Persistent Anemia Following Renal Transplantation


Mary Eng,

American Journal of Transplantation Images in Transplantation—Continuing Medical Education (CME)

Each month, the American Journal of Transplantation will feature Images in Transplantation, a journal-based CME activity, chosen to educate participants on current developments in the science and imaging of transplantation. Participants can earn 1 AMA PRA Category 1 Credit™ per article at their own pace.

This month's feature article is titled: “Persistent Anemia Following Renal Transplantation.”

Accreditation and Designation Statement

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of Blackwell Futura Media Services, the American Society of Transplant Surgeons and the American Society of Transplantation. Blackwell Futura Media Services is accredited by the ACCME to provide continuing medical education for physicians.

Blackwell Futura Media Services designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Statement of Need

Anemia after renal transplantation is a common occurrence. Common causes of anemia after renal transplantation include anemia of chronic disease, iron deficiency and medication side effects. In the immunosuppressed patient, however, other causes must be entertained to allow for appropriate treatment.

Purpose of Activity

The purpose was to improve competency in the management of persistent anemia in the renal transplant recipient, including the consideration of an unusual cause and its treatment.

Identification of Practice Gap

Anemia after renal transplantation is not uncommon. Common causes of anemia after renal transplantation include anemia of chronic disease, iron deficiency and medication side effects. Because of the immunosuppressed state of the transplant recipient, more unusual causes of anemia should be considered. Correct identification of the cause of anemia will allow for appropriate treatment.

Learning Objectives

Upon completion of this educational activity, participants will be able to:

  • • Consider this pathogen when encountered with an immunosuppressed patient with persistent anemia when more common diagnoses are excluded,
  • • Understand how this pathogen causes anemia,
  • • Appropriately treat anemia caused by this pathogen.

Target Audience

This activity has been designed to meet the educational needs of physicians and surgeons in the field of transplantation.


No commercial support has been accepted related to the development or publication of this activity. Blackwell Futura Media Services has reviewed all disclosures and resolved or managed all identified conflicts of interest, as applicable. The following authors, editors and staff reported no relevant financial relationships with respect to this activity.


Allan D. Kirk, MD, PhD, FACS


Sandy Feng, MD, PhD

Douglas W. Hanto, MD, PhD


Mary Eng, MD, Mahoney Cobb, MD, and Christopher M. Jones, MD

ASTS Staff

Mina Behari, Director of Education

This manuscript underwent peer review in line with the standards of editorial integrity and publication ethics maintained by the American Journal of Transplantation. The peer reviewers have no relevant financial relationships to disclose. The peer review process for the American Journal of Transplantation is blinded. As such, the identities of the reviewers are not disclosed in line with the standard accepted practices of medical journal peer review.

Instructions on Receiving CME Credit

This activity is designed to be completed within an hour. Physicians should claim only those credits that reflect the time actually spent in the activity. This activity will be available for CME credit for 12 months following its publication date. At that time, it will be reviewed and potentially updated and extended for an additional 12 months.

Follow these steps to participate, answer the questions and claim your CME credit:

  • • Log on to
  • • Read the learning objectives, target audience, and activity disclosures.
  • • Read the article in print or online format.
  • • Reflect on the article.
  • • Access the CME Exam, and choose the best answer to each question.
  • • Complete the required evaluation and print your CME certificate.

The patient is a 63-year-old male with diabetic nephropathy who underwent a deceased donor renal transplant from a standard criteria donor. His immediate postoperative course was unremarkable. He required no perioperative transfusion and he had immediate function of the renal allograft, with a serum creatinine 1.1 mg/dL (estimated glomerular filtration rate [eGFR] by the Modification of Diet in Renal Disease Study equation 71 mL/min/1.73 m2) by postoperative day 3. Immunosuppression included a single dose of alemtuzumab 30 mg induction, three doses of methylprednisolone (postoperative days 0–2) and maintenance therapy of tacrolimus and mycophenolate sodium. His other medications were nystatin swish/swallow, valganciclovir, trimethoprim-sulfamethoxazole, simvastatin, aspirin and insulin.

After discharge, he was found to have a steady decline in hemoglobin (hgb) (Figure 1) requiring transfusion for symptomatic anemia. Erythropoietin was initiated and mycophenolate sodium was decreased from 720 mg twice daily to 360 mg twice daily without improvement. Renal function remained stable (eGFR 85 mL/min/1.73 m2).

Figure 1.

Serum hemoglobin trend and intervention.

Laboratory tests for anemia were obtained. Results are as follows: total iron binding capacity <199 μg/dL, unsaturated iron binding capacity <10 μg/dL, serum iron 189 μg/dL, iron saturation >95%, transferrin 176 mg/dL, lactate dehydrogenase 170 mg/dL, haptoglobin 132 mg/dL, reticulocyte 0.2%, parvovirus B19 IgG 0.3, IgM 0.1, double stranded nucleic acid (DNA) polymerase-chain reaction (PCR) not detected. Bone marrow biopsy was obtained (Figure 2) and repeat parvovirus B19 DNA PCR was positive.

Figure 2.

Photograph of bone marrow biopsy at 200× magnification with two giant pronor-moblasts identified.‘A’ is an infected pronor-moblast with a central prominent red inclusion whereas the nucleus of ‘B’ has a smudged, homogenous nuclear inclusion with a peripheral rim of darker residual chromatin, also described as margination of chromatin.

Treatment was initiated and anemia resolved immediately as shown in Figure 1.


  • 1The most likely cause of this patient's anemia is
    • a. Coxsackie virus
    • b. Lyme disease
    • c. Epstein–Barr virus
    • d. Parvovirus B19 infection
  • 2The characteristic inclusions on the bone marrow biopsy ( Figure 2 ) are found on
    • a. Erythroid progenitor cell
    • b. Erythroid and myeloid progenitor cells
    • c. Plasma cell
    • d. All progenitor cells
  • 3Peripheral blood smear ( Figure 3 ) shows
    • a. Hypochromic microcytic anemia
    • b. Normochromic normocytic anemia, lacking reticulocytes
    • c. Macro-ovalcytes
    • d. Spherocytes with increased reticulocytes
  • 4Etiology of anemia is due to
    • a. Cessation of red blood cell (RBC) production
    • b. Virus-induced hemolysis
    • c. Gastrointestinal bleed
    • d. Splenic sequestration of RBC
  • 5Persistent anemia not responsive to reduction in immunosuppression can be treated with
    • a. Plasmapheresis
    • b. Acyclovir
    • c. Intravenous immunoglobulin
    • d. Erythropoietin
Figure 3.

Photograph of peripheral blood smear at 300× magnification.

To complete this activity and earn credit, please go to