Bartter syndrome is a rare autosomal recessive, salt-losing disorder 
characterized by hypokalemic hypochloremic metabolic alkalosis. A 10-year-old 
boy had severe growth retardation (height standard deviation score -8.15). He 
had a thin, triangular face, prominent ears and forehead, and big eyes. 
Megacystis, bilateral hydroureteronephrosis, and residual urine were detected in 
ultrasonography, but there was no vesicoureteral reflux. Lumbosacral magnetic 
resonance (MR) showed posterior disc bulging at L4-5. Serum sodium and chloride 
levels were normal, but mild hypokalemia was overlooked initially. During 
follow-up, hypokalemic hypochloremic metabolic alkalosis developed, with high 
urinary chloride and potassium excretion (52 and 43 mEq/L, respectively). The 
patient, with renal salt loss, was thought to have classic Bartter syndrome due 
to absence of nephrocalcinosis, presence of persistent hypercalciuria and 
sensorineural deafness, and presence of relatively mild clinical and laboratory 
findings, except polyuria initially. The child was treated with indomethacin, 
spironolactone, and oral potassium in addition to growth hormone (GH). During 
treatment, he had considerable increase in weight and height compared with the 
period of GH therapy only. We present this case because, although growth 
retardation is a major feature of Bartter syndrome, associated GH deficiency is 
rarely reported in the literature. Diagnosis of Bartter syndrome was made later, 
as our patient was followed for megacystis and megaureter secondary to the 
neurogenic bladder and GH deficiency initially; and proteinuria associated with 
focal segmental glomerulosclerosis responded to treatment for Bartter syndrome.