Prognostic importance of plasma total magnesium in a cohort of cats with azotemic chronic kidney disease

Broek, D Hendrik N van den; Chang, Yu‐Mei; Elliott, Jonathan; Jepson, Rosanne

doi:10.1111/jvim.15141

Cited by 22 publications

(30 citation statements)

References 76 publications

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“…A number of other factors have been associated with circulating FGF23 concentration. A study of cats with naturally occurring CKD observed an inverse association between plasma tMg concentration and FGF23 concentration, and it has been hypothesized that FGF23 has an effect on renal magnesium handling . In our study, tMg was not significantly different between cats with increased SDMA concentrations and those with normal SDMA concentrations, and no significant correlation was found between plasma FGF23 and tMg concentrations.…”

Section: Discussioncontrasting

confidence: 67%

Fibroblast growth factor 23 and symmetric dimethylarginine concentrations in geriatric cats

Sargent

Jepson

Chang

et al. 2019

Veterinary Internal Medicne

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Background: Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone that is increased in azotemic cats with chronic kidney disease (CKD) and predictive of the onset of azotemia in older cats. The introduction of symmetric dimethylarginine (SDMA) as a biomarker of glomerular filtration rate has led to the identification of cats in which SDMA is increased, but plasma creatinine concentrations remains within reference range. There is currently little understanding of the metabolic changes present in such cats.Objectives: To examine the relationship between plasma FGF23 and SDMA concentrations in non-azotemic geriatric cats.Animals: Records of a cross section of client-owned cats (n = 143) without azotemic CKD.Methods: Clinicopathological information was obtained from cats (≥ 9 years) from records of 2 first opinion practices. The relationship between plasma SDMA and FGF23 concentrations was examined using Spearman's correlation and variables compared using the Mann-Whitney U test.Results: Cats with increased SDMA concentrations had significantly higher plasma FGF23 (P < .001) and creatinine (P < .001) concentrations compared to cats with SDMA concentrations within reference range. A weak positive relationship was demonstrated between plasma FGF23 and SDMA concentrations (r = .35, P < .001) and between plasma FGF23 and creatinine (r = .23, P = .005) concentrations.Conclusions and Clinical Importance: More cats with increased SDMA concentrations had higher FGF23 concentrations than those with SDMA concentrations within the reference range, suggesting the presence of an alteration in phosphate homeostasis. Further studies are warranted to identify influencing factors and to explore the utility of FGF23 concentration to inform management of cats with early stage CKD. K E Y W O R D S azotemia, feline, phosphate, renal Abbreviations: 1,25 vitamin D3, 25-dihydroxyvitamin D; AKI, acute kidney injury; CKD, chronic kidney disease; CKD-MBD, chronic kidney disease mineral and bone disorder

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Section: Discussioncontrasting

confidence: 67%

Fibroblast growth factor 23 and symmetric dimethylarginine concentrations in geriatric cats

Sargent

Jepson

Chang

et al. 2019

Veterinary Internal Medicne

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“…DBA/2 mice regardless of their fetuin-A genotype had hypomagnesemia associated with elevated serum FGF23. Likewise, rats on magnesium-deficient diet had elevated serum FGF23 [50] and CKD cats had inverse association of serum Mg and FGF23 independent of serum phosphate [51]. Collectively these results suggest that serum FGF23 may be associated with hypomagnesemia in addition to the well-established association with hyperphosphatemia.…”

Section: Discussionmentioning

confidence: 75%

Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate

et al. 2020

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Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly severe soft tissue calcifications, while fetuin-A deficient C57BL/6 mice remain healthy. We employed molecular genetic analysis to identify risk factors of calcification in fetuin-A deficient mice. We sought to identify pharmaceutical therapeutic targets that could be influenced by dietary of parenteral supplementation. We studied the progeny of an intercross of fetuin-A deficient DBA/2 and C57BL/6 mice to identify candidate risk genes involved in calcification. We determined that a hypomorphic mutation of the Abcc6 gene, a liver ATP transporter supplying systemic pyrophosphate, and failure to regulate the Trpm6 magnesium transporter in kidney were associated with severity of calcification. Calcification prone fetuin-A deficient mice were alternatively treated with parenteral administration of fetuin-A dietary magnesium supplementation, phosphate restriction, or by or parenteral pyrophosphate. All treatments markedly reduced soft tissue calcification, demonstrated by computed tomography, histology and tissue calcium measurement. We show that pathological ectopic calcification in fetuin-A deficient DBA/2 mice is caused by a compound deficiency of three major extracellular and systemic inhibitors of calcification, namely fetuin-A, magnesium, and pyrophosphate. All three of these are individually known to contribute to stabilize protein-mineral complexes and thus inhibit mineral precipitation from extracellular fluid. We show for the first time a compound triple deficiency that can be treated by simple dietary or parenteral supplementation. This is of special importance in patients with advanced CKD, who commonly exhibit reduced serum fetuin-A, magnesium and pyrophosphate levels.

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“…DBA/2 mice regardless of their fetuin-A genotype had hypomagnesemia associated with elevated serum FGF23. Likewise, rats on magnesium-deficient diet had elevated serum FGF23 [47] and CKD cats had inverse association of serum Mg and FGF23 independent of serum phosphate [48]. Collectively these results suggest that serum FGF23 may be associated with hypomagnesemia in addition to the well-established association with hyperphosphatemia and morbidity.…”

Section: Discussionmentioning

confidence: 76%

Microvasculopathy And Soft Tissue Calcification In Mice Are Governed by Fetuin-A, Pyrophosphate And Magnesium

Babler

Schmitz

Büscher

et al. 2019

Preprint

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Objective -Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly severe soft tissue calcifications, while fetuin-A deficient C57BL/6 mice remain healthy. We employed molecular genetic analysis to identify risk factors of calcification in fetuin-A deficient mice. We sought to identify pharmaceutical therapeutic target that could be influenced by dietary of parenteral supplementation.Approach and Results -We studied the progeny of an intercross of fetuin-A deficient DBA/2 and C57BL/6 mice to identify candidate risk genes involved in calcification. We determined that a hypomorphic mutation of the Abcc6 gene, a liver ATP transporter supplying systemic pyrophosphate, and failure to regulate the TRPM6 magnesium transporter in kidney were associated with severity of calcification. Calcification prone fetuin-A deficient mice were alternatively treated with dietary phosphate restriction, magnesium supplementation, or by parenteral administration of fetuin-A or pyrophosphate. All treatments markedly reduced soft tissue calcification, demonstrated by computed tomography, histology and tissue calcium measurement.Conclusions -We show that pathological ectopic calcification in fetuin-A deficient DBA/2 mice is caused by a compound deficiency of three major extracellular and systemic inhibitors of calcification, namely fetuin-A, pyrophosphate, and magnesium. All three of these are individually known to contribute to stabilize protein-mineral complexes and thus inhibit mineral precipitation from extracellular fluid. We show for the first time a compound triple deficiency that can be treated by simple dietary or parenteral supplementation. This is of special importance in patients with advanced CKD, who commonly exhibit reduced serum fetuin-A, pyrophosphate and magnesium levels.

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Prognostic importance of plasma total magnesium in a cohort of cats with azotemic chronic kidney disease

Cited by 22 publications

References 76 publications

Fibroblast growth factor 23 and symmetric dimethylarginine concentrations in geriatric cats

Fibroblast growth factor 23 and symmetric dimethylarginine concentrations in geriatric cats

Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate

Microvasculopathy And Soft Tissue Calcification In Mice Are Governed by Fetuin-A, Pyrophosphate And Magnesium

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