Protein C deficiency in a uremic patient: a rare case of multivessel thromboembolism and type 5 cardiorenal syndrome

Protein C deficiency is a rare inherited disorder characterized by low levels or impaired function of protein C, a natural anticoagulant protein. Deficiency in protein C activity leads to a hypercoagulable state, predominantly resulting in venous thromboembolism. We report a case of a 69-year-old female with uremia who presented with recurrent heart failure, myocardial infarction, and extensive thromboembolism involving both arterial (coronary, abdominal aorta, renal, iliac, splenic, and femoral arteries) and venous systems (femoral, popliteal, and calf muscle veins). Progressive renal dysfunction led to a diagnosis of uremia, and genetic testing confirmed protein C deficiency. The patient ultimately succumbed to multiple organ failure, intractable ascites, and spontaneous bacterial peritonitis. This case underscores the importance of considering protein C deficiency in patients presenting with unexplained multivessel thromboembolism. For patients presenting with unexplained myocardial infarction, renal/hepatic dysfunction, extensive vascular thrombosis or calcification, acral gangrene, or persistently elevated D-dimer levels, we recommend implementing key diagnostic interventions, including protein C activity assay and genetic screening. This case suggests that protein C deficiency may be a rare potential etiology of type 5 cardiorenal syndrome, an association that requires further validation in larger cohort studies.