Defective Platelet Adhesion on Vessel Subendothelium in Uremic Patients

• Published in: Blood 1986-08, Vol.68 (2), p.337-342
• Main Authors: Castillo, Ricardo, Lozano, Teresa, Escolar, Ginés, Revert, Luis, Lépez, José, Ordinas, Antonio
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Bleeding Time; Cell Adhesion; Endothelium - physiopathology; Female; Hematocrit; Humans; Male; Medical sciences; Middle Aged; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Perfusion; Platelet Adhesiveness; Platelet Aggregation - drug effects; Renal Dialysis; Renal failure; Ristocetin - pharmacology; Uremia - blood
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V68.2.337.337

Bleeding time, platelet retention on glass beads, and risto-cetin-induced platelet agglutination (RIPA) in platelet-rich plasma were simultaneously determined for 20 patients with chronic renal failure and previous hemorrhagic history. In seven patients chosen at random out of a group of 16 in whom the three tests were abnormal, RIPA of uremic-isolated platelets in presence of normal platelet-poor plasma (PPP) and of normal platelets in presence of patient PPP were performed. In all cases, the first assay showed diminished agglutination, suggesting a platelet defect; however, uremic PPP did not inhibit the agglutination of normal platelets. In the same patients, the interaction of platelets with subendothelium was evaluated using Baum-gartner's perfusion method. The subendothelial surface covered by platelets was significantly decreased in experiments with uremic whole blood when compared to normal controls. The interaction of platelets with subendothelium was also decreased when perfusions were carried out with platelet-plasma mixtures containing either normal washed platelets and uremic PPP or uremic washed platelets and normal PPP. These results show an impaired platelet adhesion caused both by a platelet and a plasmatic abnormality. Since uremic PPP decreased the adhesion of normal platelets to subendothelium but did not inhibit RIPA, it seems probable that the plasmatic defect could result in a defective binding between vWF and subendothelium. The influence of the red cell count on the platelet adhesion to subendothelium was reconfirmed by comparing perfusions of reconstituted blood with hematocrit values of 20% to 23% and 40% to 45%. In summary, a defective platelet adhesion to subendothelium has been postulated in uremic patients, caused by platelet and plasmatic alterations that are influenced by a low hematocrit.