Hyperthyroidism is one of the most commonly diagnosed diseases of the older cat. Geriatric cats with hyperthyroidism may also have concurrent chronic kidney disease (CKD). Systemic hypertension, proteinuria, and urinary tract infection (UTI) can be consequences of either hyperthyroidism or CKD. Hyperthyroidism can increase glomerular filtration rate (GFR) in cats with CKD which can attenuate or resolve mild to moderate azotemia. In addition, serum creatinine may be decreased in cats with weight loss and decreased muscle mass. In both cases, reductions in BUN and serum creatinine concentrations make it more difficult to detect concurrent CKD. Conversely, the CKD may depress thyroid hormone concentrations (euthyroid sick syndrome) making it more difficult to diagnose hyperthyroidism. Initial treatment of cats with suspected or confirmed CKD should ideally be accomplished with a reversible anti-thyroid medication in order to assess any adverse effects on renal function. Systolic blood pressure and urine protein creatinine ratio (UP/C) should be evaluated prior to and after treatment. Urine cultures should be obtained as part of the workup of both hyperthyroidism and CKD. In either case, a concurrent UTI should be managed as a complicated UTI with long-term antibiotic treatment based on culture and sensitivity results.

Clinical Signs/Physical Examination

Classic clinical signs of hyperthyroidism include weight loss, polyuria/polydipsia (PU/PD), and polyphagia in an older cat. Fewer than 5% of cats with hyperthyroidism are less than 8 years of age; the average age at diagnosis is 12-13 years. A thyroid enlargement (thyroid slip) can often be palpated in hyperthyroid cats, although some euthyroid cats will also have enlargement of one or both glands. In cats with concurrent CKD, kidneys may be small and/or irregular. Approximately 50% of cats with hyperthyroidism will exhibit PU/PD. A primary polyuria may occur as a result of thyrotoxicosis increasing cardiac output and GFR as well as increased renal medullary blood flow which has the potential to decrease renal medullary hypertonicity and urine concentrating ability. Some cats with hyperthyroidism may also have a primary polydipsia secondary to the effects of high thyroid hormone concentrations on the thirst center. Regardless of the mechanism, decreased urine specific gravity makes interpretation of azotemia problematic (is it pre-renal azotemia superimposed on decreased concentrating ability or renal azotemia?). Systemic hypertension is another common finding in hyperthyroid cats. High blood pressure may be caused by increased cardiac output, sympathetic tone, and arteriolar resistance and if sustained, can lead to intraglomerular hypertension, glomerular sclerosis, and proteinuria. No matter what the underlying cause, hypertension can damage the eyes, brain, heart, and kidney of affected cats. For example, tachycardia murmurs, and gallop rhythms may be associated with hypertrophic cardiomyopathy. Similarly, whether proteinuria arises from hypertension or CKD, progressive renal disease is a potential consequence.

Clinicopathologic findings associated with hyperthyroidism may include a slight erythrocytosis; perhaps secondary to increased tissue oxygen consumption. Serum ALT is increased in approximately 75-90% of cats with hyperthyroidism and is thought to be associated with malnutrition, hepatic hypoxia, and/or toxic effects for thyroid hormone on hepatocytes. Azotemia is observed in approximately 25% of hyperthyroid cats and may be due to dehydration, increased protein turnover (BUN), and/or CKD. Concurrently, urine specific gravity is often decreased as discussed previously.