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. 2024 Jul-Aug;38(4):2180-2195.
doi: 10.1111/jvim.17134. Epub 2024 Jul 1.

Dietary magnesium supplementation in cats with chronic kidney disease: A prospective double-blind randomized controlled trial

Pak-Kan Tang  1 , Dirk Hendrik Nicolaas van den Broek  2 , Rosanne E Jepson  3 , Rebecca F Geddes  3 , Yu-Mei Chang  4 , Nicola Lötter  1 , Delphine Moniot  5 , Vincent Biourge  5 , Jonathan Elliott  1
Affiliations

Dietary magnesium supplementation in cats with chronic kidney disease: A prospective double-blind randomized controlled trial

Pak-Kan Tang et al. J Vet Intern Med. 2024 Jul-Aug.

Abstract

Background: Plasma total magnesium concentration (tMg) is a prognostic indicator in cats with chronic kidney disease (CKD), shorter survival time being associated with hypomagnesemia. Whether this risk factor is modifiable with dietary magnesium supplementation remains unexplored.

Objectives: Evaluate effects of a magnesium-enriched phosphate-restricted diet (PRD) on CKD-mineral bone disorder (CKD-MBD) variables.

Animals: Sixty euthyroid client-owned cats with azotemic CKD, with 27 and 33 allocated to magnesium-enriched PRD or control PRD, respectively.

Methods: Prospective double-blind, parallel-group randomized trial. Cats with CKD, stabilized on a PRD, without hypermagnesemia (tMg >2.43 mg/dL) or hypercalcemia (plasma ionized calcium concentration, (iCa) >6 mg/dL), were recruited. Both intention-to-treat and per-protocol (eating ≥50% of study diet) analyses were performed; effects of dietary magnesium supplementation on clinicopathological variables were evaluated using linear mixed effects models.

Results: In the per-protocol analysis, tMg increased in cats consuming a magnesium-enriched PRD (β, 0.25 ± .07 mg/dL/month; P < .001). Five magnesium supplemented cats had tMg >2.92 mg/dL, but none experienced adverse effects. Rate of change in iCa differed between groups (P = .01), with decreasing and increasing trends observed in cats fed magnesium-enriched PRD and control PRD, respectively. Four control cats developed ionized hypercalcemia versus none in the magnesium supplemented group. Log-transformed plasma fibroblast growth factor-23 concentration (FGF23) increased significantly in controls (β, 0.14 ± .05 pg/mL/month; P = .01), but remained stable in the magnesium supplemented group (β, 0.05±.06 pg/mL/month; P =.37).

Conclusions and clinical importance: Magnesium-enriched PRD is a novel therapeutic strategy for managing feline CKD-MBD in cats, further stabilizing plasma FGF23 and preventing hypercalcemia.

Keywords: CKD‐MBD; anti‐calcemic; calcium; fibroblast growth factor‐23; hypercalcemia; magnesium oxide.

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Conflict of interest statement

Pak‐Kan Tang received a PhD studentship funded by Royal Canin SAS. Rebecca Geddes received funding from Petplan, Royal Canin, an RVC Internal Grant, The Academy of Medical Sciences and The Everycat Foundation; has previously had a consultancy agreement with Boehringer Ingelheim; has received speaking honoraria from Boehringer Ingelheim, Idexx and Royal Canin. Rosanne Jepson received funding from PetPlan, Feline Foundation for Renal Research, RVC Internal Grant, PetSavers, and consultancy agreements: Boehringer Ingelheim, Merial, CEVA. Speaking honoraria: Boehringer Ingelheim, Hills Pet Nutrition, CEVA. Jonathan Elliott has Consultancy agreements with: Elanco Ltd, CEVA Animal Health Ltd, Boehringer Ingelheim Ltd, MSD Animal Health Ltd, Orion Incorp, Idexx Ltd, Waltham Petcare Science Institute, Invetx Inc and Zoetis Ltd received grant funding from Elanco Ltd, Waltham Centre for Pet Nutrition, Royal Canin SAS, Idexx Ltd, CEVA Animal Health. He is a member of the International Renal Interest Society which receives sponsorship from Zoetis.

Figures

FIGURE 1
FIGURE 1
A Consolidated Standards of Reporting Trials (CONSORT) flow diagram of this prospective dietary trial (MAGMA). UTI, urinary tract infection.
FIGURE 2
FIGURE 2
Scatter plots illustrating the linear change of plasma concentrations of (A) total magnesium (tMg); (B) log‐transformed fibroblast growth factor‐23 (ln[FGF23]); (C) total calcium (tCa); (D) ionized calcium (iCa); and (E) body weight in all randomized cats (n = 60) according to the allocated trial diet (“control phosphate‐restricted diet [PRD]” [crosses] vs “magnesium‐enriched PRD” [dots]) during the study period. The P‐value refers to the Group × Time interaction (as shown in Table 5) analyzed using linear mixed effects models, which assessed the difference in rate of change of the outcome variable between groups (“control PRD” vs “magnesium‐enriched PRD”) over time.
FIGURE 3
FIGURE 3
Line graphs illustrating the change of plasma concentrations of (A) total magnesium (tMg); (B) fibroblast growth factor‐23 (FGF23); (C) ionized calcium (iCa); (D) total calcium (tCa); (E) phosphate; and (F) creatinine in individual cats with chronic kidney disease (CKD) that developed hypermagnesemia (n = 6) grouped according to allocation of trial diet (“control phosphate‐restricted diet [PRD]” vs “magnesium‐enriched PRD”) during the study period of this prospective diet trial (MAGMA).
FIGURE 4
FIGURE 4
Scatter plots illustrating the linear change of plasma concentrations of (A) total magnesium concentration (tMg); (B) log‐transformed fibroblast growth factor‐23 (ln[FGF23]); (C) total calcium (tCa); (D) ionized calcium (iCa); (E) venous bicarbonate (HCO3−); and (F) body weight in the per‐protocol cats (n = 44) according to the allocated trial diet (“control phosphate‐restricted diet [PRD]” [crosses] vs “magnesium‐enriched PRD” [dots]) during the study period. The P‐value refers to the Group × Time interaction (as shown in Table 6) analyzed using linear mixed effects models, which assessed the difference in rate of change of the outcome variable between groups (“control PRD” vs “magnesium‐enriched PRD”) over time.
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