nephritis. Although modern medical advances have contributed to the development of effective treatment and management strategies (rapid cooling, extracorporeal detoxification methods, etc.), mortality in kidney damage due to general overheating has decreased slightly over the past decades. For health care and industry researchers, it is necessary to identify the harmful occupational conditions that lead to heat stress nephropathy and to develop certain occupational safety strategies.