Effect of Peritoneal Dialysis, Haemodialysis and Kidney Transplantation on Blood Platelet Function

Nenci, Giuseppe G.; Berrettini, M; Agnelli, Giancarlo; Parise, P; Buoncristiani, U; Ballatori, Enzo

doi:10.1159/000181652

Cited by 76 publications

(20 citation statements)

References 16 publications

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“…Bemiset al [19] reported findings similar to that of us, but others have described in vitro platelet aggregation as being either normal [14,15] or reduced [16][17][18] in HD patients. This has been explained on the basis that HD plasma contains certain platelet inhibitory substances [14] as well as increased levels of prostacyclin (PG12) [23].…”

Section: Discussionsupporting

confidence: 66%

“…In vivo studies have demonstrated enhanced platelet activity in this population [1][2][3][4][5][11][12][13], Conflicting data, however, have been reported regarding in vitro platelet aggregation which was found to be normal [14,15], re duced [16][17][18], and increased [19] in chronic HD patients in comparison to nonuremic controls. Our study was undertaken to reevaluate in vitro platelet aggregation in CRF subjects treated by HD.…”

Section: Introductionmentioning

confidence: 99%

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Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Viener¹,

Aviram²,

Better

et al. 1986

Nephron

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Hemodialysis patients suffer from premature atherosclerosis and various thrombotic and thromboembolic phenomena. Despite enhanced in vivo platelet activity, it is unclear whether in vitro platelet aggregation is increased or reduced in this population. We studied platelet aggregation in response to adenosine diphosphate and to epinephrine in 20 chronic hemodialysis patients and 21 controls. In the patient group the in vitro platelet aggregation was significantly enhanced in response to both aggregating agents. Our study demonstrated that in vitro platelet aggregation is enhanced in patients with chronic renal failure undergoing hemodialysis.

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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Viener¹,

Aviram²,

Better

et al. 1986

Nephron

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“…The persistence of this abnormality in the chronically dia- lyzed patients may be a reflection on the intermittency of the uremic environment, between dialyses. Alternatively, the hemodialysis procedure itself has been implicated to impair platelet function [7] and may have been responsi ble for the persistent abnormality. The lower values for membrane ATPase in the transplant recipients are more difficult to attribute to uremia.…”

Section: Discussionmentioning

confidence: 99%

“…defective platelet reten tion on glass beads [1,5], abnormal platelet aggregation [2] and poor clot retraction [2,6]. That this is a reversible phe nomenon and a consequence of the abnormal biochemical uremic environment has been documented by the observa tion that platelet function returns to normal following dial ysis or renal transplantation [6,7], Other than a brief com munication of a defect in platelet serotonin uptake and storage in uremia [8], the biochemistry of platelets in renal failure has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Biochemical Abnormalities of Platelets in Renal Failure

Eknoyan

Brown²

1981

Am J Nephrol

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The platelet content of adenosine triphosphate (ATP), adenosine diphosphate (ADP), serotonin and ouabain-insensitive, magnesium-dependent adenosine triphosphatase (ATPase) was determined in patients with chronic renal failure, patients on chronic hemodialysis, and kidney transplant recipients. Platelet ATP content was normal in all. By contrast, ADP content, expressed in μmol/l0¹¹ platelets, was significantly lower in renal failure: 1.82 ± 0.96 compared to 2.51 ± 0.97 in normals (p < 0.05), but not in dialyzed or transplanted patients: 2.27 ± 0.96 and 1.87 ± 0.87, respectively. The mean content of serotonin was also significantly lower in renal failure patients: 0.52 μg/l0⁹ platelets as compared to 0.90 μg/l0⁹ platelets in normals (p < 0.05) but was not significantly different in dialyzed and transplanted patients. ATPase was significantly lower in renal failure: 3.13 ± 1.2 μmol Pi/10⁹ platelets in whole suspension and 0.71 ± 0.22 Pi/mg protein/h in membrane preparation compared to 4.74 ± 1.1 and 1.18 ± 0.19, respectively, in normals, and was significantly lower in dialyzed and transplanted patients. Experimental azotemia (BUN 65–86 mg/l00 ml), induced by the oral ingestion of urea 2–3 g/kg body weight over 24 h, failed to induce any of these abnormalities. The abnormality in platelet ADP and serotonin content in renal failure paralleled the functional platelet defects which characterize these patients and were reversible following dialysis and transplantation.

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“…• Correct the hematocrit to >0AE30 [60,61] • Consider the use of desmopressin [34,62,63] • Consider the use of dialysis, which also have haemostatic benefits in this situation [64,65] • Only use platelet transfusions where the above methods are inappropriate or ineffective [34]. In drug-induced platelet dysfunction such as use of aspirin, NSAIDs or anti-platelet drugs, the following recommendations should be followed.…”

Section: Platelet Transfusionsmentioning

confidence: 99%

Appropriate blood component usage

Koh

Lee

Chay

2011

ISBT Science Series

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Blood transfusion (which includes FFP, platelets, cryoprecipitate and any other blood-derived product) remains an important modality of treatment across all clinical disciplines. A blood transfusion is deemed appropriate when used in an evidence-based fashion and where the effects of the transfusion are felt to outweigh any potential risks and complications that may arise from the transfusion. In certain cases, it may be the best treatment option available, for example plasma exchange in thrombotic thrombocytopenic purpura. However, blood transfusion can result in acute or delayed complications, as well as the risk of transmission of infectious agents. The inappropriate use of blood and blood products increases the risk of transfusion-related complications and adverse events to recipients. It also contributes to shortages of blood products and the possibility of it not being available when required for other patients in an appropriate setting. It is therefore necessary to reduce the unnecessary transfusions through the appropriate clinical use of blood, avoiding unnecessary transfusions, and use of alternatives to transfusion.Key words: clinical transfusion, fresh frozen plasma, guidelines, platelets, red cell, transfusion trigger. MethodsWe conducted a literature review via Pubmed and selected the articles relevant to our review and published in English or with translations provided in English. RecommendationsThese are based on the current available data; in situations where there is lack of randomized data, published reports or recommendations from previous experiences are used. Red cells transfusionThe aim of red cell transfusion is to increase oxygen carrying capacity of blood by increasing haemoglobin concentration in patients with acute or chronic anaemia.The decision to transfuse red cells should be carefully weighed on an individual basis, taking into consideration clinical evaluation of symptoms and haemodynamic status as well as laboratory parameters such as haemoglobin level. It is more relevant to consider the goal of red cell transfusion as the avoidance of tissue hypoxia rather than the correction of a laboratory parameter. In general, patients should not be transfused so as to achieve 'normal' haemoglobin (Hb) concentration [1,2]. Packed red cells should generally be provided for allogeneic transfusion where possible [3,4]. Packed red cells are preferred over whole blood to reduce the volume of transfusion and avoid the white cells ⁄ plasma that can potentially cause more febrile reaction and HLA sensitization, etc. Transfusion trigger?There is no standard fixed trigger for red cell transfusion. The trigger for transfusion should always be evaluated in the context of a multiplicity of factors including rate and amount of blood loss, cardiopulmonary reserve. The rate of development of anaemia is also an important factor.

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Effect of Peritoneal Dialysis, Haemodialysis and Kidney Transplantation on Blood Platelet Function

Cited by 76 publications

References 16 publications

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Biochemical Abnormalities of Platelets in Renal Failure

Appropriate blood component usage

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