Lungen- und Nierenversagen

Pathogenese, Wechselwirkungen und Therapie
Übersichten

Zusammenfassung

Hintergrund

Lunge und Niere stellen im Rahmen eines Multiorganversagens (MOV) bei Schock, Trauma oder Sepsis die beiden am häufigsten betroffenen Organe („acute respiratory distress syndrome“, ARDS bzw. Nierenversagen, ANV) dar mit einer für beide Organversagen nach wie vor inakzeptabel hohen Mortalität.

Pathogenese und Wechselwirkung

Auch wenn die pathophysiologischen Mechanismen des MOV noch nicht vollständig verstanden sind, scheinen Niere und Lunge ähnlichen Schädigungsmechanismen zu unterliegen sowie jeweils das Potenzial zu haben, sich gegenseitig weiter Schaden zufügen zu können („kidney-lung crosstalk“). Hierbei spielen inflammatorische Signale in beide Richtungen und eine Volumenüberladung mit konsekutiver Ödembildung in beiden Organen die vielleicht wichtigsten Rollen.

Therapieansatz

Die bei beiden Organversagen eingesetzten Organersatzverfahren können selbst wieder das jeweilig andere Organ negativ beeinflussen (Beatmungs-/Dialyttrauma). Gerade für Nierenersatzverfahren sind aber auch positive Effekte auf ein Lungenversagen durch Beeinflussung des Volumen- oder Säure-Basen-Haushalts bekannt. Neue Möglichkeiten zur sog. Low-flow-CO2-Elimination direkt am Nierenersatz könnten in Zukunft weiter helfen, ein Beatmungstrauma zu minimieren.

Schlüsselwörter

ARDS Akutes Nierenversagen Nierenersatztherapie Mechanische Beatmung Extrakorporale CO2-Elimination 

Lung and kidney failure

Pathogenesis, interactions, and therapy

Abstract

Background

The lungs and kidneys represent the most often affected organs (acute respiratory distress syndrome, ARDS or kidney failure) in multiple organ failure (MOF) due to shock, trauma, or sepsis with a still unacceptable high mortality for both organ failures.

Pathogenesis and interactions

Although the exact pathophysiological mechanisms of MOF are not completely elucidated, it appears that the lungs and kidneys share several pathophysiologic pathways and have the potential to further harm each other (kidney–lung crosstalk). Inflammatory signals in both directions and volume overload with consecutive edema formation in both organs may play a key role in this crosstalk.

Treatment

The organ replacement therapies used in both organ failures have the potential to further injure the other organ (ventilator trauma, dialyte trauma). On the other hand, renal replacement therapy can have positive effects on lung injury by restoring volume and acid–base homeostasis. The new development of “low-flow” extracorporeal CO2 removal on renal replacement therapy platforms may further help to decrease ventilator trauma in the future.

Keywords

ARDS, human Acute kidney injury Renal replacement therapy Mechanical ventilation  Extracorporeal CO2-elimination 

Notes

Einhaltung ethischer Richtlinien

Interessenkonflikt. S. John ist Mitglied eines Medical Advisory Boards zum Thema „extrakorporale CO2-Elimination“ der Fa. Baxter Gambro Renal. Er versichert, dass die Präsentation des Themas davon unabhängig und die Darstellung der Inhalte produktneutral ist. C. Willam gibt an, dass kein Interessenkonflikt besteht.

Dieser Beitrag beinhaltet keine Studien an Menschen oder Tieren.

Literatur

  1. 1.
    Uchino S, Kellum JA, Bellomo R et al (2005) Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA 294:813–818CrossRefPubMedGoogle Scholar
  2. 2.
    Oppert M, Engel C, Brunkhorst FM et al (2008) Acute renal failure in patients with severe sepsis and septic shock – a significant independent risk factor for mortality: results from the German Prevalence Study. Nephrol Dial Transplant 23:904–909CrossRefPubMedGoogle Scholar
  3. 3.
    Cooke CR, Kahn JM, Caldwell E et al (2008) Predictors of hospital mortality in a population-based cohort of patients with acute lung injury. Crit Care Med 36:1412–1420CrossRefPubMedGoogle Scholar
  4. 4.
    Liu KD, Glidden DV, Eisner MD et al (2007) Predictive and pathogenetic value of of plasma biomarkers for acute kidney injury in patients with acute lung injury. Crit Care Med 35:2755–2761PubMedCentralCrossRefPubMedGoogle Scholar
  5. 5.
    Yap SC, Lee HT (2012) Acute kidney injury and extrarenal organ dysfunction: new concepts and experimental evidence. Anesthesiology 116:1139–1148CrossRefPubMedGoogle Scholar
  6. 6.
    Doi K, Ishizu T, Fujita T et al (2011) Lung injury following acute kidney injury: kidney-lung crosstalk. Clin Exp Nephrol 15:464–470CrossRefPubMedGoogle Scholar
  7. 7.
    Texeira C, Garzotto F, Piccinni P et al (2013) Fluid balance and urine volume are independent predictors of mortality in acute kidney injury. Crit Care 17:R14CrossRefGoogle Scholar
  8. 8.
    Murugan R, Kellum JA (2011) Acute kidney injury: what’s the prognosis? Nat Rev Nephrol 7:209–217PubMedCentralCrossRefPubMedGoogle Scholar
  9. 9.
    Murugan R, Karajala-Subamanyam V, Lee M et al (2010) Acute kidney injury in non-severe pneumonia is associated with an increased immune response and lower survival. Kidney Int 77:527–535PubMedCentralCrossRefPubMedGoogle Scholar
  10. 10.
    Peng ZY, Wang HZ, Srisawat N et al (2012) Bectericidal antibiotics temporarily increase inflammation and worsen acute kidney injury in experimental sepsis. Crit Care Med 40:538–543PubMedCentralCrossRefPubMedGoogle Scholar
  11. 11.
    KDIGO (2012) Clinical practice guidelines for acute kidney injury. Kidney Int Suppl 2Google Scholar
  12. 12.
    Payen D, Pont A de, Sakr Y et al (2008) A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care 12:R74PubMedCentralCrossRefPubMedGoogle Scholar
  13. 13.
    Boyd JH, Forbes J, Nakada T et al (2011) Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med 39:259–265CrossRefPubMedGoogle Scholar
  14. 14.
    The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS), Clinical Trials Network (2006) Comparison of two fluid management strategies in acute lung injury. N Engl J Med 354:2564–2575CrossRefGoogle Scholar
  15. 15.
    Grams ME, Estrella MM, Coresh J et al (2011) Fluid balance, diuretic use, and mortality in acute kidney injury. Clin J Am Soc Nephrol 6:966–973PubMedCentralCrossRefPubMedGoogle Scholar
  16. 16.
    Druml W (2014) Nierenversagen bei Herzinsuffizienz und Hypervolämie – Bedeutung von Stauung und Rückwärtsversagen. Med Klin Intensivmed Notfmed 109:252–256CrossRefPubMedGoogle Scholar
  17. 17.
    Gritters M, Borgdorff P, Grooteman MP et al (2008) Platelet activation in clinical hemodialysis: LMWH as a major contributor to bio-incompatibility? Nephrol Dial Transplant 23:2911–2917CrossRefPubMedGoogle Scholar
  18. 18.
    Elseviers MM, Lins RL, Van der Niepen P et al (2010) Renal replacement therapy is an independent risk factor for mortality in critically ill patients with acute kidney injury. Crit Care 14:R221PubMedCentralCrossRefPubMedGoogle Scholar
  19. 19.
    John S (2014) Nierenersatztherapie als mögliches Trauma im akuten Nierenversagen. Med Klin Intensivmed Notfmed. doi:10.1007/s00063-013-0338-8Google Scholar
  20. 20.
    McIntyre CW (2010) Recurrent circulatory stress: the dark side of dialysis. Semin Dial 23:449–451CrossRefPubMedGoogle Scholar
  21. 21.
    Ferguson ND et al (2012) The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med 38:1573–1582CrossRefPubMedGoogle Scholar
  22. 22.
    Van den Akker JPC, Egal M, Groeneveld ABJ (2013) Invasive mechanical ventilation as a risk factor for acute kidney injury in the critically ill: a systematic review and meta-analysis. Crit Care 17:R98CrossRefGoogle Scholar
  23. 23.
    Ranieri VM, Giunta F, Suter PM et al (2000) Mechanical ventilation as a mediator of multisystem organ failure in acute respiratory distress syndrome. JAMA 284:43–44CrossRefPubMedGoogle Scholar
  24. 24.
    Kuiper JW, Groeneveld ABJ, Slutsky AS et al (2005) Mechanical ventilation and acute renal failure. Crit Care Med 33:1408–1415CrossRefPubMedGoogle Scholar
  25. 25.
    Brunkhorst FM, Engel C, Ragaller M et al (2008) Practice and perception – a nationwide survey of therapy habits in sepsis. Crit Care Med 36:2719–2725CrossRefPubMedGoogle Scholar
  26. 26.
    Bein T, Weber-Carstens S, Goldmann A et al (2013) Lower tidal volume strategy (≈ 3 ml/kg) combined with extracorporeal CO2 removal versus ‚conventional‘ protective ventilation (≈ 6 ml/kg) in severe ARDS: the prospective randomized Xtravent-study. Intensive Care Med 39:847PubMedCentralCrossRefPubMedGoogle Scholar
  27. 27.
    Terragni PP et al (2009) Tidal volume lower than 6 ml/kg enhances lung protection: role of extracorporeal carbon dioxide removal. Anesthesiology 111:826–835CrossRefPubMedGoogle Scholar
  28. 28.
    Forster C, Schriewer J, John S et al (2013) Low-flow CO2 removal integrated into a renal replacement circuit reduces acidosis and is paralleled by hemodynamic stabilization in critical ill, ventilated patients. Crit Care 17:R154PubMedCentralCrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Medizinische Klinik 4Universität Erlangen-NürnbergErlangenDeutschland

Personalised recommendations