Volume 58, Issue 5, Pages 788-791 (November 2010) Is Renal Living-Donor Transplantation Indicated in Adult Patients with Orthotopic Ileal Neobladder? Lessons Learned from a Clinical Case  Andrea Airoldi, Alessandro Volpe, Michele Billia, GianSilvio Marchioro, Roberta Fenoglio, Elisa Lazzarich, GianMario Sacchetti, Cinzia Baiocco, Eugenio Inglese, Alberto Menegotto, Carlo Terrone, Piero Stratta  European Urology  Volume 58, Issue 5, Pages 788-791 (November 2010) DOI: 10.1016/j.eururo.2009.05.020 Copyright © 2009 European Association of Urology Terms and Conditions

Fig. 1 Scintigraphic scans performed with 111–120 megabecquerels of 99mTc mercaptoacetyltriglycine (MAG3): (A) Left superior pole of the Camey bladder was empty with open bladder catheter in situ (red arrow), with Hilson perfusion index of 178 (normal value: <150); (B) tracer accumulated up the left superior pole of the Camey bladder with bladder catheter clamped (red arrow), while Hilson perfusion index was slightly worse at 220. European Urology 2010 58, 788-791DOI: (10.1016/j.eururo.2009.05.020) Copyright © 2009 European Association of Urology Terms and Conditions

Fig. 2 Scheme of steps leading to the respiratory compensatory mechanisms of metabolic acidosis: (A) A pH value between normal limits is obtained due to the balance between blood bicarbonate (HCO3) and carbon dioxide (CO2) concentration; (B) in simple metabolic acidosis, pH value falls, paralleling that of blood HCO3 concentration; (C) a simultaneous decrease in CO2 concentration, due to its increased pulmonary excretion, will allow partial compensation of metabolic acidosis with an increase in pH values. pCO2=partial pressure of carbon dioxide. European Urology 2010 58, 788-791DOI: (10.1016/j.eururo.2009.05.020) Copyright © 2009 European Association of Urology Terms and Conditions

Fig. 3 Synopsis of the main mechanisms responsible for posttransplant renal tubular acidosis and ileal bladder-related acidosis: (A) Renal tubular acidosis due to impaired renal acid excretion; (B) ileal cells employed in neobladder are responsible for metabolic acidosis by at least two main mechanisms: (1) the exchange of chloride urinary ions (Cl−) for bicarbonate intracellular ions (HCO3−) by the apical Cl−/HCO3− exchanger, which is present on mucosal enterocytes, leading to a significant loss of HCO3− into the urine and an increase in serum Cl−; and (2) the reabsorption of urinary ammonium (NH4) by intestinal mucosa, allowing its metabolisation in the liver to hydrogen ions (H+) and ammonia ions (NH3−). European Urology 2010 58, 788-791DOI: (10.1016/j.eururo.2009.05.020) Copyright © 2009 European Association of Urology Terms and Conditions