| Abstract|| |
Post-transplant erythrocytosis (PTE) is defined as an increase in hematocrit greater than 51%. This phenomenon affects 5 to 17% of renal transplant patients within two years of transplantation. Its etiology is not clearly known, but several factors have been implicated in its pathogenesis. We report on a 50-year-old male, known to have autosomal dominant polycystic kidney disease, diabetes mellitus and hypertension for 20 years, who underwent a living unrelated donor transplantation. Three years following renal transplantation, he was noted to have high hemogloblin and hematocrit (18.3 gm%, 53.8%). This erythrocytosis persisted for nine months during which period he underwent multiple phlebotomies before undergoing spontaneous remission. He did not develop any complications of erythrocytosis. Our patient had multiple factors to account for occurrence of PTE: diabetes mellitus, hypertension, mild allograft dysfunction, polycystic kidney disease and cyclosporin therapy. Our case suggests that multiple factors may be operative in a given patient leading to the development of PTE.
Keywords: Post transplant erythrocytosis, autosomal dominant polycystic kidney disease, hydronephrosis, chronic rejection, diabetes mellitus.
|How to cite this article:|
Ghacha R, Rafi A, Abdelrahman M, Malik TQ, Karkar A. Post-Transplant Erythrocytosis: A Disease With Multifactorial Etiology. Saudi J Kidney Dis Transpl 2006;17:54-7
|How to cite this URL:|
Ghacha R, Rafi A, Abdelrahman M, Malik TQ, Karkar A. Post-Transplant Erythrocytosis: A Disease With Multifactorial Etiology. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2016 Dec 4];17:54-7. Available from: http://www.sjkdt.org/text.asp?2006/17/1/54/32445
| Introduction|| |
Post-transplant erythrocytosis (PTE) is defined as an increase in hematocrit greater than 51%. This phenomenon affects 5 to 17% of renal transplant patients within two years of transplantation. ,, It usually undergoes spontaneous remission but may occasionally persist for years.,,, Its etiology is not clearly known, but several factors have been implicated in its pathogenesis. These include excessive erythropoietin production from the transplanted kidney due to ischemia caused by chronic rejection, renal artery stenosis and obstructive uropathy affecting the renal allograft. Cyclosporin can also cause renal ischemia resulting in over-production of erythropoietin. Native kidneys may be the source of excessive production of erythropoietin as well. In addition, hypertension, diabetes and use of diuretics can also produce spontaneous rise in hematocrit due to volume contraction 8. In this report, we describe a case of PTE which showed some atypical features.
| Case Report|| |
A 50-year-old male, known to have autosomal dominant polycystic kidney disease, diabetes mellitus and hypertension for 20 years, developed end-stage renal failure in 1990, and was started on regular hemodialysis (HD). Earlier, 20 years prior to initiation of HD, he had undergone right nephrectomy because of recurrent staghorn calculus. He received a live unrelated renal transplant two years following initiation of HD with uneventful recovery (serum creatinine 1.6 mg/dl). He presented with impaired renal function reflected by a rise of serum creatinine to 2.1 mg/dl six months after transplantation, but had good urine output without any history of fever or pain in the allograft. Ultrasound of the abdomen revealed hydronephrosis of the transplanted kidney and cystoscopy showed a urethral stricture, which was subject to dilatation. However, patient's renal function remained relatively unchanged (creatinine 1.8-2.0 mg/dl) [Table - 1]. Three years following renal transplantation, the patient's renal function was stable at around 2 mg/dl. At this stage, he was noted to have high hemogloblin and hematocrit (18.3gm%, 53.8%). This erythrocytosis persisted for nine months during which period he underwent multiple phlebotomies before undergoing spontaneous remission. During this period, the patient's renal functions remained stable and his blood sugar was under reasonable control; he was not receiving any diuretics, and was a non-smoker. He did not develop any complications of erythrocytosis. The patient's graft functioned for nine years after which he developed chronic allograft dysfunction, when he was restarted on HD.
| Discussion|| |
Post renal transplant elevation of hematocrit is a well known phenomenon in transplant recipients. The incidence varies between 5 to 15% of all transplant recipients. The onset usually occurs at different time points following kidney transplantation which varies from 1-90 months., The underlying etiology of true erythrocytosis could be due to increased over-production of erythropoietin and/or altered sensitivity of erythroid stem cells to erythropoietin. Increased production of erythropoietin may be caused by ischemia in the renal artery and/or use of cyclosporin. Native kidneys may also be the source of erythropoietin production as in acquired or hereditary polycytic kidney disease. ,,,
Although most cases of erythrocytosis are transient, prolonged elevation of hematocrit for more than five years have been described. ,,, In some patients, elevation of hematocrit is due to decreased plasma volume caused by diuresis secondary to diabetes mellitus, hypertension or use of diuretics. ,
In our patient, PTE occurred late in the course of transplant (after three years) which is rather unusual. It was probably due to multiple factors that this patient had. He was diabetic and was on insulin. His blood sugar was not very well controlled. This might have caused some contraction of blood volume. In addition, he was hypertensive and although his blood pressure was well controlled, the contribution to PTE cannot be totally excluded. Our patient was on cyclosporin at a dose of 4 mg/kg, and his trough level was within normal range. Earlier onset of reticulocytosis has been noted in patients destined to develop PTE who were treated with cyclosporin.  It is known that PTE develops more frequently in cyclosporin treated patients than in patients treated with azathioprin and steroids  as cyclosporin induces renal ischemia while azathioprin is a myelosuppressent. In this patient, the serum creatinine rose to 2.0 mg/dl at six months post-transplant and remained elevated despite correction of obstructive uropathy affecting the renal allograft. The patient subsequently developed chronic allograft dysfunction and returned to HD. It is therfore likely that earlier elevation of serum creatinine was partially due to chronic rejection and this might have contributed to PTE by causing renal ischemia. Unfortunately, allograft histology is not available to substantiate this observation. Continued production of erythropoietin by the native kidneys may also be responsible for PTE. Acquired polycystic kidney disease affecting native kidneys may be the source of erythropoietin and native kidney nephrectomy has been used as treatment for PTE.,,, In our patient, the underlying renal disease was autosomal dominant polycystic kidney disease and this native kidney might have been the source of erythropoietin and the cause of PTE.
In spite of the presence of multiple factors that could have lead to the develop-ment of PTE, the course was mild and lasted only nine months. The PTE did not produce any thromboembolic complications. PTE tends to be more aggressive in patients with good graft function. In our patient, the graft function was not normal (creatinine 2.0mg/dl at 6 months post-transplant) and this may explain the shorter duration of PTE. In conclusion, our case suggests that multiple factors may be operative in the same patient leading to the development of PTE.
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Dept. of Nephrology, Dammam Central Hospital, P.O. Box 14563 Dammam 31434
[Table - 1]