Work

Urinary hepcidin is potentially a marker of systemic infection rather than inflammation, in the setting of preserved renal function

Year: 2011

Type: article

Abstract: Urinary proteomics have recently identified hepcidin, a key regulator of iron homeostasis, as a potential marker of tubular stress [ 1 ]. It appears to be released in response to situations that predispose to acute kidney injury (AKI), and greater concentrations of hepcidin in the blood and in the urine have been associated with reduced risk of AKI [ 2 ]. Catalytic iron is a biologically plausible mechanism for the development of AKI as a consequence of tubular oxidative stress [ 3 ]. The relationship between serum creatinine, urinary hepcidin and CRP may help define whether urinary hepcidin is more likely to reflect systemic inflammation or renal events. The relationship in septic patients has not yet been described. Patients with SIRS, oliguria and a 25 μmol/l increase from baseline creatinine are known to be at an increased risk of AKI [ 4 ]. We sought to determine if hepcidin correlated more strongly with CRP or creatinine in these patients with a diagnosis of sepsis and those without.

Source: Critical Care

DOI: 10.1186/cc10377