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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 1  |  Page : 104-106
Post transplantation anemia: Re-emphasizing the use of erythropoietin

New Medical Center Specialty Hospital, Dubai, United Arab Emirates

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Date of Web Publication30-Dec-2010

How to cite this article:
Jabur WL. Post transplantation anemia: Re-emphasizing the use of erythropoietin. Saudi J Kidney Dis Transpl 2011;22:104-6

How to cite this URL:
Jabur WL. Post transplantation anemia: Re-emphasizing the use of erythropoietin. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2021 May 17];22:104-6. Available from: https://www.sjkdt.org/text.asp?2011/22/1/104/74370

   Introduction Top

One of the most common problems that are usually encountered post transplantation is anemia. [1] It is a widely recognized problem in most of the transplantation centers. The causes that invoke the anemia process in transplant patients are variable, and the morphology of anemia differs according to the underlying etiology. One of the frequently reported causes is the bone marrow suppression by the anti rejection therapies, mainly azathioprine and mycophenylate mofetil (MMF). [1] Other causes that might be responsible for the anemia in patients with normally functioning allograft include Parvo virus infection of the bone mar­row, erythropoietin deficiency, bone marrow fibrosis secondary to long standing secondary hyperparathyroidism, and rarely, primary blood diseases. [2],[3],[4],[5],[6],[7],[8]

In this case report, the probable etiology and treatment potentials for anemia post renal trans­plantation are discussed.

   Case Report Top

A 30-year-old patient, who was a renal allograft recipient, presented with a history of ane­mia of several years post transplantation. The primary cause of renal failure was unknown. There was no history of post transplant hyper­tension or diabetes mellitus. The donor was his sister and the HLA matching was 50%. Revie­wing his medical records denoted an almost normal early post transplant period with prompt allograft function and no history of delayed function or slow graft recovery. Renal function was maintained within normal limits, and se­rum creatinine ranged between 1 and 1.2 mg/dL. He had neither a history of acute clinical re­jection nor cyclosporine toxicity. He had not been monitored previously by programmed allograft biopsies. The anti-rejection regimen consisted of two pulses of methylprednisolone at the time of operation and 24 hours later, fol­lowed by tapered prednisolone dose, with the latest maintenance dose of 5 mg/day, in con­junction with cyclosporine neoral starting dose of 10 mg/kg body weight and serum cyclo­sporine C2 level of 1900 mg/L, gradually ta­pered over the past years to 483 mg/L in his later presentation and azathioprine 50 mg per day. He did not receive any medicine other­wise, except for tonics and iron supplements.

The patient's medical records showed that he was constantly anemic since early post trans­plantation time, but his anemia was not prog­ressive and the serum iron profile repeatedly showed adequate iron storage. Examination was unremarkable, except for anemia. Investigations revealed hemoglobin (Hgb) concentration of 10.5 g/dL, oversaturated iron stores with serum ferritin of 850 mg/dL, transferrin saturation of 45%, normal C-reactive protein and erythro­cyte sedimentation rate. Blood film showed normal morphology and pigmentation of red blood cells, and hemoglobin electrophoresis revealed normal pattern. Serum creatinine was 1.2 mg/dL and estimated glomerular filtration rate (eGFR) was 72 mL/min. Neither bone ma­rrow biopsy nor screening for Parvo virus in­fection was performed. Serum erythropoietin hormone level was 13.9 IU/L (normal range 5.7-19.4 IU/L).

Treatment with erythropoietin 50 units/kg body weight per week was commenced as every other day subcutaneous injections. Regular fol­low-up of the patient for blood pressure, renal function test, Hgb, and body iron store profile was continued as an out-patient on weekly bases. After 1 month, his Hgb level was 12 g/dL, and renal function and blood pressure remained normal.

   Discussion Top

Since the anemia in our patient dated back to early post transplant period, it might be related to pre-transplantation status of the bone marrow. Hyperparathyroidism might be immediately apparent in this period, but we could not point out any feature (investigational or radiolo­gical) highlighting the hyperparathyroidism. In addition, there was no evidence of pre-trans­plant hyperdynamic bone disease, and the de­tection of low serum erythropoietin level ex­cluded bone marrow resistance.

The second cause that might be important is the Parvo B19 virus infection, which may lead to profound bone marrow suppression in trans­plantation recipients. [2] However, the non-prog­ressive nature of our patient's anemia, and the low serum erythropoietin level were against this possibility.

Drug related anemia is commonly encoun­tered post transplantation, especially for aza­thioprine, MMF, and sirolimus, [3] which might directly suppress all bone marrow cellular lines, but the red blood cells' morphology in this sort of anemia is reportedly of macrocytic type with azathioprine and MMF, and micro­cytic with sirolimus. Calcineurin inhibitors may cause anemia indirectly by impairing kidney function. However, the constant tempo of ane­mia throughout the post transplant course des­pite the gradual reduction of the immunosup­pressive drug doses refutes the probability of drug related post transplant anemia.

The most important cause that we are in­clined to is the erythropoietin insufficiency post kidney transplantation. [4] Erythrocytosis is usually more expected than anemia post renal transplantation. [5] However, both conditions de­note massive derangement of erythropoietin homeostasis. In general, the reported anemia is of two kinds, either erythropoietin resistant or erythropoietin deficient. Erythropoietin resistant post transplant anemia is most probably se­condary to bone marrow permanent damage caused by pretransplant uremic toxins, hyper­parathyroidism, or primary erythroid progeni­tors disease, wherein endogenous erythropoie­tin level would be at its peak; [6] our patient revealed low serum erythropoietin level for the degree of anemia. There is a link between ery­thropoietin deficiency and the impaired GFR. [7],[8] Despite the fact that no kidney biopsy was performed in our patient because of the normal renal function, renal tubular dysfunction or in­terstitial nephritis due to low-grade immuno­logic inflammatory reaction (polyoma BK viral interstitial nephritis or CMV viral infection) that could cause erythropoietin deficiency was not ruled out.

Finally, the dramatic improvement of Hgb le­vel after commencement of erythropoietin re­placement therapy would negate the possibility of peripheral autoimmune destruction of the erythropoietin hormone. We speculate the pre­sence of the generalized erythropoietin derange­ment inflicted by the transplant procedure or the immunosuppressive medications, or a donor-recipient erythropoietin incompatibility as possible causes of anemia in the presence of nor­mal renal function.

In conclusion, this case highlights the noto­rious underestimation of the post transplant anemia secondary to erythropoietin deficiency in the kidney transplantation patients.

   References Top

1.Vanrenterghem Y, Ponticilli C, Morales JM, et al. Prevalence and management of anemia in renal transplant recipients: a European survey. Am J Transplant 2003;3:835.  Back to cited text no. 1
2.Egbuna O, Zand MS, Arbini A, et al. A cluster of parvovirus B19 infections in renal transplant recipients: a prospective case series and review of the literature. Am J Transplant 2006;6:225.  Back to cited text no. 2
3.Nayak SG, Kiran MK, Fernandes K, Gopala­krishna G, Shastry JC. Anemia in renal trans­plant recipients-a persisting problem. Indian J Nephrol 2005;15:239-42.  Back to cited text no. 3
  Medknow Journal  
4.Zadrazil J, Horak P, Horcicka V, et al. Endo­ genous Erythropoitin levels and anemia in long-term renal transplant recipients. Kidney Blood Pressure Res 2007;30:108-16.  Back to cited text no. 4
5.Charfeddine K, Zaghane S, Yaich S, et al. Factors predisposing to Post-Transplant Ery­throcytosis: A retrospective study. Saudi J Kidney Dis Transplant 2008;19:371-8.  Back to cited text no. 5
6.Joist H, Brennan DC, Coyne DW. Anemia in the kidney-transplant patient. Adv Chronic Kidney Dis 2006;13:4.  Back to cited text no. 6
7.Tukowski-Duhem A, Kamar N, Cointault O, et al. Predictive factors of anemia within the first year post renal transplant. Transplantation 2005;80(7):903-9.  Back to cited text no. 7
8.Sezer S, Ozderm F, Tutal E, Bilgic A, Haberal M. Prevalence and etiology of anemia in renal transplant recipients. Transplant Proc 2006;38 (2):537-40.  Back to cited text no. 8

Correspondence Address:
Wael Latif Jabur
New Medical Center Specialty Hospital, P.O. Box 7832, Dubai
United Arab Emirates
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PMID: 21196622

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