Erythrocytosis After Renal Transplantation

Sumrani, Nabil; Daskalakis, P.; Miles, Anne Marie V.; Sarkar, Salil D.; Markell, Mariana S.; Hong, Joon Ho; Friedman, Eli A.; Sommer, Bruce G.

doi:10.1097/00002480-199301000-00012

Cited by 15 publications

(10 citation statements)

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“…Other proposed mediators of erythrocytosis include endogenous androgens, renin–angiotensin system activation and other growth factors (710). Identified clinical risk factors that have been reported include male gender, polycystic kidney disease, smoking, immunosuppression, reduced kidney function, absence of rejection, renal artery stenosis, hydronephrosis, hypercalcemia, longer duration of dialysis, higher pretransplant hemoglobin, angiotensin‐converting enzyme genotype, hypertension and diabetes mellitus (709,710,761–765,767–778).…”

Section: Rationalementioning

confidence: 99%

“…In KTRs, erythrocytosis can be asymptomatic, or patients may complain of fatigue, headaches, plethora, dyspnea or blurred vision (709,767,776). The more serious consequences include increased risk of venous and arterial thrombosis (767,768,784). One small case control study found more thromboembolic events in patients with polycythemia (11 events in 53 patients) compared to those without erythrocytosis (0 in 49 matched controls) (767).…”

Section: Rationalementioning

confidence: 99%

See 1 more Smart Citation

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Eckardt¹,

Kasiske²,

Zeier³

2009

American Journal of Transplantation

1,205

294

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Journal compilation © 2009 The American Society of Transplantation and the American Society of Transplant Surgeons doi: 10.1111/j.1600-6143.2009.02834.x S2 American Journal of Transplantation 2009; 9 (Suppl 3): S2-S2Since the first successful kidney transplantation in 1954 It is our hope that this document will serve several useful purposes. Our primary goal is to improve patient care. We hope to accomplish this in the short term by helping clinicians know and better understand the evidence (or lack of evidence) that determines current practice. By making this guideline broadly applicable, our purpose is to also encourage and enable the establishment and development of transplant programs worldwide. Finally, by providing comprehensive evidence-based recommendations, this guideline will also help define areas where evidence is lacking and research is needed. Helping to define a research agenda is an often neglected, but very important function of clinical practice guideline development.We used the GRADE system to rate the strength of evidence and the strength of recommendations. In all, there were only 4 (2%) recommendations in this guideline for which the overall quality of evidence was graded 'A,' whereas 27 (13.6%) were graded 'B,' 77 (38.9%) were graded 'C,' and 90 (45.5%) ' and 148 (74.7%) graded '2.' There were 3 (1.5%) recommendations graded '1A,' 16 (8.1%) were '1B,' 18 (9.1%) were '1C, ' and 13 (6.6%) were '1D.' There was 1 (0.5%) graded '2A,' 11 (5.6%) were '2B,' 59 (29.8%) were '2C, ' and 77 (38.9%) BackgroundExcept perhaps for transplantation between identical twins, all kidney transplant recipients (KTRs) need immunosuppressive medications to prevent rejection. Induction therapy is treatment with a biologic agent, either a lymphocyte-depleting agent or an interleukin 2 receptor antagonist (IL2-RA), begun before, at the time of, or immediately after transplantation. The purpose of induction therapy is to deplete or modulate T-cell responses at the time of antigen presentation. Induction therapy is intended to improve the efficacy of immunosuppression by reducing acute rejection, or by allowing a reduction of other components of the regimen, such as calcineurin inhibitors (CNIs) or corticosteroids. Available lymphocytedepleting agents include antithymocyte globulin (ATG), antilymphocyte globulin (ALG) and monomurab-CD3. Basiliximab and daclizumab, the two IL2-RAs that are currently available in many parts of the world, bind the CD25 antigen (interleukin-2 [IL2] receptor a-chain) at the surface of activated T-lymphocytes and thereby competitively inhibit IL2-mediated lymphocyte activation, a crucial phase in cellular immune response of allograft rejection. Rationale• There is high-quality evidence that the benefits of IL2-RA vs. no IL2-RA (or placebo) outweigh harm in a broad range of KTRs with variable immunological risk and concomitant immunosuppressive medication regimens.• There is moderate-quality evidence that a lymphocytedepleting agent vs. no lymphocyte-depleting a...

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Section: Rationalementioning

confidence: 99%

Section: Rationalementioning

confidence: 99%

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Eckardt¹,

Kasiske²,

Zeier³

2009

American Journal of Transplantation

1,205

294

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“…In our study, among the 120 renal recipients, 22 out of the 28 renal recipients who developed erythrocytosis after transplantation were men (78.5%), and male specific rate of 23.3% compared with the female specific rate of 11.4% which point to male gender as 1 of possible predisposing factors for PTE; meanwhile PTE was independent of recipient age, donor race, and type. In accordance with these results, Sumrani et al18 found that PTE occurred more frequently in men (12.8%) than women (1.6%) and Kessler et al19 identified male gender as an important predisposing factor for PTE. Although men comprised 61% of the renal graft recipients in the United States in 1996,20 more than 80% of PTE patients reported in American studies in the mid‐1990s were men.…”

Section: Discussionmentioning

confidence: 72%

Post‐kidney transplantation erythrocytosis and its relationship to renal artery stenosis, IGF‐1, and its binding protein 3 (IGFBP‐3)

Khedr

Abdelwhab

ElSharkawy

et al. 2009

Dialysis & Transplantation

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Background Erythrocytosis is relatively common following kidney transplantation. It increases the risk of thromboembolism. Insulin‐like growth factor‐1 (IG‐1) and its binding protein 3 (IGFBP‐3) may play a role in its pathogenesis. Patients and Methods A total of 120 consecutive kidney‐transplanted patients with at least 3 month graft function were studied. Forty‐five kidney transplant patients were then selected and divided into 2 groups: 15 patients with post‐transplant erythrocytosis (PTE; group I), 30 without erythrocytosis (group II), and 15 healthy subjects matched with the cases as a control group (group III). Full medical history, clinical examination, hematological parameters, routine biochemical tests, IGF‐1, and IGFBP‐3 were measured in all subjects. Duplex ultrasonography for diagnosis of renal artery stenosis was done. Results Post‐transplant erythrocytosis developed with an incidence rate of 23.3%. The serum of IGF‐1 was significantly higher in the renal transplant recipients with and without erythrocytosis (309.4 ± 72.9, 301.6 ± 67.5 ng/mL, respectively) compared to controls (232.5 ± 95.3 ng/ml, p < 0.01), although there was no statistical difference between the first 2 groups. However, the serum of IGFBP‐3 was significantly higher in the renal transplant recipients with erythrocytosis than those without erythrocytosis and normal individuals (p < 0.001). Graft function and incidence of acute and chronic rejection were similar between the 2 groups. Conclusion Post‐transplant erythrocytosis represents an anomaly of IGF‐1 and its major binding proteins in which they may alter erythropoietin homeostatic mechanisms in the denervated transplant kidney which may be superimposed on a setting of multiple risk factors and leads to a state of erythrocytosis that is seen after kidney transplantation.

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“…In addition, cadaveric renal transplantation, as received by our patient, may cause an additional risk of antigenic challenge (Milner, Jorksky & Perloff, 1987). Post-transplant erythrocytosis (PTE) is reported to develop in between 8% and 17% of cases of renal transplant recipients (Wicke et al, 1983;Sumrani et al, 1993). PTE is normally defined as a haematocrit of 51% or greater, but the pre-transplant haematocrits in these cases averaged 30%.…”

Section: Discussionmentioning

confidence: 89%

A case of sickle-cell erythrocytosis occurring following renal transplantation

Myers

Donohue

2002

Clinical &Amp; Laboratory Haematology

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We present an unusual case of post-renal transplant 'erythrocytosis' in a patient with sickle-cell anaemia, who had developed renal failure following the effects of a phaeochromocytoma. Prior to transplantation, the patient had experienced only occasional crises. However, post-transplant, he experienced multiple and varied crises, associated with a significant increase in haemoglobin concentration. These symptoms were partially alleviated by regular venesection.

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Erythrocytosis After Renal Transplantation

Cited by 15 publications

References 0 publications

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Post‐kidney transplantation erythrocytosis and its relationship to renal artery stenosis, IGF‐1, and its binding protein 3 (IGFBP‐3)

A case of sickle-cell erythrocytosis occurring following renal transplantation

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