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A7024 - Tacrolimus and Mycophenolate Mofetil Induced Pulmonary Hypertension in a Kidney Transplant Patient
Author Block: S. Rygielski1, M. Al-Sarie1, T. Said Ahmed1, D. Hernandez2; 1University of Toledo, Toledo, OH, United States, 2Pulmonary Critical Care Sleep Medicine, University Of Toledo Medical Center, Toledo, OH, United States.
Introduction:
In kidney transplant patients, pulmonary complications, including acute respiratory failure (ARF), are associated with high mortality and graft loss rates. In these cases, it is worthwhile to consider immunosuppressant drugs as a potential cause of ARF. To our knowledge, no case reports have described tacrolimus and mycophenolate mofetil (MMF) pulmonary toxicity, as described in our case report.
Case Report:
A 68 year-old female presented to our facility with worsening dypnea over the last 4 months. Past medical history is significant for hypertension and end stage renal disease (ESRD) status-post kidney transplant 5 years prior to presentation. On presentation, patient was in mild respiratory distress and afebrile with oxygen saturation of 84% on room air. She has no known history of cardiac or lung disease. She denies any history of sick contacts or recent travel. Physical exam was significant for a loud S2 with no rales or crackles on auscultation. Her medications include amlodipine, mycophenolate, furosemide, hydralazine, metoprolol and tacrolimus. Patient denied a history of smoking, alcohol and illicit drug use.
Laboratory workup was normal except for elevated creatinine and blood urea nitrogen. Arterial blood gas revealed low pO2 and high A-a gradient. High-resolution CT scan of the chest showed no evidence of interstitial lung disease. Transthoracic echocardiogram showed a preserved left ventricular systolic function and severely elevated right heart pressures. Ventilation/Perfusion (V/Q) scan indicated low probability of a pulmonary embolism. A Nocturnal pulse oximetry was negative. Pulmonary function tests were consistent with a restrictive pattern. Right heart catheter showed a mean pulmonary arterial pressure of 37 mmHg with a normal pulmonary capillary wedge pressure (PCWP). Rheumatolgical workup including ANA, Anti SCL, and anti histone antibodies were negative.
Discussion:
Generally, the diagnosis of drug-induced pulmonary disease is one of exclusion. In our patient, we were able to reasonably exclude other potential causes of her pulmonary hypertension beside tacrolimus and/or MMF use, and the immunologic and rheumatologic testing has been negative. We did not discontinue the patient’s MMF and tacrolimus as her risk outweigh the benefits.
Conclusion:
Clinicians prescribing tacrolimus and/or MMF should be aware of the drugs’ potential pulmonary toxicity, especially in patients with poor baseline lung function. If a patient is developing respiratory distress in the absence of other causes, it is prudent to stop these medications to prevent disease progression.