When considered as biomarkers for IF <20 or > 40%, mineral metabolism markers were however neither more discriminant, nor additive when compared to renal function parameters (eGFR and proteinuria). 0. 61) but did not add to renal function prediction. T50decreased with increasing arterial lesions (r = -0. 21, p = 0. 038). The discriminative performance of T50in predicting significant vascular lesions was modest (AUC 0. 61). In summary, we demonstrated that PTH, vitamin 6H05 (TFA) D and T50are associated to interstitial fibrosis and vascular lesions in kidney allograft recipients independently of renal Slc2a3 function. Despite these associations, mineral metabolism indices do not show superiority or 6H05 (TFA) additive value to fibrosis prediction by eGFR and proteinuria in kidney allograft recipients, except for vascular lesions where T50 could be of relevance. == Intro == Renal interstitial fibrosis (IF) and arterial lesions are predictive of loss of renal function in chronic kidney disease (CKD) [13]. Kidney allografts are very prone to develop IF and vascular lesions secondary to acute or chronic rejection, and to calcineurin inhibitors toxicity [46]. Currently, IF and arterial lesions are evaluated by histopathology which necessitates kidney biopsies [710]. There are however many limitations to histopathological assessment, such as sampling error or bias, semi-quantitative and poorly reproducible scoring, biopsy complications and cost of the procedure [11]. Established noninvasive tools 6H05 (TFA) to estimate kidney IF and vascular lesions are currently not available. These would be very helpful intended for the evaluation of the whole organ without the inherent risks associated to repeated biopsies. Indeed, a better non-invasive appreciation of the formation of IF and arterial lesions in patients would allow earlier treatment adaptation and better follow-up. Amongst potential tools, phosphocalcic biomarkers are of interest. Disorders in phosphorus and calcium metabolism are common in CKD. In addition to the traditional markers such as calcium, phosphate, parathyroid hormone (PTH) and vitamin D levels, new biomarkers such as Klotho and fibroblast growth factor 23 (FGF23) are emerging. Klotho is a protein mainly expressed in kidney tubular cells. During early phases of experimental CKD, Klotho expression is downregulated [12, 13]. In humans, this early decrease in soluble Klotho can be measured [14]. Klotho downregulation plays an important role in kidney fibrosis progression by different modalities including repression of the WNT pathway [1518]. In addition , lower Klotho levels are associated with higher prevalence of cardiovascular disease, arterial stiffness and vascular calcification in the experimental setting and in some clinical observations [15, 17, 19, 20]. This could be related to Klothos direct phosphaturic properties [13] and its role as an FGF23 receptor cofactor. Klotho loss may therefore be a sensitive marker for nephron loss, early fibrosis formation and could also be an interesting marker of chronic vascular lesions. FGF23 is a key phosphaturic hormone produced by osteocytes and osteoblasts that increase early in CKD [21, 22]. The cause of this elevation is still debated, but may result from phosphate retention, Klotho loss, and kidney production of FGF23 or abnormal bone regulation. FGF23 is therefore a sensitive marker of kidney disease and cardiovascular complications in CKD. Whether 6H05 (TFA) FGF23 indicates chronic kidney histological changes has not been studied so far. All parameters of mineral metabolism are to some extent related: suppression of Klotho increases FGF23 levels, which in turn suppresses vitamin D. Increased phosphate, FGF23 and parathyroid hormone (PTH) are independent risk factor for CKD progression and cardiovascular mortality not only in primary CKD but also in kidney allograft recipients [21, 2340]. However , whether mineral metabolism components correlate with IF and vascular lesions and could be earlier markers than eGFR intended for histological lesions is not known. In addition to these new biomarkers, a blood test was recently described that measured the blood calcification propensity by monitoring the maturation 6H05 (TFA) time (T50) of calciprotein particles in serum [41]. High calcification propensity (or low T50) was closely associated with progressive aortic stiffening and increased long-term mortality in CKD patients [42, 43]. Surprisingly, T50was also predictive of renal function loss in kidney allograft recipients [44]. However , this test has not yet been studied in association with renal histological lesions. Due to the lack of data on the relation between phosphocalcic markers and chronic histological changes,.