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BMC Nephrol. 2018 Nov 15;19(1):327. doi: 10.1186/s12882-018-1114-z.

Influence of exogenous growth hormone administration on circulating concentrations of α-klotho in healthy and chronic kidney disease subjects: a prospective, single-center open case-control pilot study.

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Department of Nephrology, VU University Medical Center, De Boelelaan 1117, 1081, HV, Amsterdam, The Netherlands.
Department of Physiology, Radboud University Medical Center Nijmegen, Nijmegen, The Netherlands.
Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, Groningen, The Netherlands.
Department of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands.
Department of Nephrology, VU University Medical Center, De Boelelaan 1117, 1081, HV, Amsterdam, The Netherlands.
Amsterdam Cardiovascular Sciences (ACS), Amsterdam, The Netherlands.



The CKD-associated decline in soluble α-Klotho (α-Klotho) levels is considered detrimental. Some studies suggest a direct induction of α-Klotho concentrations by growth hormone (GH). In the present study, the effect of exogenous GH administration on α-Klotho concentrations in a clinical cohort with mild chronic kidney disease (CKD) and healthy subjects was studied.


A prospective, single-center open case-control pilot study was performed involving 8 patients with mild CKD and 8 healthy controls matched for age and sex. All participants received subcutaneous GH injections (Genotropin®, 20 mcg/kg/day) for 7 consecutive days. α-Klotho concentrations were measured at baseline, after 7 days of therapy and 1 week after the intervention was stopped.


α-Klotho concentrations were not different between CKD-patients and healthy controls at baseline (554 (388-659) vs. 547 (421-711) pg/mL, P = 0.38). Overall, GH therapy increased α-Klotho concentrations from 554 (405-659) to 645 (516-754) pg/mL, P < 0.05). This was accompanied by an increase of IGF-1 concentrations from 26.8 ± 5.0 nmol/L to 61.7 ± 17.7 nmol/L (P < 0.05). GH therapy induced a trend toward increased α-Klotho concentrations both in the CKD group (554 (388-659) to 591 (358-742) pg/mL (P = 0.19)) and the healthy controls (547 (421-711) pg/mL to 654 (538-754) pg/mL (P = 0.13)). The change in α-Klotho concentration was not different for both groups (P for interaction = 0.71). α-Klotho concentrations returned to baseline levels within one week after the treatment (P < 0.05).


GH therapy increases α-Klotho concentrations in subjects with normal renal function or stage 3 CKD. A larger follow-up study is needed to determine whether the effect size is different between both groups or in patients with more severe CKD.


This trial is registered in EudraCT ( 2013-003354-24 ).


Chronic kidney disease; Growth hormone; α-Klotho

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