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Year : 2018  |  Volume : 5  |  Issue : 2  |  Page : 30-35

Septic acute kidney injury (SAKI)

Chief, Advanced Pediatric Critical Care Centre & Head, Dept of Pediatrics, Wanless Hospital, Miraj, 416101, Maharashtra, India

Date of Submission01-Apr-2018
Date of Acceptance14-Apr-2018
Date of Web Publication30-Apr-2018

Correspondence Address:
Vinayak Patki
Chief, Advanced Pediatric Critical Care Centre & Head, Dept of Pediatrics, Wanless Hospital, Miraj, 416101,Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.21304/2018.0502.00370

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Acute kidney injury (AKI) is a common and potentially fatal complication of sepsis. Septic acute kidney injury (SAKI) remains an important challenge in critical care medicine. SAKI has a complex pathophysiology than previously anticipated. The pathophysiologic mechanisms of sepsis-induced AKI are different from non-septic AKI. Sepsis- induced systemic inflammation triggers protective mechanisms within the nephron, affecting tubular and glomerular functions. A varying degree of kidney impairment can be expected, from a small decrease in GFR to complete shutdown and permanent dysfunction, depending on the severity of the inflammatory response. It is likely that progression of septic AKI can be prevented by avoiding hypotension, fluid overload, and venous congestion. There is no specific therapy for septic AKI at present. Even though novel drugs and blood purification techniques for sepsis-induced AKI are being tested, supportive care to prevent further kidney insults is likely to allow kidney structure and function to more easily recover once the septic state has resolved.

Keywords: Sepsis, Acute kidney injury, Septic acute kidney injury, Prevention, Treatment

How to cite this article:
Patki V. Septic acute kidney injury (SAKI). J Pediatr Crit Care 2018;5:30-5

How to cite this URL:
Patki V. Septic acute kidney injury (SAKI). J Pediatr Crit Care [serial online] 2018 [cited 2020 Sep 25];5:30-5. Available from: http://www.jpcc.org.in/text.asp?2018/5/2/30/281117

  Introduction Top

Both sepsis and acute kidney injury (AKI) are diseases of major concern in critically ill patients. AKI usually complicates severe sepsis. In approximately 50% of cases of acute kidney injury (AKI) among critically ill patients is triggered by Severe sepsis. The overall incidence of septic AKI (SAKI) among all intensive care unit (ICU) admissions ranges between 15 and 20 % [1]. The incidence of AKI is as high as 16% to 25% , even in patients with less severe infections.[2] Depending on severity, SAKI is associated with mortality rates of up to 50% to 60% [3] .The characteristic of Septic AKI is a rapid and often profound decline in the kidneys’ ability to filter blood and eliminate nitrogen waste products, which usually evolves over hours to days after the onset of sepsis. Early control of infection and supportive care, with vasopressors, intravenous fluids and renal replacement therapy (RRT) seem to be logical and are likely to allow favorably outcomes among patients with septic AKI. Here some important developments in our understanding of pathogenesis, prevention and treatment of SAKI are reviewed, which have contributed to this improved prognosis or hold promise for further improvement.

  Pathophysiology of SAKI Top

The pathophysiology of SAKI is much more complex than previously anticipated. Renal dysfunction is not only a result from hypoperfusion alone but also ensues to a large extent from renal inflammation and tubular responses to various sepsis mediators. In many patients, AKI occurs without overt signs of global renal hypoperfusion and SAKI has been described in the presence of normal or even increased renal blood flow [4]. This is the reason why only correction of hemodynamic parameters often fails to prevent SAKI. The pathophysiology of SAKI is no longer based on an ischemia/reperfusion paradigm but rather it is an aggregate of inflammation, microcirculatory dysfunction, perfusion deficit, bio-energetic reactions, and tubular cell adaptation to injury.[5]

  Cellular Adaptation in SAKI Top

The adaptive mechanisms are triggered by the immune response to infections affecting the kidneys’ tubular, vascular and glomerular functions. Invading pathogens release molecules, known as pathogen- associated molecular patterns (PAMPs), like lipopolysaccharide, lipoteichoic acid, or DNA, into the blood. Additionally, cellular injury and disruption release intracellular contents, the so-called damage- associated molecular patterns (DAMPs). The pattern recognition receptors, such as Toll-like receptors, on immune cells recognize the PAMPs and DAMPs.[6] The immune cells release cytokines, chemokines and reactive oxygen (ROS) and nitrogen (RNS) species in response to this activation. The systemic inflammatory response is triggered by PAMPs from invading microorganisms and by DAMPs from damaged cells. Inflammatory mediators, ROS and RNS, are released by the activated neutrophils, which cause kidney tubular cell stress and injury. Tubules adapt to cellular stress by conserving energy through G1 cell cycle arrest. Mislocation ofNa1/K1-adenosine triphosphatase prevents energy consuming NaCl reuptake. Recruitment of glomerular shunt pathways shunt toxin-rich blood away from the kidneys to protect the tubules from further harm. [Figure 1][7]
Figure 1 : Pathophysiology of SAKI[7]

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A major portion of cardiac output (approximately one- fifth) is received by the kidneys and they filter large plasma volumes every hour. The tubules in septic patients are therefore likely to be continuously exposed to DAMPs, PAMPs, ROS, and RNS, either through blood or via its filtrate in the tubular lumen. Logically, this toxic milieu poses a threat to the nephrons and cellular stress or injury could be expected. But histologic evidence of cell injury is remarkably scarce even in the presence of complete loss of kidney function in sepsis.[8],[9] These observations suggest that important adaptive mechanisms may be at work, which, at least partly, can protect the kidneys until the septic state has resolved.

  Glomerular Hemodynamics in SAKI Top

A decreased GFR is the major functional event of septic AKI. Low GFR is a protective mechanism which guards against further insults by decreased filtration of toxins such as DAMPs and PAMPs, which limits further tubular cell toxin exposure and stress. It also means lower energy consumption, because less sodium chloride is filtered and needs to be reabsorbed. Despite normal or increased global renal blood flow during septic AKI, GFR some-times ceases completely. There are vascular pathways bypassing the glomerular capillaries (glomerular shunt pathways) which provide another possible explanation to the loss of GFR in sepsis. Recruitment of such shunt pathways may be an important defense mechanism blunting the kidneys’ exposure to PAMPs, DAMPs, ROS, and RNS.[9],[10] Raised central venous pressure (CVP) with renal venous congestion and renal interstitial edema may lead to the onset and maintenance of sepsis-induced kidney dysfunction.[11]

  Management of SAKI Top

Systemic Blood Pressure

Arterial hypotension is a frequent complication of severe infections which contributes to the development and progression of AKI . The optimal blood pressure target needed to prevent kidney damage and/or delay mortality in individual patients is not yet determined. However, in a recent multicenter, randomized controlled trial (RCT), the SEPSISPAM trial (MAP 80-85 vs 65-70 mm Hg ) found no significant difference in 90-day mortality between the hightarget and the low-target group. An important and logical result of the findings of SEPSISPAM is that norepinephrine infusion at higher doses is safe from a renal point of view, not contraindicated in septic patients with AKI, and possibly beneficial to GFR preservation in selected patients.[12]

Fluid Management and Central Venous Pressure The mainstay of treatment of septic shock is to give intravenous fluids, vasopressors and inotropes guided by physiologic endpoints. Even though such early goal-directed therapy is recommended in the Surviving Sepsis Campaign guidelines, its benefits are still to be proved.[13] In fact, in two recent large multicenter RCTs, early goal- directed therapy did not reduce mortality or prevent RRT requirements in patients with early septic shock.[14],[15] Moreover, fluid resuscitation does not reverse hemodynamic instability in a significant proportion of critically ill patients.[16] When fluid therapy does improve physiologic parameters, the effect is transient and repeated fluid boluses are required to maintain the effect. Thus, unnecessary and repeated fluid administration leads to gradual fluid retention over days. Observational studies show that fluid accumulation is associated with development and progression of AKI and increased mortality in AKI patients.[17] This association is particularly strong when CVP increases beyond 12 mm Hg. The role of venous congestion in the pathogenesis of AKI is thus supported.[18]

Vasopressor Therapy

Vasopressors can restore blood pressure reliably in most septic patients. This contrasts with fluid therapy. However, optimal timing and choice of vasopressor therapy is uncertain. In the Vasopressin and Septic Shock Trial (VASST), administration of low- dose vasopressin (0.01-0.03 U/min) instead of norepinephrine did not decrease mortality in patients with septic shock.[19] However, a secondary analysis of the VASST showed attenuated progression of AKI and decreased need for RRT in vasopressin treated patients.[20] Terlipressin, a vasopressin analog with greater selectivity for the vasopressin 1 receptor, prevented renal function worsening, compared with placebo, in patients with the hepatorenal syndrome, which has many common pathophysiologic features with sepsis-induced AKI. The benefits of terlipressin in septic shock patients need to be confirmed in future RCTs.[21]

Red Blood Cell Transfusion

Septic AKI patients treated with RRT are prone to anemia and hence to receive RBC transfusions. First, the frequent blood sampling needed to monitor electrolyte balance during RRT contributes to low hemoglobin levels. Second, both filter clotting and increased bleeding risk owing to circuit anticoagulation are recognized complications during RRT. Third, AKI is associated with disturbed red cell production because of an altered response to erythropoietin. Also, many AKI patients have chronic kidney disease with associated chronic anemia. Lastly, fluid overload is common in AKI and might dilute hemoglobin. In the Surviving Sepsis Campaign guidelines, a restrictive RBC transfusion strategy, targeting a hemoglobin of 70 g/L, is recommended and results from observational studies show that RBC transfusion in response to the anemia of critical illness is associated with increased morbidity and mortality. A recent RCT therefore explored the safety of targeting a hemoglobin level of 70 g/L compared with 90 g/L in 998 patients with septic shock, of which 12% were treated with RRT at baseline.[22] No differences in mortality, ischemic events, or further RRT requirements were found. Thus, a hemoglobin target just above 70 g/L seems to be safe and appropriate.

Renal Replacement Therapy

Continuous RRT (CRRT) rather than intermittent RRT or extended daily hemofiltration is preferred in AKI patients with severe sepsis. Although differences in survival are negligible when comparing these modalities, the rate of renal recovery is better with CRRT, most probably due to the lower rate of hypotensive episodes and better fluid homeostasis achieved with CRRT.[23] In contrast, optimal timing of CRRT initiation relative to the onset and severity of septic AKI as well as the optimal intensity of such therapy remains uncertain. In a secondary analysis of the Randomized Evaluation of Normal versus Augmented Level (RENAL) replacement therapy study, where 50% of patients had severe sepsis, the time between a doubling of serum creatinine and CRRT start had no impact on mortality. Also, early CRRT, started before conventional criteria were met, failed to improve outcomes in patients with severe sepsis. In contrast, others suggest that there is improvement in survival when CRRT has been initiated before fluid overload has evolved.[24] A CRRT intensity of 20 to 25 mL/kg per hour is recommended for critically ill AKI patients. Based on large RCTs, higher intensities do not offer additional survival benefit in general patients in the intensive care unit.[24],[25] Yet, high-volume hemofiltration (65- 70 mL/kg/h) has been suggested in patients with septic shock. [25]

Future Therapies

Alkaline phosphatase

The molecular mechanisms involved in the sepsis- induced inflammatory response are potential targets for future therapies. Alkaline phosphatase blunts the inflammatory response by detoxifying endotoxin, and by attenuating RNS production. Intravenous injection of alkaline phosphatase in patients with early septic AKI significantly improved creatinine clearance with a trend towards a reduced need for RRT. No large RCT has yet explored its efficacy in septic humans.[26]

Acetylsalicylic acid (aspirin) Several proinflammatory pathways involved in sepsis induced organ damage are triggered by activated platelets. Acetylsalicylic acid (aspirin) interferes with several of these pathways by stimulating the synthesis of anti-inflammatory molecules such as lipoxins, resolvins, and protectins. Observational data suggest that aspirin treatment before or during intensive care unit admission is associated independently with lower mortality. Animal studies also confirm an aspirin- induced resolvin mediated attenuation of AKI during endotoxemia.[27],[28]

Antihistone antibodies

Like other DAMPs, histones (nuclear gene-regulating proteins) are released by necroptotic cells. These activate the immune system and promote sepsis- induced organ injury. Activated protein C, which degrades extracellular histones, was an unsuccessful therapy for sepsis owing to lack of efficacy in a large RCT. Antihistone antibodies were recently shown to prevent death and AKI in a septic mouse model.[29] Their role as therapeutic agents in human septic AKI is yet to be determined.

Polymyxin B hemoperfusion

Removal (adsorption) of circulating endotoxin by polymyxin B hemoperfusion in patients with severe abdominal sepsis improved hemodynamics, organ function, and survival significantly as shown in a recent, small RCT. An ongoing phase 3 trial, including 650 patients with septic shock and elevated endotoxin levels, will provide more robust evidence on the potential benefits of polymyxin B hemoperfusion on clinical outcomes.[30]

Prevention of SAKI

Fluid Resuscitation

The old “credo” stating that fluid harms the lung but benefits the kidney should be revised. Liberal fluid administration is of key importance to optimize systemic hemodynamics in patients with SAKI. But there is an ongoing controversy about efficacy, nature, extent and duration of fluid therapy in septic shock.[31]

In fact, ICU physicians are faced with a “double- edged” fluid dilemma. An optimal fluid management would be to ensue a stepwise and smooth transition from initial unrestricted fluid administration (positive fluid balance) over a state of equilibrium (steady-state fluid balance) to appropriate fluid removal (negative fluid balance).[32]

Balanced crystalloids versus isotonic salt solutions Balanced crystalloid perfusions (e.g., Ringer’s lactate, Plasmalyte®) are associated with less occurrence of AKI than isotonic salt solutions. The latter contain a too high chloride load which is thought to be harmful for the kidney by inducing vasoconstriction in the renal vascular bed. It was independently associated with increased morbidity and mortality. But recent RCTs were not able to prove their efficacy.[33],[34]

Early use of continuous RRT (CRRT) Fluid overload definitely increases kidney edema and enhances severity and irreversibility of SAKI. Therefore, timely use of CRRT in case of fluid overload that is poorly responding or refractory to diuretics might be a reasonable approach to attenuate or control SAKI.[35]

Differentiating transient (functional) SAKI from structural SAKI

Urine biochemistry

SAKI may present either as a functional or structural entity. The difference is clinically relevant since functional SAKI can be reversed completely by early adequate treatment whereas structural kidney damage will mostly require RRT. However, discriminating functional from structural SAKI at the bedside, remains challenging. Low fractional excretions of sodium (FENa) and urea (FEUrea) are highly prevalent during the initial phase of sepsis. Oliguria is an earlier sign of impending SAKI than the increase in serum creatinine. It is assumed that high FENa and low FEUrea values are associated with intrinsic SAKI whereas high values of both FENa and FEUrea occur with transient or functional SAKI. However, a definite discriminative power of these urinary indices has not been established. They are also less specific than currently tested biomarkers of SAKI and less accurate for differentiating transient from persistent AKI and SAKI from non-SAKI [36]


Among various biomarker assays, neutrophil gelatinase- associated lipocalin, urine insulin-like growth factor-binding protein 7, and tissue inhibitor of metalloproteinases- 2 are the most promising. They cannot be advocated for routine guidance of therapy because of their limited availability.[37]

Oliguria vs creatinine

Oliguria is an earlier sign of impending SAKI than the increase in serum creatinine. Macedo et al. reported that oliguric episodes occurred frequently in ICU patients and allowed to identify more AKI as compared to serum creatinine. [38] In contrast, other investigators found a poor specificity of oliguria [39] To date, no biological or laboratory marker can be put forward that reliably distinguishes functional from structural SAKI.


In conclusion, the old beliefthat sepsis-induced AKI is initiated by renal ischemia because of macrovascular dysfunction has been questioned, because AKI can also develop in the presence of normal or increased renal blood flow. The simultaneous occurrence of renal inflammation and microvascular dysfunction exacerbates the adaptive response of tubular epithelial cells to injurious signals. In addition, the initiation and development of sepsis-induced AKI through the nitric oxide pathway, leukocyte adhesion, ROS, and inflammation due to endothelial cell injury is also important. Targeting tubular epithelial cells and components of the microcirculation may be an effective strategy in preventing and/or treating sepsis- induced AKI.

Acknowledgement : Dr. Rinaldo Bellomo, MD, FRACP, FCICM, Dept. ofIntesive Care, Austin Hospital, Victoria, Australia

Source of Funding - Nil

Conflict of Interest - Nil

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