Patients admitted to the Intensive Care Unit (ICU) frequently develop acute kidney injury (AKI). Changes in renal function are evaluated by blood levels of creatinine. Creatinine is a breakdown product of muscle cells which is eliminated by the kidneys via the urine. Renal function loss leads to accumulation of waste products and fluids, which may cause critical metabolic derangements. Patients with AKI may need renal replacement therapy (RRT) to correct these critical derangements. The use of RRT is frequently complicated by RRT circuit coagulation. AKI in the ICU mostly occurs due to sepsis, which is a life-threatening condition that arises when the body's response to an infection injures it's own tissues and organs. AKI was also frequently seen in COVID-19. Mechanisms leading to AKI are unclear in both sepsis and COVID-19.
This PhD thesis of Meint Volbeda illustrates that in ICU patients, renal function cannot reliably be assessed by blood creatinine due to muscle mass loss. Technical adjustments in RRT resulted in considerably less rapid RRT circuit coagulation. During the COVID-19 pandemic very rapid circuit coagulation was found, which we could substantially delay by the use of the combination of citrate and heparin for RRT circuit anticoagulation. Renal biopsies obtained after dead from patients with sepsis or COVID-19 indicated that the pathophysiological mechanisms for AKI in both entities might be different. In 93% of patients who died from COVID-19 chronic kidney disease (CKD) was found in biopsies indicating CKD is an important risk factor for a severe course of COVID-19.
