Acta Neurochir (Wien) (1993) 125:8(~91 =Acta . . N urochlrurglca 9 Springer-Verlag 1993 Printed in Austria Renal Tubular Sodium and Water Metabolism in Brain Tumour Patients Submitted to Craniotomy P. Ponce, J. Travassos, J. Cruz, P. Moreira, E. Melo Gomes, and J. Lobo Antunes Hospital CUF, Lisbon, Portugal Summary Purpose: To evaluate the effect of Brain Tomour (BT) and Neu- rosurgery (NS) on the renal handling of HzO and Na, and the ciinical importance of SIADH in this setting. Methods: Fourteen patients with BT pre-op for NS and 6 controls (C) pre-op for general surgery, were assessed in a controlled pro- spective trial. All patients were normovolaemic, with normal renal function. They received 400 mg of lithium carbonate (Li) 8 hours before each of two test periods (I and II) and a standard water load only before period II. Clearances studies were performed pre-op (period I) and 24 hours post-op (period II). Results: Serum Na was normal at all times. Despite normovo- laemia, a 1% decrement in serum osmolality and the water load, ADH dramaticaly increased from time I to II mainly in the BT group (36.2• vs 7.1 • 0.6pmol/L, p=0.02). FENa, FELi and FEUricA were significantly more elevated in the BT group pre and post-op (at time II respectively4.6 4- 1.6 vs 1.1 + 0.3%; 29.3 + 4.9 vs 22.6 • 5.5;26.0 • 8.1 vs 11.3 • 2.2, p = 0.03). Proximal and distal H20 re-absorption and distal fractional Na re-absorption were iden- tical in both groups pre and post-operatively. Conclusions: I-BT and NS always induce a SIADH. 2-There was a primary Na loss at the proximal tubule level not explained by ADH increment, that did not significantly changed H20 handling. 3-To prevent hyponatraemia, hypotonic I.V. fluids should be avoided, but more importantly saline must be provided to this po- tentially salt-wasting condition. Keywords." ADH; brain tumour; craniotomy; hyponatraemia; salt-wasting; SIADH. Abbreviations A1-Aldosterone ADH-Anti diuretic hormone UNa-Urine sodium (rnEq/1) SNa-Serum sodium (mEq/1) Creatinine clearance (CrC1) Lithium clearance (LiC1) Free water clearance (HzOC1) Uric acid clearance (UricAC1) Sodium clearance (NaCI) FENa-Fractional excretion of sodium (NaC1/CrC1) FEUricA-Fractional excretion of uric acid (UricAC1/CrC1) FELl-Fractional excretion of Lithium (LiC1/CrC1) FNa-Filtered load of sodium (CrCI*SNa/1000 mEq/min) DistNa-Distal renal tubular delivery of sodium (LiCI*SNa/1000 mEq/min) NaPR-Proximal renal tubular reabsorption of sodium (DistNa- (UNa*Urine Volume)) NaDR-Distal renal tubular sodium reabsorption (DistNa- (UNa*Urine volume)) H2OPR-Proximal renal tubular water reabsorption (CrC1-LiCr)ml/ rain H2ODR-Distal renal tubular water reabsorption (Licl-Urine vol- ume)ml/min NaPFR-Renal tubular proximal sodium fractional reabsorption (NaPR/FNa* 100)% NaDFR-Renal tubular distal sodium fractional reabsorption (NaDR/DistNa* 100)% Introduction Hyponatraemia is probably the most common elec- trolyte disorder found in patients with intracranial dis- ease, occurring in up to 33% of all patients with cran- iocerebral disorders < 10, 29 The association of hyponatraemia with an inappro- priately high natriuresis in patients with disorders of the central nervous system, originally referred to as cerebral salt wasting 9, was attributed to a defect in renal tubular reabsorption of sodium induced by the neural lesion. In 1957 Schwartz and Bartter first suggested that the hyponatraemia/hypernatriuresis observed in these patients was caused by the inappropriate secretion of ant• hormone (SIADH) 27, which induced mild extracellular volume expansion and a dilutional hyponatraemia. The renal mechanisms of this hyponatraemia and its clinical implications have not been fully elucidated.