The effect of rhGH on bone metabolism is of particular Borrelidin interest since CKD-MBD and growth retardation are often connected. However, monitoring of CKD-MBD is challenging. Bone biopsy is considered the gold standard procedure but, due to its invasiveness, currently recommended only in exceptional clinical situations.Whereas plain X rays lack sensitivity, bone density measurements are more informative but still involve repetitive exposure to radiation. Hence, serum parathormone, calcium and phosphorus constitute the mainstay of CKD-MBD monitoring in routine clinical practice. In 2006 KDIGO first recommended a detailed evaluation of emerging new biomarkers that may reflect bone cell activity in patients with CKD. For children, the particular need to investigate potential associations to linear growth was emphasized. Here, we investigated in a large pediatric CKD population a panel of serum proteins potentially reflecting the activity of different bone cell types. Bone alkaline phosphatase, an osteoblast enzyme, is a sensitive and specific marker of bone formation and remodeling. The KDIGO 2009 guidelines suggest measuring either intact serum parathormone or BAP, since markedly altered levels are informative of bone turnover. In Conantokin-R children BAP levels peak during infancy and puberty, mirroring the physiological activation of bone formation during these periods of rapid longitudinal growth. Tartrate-resistant acid phosphatase 5b degrades bone matrix proteins and is considered a specific marker of late osteoclast differentiation. The peptide sclerostin is a novel key regulator of bone turnover. It is released mainly by osteocytes as a paracrine negative feedback signal regulating bone formation by inhibiting the differentiation of osteochondral precursor cells to osteoblasts. Finally, fibroblast growth factor 23 is a key endocrine player in the regulation of bone mineral metabolism. Synthesized and released by osteocytes and osteoblasts and targeting the renal tubule, FGF-23 plays an important role in maintaining mineral and vitamin D homeostasis. Whereas the mechanisms and pathways of bone metabolism and the biological functions of the biomarker proteins are well established, their precise association to CKD-related abnormalities of bone metabolism and their role in height and growth of children with CKD is still controversial. Age- and gender-related differences and usually small available sample sizes add a further level of complexity to the interpretation of circulating bone markers in pediatric studies. Recently, pediatric reference values have been established for BAP, TRAP5b, sclerostin and c-terminal FGF-23, allowing age- and gender independent assessment of bone turnover in chronically diseased children. The 4C Study consortium is following the largest cohort of children with CKD assembled to date.