volume overload is usually secondary to an aggressive fluid resuscitation in a patient whose kidney function is still evolving . however in a small group of patients interstitial lung involvement can cause significant pulmonary involvement . we report a case of unusual pulmonary infiltrates which was thought to be secondary to mycophenolate sodium . he was evaluated and found to have end - stage kidney disease ( native kidney disease of uncertain etiology ) and was started on hemodialysis , with a temporary right internal jugular catheter and later with a left radiocephalic fistula upon maturation . he gave a history of long - standing hypertension and an ultrasound done 1 year back showed contracted kidneys . pretransplant cardiac assessment showed a normal ejection fraction echocardiographically , and a coronary angiogram on the advice of cardiologist showed complete occlusion of the right coronary artery . his preanesthetic pulmonary evaluation did not reveal any abnormality . in july 2015 , after 7 months on dialysis , he underwent a living kidney transplantation ( donor was his brother  in - law with a four antigen mismatch ) . he received 1 l of intravenous fluids during surgery and did not need any blood transfusion . the allograft attained immediate function . on the 1 postoperative day , his vitals were stable and he was diuresing well with a total urine output of more than 5 l. there was no clinical evidence of fluid overload . he received basiliximab as induction with tacrolimus , mycophenolate sodium , and steroids as his maintenance immunosuppression . the tacrolimus ( 0.1 mg / kg / day in two divided doses ) and mycophenolate sodium ( 720 mg twice a day ) was started 48 h before the transplantation surgery . the chest x - ray was suggestive of pulmonary edema , and consequently , he was started on diuretics , and his fluid intake was restricted . his central venous pressure was 11 cm of water , and his electrocardiogram and echocardiogram did not show any fresh changes . his respiratory condition continued to worsen and a computed tomography ( ct ) scan of the chest was done which showed patchy right lower lobe consolidation , bilateral ground - glass densities with minimal left pleural effusion [ figure 1 ] . cultures for bacteriological , mycobacterial , and fungal isolation were sent and antibiotics were started . the pulmonologist opinion was that of noncardiogenic pulmonary edema , and he suggested continuation of diuretics . despite adequate diuresis and antibiotics , his oxygen saturation continued to deteriorate . besides antibiotics , treatment for possible fungal , cytomegaloviral , and pneumocystis infection was started and bronchoscopy was done . initial computed tomography done on the 1 postoperative day showing right lower lobe consolidation and left pleural effusion because of his persistent pulmonary infiltrates , the second dose of basiliximab ( day 4 ) was not given . on the 8 postoperative day in view of his worsening clinical condition , he was put on noninvasive ventilation and a repeat ct scan of the chest was done . the ct scan showed confluent ground - glass densities in both the lungs with smooth interlobar septal thickening . certain parts of the parenchyma were spared giving a crazy pavement pattern [ figure 2a and b ] . as there was no radiological evidence of infection and fluid overload , a diagnosis of interstitial pneumonitis was considered . a drug - induced etiology of the lung pathology was considered secondary to mycophenolate sodium ( idiosyncratic reaction as there was no skin rash , arthralgia , or blood eosinophilia ) and the drug was withdrawn . over the next 4 days , he showed progressive improvement . his oxygen requirement came down dramatically , and he was discharged on day 14 in stable clinical condition without any oxygen requirement . a repeat ct scan of the chest after 4 weeks showed considerable improvement in the pulmonary infiltrates . [ figure 3a and b ] the patient is doing well after 6 months posttransplantation . ( a ) confluent ground - glass densities in both the lungs noted in the computed tomography scan done on the 8 postoperative day . ( b ) extensive pulmonary infiltrates in the coronal images ( a ) near total resolution of pulmonary infiltrates on follow - up after 4 weeks . pulmonary infiltrates presenting in a renal allograft recipient early in the course of transplant is often considered to be a pulmonary infection and early antibiotics are started . even though the incidence of bacterial pneumoniae is decreasing , multidrug - resistant bacteria are emerging as growing threat . some reports have revealed that the use of newer immunosuppressive medications ( tacrolimus , mycophenolate mofetil , induction therapy ) and inappropriate use of antibiotics have led to an increased rates of bacterial pulmonary infection . some studies have shown that consistent use of antiviral / antifungal prophylaxis reduces the incidence of cytomegalovirus and pneumocystis infections . however , there are other studies which have shown an increasing trend of fungal infection in renal allograft recipients , which is a major cause of posttransplant mortality . in many instances , the bacterial pathogen remains unidentified . in our patient also , the early sputum and bronchial lavage did not yield any organism and he was treated empirically with broad - spectrum antibiotics . one of the major issues to be considered in the differential diagnosis of worsening pulmonary infiltrates in a renal allograft recipient is to consider noninfectious causes of the pulmonary pathology . pulmonary edema , pulmonary hemorrhage , and interstitial pneumonitis are seen in renal allograft recipients and should be part of the differential diagnoses of pulmonary infiltrates in renal transplant recipients . there are several reports regarding target of rapamycin inhibitors and interstitial lung disease , following kidney transplantation . though rare , there are a few reports of pulmonary toxicity secondary to the use of azathioprine   and mycophenolate mofetil . in our patient , the dramatic improvement in the pulmonary infiltrates following withdrawal of mycophenolate sodium led us to believe that mycophenolate sodium was the cause of the lung infiltrates in our patient . it acts as an inhibitor of inosine monophosphate dehydrogenase isoform 2 and selectively inhibits t and b lymphocytes and is effective in preventing early acute rejection . very little information regarding pulmonary toxicity exists in literature and it is unclear whether pulmonary toxicity occurs along with other known side effects or it manifests as a solitary phenomenon . some studies have shown that there is an association between the drug level and side effects of the drug , but the clinical benefit of drug level monitoring is still of questionable value in such situation where the adverse effect is considered to be an idiosyncratic reaction . in a patient with worsening pulmonary infiltrates , which can not be related to infections and fluid overload , consideration should be given to interstitial lung injury . drugs are known to cause interstitial lung injury , and immunosuppressive agents are being recognized as potential causes for persistent pulmonary pathology in a solid organ recipient . no added information as the authors have not received any honorarium from any pharmaceutical company . there are no conflicts of interest . no added information as the authors have not received any honorarium from any pharmaceutical company .
a renal allograft recipient developed cough with hemoptysis on the 1st postoperative day . 
 a chest x - ray was performed which was suggestive of fluid overload . 
 his fluid was restricted and diuretics were added . on the same day , his pulmonary infiltrates worsened and a computed tomography ( ct ) of the chest was carried out , which was suggestive of the right lower lobe consolidation and left pleural effusion . 
 he underwent a bronchoscopy and the lavage was sent for cultures , which did not grow any infective organism . besides routine antibiotics , treatment for possible cytomegalovirus , fungal infections , and pneumocystis infection was instituted . 
 noninvasive ventilation was started on day 8 . 
 a repeat ct of the chest on the postoperative day 8 showed further worsening of the pulmonary infiltrates . 
 as all the initial cultures and serology were negative , a possibility of interstitial pneumonitis was considered . 
 mycophenolate sodium was considered as a possible cause of the lung infiltrates and was withdrawn . 
 the patient showed progressive improvement . 
 his antibiotics were withdrawn . 
 he was discharged on day 14 . 
 a repeat ct 4 weeks post transplant showed significant improvement in his pulmonary pathology . 
 the acute lung injury was considered to be a drug reaction secondary to mycophenolate sodium . in a renal allograft recipient with persistent pulmonary infiltrates , interstitial involvement secondary to drugs 
 should be considered if the patient does not improve with the standard treatment measures .