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Abstract: TH-PO165

Effect of Gastrointestinal Factors on Bone Turnover Markers in ESRD

Session Information

Category: Bone and Mineral Metabolism

  • 502 Bone and Mineral Metabolism: Clinical


  • Jørgensen, Morten Buus, Rigshospitalet, Department of Nephrology, Copenhagen, Denmark
  • Mace, Maria Lerche, Rigshospitalet, Department of Nephrology, Copenhagen, Denmark
  • Knop, Filip K., Gentofte Hospital, Center for Clinical Metabolic Research, Gentofte, Denmark
  • Idorn, Thomas, Novo Nordisk A/S, Søborg, Denmark
  • Jørgensen, Niklas Rye, Rigshospitalet, Department of Clinical Biochemistry, Glostrup, Denmark
  • Hartmann, Bolette, University of Copenhagen, Department of Biomedical Sciences, Copenhagen, Denmark
  • Holst, Jens Juul, University of Copenhagen, Department of Biomedical Sciences, Copenhagen, Denmark
  • Hornum, Mads, Rigshospitalet, Department of Nephrology, Copenhagen, Denmark
  • Feldt-Rasmussen, Bo, Rigshospitalet, Department of Nephrology, Copenhagen, Denmark

Chronic kidney disease - mineral and bone disorder (CKD-MBD) is a serious but not yet fully understood complication to CKD. Recent studies show that an oral glucose challenge affects bone resorption to a larger extent than intravenously administered glucose – the so-called gut-bone axis. Here, we investigated the effect of gastrointestinal factors on bone-turnover in end-stage renal disease.


Plasma samples from a previously published study involving 10 patients receiving chronic hemodialysis treatment (ESRD) and 11 healthy controls (CTRL) with normal glucose tolerance were analyzed post hoc. On two separate examination days, participants were studied in a fasted state with a 3h oral glucose tolerance test (OGTT) and an isoglycemic intravenous glucose infusion (IIGI) mimicking the plasma glucose excursions on the OGTT day. Carboxy-terminal collagen type 1 crosslinks (CTX), procollagen type I N-terminal propeptide (PINP), bone-specific alkaline phosphatase (BAP) and intact parathyroid hormone (PTH) were measured at baseline and every 30 minutes during OGTT and IIGI. All bone-turnover marker concentrations were evaluated relative to baseline levels and average excursions calculated using baseline-subtracted area under the curve (AUC). Values are expressed as median [IQR] or mean (95% CI).


Median baseline concentrations of CTX (2.3 [1.9;4.9] (ESRD) vs. 0.4 [0.4;0.8] ng/ml (CTRL), P = 0.014) and PTH (292 [146;500] (ESRD) vs. 44 [32;73] pg/ml (CTRL), P = 0.003) were significantly elevated in patients compared to controls while PINP (142 [54;274] (ESRD) vs. 67 [60;78] ng/ml (CTRL)) and BAP (13.4 [10.8;20.5] (ESRD) vs. 15.3 [11.4;17.1] µg/l (CTRL)) were comparable.
CTX was significantly suppressed during OGTT in both groups but to a significantly lesser extent in ESRD compared to CTRL (-15 (-20;-9)%) vs. (-43 (-50;-36)%; P < 0.001). During IIGI, CTX was significantly suppressed in CTRL (-15 (-21;-9)%) but not in ESRD (-1 (-6; 4)%). Neither P1NP nor BAP changed from baseline in response to OGTT or IIGI whereas PTH showed significant suppression in response to OGTT (but not to IIGI) in CTRL (-9 (-15;-4)%).


Suppression of the bone resorption marker CTX in response to OGTT is impaired in ESRD indicating that gastrointestinal factors may play a role in CKD-MBD.


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