What is the SIADH?
SIADH refers to ADH secretion that persists in the absence of an osmotic or hemodynamic stimulus. Other potential etiologies of hyponatremia including adrenal or glucocorticoid insufficiency, heart failure, liver failure, hypothyroidism, advanced kidney disease, or diuretics (usually thiazide) should be ruled out. Although CHF and cirrhosis patients can have persistent ADH secretion despite hypotonicity, such patients as well as individuals with advanced kidney failure (due to intrinsic defects in urinary dilution) are excluded by convention from the diagnosis of SIADH. Patients with SIADH classically present with hypotonic, euvolemic hyponatremia and U Osm >100 mOsm/kg H 2 O. The urine osmolality need not be higher than plasma osmolality; it only need be greater than maximally dilute. The modest intravascular volume expansion that results from ADH-induced water retention results in decreased renin angiotensin aldosterone system (RAAS) activity and sodium reabsorption. Assuming a normal dietary sodium intake, the urine sodium concentration is consequently >30 mmol/L. Likewise, an associated serum uric acid level of less than 4 mg/dL reflects increased urinary urate excretion. BUN and creatinine tend to be low normal or normal; a high normal or elevated BUN should make clinicians consider volume depletion or diminished effective arterial volume as the cause of hyponatremia. Directly measuring vasopressin levels is in general of very limited utility, as urine osmolality is an adequate surrogate measure of ADH activity. Furthermore, ADH levels will be elevated in patients with hypervolemic or hypovolemic hyponatremia, so levels do not help distinguish among these disorders. SIADH can arise in a variety of malignancies, pulmonary disorders, and central nervous system (CNS) disease. Many medications, most notably selective serotonin reuptake inhibitors, narcotics, and antipsychotics, can also cause SIADH.