“…In the native kidney, human studies have reported various markers associated with increased kidney stiffness: estimated glomerular filtrate rate (eGFR) [23,28,29], urinary albumin / creatinine or protein / creatinine ratio [30,33], serum creatinine [23,29], urea nitrogen [23], elasticity values in healthy native kidneys [23][24][25][26][27][28][29][30][31][32][33]35], kidney biopsies [25], other imaging tests etc [24,26,35]. Thus, there are studies finding no significant correlation between markers of chronic kidney injury and elasticity of renal parenchyma in native [27] or transplanted kidney [48,51], and also studies which could not prove a significant difference of elasticity between different stages of CKD [23,25]; in addition, it has been reported an increased intra-subject variability of results in CKD versus healthy controls [33] or a higher influence of arteriosclerosis markers, such as pulsatility index or resistivity index, on kidney stiffness than eGFR [28]. Such discrepancies may be explained not only by the heterogeneity of the markers utilized for the presence of fibrosis, by anatomic features of the kidney or by several confounders (age, BMI, technique variations etc), but also by the heterogeneity of primary kidney diseases which may be accompanied, in different stages of evolution, by inflammation, as it happens in the early phase of graft rejection or in vesicoureteral reflux.…”