abdominal ultrasound was normal. C. difficile and C. Tropicalis were found in stool cultures. 2 consecutive sweat tests were performed, showing borderline values: 61,25 mmol/l; 67,7 mmol/l. There was no polyuria or excessive chloride loss in urine, which are typical features of Bartter's syndrome. Diarrhea was not present at birth, no watery stools were observed and the failure to thrive was not significant prior to admission, making the diagnosis of congenital chloride diarrhea unlikely. Genetic testing for CF showed that the infant was a delF508 mutation and G178r mutation compound heterozygote.The child showed no clinical symptoms of hypokalemia. No hyponatremia seizures were observed. Diarrhea was persistent. Rehydration therapy and antibiotic treatment significantly improved the condition.Patients who are compound heterozygous for the milder CFTR mutations (classes IV and V) experience partial CFTR function, resulting in atypical featuressuch as borderline sweat chloride concentrations, unlike our patient who is a compound heterozygous with class II and III mutation, where high amount of chloride in sweat is more commonly seen. Such patents are more likely to experience severe CF. Therefore making early diagnosis is crucial to further normal growth and development as therapy could be started early in life.