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Abstract: FR-PO277

Acute Tubulointerstitial Nephritis and Minimal Change Disease After Administration of Lenalidomide

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Du, Xuanling, University of South Florida, Tampa, Florida, United States
  • Russell, Charles, University of South Florida, Tampa, Florida, United States
  • Punchayil Narayanankutty, Naveen, University of South Florida, Tampa, Florida, United States

Several case reports have raised concern regarding association between lenalidomide and acute tubulointerstitial nephritis (ATIN) or minimal change disease (MCD), mostly described in patients with plasma cell dyscrasia. Here we report a case of concomitant ATIN with MCD after lenalidomide initiation for a patient with myelodysplastic syndrome (MDS).

Case Description

A 68-year-old male with a history of MDS, hypertension, and coronary artery disease presented with a 2-week history of right flank pain, anasarca, and dark urine. He reported a 40-pound weight gain since the symptoms began. He had been taking lenalidomide for 7 months and was awaiting allogeneic hematopoietic stem cell transplantation. He was taking ibuprofen 2-3 tabs (200mg) per week over the last few years and denied other medication changes or contrast exposure.
On admission, serum creatinine was 6.9 mg/dl (baseline 0.6-0.8 mg/dl) with albumin of 1.5 g/dL (baseline 3.5 g/dL). A urinalysis showed a specific gravity of 1.045, 51-100 WBC/hpf, 51-100 RBC/hpf, and many granular casts. Urine protein quantification was > 2000 mg/dl. Renal ultrasound showed medical renal disease.
Hospital course was complicated by continued renal deterioration requiring initiation of hemodialysis. His renal biopsy showed mild acute tubulointerstitial nephritis with scattered eosinophils and some chronic ischemic changes. Ultrastructural studies revealed diffuse podocyte injury and extensive foot process effacement consistent with minimal change disease.
The patient was started on prednisone 60mg daily with an ensuing taper initiated at discharge. At 13 weeks the patient reported near total renal recovery with cessation of hemodialysis needs.


Lenalidomide has been reported to induce ATIN. To the best of our knowledge, there is only one case report of MCD associated with lenalidomide administration in a patient with Waldenström macroglobulinemia. NSAIDs can cause acute renal failure, ATIN and nephrotic syndrome, including MCD. NSAID-associated MCD may be present with or without ATIN, usually after long-term use. The elements of the history in our case suggests that consistent use of lenalidomide might have triggered the development of MCD with concurrent ATIN on a background of minimal NSAID use. Furthermore, rarely has MCD been reported in the setting of both MDS and lenalidomide exposure.