Chronic kidney disease begins with acute kidney injury

Abstract

The paper discusses the development of chronic kidney disease (CKD). It is postulated that acute kidney injury (AKI) may be the onset of CKD formation. The pathogenesis of acute kidney injury transition to acute kidney disease is based on the restriction of sodium reabsorption in the tubules, stimulation of the intrarenal renin-angiotensin system and restriction of blood flow in the nephron. The authors express the opinion that the practical aspect of this mechanism is the correction of hyponatremia, which leads to the restoration of normal blood supply to the nephron. Thus, the iatrogenic restriction of sodium chloride in the diet of AKI patients may be erroneous. The authors present the pathogenetic stages of CKD development from hypoxia to ischemia and the formation of sclerosis. It is emphasized that there are 3 categories of nephrons. The first one with normal function, the second one with limited function and the third — sclerosed ones. Restoration of blood flow is accompanied by an increase in the glomerular filtration rate, which characterizes the functional renal reserve. Its value determines the kidney ability to respond to negative factors and to realize the effectiveness of therapy for primary kidney disease. The article pre­sents the latest International Society of Nephrology guidelines on the use of steroidal and non-steroidal mineralocorticoid receptor antagonists. The authors also present a scheme for determining the effectiveness of therapy depending on the functional renal reserve against the background of glomerular filtration rate, albuminuria level and existing hypertension.