Management of acute kidney injury in cirrhosis

Abstract

Acute kidney injury (AKI) is a relatively frequent problem, occurring in approximately 20 % of hospitalized patients with cirrhosis. Although serum creatinine (S Cr) is the most commonly used method to determine AKI because of easy availability and low cost, practically it underestimates the extent of kidney injury in patients with chronic liver disease. AKI is defined as an abrupt rise in S Cr of 0.3 mg/dl or more (>26.4 mmol/l) or an increase of 150 % or more (1.5-fold) from baseline. The cause of AKI in cirrhosis is multifactorial and is unique in terms of pathogenesis. The most common causes of AKI in cirrhosis can be subdivided into either functional or structural. The functional group includes volume-responsive (prerenal azotemia) and volume-unresponsive states (hepatorenal syndrome). Volume responsive is the most common type of AKI due to frequent use of diuretics, large volume abdominal paracentesis and gastrointestinal bleeding in patients with liver disease. The structural causes include acute tubular necrosis, tubulointerstitial and glomerular diseases. Patients with decompensated cirrhosis are in a vasodilatory state leading to a decrease in effective arterial blood volume, predisposing to AKI. Therefore, management of AKI depends on the underlying cause, and therapy should be directed toward removal of the cause. The outcome in cirrhosis when patients are on dialysis is very dismal. Every effort should be made to prevent AKI.

Acute kidney injury in children with chronic liver disease

“…The predominant causes of AKI in cirrhosis can be either functional or structural. Functional causes include pre-renal azotemia and hepatorenal syndrome (HRS), while structural causes are predominantly due to intrinsic renal disease which may be tubulo-interstitial or glomerular in origin [26]. The importance of etiopathological diagnosis was demonstrated by Martín-Llahí et al, who found that the most common causes of AKI in cirrhosis were pre-renal azotemia, acute tubular necrosis (ATN) and HRS [27].…”

“…Injury to hepatocytes is known to produce DAMP (damage-associated molecular pattern) molecules, such as high-mobility group box-1 (HMGB1) proteins, which further increase the inflammatory response [13, 26]…”

“…Increased cytokine production upregulates NO synthase leading to increased production of NO and ultimately to exaggerated splanchnic vasodilation [ 50 ]. Injury to hepatocytes is known to produce DAMP (damage-associated molecular pattern) molecules, such as high-mobility group box-1 (HMGB1) proteins, which further increase the inflammatory response [ 13 , 26 ]…”

Cirrhosis and Renal Dysfunction

“…Hastanede takip edilen siroz hastalarının yaklaşık %20' sinde AKI gelişmektedir (6 (10). AKI gelişen 83 sirozlu hastanın değerlendirildiği bir çalışmada %53 ATN, %6 prerenal böbrek hasarı ve %22 HRS tespit edilmiştir (11).…”

Role of renal dysfunction in development of cirrhosis complications

“…Оба состояния характеризуются снижением почечного кровотока и могут привести к развитию почечной недостаточности. Отдельно выделяют гипонатриемию, в основе которой лежит задержка жидкости, непропорциональная задержке натрия, из-за чего снижается его относительная концентрация в крови -гиперволемическая гипонатриемия [9,12].…”