Tolvaptan corrects hyponatremia and relieves the burden of fluid/dietary restriction and hospitalization in hyponatremic patients with terminal lung cancer: a report of two cases.

Case 1: A 45-year-old man, admitted for symptomatic hyponatremia, was diagnosed with advanced small-cell lung cancer and severe hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. In addition to chemotherapy, the patient was treated with increased dietary salt intake (15 g/day), fluid restriction of 500 mL/day, and amino acid supplementation to maintain a urea load of 31 g/day. Due to the difficulty in changing his habit of drinking 2-3 L/day after discharge, tolvaptan was started. This resulted in correction of hyponatremia, which facilitated earlier discharge and improved his quality of life by eliminating the need for dietary restriction.Case 2: An 88-year-old man with asymptomatic hyponatremia was admitted for assessment of pleural effusion. He was diagnosed with small-cell lung cancer with mild hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. He was treated with best supportive care and dietary modification (salt intake of 15 g/day and fluid restriction of 400 mL/day). He found it difficult to comply with the dietary changes, and prolonged hospitalization was required for hyponatremia correction. Therefore, tolvaptan was initiated, which corrected his hyponatremia, and the patient was discharged.In summary, tolvaptan results in stable correction of hyponatremia in patients with terminal small-cell lung cancer complicated by the syndrome of inappropriate secretion of antidiuretic hormone. Furthermore, it improves the quality of life of these patients by relieving the burden of strict dietary modifications and prolonged hospitalization.

The neonatal variant of Bartter syndrome and deafness: preservation of renal function.

BACKGROUND: A subtype of antenatal Bartter syndrome and sensorineural deafness (BSND) was originally described among families from southern Israel, and its gene (Barttin, OMIM #606412) has recently been identified. A report has suggested that these children develop chronic renal insufficiency during childhood attributable to chronic tubulointerstitial fibrosis and atrophy. METHODS: Data from 13 infants with BSND, who were born during a 20-year period in our institution, were retrospectively analyzed. RESULTS: All pregnancies were complicated by polyhydramnion and premature birth. All patients have sensorineural deafness, as well as hypokalemic metabolic alkalosis. Persistent hypercalciuria or nephrocalcinosis were absent in most children. All children have been treated with indomethacin (2 mg/kg/d) and potassium supplementation. The current average serum creatinine and calculated creatinine clearance from the older group (n = 8; mean age: 8.8 +/- 1.4 years) is 60.8 +/- 16.5 micro mol/L and 95 +/- 20 mL/min/1.73m(2), respectively. Kidney biopsies from two 7-year-old patients revealed mild focal tubulointerstitial fibrosis and minimal mesangial proliferation but no glomerulosclerosis. CONCLUSIONS: Early renal function deterioration is not a uniform finding among children with BSND mutations.