Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study

Abstract

IntroductionThe role of systemic hemodynamics in the pathogenesis of septic acute kidney injury (AKI) has received little attention. The purpose of this study was to investigate the association between systemic hemodynamics and new or persistent of AKI in severe sepsis.MethodsA retrospective study between 2006 and 2010 was performed in a surgical ICU in a teaching hospital. AKI was defined as development (new AKI) or persistent AKI during the five days following admission based on the Acute Kidney Injury Network (AKIN) criteria. We studied the association between the following hemodynamic targets within 24 hours of admission and AKI: central venous pressure (CVP), cardiac output (CO), mean arterial pressure (MAP), diastolic arterial pressure (DAP), central venous oxygen saturation (ScvO2) or mixed venous oxygen saturation (SvO2).ResultsThis study included 137 ICU septic patients. Of these, 69 had new or persistent AKI. AKI patients had a higher Simplified Acute Physiology Score (SAPS II) (57 (46 to 67) vs. 45 (33 to 52), P < 0.001) and higher mortality (38% vs. 15%, P = 0.003) than those with no AKI or improving AKI. MAP, ScvO2 and CO were not significantly different between groups. Patients with AKI had lower DAP and higher CVP (P = 0.0003). The CVP value was associated with the risk of developing new or persistent AKI even after adjustment for fluid balance and positive end-expiratory pressure (PEEP) level (OR = 1.22 (1.08 to 1.39), P = 0.002). A linear relationship between CVP and the risk of new or persistent AKI was observed.ConclusionsWe observed no association between most systemic hemodynamic parameters and AKI in septic patients. Association between elevated CVP and AKI suggests a role of venous congestion in the development of AKI. The paradigm that targeting high CVP may reduce occurrence of AKI should probably be revised. Furthermore, DAP should be considered as a potential important hemodynamic target for the kidney.

Detrimental Cross-Talk Between Sepsis and Acute Kidney Injury: New Pathogenic Mechanisms, Early Biomarkers and Targeted Therapies

“…This relative venous hypertension may induce microvascular congestion and tissue edema, thus affecting GFR. In support of this hypothesis, a retrospective analysis of 105 ICU patients found a linear correlation between the CVP and AKI incidence or duration [10]. Moreover, it has been shown that fluid overload in septic patients is independently associated with death and worse renal outcomes [11].…”

The Beneficial Effects of Agomelatine in Experimental Model of Sepsis Related Acute Kidney Injury

“…[5,6] Pathophysiology of AKI is not clear, though multifactorial mechanisms containing ischemia-reperfusion injury, direct inflammatory injury, coagulation, endothelial cell dysfunction, and apoptosis are generally considered to be causes. [7] Agomelatine, N-[2-(7-Methoxy-1-naphthyl)ethyl]acetamide, is specified for the treatment of major depression, with dual effects on sleep problems and depressive disorders.…”

Vasopressin versus noradrenaline as initial therapy in septic shock. Is vasopressin-related renal protection doomed to “vanish” in the haze?

“…However, an unrestrained preload increase may adversely affect the kidneys by enhancing venous congestion and blocking venous outflow (14). Such augmentation in kidney "afterload" was found to be associated with an increased incidence and mortality of SAKI (15,16). Being encapsulated, the kidneys are also extremely vulnerable to compression by evolving edema.…”