From the Research
Increased renal excretion of phosphate in hyperthyroidism occurs primarily due to the direct effects of excess thyroid hormones on kidney function, leading to increased glomerular filtration rate and reduced tubular reabsorption of phosphate in the proximal tubules, as supported by the most recent study 1. The pathophysiology of hyperthyroidism involves the excessive production of thyroid hormones, which can affect various bodily systems, including the renal system. In hyperthyroidism, elevated levels of thyroid hormones (T3 and T4) enhance the metabolic activity throughout the body, including the kidneys.
- This leads to increased glomerular filtration rate, which allows more phosphate to be filtered out of the blood and into the urine.
- Reduced tubular reabsorption of phosphate in the proximal tubules also contributes to increased renal excretion of phosphate, as thyroid hormones downregulate sodium-phosphate co-transporters in the proximal tubule, which are responsible for phosphate reabsorption. Additionally, hyperthyroidism may increase parathyroid hormone (PTH) sensitivity in the kidneys, further promoting phosphaturia, as noted in the study 1.
- The heightened metabolic state also increases bone turnover, releasing more phosphate into the circulation, which contributes to the phosphate load that must be excreted. This increased renal phosphate excretion can sometimes lead to hypophosphatemia in patients with severe or prolonged hyperthyroidism, though this is not always clinically significant, and management options should be guided by the most recent and highest-quality evidence, such as the study published in The lancet. Diabetes & endocrinology 1.