Saudi Journal of Kidney Diseases and Transplantation

: 2021  |  Volume : 32  |  Issue : 1  |  Page : 9--18

Essence Core: Fluid Management in Acute Kidney Injury

Fatma Ibrahim Albeladi 
 Department of Nephrology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia

Correspondence Address:
Fatma Ibrahim Albeladi
Department of Nephrology, Faculty of Medicine, King Abdulaziz University, Jeddah
Saudi Arabia


Acute kidney injury (AKI) is a heterogeneous disorder characterized by sudden decrease in kidney functioning, with increased serum creatinine levels and impairment of vital kidney functions such as fluid, electrolyte, and acid-base homeostasis. The key to perioperative AKI management is accomplishing optimal intravenous fluid therapy, involving guided fluid resuscitation and fluid balance management including proper fluid removal. In the present review, we highlighted the importance of fluid-based management of AKI, which is a critical process, as both reduced and increased levels of body fluids can have detrimental effects on the patient. While fluid depletion is commonly the targeted approach for fluid management, fluid overload is also largely recognized as a major contributor to worsening the outcomes. With the wide range of available fluid types, such as colloids and crystalloids, detailed knowledge and role of each are necessary before making the choice of a treatment strategy to be employed. While each of these has associated pros and cons, crystalloids are largely accepted as the treatment of choice due to better outcomes and affordability. Nevertheless, the dose and choice of fluid therapy must be goal irected and customized based on the patient's condition, ruling out the confounding factors.

How to cite this article:
Albeladi FI. Essence Core: Fluid Management in Acute Kidney Injury.Saudi J Kidney Dis Transpl 2021;32:9-18

How to cite this URL:
Albeladi FI. Essence Core: Fluid Management in Acute Kidney Injury. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2021 Aug 4 ];32:9-18
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Full Text


Acute kidney injury (AKI) is a heterogeneous disorder characterized by sudden decrease in kidney functioning, with increased serum creatinine (SCr) levels and impairment of vital kidney functions such as acid-base, fluid, and electrolyte homeostasis.[1]

AKI, formerly known as acute kidney disease, lacked proper definition and criteria until 2012, when Kidney Disease Improving Global Outcomes (KDIGO) committee put forth well-defined guidelines based on the RIFLE (Risk, Injury, Failure; Loss; and End-stage kidney disease) criteria, which has improved the detection and management of AKI since then [Table 1].[2] As a result, AKI is considered a spectrum of disorders that includes both less severe to advanced forms of injuries. Furthermore, for improved classification of small children with acute-on-chronic disease, additional modifications have been suggested.[2] In children, however, reaching SCr 4.0 mg/dL is uncommon due to low muscle mass; therefore, several modifications have been suggested in the criteria for classification in children.[2]{Table 1}

The diagnosis of AKI relies on measuring levels of SCr, urine output, as well as biomarkers reflecting tubular injury (e.g., interleukin 18, kidney injury molecule 1, neutrophil gelatinase-associated lipocalin, and liver-type fatty acid binding protein) and kidney stress (e.g., insulin-like growth factor binding protein 7 and tissue injury metallo-proteinase 2). The latter has been FDA approved for Stage 2 or 3 AKI-risk patients.[3],[4]

Classically, AKI can also be classified as prerenal (e.g., hypovolemia, impaired cardiac function, systemic vasodilation, or increased vascular resistance), intrinsic renal (e.g., tubular damage, glomerular damage, interstitial damage, or vascular damage), or post-renal AKI. While intrinsic renal refers to a proper kidney disease, pre- and post-renal AKI result due to extrarenal diseases which leads to reduced glomerular filtration rate levels and if prolonged, can cause cellular damage and thus intrinsic renal disease.[5]

AKI is a major problem in developing countries with ~15% prevalence in inpatients and ~60% in critically ill patients.[5],[6],[7],[8],[9],[10],[11] Although less common, community AKI has been reported in as much as 4.3% of adult hospitalized patients.[12] In children aged one to three years, the risk for post-AKI chronic kidney disease was found to be as high as 46.8% in the intensive care.[13] The high prevalence rate is attributable to its association with several surgical complications which further increases the risk and cost of healthcare. Neonates and children exhibit a high mortality rate following AKI requiring critical care or dialysis, and AKI is more commonly linked with systemic/multiorgan disease than the primary renal disease in this population.[14] However, it is observed that, as compared to adults, children who had an AKI episode exhibited improved prognosis. For example, Askenazi reported that three to five-year survival in children who have survived AKI was 80% and two-third deaths occurred in the first two years, suggesting improved life expectancy after that.[15]

Body fluids are affected the most by AKI; therefore, monitoring and restoring fluid balance are the key to perioperative AKI management. Accomplishing optimal intravenous fluid therapy involves strategies such as guided fluid resuscitation, fluid balance management, and proper fluid removal.[16]

Several have described the management of AKI, especially focused either on adults or children; however, reports describing the complete picture of fluid management in both these populations are scarce. Therefore, in the present review, we have addressed fluid management in both adult and children population. We believe our review would help giving true knowledge of fluid-based AKI management, thus helping both patients and caregivers achieve improved clinical outcomes and better quality of life.


Literature relating to AKI management was searched from two sources: PubMed (till 2020) and Google Scholar, with emphasis on fluid management. The keywords for searching articles were “acute kidney injury,” “management,” and “fluid management” as titles or in the manuscript. Studies including fluid-based therapy for the management of AKI in human adults or children were included, and all studies in other organisms were excluded. Furthermore, studies describing fluid-based therapy for patients other than AKI, such as cardiac surgery or liver diseases, were excluded. From the selected articles, references matching the inclusion criteria were also selected and analyzed for relevant data. After comprehensive analysis of each article, the relevant information was placed in a word document, and significant findings were discussed.


Management of AKI is a challenging process; therefore, careful assessment of the fluid status is required at every step.

Fluid imbalance

Fluid balance is one of the key interventions in hospitalized patients, especially those with AKI, who have impaired ability to regulate fluid volume. A large variation in fluid imbalance is often reported in patients after acute trauma. While cases with depleted fluids are frequently reported, inappropriate fluid resuscitation can often lead to fluid overload (FO), observed as venous pressure increase and interstitial space expansion, leading to tissue edema, organ dysfunction, and adverse effects.[17] Primarily, FO, when more than 10%, can result in adverse effects.[3],[18] Sutherland et al[19] evaluated FO associated mortality in 297 children and reported that mortality rates corresponding to FO at 10%, 10%–20%, and >20% were 29.6%, 43.1%, and 65.6%, respectively. Another study by Wang et al[20] reported that FO in small degrees was also associated with increased risk for AKI and mortality. Bagshaw et al[21] reported a direct link between FO at >5% bodyweight from 24 h before renal replacement therapy (RRT) and the risk for hospital mortality. Furthermore, some studies have reported a link between FO and worsened patient outcomes and increase in the risk of complications such as delayed wound healing and infection rate.[22]

Not only the level of FO but also its timing and duration are associated with adverse patient outcomes.[23] A study by Gist et al[22] reported improved patient outcomes when fluid accumulation was managed before day 3 of intensive care unit (ICU) admission. FO is also associated with increased requirement for medical interventions[24] such as decreased mobility[25] and need for RRT or mechanical ventilation.[20] Bouchard et al[23] evaluated FO in critically ill patients with AKI. The survivors displayed less fluid accumulation at ICU admission than that of the no survivors. At 10% FO, the 30- and 60-day mortality increased from 25% to 37% and 35% to 48%, respectively. Furthermore, fluid buildup was directly associated with mortality. Payen et al[26] reported that patients with sepsis and AKI displayed higher 60-day mortality when associated with FO. Another study reported a direct relation between FO at the beginning of RRT and reduced one-year renal recovery.[27] Vaara et al[28] evaluated 226 RRT-treated critically ill patients and reported that the presence of FO (fluid accumulation >10%) at RRT increased the chances of 90-day mortality by two-fold.

Therefore, fluid administration should be done before procedures that are time-bound, such as radiological contrast and continue for a few hours after that.[18] Furthermore, a careful balance between administering diuretics, increasing urine flow, and vigorously replenishing fluids can help reduced nephropathy.[29] Therefore, optimizing fluid management is imperative for improving patient outcomes.

Detection of fluid imbalance

The primary step in achieving fluid balance is evaluating the fluid status. This can be achieved by accurate and timely monitoring of patient’s fluid levels. Educating the staff to regularly document and follow simple interventions is essential for improving AKI recognition and management. Davies et al[30] have reported the benefits of a chart-based system in reducing the rate of AKI. The study highlighted that by documenting fluid status in charts calculating AKI alerts every month, training the staff by meetings and e-learning, and informing the patients by educational posters significantly reduced the rate of AKI by 33%.

Different approaches have been reported to document fluid levels in patients. As a quality improvement project, Address drugs, Boost blood pressure, Calculate fluid balance, Dip urine, Exclude obstruction (ABCDE) checklist was introduced by Forde et al[31] in a district general hospital to evaluate AKI recognition and management. The study reported that post multidisciplinary education, AKI recognition improved to 100% as compared to 31% previously. Similarly, Bhagwanani et al[32] reported the role educating the staff of the DONUT bundle involving six interventions: Dehydration, obstruction, nephrotoxins, urine, think sepsis, in improving AKI management. Several warning systems have also been developed to assess the risk in patients with AKI. For example, the Sequential Organ Failure Assessment (SOFA) score was developed for patients with AKI that were transferred from other hospitals, a high score highlighting emergent actions within 24 h.[33] Similarly, the Modified Early Warning System (MEWS) score incorporated the features of SOFA along with the added benefit of coordinating physiological evaluation in the institution.[34]

Regular monitoring for efficient AKI management can be achieved by multiple approaches. [Table 2] highlights the parameters for evaluating FO,[18] including clinical, Para clinical, static, and dynamic measures.{Table 2}

Fluid resuscitation

The composition of intravenous (IV) fluid has significant effect on organ function and patient outcomes; therefore, the choice of fluids plays a key role in maintaining and restoring fluid balance. A UK-based study reported that 20% cases suffered adverse effects due to inadvisable fluid use.[35] Therefore, following requirement-based fluid administration is imperative. The 12th Acute Dialysis Quality Initiative highlighted the significance of well-defined outline for fluid therapy rather than following a general approach for all. These comprise evaluation of the need and time for fluid administration as well as regular assessment of the response.[36] Concerning the type of fluid, numerous options can be opted including gelatin or albumin, crystalloids (saline or buffered), and colloids [e.g., synthetic hydroxyethyl starch (HES)] [Table 3].{Table 3}

Several studies have assessed the superiority and safety of different fluids and evaluated their effects on AKI, adverse effects, mortality, etc. However, the results have been found contradicting in several cases possibly due to the vast heterogeneity in patient population and the volume of fluid.[18]

The choice of fluid largely depends on the type of intervention. For example, situations such as inflammation, where vascular permeability increases, HES, albumin, and gelatin might not be much effective since their mechanism of action involves selectively expanding intravascular space.[3] Albumin has shown mixed effects in previous studies. For example, the saline versus albumin fluid evaluation trial reported no renal or mortality advantage in patients administered 4% albumin; however, the albumin group required less volume for resuscitation, thus suggesting possible advantage of employing albumin-based therapy in conditions such as septic shock and cirrhosis, where the volume of IV fluids can substantially increase.[38] Only few studies have shown the link between gelatin risk for AKI.[3]

HES is available in various molecular weights and tonicities which are more affordable than albumin. While studies such as colloids versus crystalloids for the resuscitation of the critically ill reported beneficial effects of using HES in reducing 90-day mortality and requirement for mechanical ventilation and vasopressor,[39] other studies have reported HES to cause proximal tubule vacuolization and swelling, thus resulting in renal toxicities. The 6S trial reported increased risk of mortality in patients with sepsis upon HES administration.[40] However, iso-oncotic HES preparations are considered less nephrotoxic than hyper oncotic preparations.[3] Several studies have reported a dose-dependent effect of HES on renal function. The crystalloid versus hydroxyethyl starch study compared outcomes in ICU patients who were administered iso-oncotic 6% HES or saline solution and the risk significantly increased in the former group. As a result, additional warnings have been added by the FDA to the packaging of HES, and the use of HEK is restricted.[3] Recent studies such as FENICE trial have supported the preferential use of buffered crystalloids for fluid management.[41] Therefore, it is suggested that the outcomes due to colloids are largely dependent on the timing of administration; however, data supporting their routine use are insufficient.

Furthermore, some studies have reported the association between saline (0.9% sodium chloride) and AKI with increased incidence of death, RRT, and reduced kidney functioning. This is possibly attributed to the significantly high chloride content than the extracellular space, which increases the risk for hyper-chloremic metabolic acidosis.[3] Bellomo et al[42] reported that, in patients admitted to ICU, beneficial effect of restricting IV chloride administration was seen in decreasing AKI incidence. In the case of sepsis, saline is also linked with higher risk of AKI and death. The major side effects associated with saline administration include renal vasoconstriction and reductions in salt–water retention, glome-rular filtration rate, renal cortical perfusion, and renal artery flow velocity.[43]No large-scale studies have reported better clinical outcomes for saline or balanced solutions. For example, the SPLIT trial analyzed outcomes for 2262 patients who were administered ICU fluid therapy with 0.9% saline or Plasma-Lyte® 148. The study reported no significant difference in terms of AKI development; the results were however found unreliable due to inaccurate representation of ICU patient population.[44] Therefore, saline is still a part of standard care for AKI management due to limited evidence showing the superiority of other fluids.

Acute kidney injury management guidelines Kidney Disease Improving Global Outcomes

AKI imposes a significant financial burden on the patients with morbidity and mortality risk. Consequently, prevention, timely detection, and treatment are imperative. In 2012, the KDIGO Clinical Practice Guideline was published aimed at improving the care for patients with AKI.[2] These guidelines describe several aspects of related to the definition, assessment, management, etc., of AKI. The guidelines pertaining to fluid management have been briefly discussed below (Section 2–Section 5), and the full version is available on the KDIGO website.[2]

Section 2. Acute kidney injury Definition

Section 2.1 Definition and classification of AKI

Section 2.1.1 defines AKI as:

- Increase in SCr by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 h or

- Increase in SCr to ≥1.5 times baseline, to be occurred within 7 days or

- Urine volume <0.5 mL/kg/h for 6 h.

Section 2.1.2 describes the stages of AKI severity

As previously stated, depending on the severity, stages of AKI are:

- Stage 1: SCr ≥0.3 mg/dL (≥26.5 mmol/L) or >1.5–1.9 times from baseline urine volume <0.5 mL/kg/h for 6–12 h

- Stage 2: SCr 2.0–2.9 times baseline, urine volume <0.5 mL/kg/h for ≥12 h

- Stage 3: SCr 3 times baseline, increase in SCr to ≥4.0 mg/dL (≥353.6 μmol/L) OR initiation of RRT, OR in patients <18 years, decrease in eGFR to 35 mL/min per 1.73 m2 OR, urine volume <0.3 mL/kg/h for ≥24 h OR anuria for ≥ 12 h).

Section 2.1.3 When feasible, the reason of AKI should be determined.

Section 2.2 Risk assessment

Section 2.2.1 Patients should be classified for the risk of AKI based on their susceptibilities and exposures.

Section 2.2.2 Patients should be managed based on the abovementioned stratification to reduce the risk for AKI.

Section 2.2.3 Patients should be tested based on SCr and urine output levels, and monitoring should be individualized.

Section 2.3 Evaluation and general management of patients with and at risk for AKI

Section 2.3.1 Patients should be promptly evaluated for cause, especially reversible causes.

Section 2.3.2 Patients should be monitored to measure SCr and urine output for assessment of severity.

Section 2.3.3 Patients should be managed depending on the stage and cause.

Section 2.3.4 Patients should be evaluated at 3 months post AKI for resolution, new onset, or worsening of pre-existing CKD.

Section 3. Prevention and Treatment of Acute kidney injury

Section 3.1 Hemodynamic monitoring and support for prevention and management of AKI

Section 3.1.1: Patients without hemorrhagic shock should be administered isotonic crystalloids instead of colloids (albumin or starches) as initial management for expansion of intravascular volume.

Section 3.1.2: Patients with vasomotor shock with, or at risk for, AKI should be administered a combination of vasopressors and fluids. The need for vasopressor is found to be highly associated with AKI in patients having sepsis or sepsis shock.

Section 4.1 AKI should be defined and staged postadministration of IV contrast media.

Section 4.2 Assessment of the population at risk for Contrast-induced AKI (CI-AKI)

Section 4.2.1 Risks for CI-AKI should be evaluated, especially pre-existing kidney function impairment.

Section 4.2.2 Alternative imaging methods should be considered for high risk patients of CI-AKI.

Section 4.3 Nonpharmacological prevention strategies of CI-AKI

Section 4.3.2 Iso- or low-osmolar compared with high-osmolar iodinated contrast media is advised for high-risk patients of CI-AKI.

Section 4.4 Pharmacological prevention strategies of CI-AK

Section 4.4.2 Oral fluids alone are not advised for patients at increased risk of CI-AKI.

Section 4.4.3 Oral NAC together with IV isotonic crystalloids are advisable for patients at increased risk of CI-AKI.

Section 5.1 Timing of renal replacement therapy in AKI

Section 5.1.1 RRT should be emergently initiated in cases of life-threatening changes in fluid, electrolyte, and acid-base balance.


AKI is a complex renal disease associated with a range of disorders, such as renal dysfunction, and is highly prevalent affecting 5%–20% patients admitted in the hospital. Of these, cases with severe AKI requiring RRT are estimated to be 49%. The mortality rate varies with the patient population studied but lies in the range of 10%–80% in hospitalized cases and ~50% in cases reporting AKI and multiorgan failure, which increases further to ~80% if RRT is required.[45]

AKI development postmajor vascular surgery is directly related to complications, such as infection, cardiovascular events, rates of tracheostomy, and mechanical ventilation requirement. Conditions developing post AKI and chronic kidney disease development, such as dialysis dependency, are also more frequent. Furthermore, in cases where AKI overlaps with other major diseases, such as acute respiratory distress syndrome, the mortality rates, length of hospital stay, and management complexity are higher.[46]

The high incidence of AKI is partly attributable to increased comorbidities and employing high-risk diagnostic and therapeutic interventions that ultimately favor AKI. The financial burden associated with the treatment of AKI, as well increased mortality, cardiovascular events, and chronic kidney diseases, are a major concern and are of prime importance in efficient management of the disease and improving patient’s quality of life.[37]

Since, AKI results in high risk of short/long-term morbidity and mortality, chronic kidney disease, and dialysis, and due to the lack of specific approved therapies for AKI treatment, prompt diagnosis, and management are imperative. This requires early recognition, hyper-volemia correction, and treating reversible causes such as sepsis or obstruction.[1]

Accurate data are vital for preventing AKI and the common practice of irregular observations or alerting post a warning score has been recognized. However, in the last few years, increased caution toward fluid balance and urine output has been the focus of some studies and regular monitoring has been stresses upon. Due to the absence of well-defined treatment for AKI, awareness of the disease and regular evaluation of the clinical parameters is vital. Since the entire multi-disciplinary team is responsible for the management of AKI, increasing awareness for all has been much emphasized. For the same, several educational programs, evaluation charts, and electronic data systems have been proposed; however, these require further validation in large-scale studies.[31]

Optimization of body fluids is the primary goal in the maintenance of the hemolytic balance in AKI. In the present review, we highlighted the importance of fluid-based management of AKI. Fluid-based management of AKI is a critical process as both reduced and increased levels of body fluids can have detrimental effect on the patient. While fluid depletion is commonly the targeted approach for fluid management, FO is also largely recognized as a major contributor to worsening the outcomes. Furthermore, despite the known parameters to look for and the awareness of regular monitoring for prevention of AKI, the scenario is challenging in clinical practice due to several reasons. For example, accurately estimating FO is not feasible and is therefore, calculated as percentage gain in body weight since ICU admission. Furthermore, it is unclear whether the adverse effects of FO are specific as the effects of excessive fluid accumulation can differ with those due to excessive crystalloid therapy.[31] The relationship between FO and AKI associated mortality is also complicated, and it is not clear whether FO is the cause or result of severe illness. Some investigators have reported FO to be an independent risk factor for the development of adverse outcomes in patients with AKI,[20] others have reported contradicting results. AKI increases the risk for fluid accumulation and vice versa, and not all patients with AKI exhibit fluid accumulation, or fluid accumulation not always leads to severe AKI. For example, hypotension is commonly found in patients with AKI and when clubbed with severe illness, it can lead to fluid accumulation. Furthermore, fluids dilute serum creatinine concentration, thus making the relationship between AKI and FO more complex.[22]

Therefore, the approach should be goal-directed and customized based on the patient’s condition, ruling out the confounding factors. With the wide range of available fluid types, such as colloids and crystalloids, detailed knowledge and role of each are necessary before making the choice of a treatment strategy to be employed. For example, crystalloids are preferred in conditions of hypovolemia, and colloids are less preferred to the lack of confirmatory data on their safety and clinical benefits.

Although each of these strategies has associated pros and cons, crystalloids are largely accepted as the treatment of choice due to better outcomes and affordability. Nevertheless, the dose and choice of fluid therapy should be customized depending on the specific requirements of the patient. Certain fluid regimens have reportedly shown adverse effects on AKI and patient outcomes. Therefore, spreading awareness and customizing treatment strategies depending on the patient’s health status can help improve patient outcomes and reduce morbidity and mortality.

Our study had a few limitations. First, this research was biased to search for fluid-based management lowering the risk for AKI. Therefore, we might have missed some studies focusing on the complications in the management of AKI and not included. Nevertheless, our review provides a comprehensive analysis of the possible strategies to be employed for the management of AKI, especially fluid management, thereby improving patient outcomes.

Conflict of interest: None declared.


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