Creatine homeostasis and the kidney: comparison between kidney transplant recipients and healthy controls.


Journal

Amino acids
ISSN: 1438-2199
Titre abrégé: Amino Acids
Pays: Austria
ID NLM: 9200312

Informations de publication

Date de publication:
13 Jun 2024
Historique:
received: 19 03 2024
accepted: 29 05 2024
medline: 13 6 2024
pubmed: 13 6 2024
entrez: 13 6 2024
Statut: epublish

Résumé

Creatine is a natural nitrogenous organic acid that is integral to energy metabolism and crucial for proper cell functioning. The kidneys are involved in the first step of creatine production. With kidney transplantation being the gold-standard treatment for end-stage kidney disease, kidney transplant recipients (KTR) may be at risk of impaired creatine synthesis. We aimed to compare creatine homeostasis between KTR and controls. Plasma and urine concentrations of arginine, glycine, guanidinoacetate, creatine and creatinine were measured in 553 KTR and 168 healthy controls. Creatine intake was assessed using food frequency questionnaires. Iothalamate-measured GFR data were available in subsets of 157 KTR and 167 controls. KTR and controls had comparable body weight, height and creatine intake (all P > 0.05). However, the total creatine pool was 14% lower in KTR as compared to controls (651 ± 178 vs. 753 ± 239 mmol, P < 0.001). The endogenous creatine synthesis rate was 22% lower in KTR as compared to controls (7.8 ± 3.0 vs. 10.0 ± 4.1 mmol per day, P < 0.001). Despite lower GFR, the plasma guanidinoacetate and creatine concentrations were 21% and 41% lower in KTR as compared to controls (both P < 0.001). Urinary excretion of guanidinoacetate and creatine were 66% and 59% lower in KTR as compared to controls (both P < 0.001). In KTR, but not in controls, a higher measured GFR was associated with a higher endogenous creatine synthesis rate (std. beta: 0.21, 95% CI: 0.08; 0.33; P = 0.002), as well as a higher total creatine pool (std. beta: 0.22, 95% CI: 0.11; 0.33; P < 0.001). These associations were fully mediated (93% and 95%; P < 0.001) by urinary guanidinoacetate excretion which is consistent with production of the creatine precursor guanidinoacetate as rate-limiting factor. Our findings highlight that KTR have a disturbed creatine homeostasis as compared to controls. Given the direct relationship of measured GFR with endogenous creatine synthesis rate and the total creatine pool, creatine supplementation might be beneficial in KTR with low kidney function.Trial registration ID: NCT02811835.Trial registration URL: https://clinicaltrials.gov/ct2/show/NCT02811835 .

Identifiants

pubmed: 38869518
doi: 10.1007/s00726-024-03401-w
pii: 10.1007/s00726-024-03401-w
doi:

Substances chimiques

Creatine MU72812GK0
glycocyamine GO52O1A04E
Glycine TE7660XO1C
Creatinine AYI8EX34EU

Banques de données

ClinicalTrials.gov
['NCT02811835']

Types de publication

Journal Article Comparative Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

42

Subventions

Organisme : Top Institute Food and Nutrition
ID : A-1003

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Adrian Post (A)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands. a.post01@umcg.nl.

Dion Groothof (D)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.

Daan Kremer (D)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.

Tim J Knobbe (TJ)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.

Willem Abma (W)

Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, 9713 GZ, the Netherlands.

Christa A Koops (CA)

Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, 9713 GZ, the Netherlands.

Dimitrios Tsikas (D)

Institute of Toxicology, Core Unit Proteomics, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.

Theo Wallimann (T)

Department of Biology, ETH Zurich, Zurich, Switzerland.

Robin P F Dullaart (RPF)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.

Casper F M Franssen (CFM)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.

Ido P Kema (IP)

Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, 9713 GZ, the Netherlands.

M Rebecca Heiner-Fokkema (MR)

Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, 9713 GZ, the Netherlands.

Stephan J L Bakker (SJL)

Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.
Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, Groningen, 9700 RB, the Netherlands.

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