Renal Function and Hyperthyroidism
Renal function is profoundly influenced by thyroid status (van Hoek and Daminet, 2009). Through their ino- and chronotropic effects, excessive thyroid hormone concentrations can lead to an increased cardiac output.
Further, hyperthyroidism diminishes peripheral vascular resistance by dilating arterioles of the peripheral circulation. The increased glomerular filtration rate (GFR) associated with hyperthyroid states is thought to result from the increased cardiac output and intrarenal vasodilatation and leads to a decline in blood-urea-nitrogen (BUN) and serum creatinine concentrations. With effective treatment, a marked decline of renal function has been reported (van Hoek et al. 2009), which is “normalization” of renal function rather than a “decline.”Chronic kidney disease (CKD) and hyperthyroidism are both frequently encountered diseases in geriatric cats and thus finding both diseases in one cat is common. As renal function can decline (“normalize”) after treatment of hyperthyroidism, this can unmask renal disease in some cats. Decreased muscle mass associated with emaciation and therefore decreased production of creatinine can contribute to the declined serum creatinine concentrations observed in untreated hyperthyroid cats. The presence of a hyperthyroid state could contribute to the development or progression of CKD. Systemic hypertension can lead to intra-glomerular hypertension, hyper-filtration and contribute to the development of glomerulosclerosis.
Pre-existing Azotemia in a Newly Diagnosed Hyperthyroid Cat
In such a case, the diagnosis of hyperthyroidism can be somewhat complicated by a decline in thyroid hormones (euthyroid sickness) within the reference range and given the further decline in GFR to be expected after resolution of the hyperthyroid state, it is important to start an azotemic hyperthyroid cat with a reversible anti-thyroid therapy. This allows assessing the impact of anti-thyroid therapy on renal function.
These patients should be monitored every 2 weeks. Dosage adjustments should be made prudently. In such cases, a compromise between improved renal function and persistence of hyperthyroidism may be required to optimize quality of life.Development of Azotemia after Treatment of Hyperthyroidism
Resolution of the hyperthyroid state can unmask CKD. Excess thyroid hormones increase GFR and treatment of hyperthyroidism will decrease GFR, leading to an increase in BUN and creatinine values. Up to 30% of the patients, develop overt azotemia after treatment of hyperthyroidism. Post-treatment development of azotemia does not seem to decrease the survival of hyperthyroid cats after treatment. The appearance of mild stable azotemia should not affect treatment advice for hyperthyroidism given to clients. As long as TT4 and renal parameters are monitored closely, there is no reason to stop or reduce anti-thyroid drug treatment in azotemic cats in order to normalize creatinine concentration. However, as these cats carry a similar prognosis to cats not developing post-treatment azotemia and are unlikely to increase more than one IRIS stage, a recent “consensus panel” did not recommend routine use of a therapeutic trial in non-azotemic hyperthyroid cat to assess effect on renal function (Daminet et al. 2014).