In our earlier studies, we have shown that the markers of endothelial dysfunction and increased vascular leak (angiopoietin-2 and soluble fms-like tyrosine kinase-1) as well as the markers of kidney injury (neutrophil gelatinase-associated lipokalin in urine and in serum) are significantly associated with acute kidney injury in the early phase of AP as well as with subsequent severe course of AP [11,12,13,14]. The gene discussed is FLT1; the disease is alkaline phosphatase measurement.