Plasma thrombopoietin levels in patients with chronic renal failure

Linthorst, Gabor E.; Folman, Claudia C.; Olden, R. W. van; Borne, A. E. G. K. Von Dem

doi:10.1038/sj.thj.6200153

Cited by 25 publications

(24 citation statements)

References 18 publications

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“…The authors of the previous study speculate that the lower serum levels of TPO observed in the transplant group may be partially caused by decreased production (since TPO is produced partially by the kidney), yet no significant correlation was revealed between TPO levels and serum creatinine levels [22]. This notion also seems inconsistent with other studies that have noted that TPO production remained normal in patients with severe kidney function (without a transplant) [23] and were elevated in hemodialysis patients [24,25]. While the literature is seemly scant with respect to studies on TPO in renal transplants, a number of studies have involved liver transplant recipients.…”

Section: Discussioncontrasting

confidence: 55%

Association between Circulating Thrombopoietin Levels and Cardiovascular Risk Prediction Scores in Renal Transplant Recipients

Mansell

Elmoselhi²,

Shoker³

2015

Am J Nephrol

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Background/Aims: The 7-year Major Adverse Cardiovascular Events Calculator (CRCRTR-MACE) predicts cardiovascular events (CVE) in renal transplant recipients (RTR), and thrombopoietin (TPO) is a humoral inflammatory factor implicated in cardiovascular disease (CVD). The aim of the study was to determine if circulating TPO levels in stable RTR are positively associated with variable(s) in the CRCRTR-MACE score. Methods: CRCRTR-MACE scores were calculated in 95 stable RTR. TPO levels were measured by multiplexed fluorescent bead-based immunoassay in all patients and 48 controls. Multivariate analysis (MVA) was performed between TPO and CV risk variables and patient demographics. Stepwise regression with backward elimination of insignificant variables estimated the impact of risk variables on TPO levels. Significance was defined at p < 0.05. Normalized data were presented as mean ± SD and non-normalized data as median (maximum to minimum). Results: The risk of a CVE within 7 years as predicted by the median was 9.97% (range 1.93-84.2). The percentage of patients who were above 20% risk for a CVE was 28.4%. Control TPO level of 170.41 (4.4-995.9) pg/ml was significantly lower than that of 237.90 (32.77-1,386.79) pg/ml in RTR (p = 0.010). TPO level correlated significantly with the total CRCRTR-MACE score (R = 0.310, p = 0.004), smoking (p = 0.009) and eGFR (R = -0.275, p = 0.012) but not with age, diabetes, LDL level or history of CVE. Only the total CRCRTR-MACE score (p = 0.013) and smoking (p = 0.009) remained significant in the MVA. Stepwise regression estimated that smoking increased TPO levels by 206.28 pg/ml and each 10% increase in CRCRTR-MACE score increased TPO levels by an additional 44.4 pg/ml. Conclusion: TPO levels are increased in RTR with high CRCRTR-MACE, particularly in smokers with diminished eGFR. Circulating TPO may serve as a biomarker and treatment target for CVD in RTR.

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Section: Discussioncontrasting

confidence: 55%

Association between Circulating Thrombopoietin Levels and Cardiovascular Risk Prediction Scores in Renal Transplant Recipients

Mansell

Elmoselhi²,

Shoker³

2015

Am J Nephrol

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“…In continuous ambulatory peritoneal dialysis patients, platelet counts have been reported to be closer to the normal range. 2 Platelet survival in hemodialysis patients is thought to be of normal duration, although the only paper examining this was published in 1967. 3 The megakaryocyte number in bone marrow is normal, 1 but the reticulated platelet count, a measure of thrombopoiesis, is reduced, despite elevated thrombopoietin levels.…”

Section: Platelet Number Survival and Function In Chronic Kidney DImentioning

confidence: 97%

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Daugirdas

Bernardo

2012

Kidney International

162

149

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Substantial activation of platelets can occur in the course of hemodialysis. Platelet surface markers show evidence of platelet degranulation. Some activation occurs due to exposure of blood to the roller pump segment and microbubbles may play a role. Platelet activation seems to be reduced with reused dialyzers or with those containing synthetic versus cellulosic membranes. Nevertheless, a substantial degree of platelet activation can be demonstrated with polysulfone and other synthetic membranes; the amount of activation may differ substantially among polysulfone membranes, depending on the manufacturer and the polyvinylpyrrolidone content. Platelet-platelet and platelet-leukocyte aggregates have been detected in the dialyzer blood outflow line and the consequences of these to the microcirculation are unknown. Typically, the platelet count decreases slightly during the first hour of dialysis, but mostly returns to initial values by the end of dialysis. A number of chronic hemodialysis patient cases have been reported in which a marked decrease in platelet count (50% or more) during dialysis was observed, resulting in mild degrees of predialysis thrombocytopenia. In only one case was the decrease in platelet count associated with bleeding. Dialyzer hypersensitivity symptoms are infrequently associated with a fall in platelet count. Most recent cases of dialysis-associated thrombocytopenia have been with polysulfone membranes, especially polysulfone membranes sterilized by electron beam. The exact cause of these reactions remains unknown.

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“…1 The mechanisms for decreased antiplatelet drug effects in patients with chronic kidney disease are poorly understood and could be explained by a number of disturbances found in chronic kidney disease and possibly leading to altered platelet function and reduced sensitivity to antiplatelet drugs. This includes an increase in the platelet turnover rate 18 by means of increased levels of thrombospondin 19,20 ; poor bioavailability of the active clopidogrel metabolite caused by impaired absorption or drug metabolization 21,22 ; procoagulant factors, such as thrombin-antithrombin III complex, D-dimer, fibrinogen, fibrinopeptide A, and von Willebrand factor 23,24 ; altered metabolism of prostaglandin 25 ; changes in thromboxane A2-dependent platelet activation and altered expression of platelet surface receptors 26,27 ; and extrinsic factors such as uremic toxin, anemia, and abnormality of nitric oxide synthesis. 28,29 We are aware of several limitations associated with this study.…”

Section: Discussionmentioning

confidence: 99%

Low Responsiveness to Clopidogrel Increases Risk among CKD Patients Undergoing Coronary Intervention

Htun

Fateh-Moghadam

Bischofs

et al. 2011

Journal of the American Society of Nephrology

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Plasma thrombopoietin levels in patients with chronic renal failure

Abstract: These results confirm the increased platelet turnover in patients with chronic renal failure. Moreover this study shows that the kidney does not seem to play a major role in the overall Tpo production in the body.

Cited by 25 publications

References 18 publications

Association between Circulating Thrombopoietin Levels and Cardiovascular Risk Prediction Scores in Renal Transplant Recipients

Association between Circulating Thrombopoietin Levels and Cardiovascular Risk Prediction Scores in Renal Transplant Recipients

Hemodialysis effect on platelet count and function and hemodialysis-associated thrombocytopenia

Low Responsiveness to Clopidogrel Increases Risk among CKD Patients Undergoing Coronary Intervention

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