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Parathyroid hormone concentration in geriatric cats with various degrees of renal function

Natalie C. Finch BVSc, PhD1, Harriet M. Syme BVetMed, PhD, DACVIM2, and Jonathan Elliott VetMB, PhD3
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  • 1 Royal Veterinary College, University of London, London, NW1 0TU, England.
  • | 2 Royal Veterinary College, University of London, London, NW1 0TU, England.
  • | 3 Royal Veterinary College, University of London, London, NW1 0TU, England.

Abstract

Objective—To determine whether cats in the nonazotemic stages of chronic kidney disease have increased plasma parathyroid hormone (PTH) concentrations as a compensatory physiologic mechanism to maintain plasma phosphate concentration within the reference interval.

Design—Prospective longitudinal study.

Animals—118 client-owned geriatric cats with various degrees of renal function.

Procedures—For each cat, a blood sample was obtained for plasma biochemical analysis and determination of plasma PTH concentration, and a urine sample was obtained for determination of urine specific gravity at study entry (baseline) and after 12 months. For a subset of 30 cats, plasma calcitriol concentration was determined at baseline. Cats were categorized into 1 of 3 groups on the basis of kidney function at the end of 12 months. At baseline and after 12 months, plasma concentrations of variables associated with calcium homeostasis were compared between the 3 groups and also within groups over time. Multivariable linear regression was used to identify variables associated with plasma PTH concentration.

Results—Plasma PTH concentration was significantly increased in cats that developed azotemia, compared with PTH concentration in cats that remained nonazotemic, and PTH concentration increased before changes in plasma calcium and phosphate concentrations were detected. A moderate positive association between plasma calcitriol and PTH concentrations was identified. Plasma PTH concentration was associated with age and plasma urea, creatinine, and total calcium concentrations in the final multivariable model.

Conclusions and Clinical Relevance—Results suggested that renal secondary hyperparathyroidism can develop prior to azotemia in cats, even in the absence of hyperphosphatemia and hypocalcemia.

Abstract

Objective—To determine whether cats in the nonazotemic stages of chronic kidney disease have increased plasma parathyroid hormone (PTH) concentrations as a compensatory physiologic mechanism to maintain plasma phosphate concentration within the reference interval.

Design—Prospective longitudinal study.

Animals—118 client-owned geriatric cats with various degrees of renal function.

Procedures—For each cat, a blood sample was obtained for plasma biochemical analysis and determination of plasma PTH concentration, and a urine sample was obtained for determination of urine specific gravity at study entry (baseline) and after 12 months. For a subset of 30 cats, plasma calcitriol concentration was determined at baseline. Cats were categorized into 1 of 3 groups on the basis of kidney function at the end of 12 months. At baseline and after 12 months, plasma concentrations of variables associated with calcium homeostasis were compared between the 3 groups and also within groups over time. Multivariable linear regression was used to identify variables associated with plasma PTH concentration.

Results—Plasma PTH concentration was significantly increased in cats that developed azotemia, compared with PTH concentration in cats that remained nonazotemic, and PTH concentration increased before changes in plasma calcium and phosphate concentrations were detected. A moderate positive association between plasma calcitriol and PTH concentrations was identified. Plasma PTH concentration was associated with age and plasma urea, creatinine, and total calcium concentrations in the final multivariable model.

Conclusions and Clinical Relevance—Results suggested that renal secondary hyperparathyroidism can develop prior to azotemia in cats, even in the absence of hyperphosphatemia and hypocalcemia.

Contributor Notes

Dr. Finch's present address is School of Veterinary Sciences, University of Bristol, Langford, Bristol, BS40 5DU, England.

Supported by Waltham Centre for Pet Nutrition and Royal Canin SAS.

Presented as an oral presentation at the 19th Annual Congress of the European College of Veterinary Internal Medicine, Porto, Portugal, September 2009.

Address correspondence to Dr. Finch (natalie.finch@bristol.ac.uk).