Abstract

Background: Uremia results in a characteristic breath odor (uremic fetor) which is largely due to its high ammonia content. Earlier studies have shown a strong correlation between breath ammonia and blood urea levels and a 10-fold reduction in breath ammonia after hemodialysis in patients with chronic kidney disease. Potential sources of breath ammonia include: (i) local ammonia production from hydrolysis of urea in the oropharyngeal and respiratory tracts by bacterial flora, and (ii) release of circulating blood ammonia by the lungs. While the effects of uremia and hemodialysis on breath ammonia are well known while their effects on blood ammonia are unknown and were explored here. Methods: Blood samples were obtained from 56 hemodialysis patients (immediately before and after dialysis). Blood levels of ammonia, creatinine, arterial blood gases, and electrolytes were measured. Results: There was significant fall in serum creatinine following hemodialysis with significant increase in blood ammonia. Moreover, cirrhotic patients with highbicarbonate showed a significant more increase in ammonia and significant increase in incidence of hyper-ammonemia to that of non-cirrhotic and low-bicarbonate. Furthermore, the increase in serum bicarbonate showed a significant correlation to the change of blood ammonia following dialysis. Conclusion: The fall in blood creatinine concentration following hemodialysis is paradoxically accompanied by a rise in blood ammonia in hemodialysis subjects, contrasting the reported effect on breath ammonia. The mechanism of the posthemodialysis rise in blood ammonia may be due alkalotic change in PH. The observed rise in blood ammonia level was directly related to the rise in blood bicarbonate and with aggravation of alkalotic state in cirrhotic patients. The rise in blood bicarbonate is associated with increased incidence of hyper-ammonemia among cirrhotic patients.

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