Transition from acute kidney injury to chronic kidney disease in liver cirrhosis patients: Current perspective

Table 1 Important issues involving transition of acute kidney injury to chronic kidney disease in patients with liver cirrhosis

Factors	Description
Risk factors for CKD transition	AKI characteristics: Recurrent AKI, severe AKI, acute kidney disease
	Metabolic factors: Diabetes mellitus, hypertension, metabolic dysfunction-associated steatotic liver disease
	Cirrhosis factors: Higher model for end-stage liver disease scores, neuro-hormonal alterations
	Etiological factors: Alcohol, hepatis B virus and hepatitis C virus (glomerulonephritis)
Putative mechanisms for chronic liver disease transition	Maladaptive repair mechanism: Cell cycle arrest and cellular senescence
	Inflammation and fibrosis: Profibrotic cytokines, myofibroblast generation, and increase in extracellular matrix
Clinical impacts of CKD	Refractory ascites and increased frequency of bacterial infection
	Increased frequency of AKI
	Need for dialysis and need for liver transplantation and simultaneous liver and kidney transplantation
	Higher mortality risk
Novel biomarkers for AKI-CKD	Kidney injury molecule-1
	Neutrophil gelatinase-associated lipocalin
	Tissue inhibitor of metalloproteinases-2
	Uromodulin and dimethylarginine
	Liver type-fatty acid binding protein
Future potential therapies	Targeted transforming growth factor-β inhibition
	Modulation of renin-angiotensin-aldosterone system, endothelial dysfunction and oxidative stress biomarker driven therapy
	Hypoxia inducible factor stabilizers
	Mesenchymal stem cell therapies

AKI: Acute kidney injury; CKD: Chronic kidney disease.