SCM15: Hyponatremia and Vaptan Use
NKF Meeting: Saturday March 28, 2015
Session: Hyponatremia and Vaptan Use
Today, Drs. Biff Palmer, Richard Sterns, and myself provided an overview of hyponatremia and therapy. The session started with Dr. Palmer providing an overview of the pathogenesis of hyponatremia and he stressed the importance of impaired renal water excretion. He noted that hyponatremia was the most common electrolyte disorder and in one study was found in over 25% of hospitalized patients and when encountered is associated with increased mortality and morbidity. He discussed a standardized algorithm for the diagnosis of hyponatremia and presented a study from the American Journal of Medicine showing that proper use of the algorithm (based upon classification of serum and urine osmolality) was associated with attaining the correct diagnosis in the majority of cases. He did point out that the algorithm may not be as useful in patients on diuretics (where he recommended the use of the fractional excretion of urea over urine sodium) or in patients with psychogenic polydipsia where there may be some vasopressin secretion and the urine osmolality may be between 100-200 mOsm/kg.
I spoke next and gave an overview of the therapies for hyponatremia as well as delineating some possible clinical scenarios where vaptans may be of benefit. I discussed that water restriction may fail when the urine osmolality is > 500 mOsm/kg, when urine output < 1500 mL/day or when the urine sodium and potassium are greater than the serum sodium. The use of loop diuretics along with sodium supplementation may useful and allows for net water excretion. The vaptans (tolvaptan and conivaptan) are direct vasopressin receptor antagonists and they increase free water. However, they are expensive and may be associated with liver toxicity. Thus, there use may be limited and I gave three clinical scenarios: (1) patients awaiting liver transplantation with severe hyponatremia where there is a risk for post-operative osmotic demyelination; (2) refractory heart failure with worsening hyponatremia; and (3) severe SIADH where the urine osmolality is high (often in the setting of malignancies). In those cases, individualized therapy assessing risks and benefits is warranted and the vaptans may be tools to help.
Last, Dr. Sterns discussed guidelines for the rate of correction of hyponatremia. In the acute setting he showed data that 5 mEq/L rises in serum sodium lower intracranial pressure by 40% and that this is a reasonable acute goal and can be best achieved with 3% saline. In general, 1 mL of 3% saline per kg will raise the serum sodium by 1 mEq/L/hour but there may be variability. In the chronic setting, he stated that a reasonable goal for correction would be 5-6 mEq/L rise in serum sodium in the first 24 hours. He stressed that there are clinical situations where the impairment of renal water excretion may be reversible and in those cases, the serum sodium may start to correct very quickly. He described his institutions use of a combination of DDAVP (desmopressin) and 3% saline to correct serum sodium and showed excellent outcomes with this therapy. He also showed European data with the use of urea to increase renal water excretion and finally, showed some animal data on new urea transport inhibitors that may be of future use in the therapy of hyponatremia.
Post written by Dr. Mitchell Rosner, Feature Editor for AJKD’s In Translation.
Check out more AJKD blog coverage of the NKF’s 2015 Spring Clinical Meetings!
If hyponatremia is both so common and so important (associated with increased mortality and morbidity) where is the rigorous (RCT) data showing the benefits of correcting mild to moderate, mostly asymptomatic, hyponatremia?