Haemorrhage, Platelet Dysfunction and other Coagulation Defects in Uraemia

Cheney, Kelly M.; Bonnin, J. A.

doi:10.1111/j.1365-2141.1962.tb06514.x

Cited by 81 publications

(33 citation statements)

References 12 publications

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“…The first report which described such an abnormality was by Lewis, Zucker, and Ferguson in 1956 (27). Although there were later reports of similar abnormalities in patients with renal insufficiency (28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39), some investigators did not find any qualitative disturbance of platelet phospholipids in uremics (40)(41). Even with the newer, more specific techniques, there has been difficulty in definitely establishing the incidence of PF3 deficiency in these patients (3).…”

Section: Discussionmentioning

confidence: 99%

Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's plateletrich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1: 8). The second test was similar but used "frozen and thawed" platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the nonbleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material.Dr. Hrodek's present address is 2nd Pediatric

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Section: Discussionmentioning

confidence: 99%

Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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“…Decreased factor III activity, abnormal platelet aggregation and adhesiveness and impaired prothrombin consumption contribute to the clotting defect in uremia. 22 Although hemostatic defects in uremia are often complex, it is probable that platelet dysfunction is the most consistent and clinically the most important feature. 23 Macrocytosis in chronic hemodialysis patients may be associated with increased mortality.…”

Section: Discussionmentioning

confidence: 99%

Hematological changes in patients of chronic renal failure and the effect of hemodialysis on these parameters

2017

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Background: Chronic kidney disease (CRD) is a global public health problem, where slowly progressive deterioration in kidney function lead to numerous hematological and biochemical dysfunction which further make the patients vulnerable to cardiovascular morbidity and mortality if appropriate measures is not taken for their control. The aim of present study was to find out the common hematological dysfunction that may occur in the patients of chronic renal failure (CRF) and in the process of dialysis and suggest appropriate measures for their management.Methods: Forty-two patient with CRF and on regular maintenance dialysis and 40 healthy adults were recruited into the study. Hemoglobin concentration, total red cell count, total white blood cell count and platelet count and ESR were assessed for the subjects and controls. Results were analyzed using SPSS 21.0 version.Results: showed that the RBC count, hemoglobin levels and platelets counts are significantly reduced in the patients of chronic renal failure and the process of hemodialysis further decreases the level of all the above mentioned hematological parameters whereas there is slight increase in total leucocyte count but significant increase in ESR was detected.Conclusions: Chronic renal failure is associated with different degrees of abnormality in hematological parameters that needs careful evaluation and management.

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“…These new insights stimulated the research on the pathogenesis of bleeding tendency in renal failure. This complication frequently observed in uremia could not be fully explained by the well-known defective platelet function [4,6,18]. In 1977 Remuzzi et al [27] studied the PGP synthesis of venous specimens from 2 patients with acute renal failure and of 1 patient with chronic renal insufficiency.…”

Section: Increased Vascular Pgp Releasementioning

confidence: 99%

“…It is a well-known fact that platelet function is fre quently disturbed in patients suffering from terminal renal failure [4,6,18,36]. This alteration is rather com plex and includes a decreased platelet factor 3 availabil ity [18], depressed retention by glass beads [36], and decreased platelet aggregation to various exogenous stimuli in vitro [4,6,36], In 1975 Lindsay et al [20] studied the platelet function in dialyzed and nondialyzed patients with chronic renal failure.…”

Section: Defective Platelet Functionmentioning

confidence: 99%

“…This alteration is rather com plex and includes a decreased platelet factor 3 availabil ity [18], depressed retention by glass beads [36], and decreased platelet aggregation to various exogenous stimuli in vitro [4,6,36], In 1975 Lindsay et al [20] studied the platelet function in dialyzed and nondialyzed patients with chronic renal failure. They examined plate let aggregation by ADP as well as platelet adhesiveness using dialysis membranes in a test cell system.…”

Section: Defective Platelet Functionmentioning

confidence: 99%

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Eicosanoids of Platelets and Vascular Wall in Chronic Renal Insufficiency

Sinzinger

Leithner²

1987

Am J Nephrol

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There is good evidence that retention products accumulating in chronic renal insufficiency influence prostaglandin (PG) synthesis, thus affecting platelet-vascular wall interaction. The vascular PGI2 synthesis is increased and prolonged in vitro, the plasma factor activity enhanced. A defective platelet function is frequently observed; it is completely restored by peritoneal dialysis, but only partially by hemodialysis. The sensitivity of platelets to PGI2 and its plasmatic degradation are unchanged. There is evidence of a shift of arachidonic acid metabolism from cyclooxygenase to lipoxygenase. These changes may be attributed to undialyzable plasma constituents, the ‘middle molecules’.

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Haemorrhage, Platelet Dysfunction and other Coagulation Defects in Uraemia

Cited by 81 publications

References 12 publications

Platelet factor 3 in normal subjects and patients with renal failure

Platelet factor 3 in normal subjects and patients with renal failure

Hematological changes in patients of chronic renal failure and the effect of hemodialysis on these parameters

Eicosanoids of Platelets and Vascular Wall in Chronic Renal Insufficiency

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