234 Effect of Dialysate Baths on Serum Bicarbonate Levels in Hemodialysis Patients

Abstract

HYPONATREMIA AFTER HEAD INJURY: A COMPLEX CEREBRORENAL CONNECTION BEYOND SIADH Uma Pakkivenkata, Kambhampati Ganesh, Gurjit Dhatt, Amir Kazory Division of Nephrology, University of Florida, Gainesville, Florida, USA A 76-year-old female who was admitted for subdural hematoma secondary to a fall presented with hyponatremia of 120 mmol/l. The blood pressure was 149/73, pulse 80, and she appeared euvolemic. The brain CT scan revealed a stable subdural hematoma which was managed conservatively. Since the lab data (urine Na 48meq/L, urine osm 401mosm/kg, and serum osm 250mosm/kg) was consistent with the diagnosis of SIADH in the context of recent head injury, the patient was placed on free water restriction. However, this was followed by worsening of hyponatremia to 117 mmol/l and alteration in mental status. A repeat brain CT scan showed worsening hematoma, and she underwent a surgical drainage. Review of the lab results revealed characteristics compatible with increased ADH release associated with features of renal proximal tubulopathy: persistent high urinary levels of electrolytes (e.g. K, Mg, and Phos) despite very low serum levels. Therefore the diagnosis of cerebral salt wasting (CSW) was made and the patient was started on hypertonic saline, which was followed by progressive improvement in serum sodium levels. Two days after resolution of hyponatremia, serum and urine studies were rechecked: serum uric acid remained very low (1.4 mg/dl) and fractional excretion of uric acid did not normalize; a finding that further supported the diagnosis of CSW, rather than SIADH. Other manifestations of proximal tubulopathy (e.g. hypokalemia and hypo-phosphatemia) gradually improved. Hyponatremia after head injury is possibly the manifestation of a complex cerebro-renal connection, with poorly understood underlying mechanisms. In CSW, an unidentified mediator released from the brain disrupts the function of the proximal tubules and leads to leakage of electrolytes into the urine. Interestingly, ADH levels are also increased in CSW; hyponatremia is related to “appropriate” ADH secretion in response to intravascular volume depletion secondary to excessive tubular sodium excretion. As such, CSW and SIADH share several features and represent the biological consequences of a primary insult to the brain that can either be predominant in the brain (SIADH) or in the kidney (CSW). It is of utmost importance to appreciate the subtle differences existing between CSW and SIADH in order to avoid instauration of potentially-harmful management strategies such as this case.