CLINICAL, ETIOLOGICAL AND PROGRESSIVE ASPECTS OF ACUTE TUBULAR NECROSIS OF TOXIC ORIGIN AT THE SAMARKAND STATE MEDICAL UNIVERSITY HOSPITAL CENTER

Abstract

Acute kidney injury (AKI) is defined as an increase in serum creatinine of 50% in 7 days, or 3 mg/L in 2 days, or oliguria [1] . In practice, it is a rapid decline in renal function occurring over several hours or several days, characterized by metabolic disturbances, which, if major, can quickly have lethal consequences [2] . It is staged in 3 stages depending on its severity [3] . Pathophysiologically, we distinguish 3 types of AKI: pre-renal AKI, intrinsic renal AKI and post-renal AKI with various etiologies [4] . In Sub-Saharan Africa, the intra-hospital incidence rate of AKI is estimated at 25.3% [5] . And the acute tubular necrosis (ATN) toxic origin is the second cause of AKI after infections [6] . Indications for dialysis are common [7] [8] . In the Republic of Congo, the intra- hospital incidence of AKI is reported at 13.4% [7] , dehydration and ATN of toxic origin are the main causes [7] . Intrinsic renal AKI is a risk factor for chronic kidney disease (CKD) [9] . Dialysis centers are rare in Congo [7] [8] , so it is necessary to place an emphasis on prevention. Prevention of ATN involves controlling its etiologies, and therefore toxic substances, in order to avoid them. Our study had two objectives of describing the clinical profile of toxic ATN and determining the toxic substances at the origin of ATN in Samarkand, the evolutionary aspects and the factors associated with healing.