Additional mutations in the calreticulin (CALR) gene (typically in exon 9) and the myeloproliferative leukemia virus oncogene (MPL), which encodes the thrombopoietin receptor (TPO-R), have also been associated with increased thrombotic risk and endothelial damage—two major contributors to renal dysfunction [7]. This evidence concerns the gene CALR and Abnormal renal physiology.