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Critical Care Nephrology and Acute Kidney Injury
Open Access

Sepsis Management for the Nephrologist

Sharad Patel, Nitin Puri and R. Phillip Dellinger
CJASN May 2022, CJN.14381121; DOI: https://doi.org/10.2215/CJN.14381121
Sharad Patel
1Department of Critical Care, Rowan University Cooper Medical School, Camden, New Jersey
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Nitin Puri
2Department of Critical Care, Cooper Hospital University Medical Center, Camden, New Jersey
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R. Phillip Dellinger
2Department of Critical Care, Cooper Hospital University Medical Center, Camden, New Jersey
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    Figure 1.

    The evolution of sepsis definitions. SIRS, systemic inflammatory response.

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    Figure 2.

    Antibiotic timing. The timing of antibiotics depends on the presence of shock and the probability of sepsis. Patients with a high probability of sepsis should receive antibiotics within 1 hour. In patients with possible sepsis, antibiotics should be initiated within an hour if shock is present and within 3 hours if they are hemodynamically stable. Reprinted from ref. 4, with permission.

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    Figure 3.

    In sepsis, the afferent arteriole undergoes vasoconstriction, whereas the efferent arteriole vasodilates, leading to a reduction in glomerular filtration pressure. The differences in resistance between the two arterioles predispose to glomerular shunting via periglomerular shunting pathways. Both mechanisms lead to a reduction in GFR, despite an increase in renal blood flow early in sepsis.

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    Figure 4.

    Sepsis-related kidney injury can be divided into primary and secondary mechanisms. The primary mechanisms include damage-associated molecular patterns (DAMPS) and pathogen-associated molecular patterns (PAMPS), leading to an innate immune response with consequential systemic vasodilation, disseminated intravascular coagulopathy (DIC), and cellular reprogramming of renal tubular epithelial cells. The innate immune response further contributes to microvascular changes and glomerular microthrombi, resulting a net reduction in GFR. Secondary injury occurs due to fluid resuscitation that can lead to venous congestion and intra-abdominal hypertension, which further contributes to AKI.

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    Figure 5.

    The figure illustrates the relationship between oxygen delivery (DO2) and oxygen consumption (VO2). As DO2 decreases, VO2 remains relatively constant until it reaches a critical O2 supply dependence threshold, at which point there will be a significant drop in VO2. Lactate rises prior to the O2 supply dependence threshold are independent of the DO2-VO2 relationship, whereas below the threshold, they become DO2-VO2 dependent.

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Clinical Journal of the American Society of Nephrology: 17 (5)
Clinical Journal of the American Society of Nephrology
Vol. 17, Issue 5
May 2022
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Sepsis Management for the Nephrologist
Sharad Patel, Nitin Puri, R. Phillip Dellinger
CJASN May 2022, CJN.14381121; DOI: 10.2215/CJN.14381121

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Sepsis Management for the Nephrologist
Sharad Patel, Nitin Puri, R. Phillip Dellinger
CJASN May 2022, CJN.14381121; DOI: 10.2215/CJN.14381121
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  • Article
    • Abstract
    • Introduction
    • Definitions
    • Antibiotics
    • Pathophysiology
    • Resuscitation and Kidney Function
    • Fluid Type
    • Lactate/Oxygen Delivery/Oxygen Consumption
    • Blood Purification
    • Conclusion
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More in this TOC Section

  • Low-Flow Acute Kidney Injury
  • Overview of Diagnostic Criteria and Epidemiology of Acute Kidney Injury and Acute Kidney Disease in the Critically Ill Patient
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Keywords

  • Critical Care Nephrology and Acute Kidney Injury Series
  • sepsis
  • acute kidney injury
  • septic shock

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