Bartter syndrome, a group of disorders that encompasses multiple genetic defects 
with similar clinical presentation, has been divided into six different 
genotypes, according to different genetic defects, and into three main clinical 
variants (or phenotypes). Classic laboratory findings in all variants include 
hypochloremia, hypokalemia, and metabolic alkalosis with excessive excretion of 
chloride and potassium. Classic Bartter syndrome, neonatal Bartter syndrome, and 
Gitelman syndrome are the three main clinical variants. Classic Bartter syndrome 
and neonatal Bartter syndrome have defects in genes that affect transport 
channels in the ascending loop of Henle, where as in Gitleman syndrome the 
defect occurs in the transport channels of the distal convoluted tubule. Classic 
Bartter syndrome and neonatal Bartter syndrome have similar presenting symptoms, 
potential outcomes, and treatment, but different ages at presentation. Gitelman 
syndrome, a more benign condition than the other clinical variants, has the 
classic hallmark finding of hypomagnesemia and low to normal excretion of 
calcium. This differentiates it from the classic and neonatal variants of the 
disease. With early diagnosis and proper treatment, Bartter syndrome has a good 
prognosis. But failure to identify it can lead to tubulointerstitial nephritis 
and renal failure. We present a case of a 6-month-old boy with Bartter syndrome 
who presented with poor weight gain and an abdominal mass.