sepsis and the kidney.pdf - SASSiT

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klenzak & himmelfarb
renal tubule-assist device, and then infused with endotoxin. Again, IL-10 levels
were higher in the renal tubule-assist device–treated group, as was mean arterial
pressure. Survival data were not published [39]. To assess whether the renal
tubule-assist device ameliorates the course of sepsis before renal failure, the
investigators assessed it in pigs administered E. coli intraperitoneally, which were
immediately started on CVVHF with or without renal tubule-assist device. All of
the animals developed ARF within hours. This study demonstrated a significant
increase in survival time, associated with better systemic hemodynamic
measurements and renal artery blood flow. IL-6 and interferon-g levels were
lower in renal tubule-assist device–treated animals, but most cytokines measured
did not demonstrate significant differences between renal tubule-assist device and
sham-treated animals [40].
Summary
When renal failure occurs, the systemic and local dysregulation of sepsis is
compounded by loss of metabolic, fluid, and electrolyte homeostasis. The loss of
renal function increases mortality, and those who do survive likely do so with the
return of renal function. The interplay between systemic host responses and local
injury and activity in the kidney affects the vascular bed, the immune system, and
plays a role in the development of MOSF. Patients with end-stage renal disease
and sepsis have a lower mortality rate than those who develop ARF in the setting
of sepsis. Despite advances in RRT and critical care, mortality rates have
remained fairly stable over the last two decades for sepsis-associated ARF. There
is little conclusive evidence from human trials of great benefit from the myriad of
original therapies tested to date.
For these reasons, it is important to learn more about the human response to
sepsis and ARF, and to clarify the differences between patients who develop renal
failure and those who do not; and to clarify the differences between those who
survive, and those who do not. It is these variables, in the ICU, which may serve
to aid in designing rational therapies for the restoration of metabolic balance and
the return of renal function.
References
[1] Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory
response syndrome (SIRS): a prospective study. JAMA 1995;273:117–23.
[2] Clermont G, Acker CG, Angus DC, et al. Renal failure in the ICU: comparison of the impact
of acute renal failure and end-stage renal disease on ICU outcomes. Kidney Int 2002;62:986–96.
[3] Lugon JR, Boim MA, Ramos OL, et al. Renal function and glomerular hemodynamics in
male endotoxemic rats. Kidney Int 1989;36:570–5.
[4] Kashgarian M, Siegel NJ, Ries AL, et al. Hemodynamic aspects in development and recovery
phases of experimental postischemic acute renal failure. Kidney Int Suppl 1976;6:S160–8.