Therapeutische Implikationen und pathophysiologische Rolle von Calprotectin beim akuten Nierenversagen

• Antragsteller: Professor Dr. Kai Schmidt-Ott; Professor Dr. Timm H. Westhoff
• Fachliche Zuordnung: Nephrologie
• Förderung: Förderung von 2011 bis 2018
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 152203169

Acute kidney injury (AKI) is classified according to its origin. There are hemodynamic (prerenal) and non-hemodynamic causes (intrarenal, postrenal). The prognosis of AKI crucially depends on an early diagnosis and immediate onset of therapy. The differential diagnosis of hemodynamic and intrarenal AKI, however, may be difficult. Unfortunately, there is no reliable marker for the non-invasive differentiation of these two entities. The present project investigates the use of urinary calprotectin as a new biomarker for the differentiation of hemodynamic and non-hemodynamic AKI. Calprotectin is a calcium-binding protein that is derived predominantly from neutrophils and monocytes. Being part oft the innate immune system, it is released as a ”damage-associated molecular pattern protein (DAMP)“ in a variety of inflammatory processes. In gastroenterology, fecal calprotectin concentration is a well established marker for the differentiation of inflammatory bowel disease and irritable bowel syndrome. Preliminary results of our group indicate that urinary calprotectin concentrations in patients with hemodynamic AKI is almost identical to healthy controls, whereas urinary calprotectin concentrations are approximately 1000 times higher in intrarenal AKI. If the preliminary results of our pilot study are confirmed by the current project, these findings will be of outstanding clinical relevance: A differentiation between hemodynamic and non-hemodynamic AKI would be available within minutes. “Calprotectin-negative” patients with hemodynamic AKI will immediately receive fluid repletion, whereas “calprotectin-positive” patients with intrarenal failure may require renal biopsy and specific treatment.

• DFG-Verfahren: Forschungsgruppen
• Teilprojekt zu: FOR 1368: Hemodynamic Mechanisms of Acute Kidney Injury
• Beteiligte Personen: Professor Dr. Thomas Vogl, Ph.D.; Professor Dr. Walter Zidek