From the Research
Uric acid serves as a useful marker for Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) due to its decreased levels in this condition, which can help distinguish it from other causes of hyponatremia. The physiology behind uric acid as a marker for SIADH is rooted in the effects of excessive antidiuretic hormone (ADH) on the kidneys. In SIADH, ADH causes water retention and dilutional hyponatremia, leading to increased renal clearance of uric acid and subsequent hypouricemia, often with levels below 4 mg/dL 1. This occurs because volume expansion in SIADH reduces proximal tubular reabsorption of uric acid, resulting in increased uric acid excretion. Additionally, ADH directly stimulates uric acid excretion by affecting urate transporters in the renal tubules. Some key points to consider when evaluating uric acid in the context of SIADH include:
- The decrease in uric acid levels is due to increased renal clearance, which is a result of the body's attempt to eliminate excess water and electrolytes 2.
- The use of fractional excretion of uric acid (FE-UA) can be a useful diagnostic tool, particularly in patients taking diuretics, as it can help distinguish SIADH from other causes of hyponatremia with high sensitivity and specificity 1.
- Uric acid levels typically normalize once the underlying SIADH is treated, making it a valuable marker for both diagnosis and monitoring treatment response. It is essential to consider the clinical context and other laboratory findings, such as serum osmolality, urine osmolality, and electrolyte levels, when interpreting uric acid levels in patients with suspected SIADH 3, 4.