Intensive Care Medicine

, Volume 36, Issue 3, pp 471–478

Histopathology of septic shock induced acute kidney injury: apoptosis and leukocytic infiltration

Authors

    • Département de Réanimation Médicale et de Médecine HyperbareCentre Hospitalo-Universitaire d’Angers
    • Faculté de MédecineUniversité Paris Descartes
    • Service de Réanimation MédicaleHôpital Européen Georges Pompidou
  • Dominique Nochy
    • Faculté de MédecineUniversité Paris Descartes
    • Laboratoire d’Anatomopathologie, Assistance Publique–Hôpitaux de ParisHôpital Européen Georges Pompidou
  • Emmanuel Guérot
    • Faculté de MédecineUniversité Paris Descartes
    • Service de Réanimation MédicaleHôpital Européen Georges Pompidou
  • Patrick Bruneval
    • Faculté de MédecineUniversité Paris Descartes
    • Laboratoire d’Anatomopathologie, Assistance Publique–Hôpitaux de ParisHôpital Européen Georges Pompidou
  • Jean-Yves Fagon
    • Faculté de MédecineUniversité Paris Descartes
    • Service de Réanimation MédicaleHôpital Européen Georges Pompidou
  • Jean-Luc Diehl
    • Faculté de MédecineUniversité Paris Descartes
    • Service de Réanimation MédicaleHôpital Européen Georges Pompidou
  • Gary Hill
    • Laboratoire d’Anatomopathologie, Assistance Publique–Hôpitaux de ParisHôpital Européen Georges Pompidou
Original

DOI: 10.1007/s00134-009-1723-x

Cite this article as:
Lerolle, N., Nochy, D., Guérot, E. et al. Intensive Care Med (2010) 36: 471. doi:10.1007/s00134-009-1723-x

Abstract

Purpose

Septic shock is one of the leading causes of acute kidney injury. The mechanisms of this injury remain mostly unknown notably because of the lack of data on renal histological lesions in humans.

Methods

Kidney biopsy was performed immediately post-mortem in consecutive patients who died of septic shock. Comparisons were made with specimens from eight patients who died of trauma on scene and nine ICU patients that died of non-septic causes.

Results

Nineteen septic patients were included, 11 were male, and age was 72 ± 12 years. Anuria occurred in all patients 2.2 ± 1.4 days before death. Seven patients had disseminated intravascular coagulation. In all patients we observed (1) acute tubular lesions whose intensity correlated with blood lactate concentration; (2) intense infiltration by leukocytes, mainly monocytic, in glomeruli and interstitial capillaries as compared to controls; (3) presence of tubular cell apoptosis proved by the presence of apoptotic bodies (2.9% of tubular cells) significantly more frequently than in controls and confirmed by TUNEL and activated caspase-3 staining. Arteriolar/arterial thromboses were observed in only 4 of 19 patients, without any association with presence of disseminated intravascular coagulation.

Conclusions

Kidney lesions in septic shock go beyond those associated with simple acute tubular injury, notably capillary leukocytic infiltration and apoptosis. Vascular thrombosis, however, did not appear to play a major role in the majority of patients. The extent to which these lesions are specific to sepsis or are common to all multi-organ failure independent of its cause is yet to be elucidated.

Keywords

Kidney pathologySeptic shockCritical care medicineAcute kidney injuryApoptosisAcute tubular necrosis

Supplementary material

134_2009_1723_MOESM1_ESM.doc (96 kb)
Supplementary material 1 (DOC 96 kb)
134_2009_1723_MOESM2_ESM.ppt (1.5 mb)
Supplementary material 1 (PPT 1555 kb)
134_2009_1723_MOESM3_ESM.doc (50 kb)
Supplementary material 1 (DOC 50 kb)

Copyright information

© Copyright jointly hold by Springer and ESICM 2009