Patients with chronic kidney disease (CKD) develop hemostatic disorders mainly in the form of bleeding diatheses. Platelet dysfunction is the main factor responsible for hemorrhagic tendencies in advanced kidney disease. Anemia, dialysis, the accumulation of medications due to poor clearance, and anticoagulation used during dialysis have some role in causing impaired hemostasis in CKD patients. Platelet dysfunction occurs both as a result of intrinsic platelet abnormalities and impaired platelet-vessel wall interaction. The normal platelet response to vessel wall injury with platelet activation, recruitment, adhesion, and aggregation is defective in advanced renal failure. Dialysis may partially correct these defects, but cannot totally eliminate them. The hemodialysis process itself may in fact contribute to bleeding. Hemodialysis is also associated with thrombosis as a result of chronic platelet activation due to contact with artificial surfaces during dialysis.

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We reported a 64-year-old woman was admitted to Emergency Department of dr.Soetomo hospital with fainting and previous chest discomfort, then we diagnosed this patient with Non ST Elevation Myocard Infarct, diabetes mellitus, hypertension stage II, and long QT syndrome (LQTS) with torsades de pointes episodes.  There are two important tests to determine LQTS, electrocardiogram (ECG) and a genetic test. Two kinds of LQTS, congenital LQTS is caused by mutations in genes coding, and acquired LQTS often is associated with drugs or metabolit abnormalities.  Myocardial ischemia could change QT interval regionally in the area of ischemia, and these changes are related to extent and severity of coronary atherosclerosis. There are two major treatment options for patients with LQTS, medications and ICD/pacemaker implantation. Beta-blockers are the drugs of choice.