Острое повреждение почек при пневмонии

Abstract

Mutual complications of impaired lung and kidney function in severe pneumonia (SP) complicated by acute kidney damage (AKP) are considered. The lungs and kidneys perform some similar functions, such as detoxification and regulation of acid-base balance. Lung damage is complicated by dysfunction or impaired renal function, and vice versa, AKI depressively affects lung function. Initially, all organs and tissues, including the kidneys, suffer from hypoxemic respiratory failure. SP is characterized by increased production of inflammatory mediators, decay products of microorganisms and their toxins and ejection them into the bloodstream. Endothelial vascular insufficiency, disseminated microvascular thrombosis, central hemodynamic disorders develop, and as a result, multiple organ failure develops. With the development of AKI, the elimination of uremic toxins and water is disrupted, hyperhydration is formed with an increase in the volume of extravascular water in the lungs on the background of the already existing broken airborne barrier. Uremic toxins depressively affect the heart muscle on the background of an acute pulmonary heart. There is evidence of a negative effect of mechanical ventilation on kidney function, and, conversely, of an adverse effect of AKI on the need and duration of ventilation. The progression of TP and AKP disrupts the acid - base balance due to excess CO2, impaired H+ ion release, and impaired synthesis of HCO3. The pathophysiological mechanisms underlying these relationships are complex, and their effect on the course of the disease is significant.