Acute Kidney Injury in Cirrhotic Patients with Portal Hypertension

So Mi Kim; Il Han Song

doi:10.4166/kjg.2016.68.5.237

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Kim and Song: Acute Kidney Injury in Cirrhotic Patients with Portal Hypertension

Review Article

Korean J Gastroenterol 2016;68(5):237-244.

Published online: 4 October 2016

DOI: https://doi.org/10.4166/kjg.2016.68.5.237

Acute Kidney Injury in Cirrhotic Patients with Portal Hypertension

So Mi Kim, Il Han Song

Department of Internal Medicine, Dankook University College of Medicine, Cheonan, Korea

Correspondence to: Il Han Song, Department of Internal Medicine, Dankook University Hospital, 201 Manghyang-ro, Dongnam-gu, Cheonan 31116, Korea. Tel: +82-41-550-3924, Fax: +82-41-556-3256, E-mail: ihsong21@dankook.ac.kr

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Acute kidney injury (AKI) is one of the most common manifestations encountered in clinical practice. It is associated with high morbidity and mortality in cirrhotic pre- and post-transplantation patients. Hepatorenal syndrome (HRS), a special form of AKI in cirrhotic patients, was recognized as a consequence of renal vasoconstriction from systemic/renal hemodynamic alterations developed in advanced cirrhosis with portal hypertension. Recently, multiple factors— such as infection/inflammation, underlying glomerulonephritis, bile cast, or increased abdominal pressure— have been considered to contribute to renal dysfunction in cirrhotic patients, which were presumed to induce HRS. Moreover, in addition to changing the definition of AKI in the nephrologic guidelines, the new AKI definition for early diagnosis and intervention based on characteristics of liver cirrhosis has been proposed in an international meeting. This article provides a comprehensive and recent review of AKI definition, laying out the topics in accordance with the pathophysiologic mechanisms and therapeutic interventions of AKI in cirrhotic patients with portal hypertension.

Keywords: Acute kidney injury, Hepatorenal syndrome, Liver cirrhosis, Portal hypertension

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Fig. 1.

Traditional and potential mechanisms of the development of acute kidney injury in cirrhotic patients with portal hypertension. NO, nitric oxide; CO, carbon monoxide; iNOS, inducible NO; TLR, toll like receptor; TNF, tumor necrosis factor; IL, interleukin; RAA, renin-angiotensin- aldosterone; SNS, sympathetic nervous system; PGE2, prostaglandin E2;6-keto PGF1, 6-keto-prostaglandin F1.

Table 1.

A Comparison of the Diagnostic Criteria of AKI in General Population and Cirrhotic Patients

	RIFLE	AKIN	KDIGO	ICA-AKI
Definition	↑ sCr×1.5 within 7 days or ↓ GFR ＞25% or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or
	↓ UO ＜0.5 mL/kg/hr for 6 hr	↑ sCr ≥150–199% within 48 hr or ↓ UO ＜0.5 mL/kg/hr for 6 hr	↑ sCr×1.5 time baseline to have occurred within 7 days or	↑ sCr×1.5, baseline to have occurred within 7 days
			↓ UO ＜0.5 mL/kg/hr for 6 hr
Staging	Risk	Stage 1	Stage 1	Stage 1
	↑ sCr×1.5 within 7 days or ↓ GFR ＞25% or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or	↑ sCr ≥26.5 μ mol/L (0.3 mg/dL) within 48 hr or
	↓ UO ＜0.5 mL/kg/hr for 6 hr	↑ sCr ≥150–199% within 48 hr or ↓ UO ＜0.5 mL/kg/hr for 6 hr	↑ sCr×1.5 baseline to have occurred within 7 days or	↑ sCr×1.5 baseline to have occurred within 7 days
			↓ UO ＜0.5 mL/kg/hr for 6 hr
	Injury	Stage 2	Stage 2	Stage 2
	↑ sCr×2 or	↑ sCr ≥200–229% within 48 hr or	↑ sCr×2 or	↑ sCr×2
	↑ GFR ＞50% or	↓ UO ＜0.5 mL/kg/hr for 12 hr	↓ UO ＜0.5 mL/kg/hr for 12 hr
	↓ UO ＜0.5 mL/kg/hr for 12 hr
	Failure	Stage 3	Stage 3	Stage 3
	↑ sCr×3 or GFR ＞75% or	↑ sCr ≥300% or	↑ sCr×3 or	↑ sCr×3 or
	If baseline	If baseline	If baseline	If baseline
	↑ sCr ≥353.6  mol/L (4.0 mg/dL) with ↑ sCr 44.2  mol (0.5 mg/dL) or ↓ UO ＜0.3 mL/kg/hr for 24 hr or anuria for 12 hr	↑ sCr ≥353.6  mol/L (4.0 mg/dL) with ↑ sCr 44.2  mol (0.5 mg/dL) or ↓ UO ＜0.3 mL/kg/hr for 24 hr or anuria for 12 hr or	↑ sCr ≥353.6  mol/L (4.0 mg/dL) or ↓ UO ＜0.3 mL/kg/hr for 24 hr or anuria for 12 hr	↑ sCr ≥353.6  mol/L (4.0 mg/dL) with ↑ sCr 44.2  mol (0.5 mg/dL) Initiation of RRT
		Initiation of RRT
Outcomes	Loss of kidney function			Response to treatment
	Complete loss ＞4 weeks			No response
	End-stage kidney disease			No regression of AKI
	Complete loss ＞3 months			Partial response
				Regression of AKI stage with reduction of sCr ≥26.5  mol/L (0.3 mg/dL)
				Full response
				Return to sCr to a value within 26.5  mol/L (0.3 mg/dL) of baseline value

AKI, acute kidney injury; RIFLE, Risk, Injury, Failure, Loss, End-stage kidney disease; AKIN, Acute Kidney Injury Network; KDIGO, Kidney Disease Improving Global Outcome; ICA, International Club of Ascites; sCr, serum creatinine; GFR, glomerular filtration rate; UO, urine output; RRT, renal replacement therapy.

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