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Updated: Aug 14, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
[Case of uremic platelet dysfunction]
Mioko Ohzeki1, Tatsuo Fukushima, Sayaka Arakawa
1Kawasaki Medical School, Department of Medicine, Division of Nephrology, Okayama, Japan.
Abstract:
The present case was a 59-year-old woman who underwent a right nephrectomy at 30 years of age, and in whom renal dysfunction occurred at 51 years of age. In November 199X, when her creatinine level reached 7 mg/dl, renal replacement therapy was recommended. She refused this therapy and began her own diet therapy, which consisted of taking only supplement beverage, but no food. Afterwards she became unable to do daily work, and entered our hospital in July of the next year. On admission, her bleeding time was over 10 minutes, but coagulation function tests showed normal values. Platelet function tests showed that coagulation with the addition of ADP was mildly decreased and that coagulation with the addition of aggregation was severely decreased. These data and her bleeding tendency improved with hemodialysis. Therefore, a diagnosis of aggregation non-responsive uremic platelet dysfunction was made. On admission, we were not able to insert a catheter for hemodialysis because of her severe bleeding tendency. A platelet transfusion was made so that we could insert the catheter without severe bleeding. However, this hemostatic effect lapsed after about five to six hours. Six hours after insertion of the catheter, oozing from the orifice of the catheter was seen and a red blood transfusion was necessary. Three days after beginning hemodialysis, the bleeding tendency was no longer seen. Her platelet function and coagulation test results also improved. We can make two conclusions regarding this case. The first is when the physician's medical strategy cannot be carried out due to uremic platelet dysfunction, a platelet transfusion can temporarily eliminate the bleeding tendency. The second is that the pathophysiology of uremic platelet dysfunction involves suppression of the primary step of platelet aggregation with collagen. Experience with the present case revealed the appropriate therapeutic strategy for the pathophysiology of uremic platelet dysfunction.
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