COMPLICATIONS - METABOLIC

J. Klassen
Nephrology, University of Calgary, Calgary/AB/CANADA

Body:
A 54-year-old female patient presented to the hospital in November 2009 in acute hypoxic respiratory failure. She gave a history of developing end stage renal disease secondary to IgA nephropathy. She received a cadaveric renal transplant in November 1996. She had normal renal function (creatinine 64) prior to presenting to the Emergency room. She gave a history of feeling increasing unwell for three weeks prior with increasing dyspnea but no fever, chest pain or bone pain. She was admitted to the Intensive Care Unit and intubated. She had massive anasarca with large pleural and pericardial effusions. 600 c.c.s of pleural fluid were aspirated but it reaccumulated quickly. She required 6 litres of oxygen by mask. Investigation of the pleural effusion revealed it to be an exudate but analysis of this did not reveal a diagnosis. Therefore a diagnosis of edema secondary to rapamycin was made. Cyclosporine was substituted for the rapamycin, the levels of which had ranged from 4.3 to 7.4. The edema cleared over the next two or three months. Her renal function had remained normal throughout. Cardiac function was also not impaired. A 61-year-old female presented in May of 2006 to the clinic with a vague history of increasing dyspnea. She had developed end stage renal disease secondary to glomerulonephritis. She received a cadaveric renal transplant in 1989. A chest x-ray revealed bilateral pleural effusions and an echocardiogram showed a large pericardial effusion with normal ventricular function however. Her serum creatinine at this time was 64 µmols/L. A pericardiocentesis was done and 885 mL of fluid was removed. The fluid reaccumulated quickly. Analysis did not reveal any etiology. The rapamycin levels were at 6.1 to 9.5. A diagnosis of rapamycin induced edema was made so drug was stopped and cyclosporine was substituted. Over a period of several months the effusions cleared completely. Pleural and pericardial effusions are quite common after organ transplants especially after cardiac transplants. They are also considerably more common with rapamycin. Pedal edema unilateral or bilateral can also occur. However what was unexpected in these two cases was the late presentation in these patients with stable renal function on relatively low doses of rapamycin some thirteen and fifteen years post transplant. Even more unusual was the development of anasarca in the second patient. Again, no identifying triggering event could be identified in either patient. It took several months for the edema to disappear once the drug is stopped. A number of theories have been proposed for the mechanism of the edema production secondary to rapamycin.

Disclosure: All authors have declared no conflicts of interest.