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Hyperthyroidism and kidney disease in cats

Williams TL, Elliott J and Syme HM. Calcium and phosphate homeostasis in hyperthyroid cats – associations with development of azotaemia and survival time. J Small Anim Pract. 2012; 53: 561-71. 

Hyperthyroidism and chronic kidney disease (CKD) are common conditions of older cats that frequently occur concurrently. Hyperthyroid cats often have increased plasma phosphate concentrations and concomitantly increased plasma parathyroid hormone (PTH) concentrations. PTH is regarded as a uremic toxin and elevated levels have been postulated to contribute to renal damage or increased morbidity and mortality in feline hyperthyroidism. In addition, secondary renal hyperparathyroidism may also contribute to the progression of CKD in cats. Fibroblast growth factor-23 (FGF-23) is a phosphatonin secreted by osteoblasts in response to increased plasma phosphate and calcitriol concentrations. FGF-23 inhibits renal phosphate reabsorption, increasing phosphate urinary loss. In humans, serum FGF-23 concentrations predict the progression of CKD and both PTH and FGF-23 concentrations have been positively associated with all-cause mortality. It is unclear whether PTH and FGF-23 represent biomarkers of or mediate renal disease progression. Nevertheless, the association of PTH and FGF-23 with renal disease progression warrants evaluation of their concentration in hyperthyroid cats before and after treatment.

This study evaluated calcium and phosphate homeostasis in 207 hyperthyroid cats before and after treatment for hyperthyroidism by measuring plasma calcium, phosphate, PTH and FGF-23 concentrations. Patient selection was from records obtained from two London-based first-opinion practices between 1999 and 2009 and from newly diagnosed hyperthyroid cats. Twenty-eight healthy non-azotemic geriatric cats were also recruited in the study as controls. Hyperthyroid cats were treated with anti-thyroid medications (carbimazole or methimazole) alone or in combination with thyroidectomy. Hyperthyroid cats were divided into three groups: cats with pre-existing azotemia, cats that developed azotemia within 240 days after treatment and maintained euthyroidism, and cats which remained non-azotemic for at least 240 days after treatment and maintained euthyroidism. 

Results suggest that approximately 60% of hyperthyroid cats have elevated plasma PTH concentrations. Hyperthyroid cats without azotemia had hypocalcemia and hyperphosphatemia that would elevate PTH; however, the cause of decreased calcium and increased phosphate is unknown. There was no statistical difference in PTH levels for the three groups of hyperthyroid cats before treatment. PTH concentrations decreased following treatment in hyperthyroid cats that remained non-azotemic and remained elevated in cats that were or developed azotemia, suggesting secondary renal hyperparathyroidism in cats with azotemic CKD. 

FGF-23 concentrations were significantly higher in hyperthyroid cats with azotemia or that developed azotemia compared with cats that remained non-azotemic. Unexpectedly, plasma FGF-23 concentrations increased following treatment in cats with or without azotemic CKD independent of plasma phosphate concentrations, suggesting FGF-23 levels are suppressed in feline hyperthyroidism. The authors speculate that this increase in FGF-23 levels occurs secondary to the reduction in glomerular filtration rate after control of the hyperthyroid condition. FGF-23 was shown to be negatively associated with survival time when adjusted for age, creatinine, total calcium, phosphate, and PTH, but this association was lost when further adjustment factors were considered. Interestingly, omission of packed cell volume (PCV) as an explanatory variable resulted in FGF-23 again being associated with all-cause mortality, suggesting that FGF-23 influences survival time possibly by causing a reduction in PCV. [GO]

See also: Williams TL, Peak KJ, Brodbelt D, Elliott J and Syme HM. Survival and the development of azotemia after treatment of hyperthyroid cats. J Vet Intern Med. 2010; 24: 863-9.