TY - JOUR
T1 - Deranged platelet calcium homeostasis in diabetic patients with end- stage renal failure
T2 - A possible link to increased cardiovascular mortality?
AU - Vicari, Aurelio M.
AU - Melandri, Marco
AU - Taglietti, Maria V.
AU - Galli, Laura
AU - Pellegatta, Fabio
AU - Ronchi, Paola
AU - Spotti, Donatella
AU - Folli, Franco
PY - 1996/10
Y1 - 1996/10
N2 - OBJECTIVE - Platelet hyperfunction is a typical feature of the prothrombotic state that frequently complicates the natural history, of diabetes. In uremia, a bleeding diathesis is present, which principally involves the primary phase of hemostasis. Thus, in patients with uremia of diabetic origin, the infrequent coexistence of two opposite alterations of hemostasis takes place. In patients with uremia, an increased incidence of cardiovascular events and related mortality is observed. This phenomenon is greatly amplified in uremia of diabetic origin. Calcium homeostasis is a critical aspect of platelet function, which has recently become available in human diseases. The aim of this study was to evaluate calcium homeostasis in platelets from patients with uremia of diabetic and nondiabetic origin. RESEARCH DESIGN AND METHODS - We evaluated, by means of Fura 2, the intracellular concentration of ionized calcium ([Ca2+](i)) in platelets from 18 patients with uremia of diabetic origin, 12 patients with uremia of nondiabetic origin, and 16 healthy control subjects. [Ca2+](i) was evaluated in resting conditions and after stimulation with 0.05, 0.1, 0.5 U/ml thrombin. RESULTS - Platelets from uremic patients with diabetes had higher resting [Ca2+](i) than both control subjects (P = 0.01) and uremic patients without diabetes (P = 0.001). Similarly, after stimulation with thrombin, the absolute increase of [Ca2+](i) was higher (P < 0.05) in platelets from uremic patients with diabetes compared with both control subjects and uremic patients without diabetes. The relative increase of [Ca2+](i) was higher (P < 0.05) than normal in platelets from uremic patients after weak or intermediate strength thrombin. No correlation were present between [Ca2+](i), values and other clinical and laboratory variables potentially associated with platelet hyperfunction. CONCLUSIONS - Diabetes and uremia in combination further deteriorate the abnormal platelet calcium homeostasis observed in uremia.
AB - OBJECTIVE - Platelet hyperfunction is a typical feature of the prothrombotic state that frequently complicates the natural history, of diabetes. In uremia, a bleeding diathesis is present, which principally involves the primary phase of hemostasis. Thus, in patients with uremia of diabetic origin, the infrequent coexistence of two opposite alterations of hemostasis takes place. In patients with uremia, an increased incidence of cardiovascular events and related mortality is observed. This phenomenon is greatly amplified in uremia of diabetic origin. Calcium homeostasis is a critical aspect of platelet function, which has recently become available in human diseases. The aim of this study was to evaluate calcium homeostasis in platelets from patients with uremia of diabetic and nondiabetic origin. RESEARCH DESIGN AND METHODS - We evaluated, by means of Fura 2, the intracellular concentration of ionized calcium ([Ca2+](i)) in platelets from 18 patients with uremia of diabetic origin, 12 patients with uremia of nondiabetic origin, and 16 healthy control subjects. [Ca2+](i) was evaluated in resting conditions and after stimulation with 0.05, 0.1, 0.5 U/ml thrombin. RESULTS - Platelets from uremic patients with diabetes had higher resting [Ca2+](i) than both control subjects (P = 0.01) and uremic patients without diabetes (P = 0.001). Similarly, after stimulation with thrombin, the absolute increase of [Ca2+](i) was higher (P < 0.05) in platelets from uremic patients with diabetes compared with both control subjects and uremic patients without diabetes. The relative increase of [Ca2+](i) was higher (P < 0.05) than normal in platelets from uremic patients after weak or intermediate strength thrombin. No correlation were present between [Ca2+](i), values and other clinical and laboratory variables potentially associated with platelet hyperfunction. CONCLUSIONS - Diabetes and uremia in combination further deteriorate the abnormal platelet calcium homeostasis observed in uremia.
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U2 - 10.2337/diacare.19.10.1062
DO - 10.2337/diacare.19.10.1062
M3 - Article
C2 - 8886550
AN - SCOPUS:10144222647
SN - 1935-5548
VL - 19
SP - 1062
EP - 1066
JO - Diabetes Care
JF - Diabetes Care
IS - 10
ER -