Post Transplant Erythrocytosis in Hypercalcemic Renal Transplant Recipients

Kurella, Manjula; Butterly, David W.; Smith, Stephen R.

doi:10.1034/j.1600-6143.2003.00131.x

Cited by 13 publications

(9 citation statements)

References 24 publications

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“…The incidence of erythrocytosis varies from 8% to 22% among reports identified from earlier clinical practice guideline publications (627,708–710). More recent studies document that erythrocytosis still occurs in KTRs (761–765). Many studies do not differentiate between increased red cell mass or reduced plasma volume.…”

Section: Rationalementioning

confidence: 99%

“…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%

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

1,130

257

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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

1,130

257

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“…Furthermore, recently some AA reported that posttransplant erythrocytosis is 2-3 times more frequent in KTx patients who have higher serum calcium levels as compared with normocalcemic patients [47, 48]. However, there are as yet no data demonstrating that the correction of HC might translate into a correction of posttransplant erythrocytosis.…”

Section: Clinical Consequences Of Hc In Ktxmentioning

confidence: 99%

Clinical Impact of Hypercalcemia in Kidney Transplant

Cafforio

Alfieri

2011

International Journal of Nephrology

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Hypercalcemia (HC) has been variably reported in kidney transplanted (KTx) recipients (5–15%). Calcium levels peak around the 3rd month after KTx and thereafter slightly reduce and stabilize. Though many factors have been claimed to induce HC after KTx, the persistence of posttransplant hyperparathyroidism (PT-HPT) of moderate-severe degree is universally considered the first causal factor. Though not proven, there are experimental and clinical suggestions that HC can adversely affect either the graft (nephrocalcinosis) and other organs or systems (vascular calcifications, erythrocytosis, pancreatitis, etc.). However, there is no conclusive evidence that correction of serum calcium levels might avoid the occurrence of these claimed clinical effects of HC. The best way to reduce the occurrence of HC after KTx is to treat as best we can the secondary hyperparathyroidism (SHP) during the uraemic stages. The indication to Parathyroidectomy (PTX), either before or after KTx, in order to prevent or to treat, respectively, HC after KTx, is still a matter of debate which has been revived by the availability of the calcimimetic cinacalcet for the treatment of PT-HPT. However, we still need to better clarify many points as regards the potential adverse effects related to either PTX or cinacalcet use in this clinical set, and we are waiting for the results of future randomized controlled trials to achieve some more definite conclusions on this topic.

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“…Future will show to what extent calcimimetics will displace calcitriol in the management of hyperparathyroidism and how this will affect requirements of erythropoietic agents. A recent retrospective analysis found erythrocytosis following renal transplantation to be more common in hypercalcaemic patients, and serum calcium was a strong independent predictor of maximum haematocrit after transplantation [35]. Further studies should dwell on the interplay of calcium, calcitriol, parathyroid hormone and erythropoietin at the haematon level.…”

Section: Calcitriolmentioning

confidence: 99%

Hormonal adjuvants for the treatment of renal anaemia

Deicher

Hörl

2005

Eur J Clin Investigation

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Hormonal adjuvants, besides being erythropoietic agents, broaden the spectrum of therapeutic options for the treatment of the anaemia of chronic kidney disease (CKD). Lowering elevated parathyroid hormone levels by oral calcium supplementation and phosphate restriction, by varying dialysate calcium concentrations, by administration of vitamin D3 derivatives and, in the near future, by treatment with calcimimetics may prove efficient in some patients to fight extensive requirements of erythropoietic agents. Clinical evidence for a principal role of secondary hyperparathyroidism in resistance to erythropoietin, however, is lacking. Active vitamin D3 derivatives, in addition to their beneficial effects on secondary hyperparathyroidism, appear to exert a direct, stimulatory action on erythroid precursor cells and possibly also an inhibitory action on collagen synthesis by bone marrow stromal cells. Growth hormone (GH) induces insulin-like growth factor (IGF)-1, which in turn counteracts apoptosis similarly to erythropoietin, and fosters proliferation of burst- and colony-forming units-erythroid (BFU-E, CFU-E). If erythropoietic agents improve survival of CKD patients, a similar benefit should apply for strategies that increase synthesis and bioavailabilty of IGF-1. The latter appears to be reduced in CKD patients, and zinc supplementation potentially enhances it via an increase in free IGF-1. Finally, androgens also exert anti-anaemic effects. Nandrolone decanoate constitutes the only androgen currently applicable for selected male dialysis patients over the age of 50 years. It should not be given to women, however, because of serious side effects. Collectively, hormonal interventions offer the potential to reduce requirements of erythropoietic agents, and some may also improve physical performance.

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Post Transplant Erythrocytosis in Hypercalcemic Renal Transplant Recipients

Cited by 13 publications

References 24 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

Clinical Impact of Hypercalcemia in Kidney Transplant

Hormonal adjuvants for the treatment of renal anaemia

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