Nermien Yousef Selim1, Hazem Farag Mannaa2, Ola Atef Sharaki3, Tayseer Zaytoun4, Noha Elkholy5, Waleed Arafat6. 1. Medical Research Center, Faculty of Medicine, University of Alexandria, Egypt. 2. Medical Biochemistry Department, Faculty of Medicine, University of Alexandria, Egypt. 3. Clinical Pathology Department, Faculty of Medicine, University of Alexandria, Egypt. 4. Critical Care Medicine center, Faculty of Medicine, University of Alexandria, Egypt. 5. Nephrology Department, Faculty of Medicine, University of Alexandria, Egypt. 6. Clinical Oncology Department, Faculty of Medicine, University of Alexandria, Egypt.
Abstract
BACKGROUND: Many animal studies suggested that the uremic toxin indoxyl sulphate can add to renal damage following induced nephrotoxicity and this effect has not been proved in patients with such complication. METHODS: This is a prospective, case-control, and an observational study conducted on 74 critically ill patients with acute nephrotoxicity. It was designed to measure serum levels of indoxyl sulphate on the day of enrollment and over the course of their illness using high performance liquid chromatography (HPLC-UV) and to test the correlation between these levels and patient's demographics, clinical characteristics, physiological variables, and their outcomes. RESULTS: Critically ill patients with acute nephrotoxicity had significantly higher total (tIS) and free (fIS) indoxyl sulphate than healthy controls and significantly lower than patients with end-stage renal disease (ESRD). Although, no correlation was found between tIS or fIS and mortality, among survivors, tIS, fIS, creatinine and eGFR were independently associated with no renal recovery. CONCLUSION: Serum indoxyl sulphate levels were elevated in critically ill patients with acute nephrotoxicity. There is an association between high levels of indoxyl sulphate and no renal-recovery outcome among survivors of acute nephrotoxicity. Early removal of indoxyl sulphate from patients' blood may improve their outcomes.
BACKGROUND: Many animal studies suggested that the uremic toxin indoxyl sulphate can add to renal damage following induced nephrotoxicity and this effect has not been proved in patients with such complication. METHODS: This is a prospective, case-control, and an observational study conducted on 74 critically ill patients with acute nephrotoxicity. It was designed to measure serum levels of indoxyl sulphate on the day of enrollment and over the course of their illness using high performance liquid chromatography (HPLC-UV) and to test the correlation between these levels and patient's demographics, clinical characteristics, physiological variables, and their outcomes. RESULTS: Critically ill patients with acute nephrotoxicity had significantly higher total (tIS) and free (fIS) indoxyl sulphate than healthy controls and significantly lower than patients with end-stage renal disease (ESRD). Although, no correlation was found between tIS or fIS and mortality, among survivors, tIS, fIS, creatinine and eGFR were independently associated with no renal recovery. CONCLUSION: Serum indoxyl sulphate levels were elevated in critically ill patients with acute nephrotoxicity. There is an association between high levels of indoxyl sulphate and no renal-recovery outcome among survivors of acute nephrotoxicity. Early removal of indoxyl sulphate from patients' blood may improve their outcomes.
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