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| Year : 2008 | Volume
: 19
| Issue : 4 | Page : 559-563 |
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| Risk Factors of Erythrocytosis Post Renal Transplantation |
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Effat Razeghi1, Alireza Kaboli1, Mahboob Lessan Pezeshki2, Ali Pasha Meysamie3, Mohammad Reza Khatami2, Patricia Khashayar1
1 Sina Hospital, Tehran, Iran
2 Imam Khomeini Hospital, Tehran, Iran
3 Social Medicine Division, Medical Sciences/University of Tehran, Tehran, Iran
Click here for correspondence address and email
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 Abstract | | |
Post-transplant erythrocytosis (PTE) is characterized by persistently elevated hematocrit level 0 51%. This complication is reported to develop in 10-20% of renal allografts recipients, mostly 2 years after kidney transplantation. PTE is self-limited in 25% of the patients; however it may persist in patients with an increased susceptibility for thrombosis and potential fatal outcome. To evaluate the prevalence and risk factors of PTE in our center, we reviewed the records of 235 patients who received renal allografts from 1999 to 2004. Polycythemia was found in 45 (19%) patients. There was no significant correlation of polycythemia and age, history of hypertension, diabetes, pretransplant hematocrit level, pre-transplant history of transfusion, graft's function, and source of kidney. A significantly higher proportion of PTE patients were males, patients with history of polycystic kidney disease, and patients with glomerulonephritis. We conclude that PTE is an important complication of kidney transplantation. There are several risk factors that should be addressed to prevent this complication. Keywords: Erythrocytosis, Renal Transplantation, Thrombosis, Polycythemia
How to cite this article:
Razeghi E, Kaboli A, Pezeshki ML, Meysamie AP, Khatami MR, Khashayar P. Risk Factors of Erythrocytosis Post Renal Transplantation. Saudi J Kidney Dis Transpl 2008;19:559-63 |
How to cite this URL:
Razeghi E, Kaboli A, Pezeshki ML, Meysamie AP, Khatami MR, Khashayar P. Risk Factors of Erythrocytosis Post Renal Transplantation. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2021 Jan 23];19:559-63. Available from: https://www.sjkdt.org/text.asp?2008/19/4/559/41314 |
| Introduction | |  |
Post transplant erythrocytosis (PTE) is one of the complications that occur in 10 to 20% of the recipients of renal allografts, most often during the first 2 years following transplantation. It is defined as a constantly elevated level of hematocrit 0 51%. Spontaneous recovery is reported in 25% of the patients within 2 years from the onset of this problem, while the rest continue to have elevated hematocrit levels for several years or until the occurrence of rejection. Male gender, non-nephrectomized failed native kidneys, diabetes mellitus, and dysfunction or arterial stenosis in the transplanted kidney are known risk factors for PTE. [1],[2],[3] Although smoking is not believed to be an essential factor, it is considered to be an important one. Some studies have not revealed any relation between drug consumption, especially corticosteroids, and PTE, [3] while others noted a higher prevalence of erythrocytosis in patients receiving cyclosporine compared with azathiopurine and prednisolone. [4],[5]
Thromboembolic accidents were reported in 10-30% of these patients, which may lead to death in 1-2% of them. [1],[6] Considering the relatively high incidence of PTE and its potential fatal outcome, in-time diagnosis and treatment would play an important role in preventing the these complications.
The purpose of this study is to assess the prevalence and the risk factors of PTE in our center.
| Material and Methods | | |
We reviewed the records of 235 stable renal transplant patients who received renal allografts at Sina Hospital, and Imam Khomeini Hospital, University of Tehran, Tehran, Iran, from 1999 to 2004. The transplant was performed for all the subjects at least 3 months prior to this study.
Patients with a positive history of polycythemia hematocrit levels (hct) > 51% prior to transplant, apparent pulmonary disease, and polycythemia vera (thrombocytosis plus leukocytosis and splenomegaly) were excluded.
We found 45 (19%) patients who satisfied the criteria for diagnosis of PTE and considered as the case group. We compared this group to 90 sex and age matched nonPTE transplant patients.
The risk factors considered in the study included age, gender, source of allografts, immunosuppressive therapy, smoking habits, co-morbid disease such as hypertension and diabetes mellitus, phlebitis, pulmonary emboli, cerebrovascular accidents, underlying renal disease such as renal artery stenosis and obstruction of urinary tract, nephrectomy, splenectomy, parathyroidectomy, and history of blood transfusion before transplant (0, 1-3, 4-6 and more than 6 times).
The studied laboratory parameters consisted of hemoglobin and hematocrit rates prior to transplant, liver enzymes, and serum creatinine (creatinine > 1.5 was considered as a low performance).
Statistical analysis
Results were analyzed with SPSS version 11.5 using chi-square, student t-test and Mann-Whitney tests. In addition, in order to assess the effect of risk factors on development of erythrocytosis, Binary Logistic Regression analysis was carried out. P value less than 0.05 was considered significant.
| Results | | |
The mean age of the case and control groups were 41.5 ± 12.1 and 38.4 ± 14.1, respectively, (p= 0.182). There was no significant difference between the mean age of male and female patients (40.5 ± 13.5 vs. 37.5 ± 13.5, p= 0.2). Forty two out of 86 male (48.8%) and 3 (6.1%) female patients developed PTE (p < 0.001).
PTE was found in 10 of the 17 (58.8%) smokers and 35 of the 118 (29.7%) nonsmokers (p= 0.017). It should be noted that only one member of the smoker group was female, demonstrating a meaningful difference between smoking habits in different genders (p= 0.005). Mantel-Haenszel test revealed gender to have an altering effect on the relation between smoking habit and the incidence of erythrocytosis (OR= 13.24, CI 95%: 3.77-46.5). Accordingly, smoking indirectly influenced the development of PTE and male gender was the real risk factor.
[Table 1] shows the characteristics of patients developing PTE. There was no statistically significant relation between any of these risk factors and PTE. Mann Whitney test did not reveal any relation between PTE and number of previous transfusions (p= 0.85).
[Table 2] shows no difference in the hemoglobin and hematocrit prior to transplantation between the case and control groups. Mild elevation in liver enzymes occurred in 6 (4.4%) patients, of whom 2 developed PTE.
When underlying renal diseases were addressed, it was noted that 16 of 22 (72.7%) subjects with glomerulonephritis and 6 of 8 (75%) patients with polycystic kidney disease (PKD) developed PTE (p= 0.001and 0.01, respectively).
[Table 3] shows the different underlying renal diseases in the study groups. None of the study patients had nephrectomy of their native kidneys.
Doppler ultrasonography to rule out renal artery stenosis was performed in 101 cases. None of the 27 patients with PTE revealed renal artery stenosis versus 6 (8.1%) patients in the non-PTE (p= 0.189).
Three patients (2.2%) who had strictures in their urinary tract were all in the nonPTE group. Parathyroidectomy was not performed on any of our study patients. History of splenectomy was found in 7 (5.2%) of the cases, of whom 3 (42.9%) developed PTE (p= 0.686). Hydronephrosis was reported in only 3 (2.2%) non-PTE patients.
Our study patients received one of three different immunosuppressive regimens that included PMC (prednisolone, mycophenolate mofetil, cyclosporine), PIC (prednisolone, azathioprine, cyclosporine) and PC (prednisolone, cyclosporine). Analysis did not reveal any relation between therapeutic regimen and PTE (p= 0.097).
Evaluation for PTE related complications revealed that cerebrovascular accident (CVA) occurred in one case of PTE and another case of non-PTE. In addition, thrombophlebitis was reported in one case in the PTE group (p= 0.319).
The Binary Logistic Regression test revealed that men developed PTE 13.8 times more than women. Moreover, patients with PKD and glomerulonephritis developed PTE 9.6 and 7.9 times more than other underlying kidney diseases, and the use of PIC immunosuppressive regimen was associated with 3.5 times higher risk of developing PTE that other regimens.
| Discussion | | |
According to the results of this study male gender was the most important risk factor for PTE. Other studies demonstrated that 50% of PTE patients were men. [1],[2],[3]
Although smoking was associated with higher risk of PTE in the primary analysis, final revisions proved the contrary. Actually, fewer women were smokers compared to men and male gender was the real risk factor influencing PTE in this group. However, several other studies have mentioned smoking as a main risk factor. [1],[2],[3]
In our study, patients with PKD were found to have a higher risk of PTE; anemia occurs less often in these patients when they reach end-stage renal disease than other kidney diseases. Structural changes in the kidney of this group of patients may activate renin-angiotensin-aldestrone and results in the development of PTE. Similar explanation for glomerulonephritis is not available. [7],[8]
PTE was more frequently reported in patients receiving PIC regimen. Though, azathioprine (Imuran) is suggested to be the culprit, Perazella's [1] proposed that cyclosporine might be the cause of PTE. However, Koziak and others found no difference in the level of hematocrit of patients using these cytotoxic agents. [2],[3]
In the present study, PTE did not result in a high incidence of thromboembolic accidents; however, other studies have found that 10-30% of PTE patients were at risk of these complications. [4],[5] The lower incidence of thromboembolic complications in our study may be due to early diagnosis and treatment.
We conclude that despite all limitations, our study indicated several factors that influence PTE. Modification of these factors may reduce complications. However, large and prospective studies are required in order to identify and investigate all the risk factors.
| References | | |
| 1. | Vlahakos DV, Marathias KP, Agroyannis B, Madias NE. Post transplant erythrocytosis. Kidney Int 2003;63(4):1187-94.  |
| 2. | Einollahi B, Lessan pezeshki M, Nafar M, et al. Erythrocytosis after renal transplantation: Review of 101 cases. Transplant Proc 2005;37(7):3101-2. |
| 3. | Wickre CG, Norman DJ, Bennion A, Barry JM, Bennet WM. Post renal transplant erythrocytosis: a review of 53 patients. Kidney Int 1983;23(5):731-7. |
| 4. | Panjwani DD, Sabawi NM, White AG, Kumar MS, Aref MS, Abouna GM. Post renal transplant erythrocytosis: Existence of two distinct types. Clin Transplant 1990;4:23-5. |
| 5. | Macdougall IC, Karim S, Amos R, Baker Lri, Raine AE. Polycythemia in renal transplant recipients is not mediated solely by enhanced erythropoietin activity. J Am Soc Nephrol 1992;3:428. |
| 6. | Kazory A. Post transplant erythrocytosis and thromboembolic events: an error. Nephrol Dial Transplant 2004;19:260-1. |
| 7. | Yildiz A, Yazici H, Ine N, et al. Angio tensin converting enzyme gene polymorphism and development of posttransplant erythrocytosis. J Nephrol 2003; 16(3):399-403. |
| 8. | Glicklich D, Burris L, Urban A, et al. Angiotensin converting enzyme inhibition induces apoptosis in erythroid precursors and affects insulin- like growth factor-1 in post transplantation erythrocytosis. J Am Soc Nephrol 2001;12(9):1958-64. |
Correspondence Address:
Effat Razeghi
Urology Research Center, Sina Hospital, Imam Khomeini St. 11367-46911 Tehran
Iran
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PMID: 18580013 
[Table 1], [Table 2], [Table 3] |
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