A patient with end-stage renal disease (ESRD) developed metabolic alkalosis and alkalemia from protracted vomiting. As a result of the absence of the alkali excretory capacity in this patient with ESRD, the alkaline load accumulated rapidly. Once the amount of acid lost from vomiting exceeded the amount of acid gained from metabolism, alkalemia supervened. The initial arterial blood gas on room air revealed hypercarbia, hypoxia and alkalemia. Her serum bicarbonate was greater than 50 mEq/l. Compensatory hypoventilation occurred. In this report, the extent of compensatory hypoventilation in the setting of metabolic alkalosis in patients treated for ESRD and therapeutic approaches to this problem will be discussed. Treatment was aimed at correcting the primary disorder, namely metabolic alkalosis. Conventional bicarbonate dialysis was shown to be effective in improving acid-base homeostasis in this patient.