Acute Kidney Damage: Definition, Classification and Optimal Time of Hemodialysis

Abstract

Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated.

Basic Principles of Antibiotics Dosing in Patients with Sepsis and Acute Kidney Damage Treated with Continuous Venovenous Hemodiafiltration

“…Severe sepsis progresses to a septic shock, which is defined as a persistent hypotension that does not repair after resuscitation with 0.9% NaCl solution of crystalloid at a dose of 40-60 mL/kg in the first hour, requiring the use of the vasopressor norepinephrine in a dose > 5 μg/kg/min for maintenance of mean arterial blood pressure at values ≥ 65 mmHg, associated with clinical data for hypoperfusion (serum lactate concentration greater than 2.0 mmol/L) and organ dysfunction (SOFA score ≥ 2.0) [3,4]. The mortality rate of patients with severe sepsis, septic shock and acute kidney damage is 50-80% [5][6][7][8][9]. Patients in intensive care units with severe sepsis, septic shock and acute kidney damage require extended hospitalization, kidney replacement therapy, have high cost of treatment and an increased risk of developing insufficiency of multiple organ systems and unwanted outcomes [5][6][7][8][9].…”

“…The mortality rate of patients with severe sepsis, septic shock and acute kidney damage is 50-80% [5][6][7][8][9]. Patients in intensive care units with severe sepsis, septic shock and acute kidney damage require extended hospitalization, kidney replacement therapy, have high cost of treatment and an increased risk of developing insufficiency of multiple organ systems and unwanted outcomes [5][6][7][8][9]. Early detection of sepsis and acute kidney damage, early target therapy, early administration of antibiotics at an appropriate dose, and early extracorporeal therapy to replace the kidney function and removing the inflammatory mediators can correct the outcome in patients with sepsis in intensive care units [5][6][7][8][9].…”