An approach to Acute Kidney Injury – The Kidney 7

The recognition of sepsis, with the introduction of sepsis care bundles – most notably the “Sepsis 6” – together with widespread sepsis education has led to a significant decrease in sepsis associated morbidity and mortality. Education and research has focused on the importance of initiating simple recognition/treatment of suspected sepsis in a timely fashion (typically <60mins).

In the world of Nephrology, acute kidney injury (AKI) remains a similarly troublesome disease process for medical clinicians. However, unlike sepsis, AKI has not yet benefited from as much of a clearly defined recognition pathway as the sepsis 6. This post summarizes an approach to dealing with AKI and its ramifications – titled here as ‘The Kidney Seven’ – clever, right! The ‘Kidney Seven’ provides a framework to structure your thought processes when working up a suspected AKI. This approach can also be helpful for the intern/resident managing a patient with low urine output or rising creatinine.

Definition:

Acute kidney injury is defined as a rapid decrease in the GFR, occurring over a period of hours to days and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately.

Background: 5 simple AKI facts

  1. AKI is common.

In large tertiary care hospitals = approximately one in five patients will be admitted with AKI or develop AKI during their hospital admission. The severity of AKI will vary significantly depending on a variety of background factors

2. AKI is bad for you.

The occurrence of AKI has very direct implications for morbidity and mortality.

  • AKI Grade 1 – 8% (Mortality Risk)
  • AKI Grade 2 – 16-28%
  • AKI Grade 3 – 35 – 65%.
f2-large
Acute Kidney Injury & Mortality (Study Link)

Remember that acute kidney injury is rarely an isolated disease process – it is commonly a manifestation of the patient’s severe systemic response to known medical conditions.

3. AKI is a disease of the old and the sick (think ‘failure’)

  • Age: 65 – 85 yrs of age
  • Renal failure – (i.e. Pre-existing CKD)
  • Heart failure
  • Liver failure
  • Being chronically sustained on a medication which is potentially nephrotoxic (interferes with renal autoregulation) – Note: ‘Chronically sustained’ includes a patient who has been taking an NSAID or ACEi etc for months, not a patient who was given an NSAID a week ago for 2 days.

4. AKI is easily recognisable and easily stratifiable

Two well validated grading systems for AKI exist – The Rifle criteria [1] and the AKIN grading system [2]. You may use whichever system you feel more comfortable with. The first 3 stages of RIFLE correspond to the 3 stages of AKIN.

rifle-criteria
Grades: AKI 1 = Risk, AKI 2 = Injury, AKI 3 = Failure (respectively)

5. AKI is most commonly caused by PRE-RENAL causes (80 – 85%)

  • Prerenal (80 -85%)

Severe sepsis, Acute CHF, Shock from any cause, ECF volume depletion, Medications: NSAIDs, ACEi’s, Diuretics (85%)

  • Post Renal (10-15%)

aka. Obstruction – if you are unsure if this is Pre-Renal – do an ultrasound

  • Intra-renal (5 – 10%):

Blood + Protein in the urine – least common, most needing intervention, call nephrology…


 

Management Approach: The Kidney 7

  1. History/Nephrotoxins.
  2. Volume status/Blood pressure.
  3. Urine output.
  4. Obstruction.
  5. Urinalysis.
  6. Electrolytes/acid base.
  7. Dialysis.

 

1. History/Nephrotoxins

A detailed patient history and assessment of the drug chart should leave you with the following pieces of information

  • Risk factor profile for developing AKI (Age, Chronic ‘failure’ of any kind – Renal, Liver, Heart)
  • Nephrotoxins (recent contrast CT, NSAIDs, ACEi, Diuretic?)
  • Recent Surgery, Blood loss, Sepsis

 

2. Assess Volume Status (ECF volume increased or decreased?)

Do I give IV fluids or send the patient for renal replacement therapy? An assessment of volume status is crucial to guiding decisions around the dichotomy of fluid resuscitation versus renal replacement therapy.

Fluid status can be assessed both clinically and biochemically. The following clinical signs are individually predictive of overload (many other signs exist).

  • Peripheral Edema
  • Raised JVP
  • Blood Pressure
  • Crackles on Pulmonary Examination
  • Increased RR (>24)

Biochemical indicators of overload/hypovolemia

  • BUN, Sodium, Fe:Na, Fe:Urea

Note: Well intentioned but overly aggressive fluid resuscitation has been associated with increased complications, increased length of ICU and hospital stay, and increased mortality. A 250ml IV NaCl bolus over 10 mins – if the patient is hypovolemic, followed by re-assessment for the clinical signs above is a safe approach. Blood pressure and urine output are important for further assessing volume status and may indicate if a patient is ‘dry’.

 

3. Urine output

Monitor Urine Ins & Outs – Place a Foley catheter

fig4
Remember the urine outputs for AKI 1,2 & 3

 

Creatinine and Urine output are the ‘Lactate and CRP’ of sepsis. Do not underestimate the clinical use of urine output – it is both sensitive and specific for the early recognition of AKI – is easily measurable and allows you to assess response to treatment within a short time frame.

4. Rule out Obstruction

As noted above – if you are unsure if the cause of AKI is Pre-Renal – book an ultrasound of kidneys, ureters and bladder to assess for kidney size/obstruction/hydronephrosis

5. Urinalysis

A urine dipstick is a quick and simple bedside test with high potential diagnostic yield. If positive for microscopic hematuria and proteinuria it may point towards a diagnosis of glomerulonephritis. Involve senior help/nephrology if positive in the setting of AKI.

6. Electrolytes/Acid Base

Assess major electrolytes – in both the urine and the serum.

  • Serum K+ to ensure no risk of arrythmia
  • Serum and Urine Na+ & Creatinine – to assess the FeNa+ – A value less than 1% indicates a pre-renal cause of acute kidney injury, whereas a value greater than 2% indicates an intrinsic renal cause. (Calculator + Description)
labsaki
Trends in AKI

 

7. Assess the need for Dialysis

A-Acidosis (pH <7.1)
E-Electrolyte (K+ >7)
I-Intoxication (Certain alcohols + drugs)
O-Overload of volume (Refractory to treatment)
U-Uremia (Symptomatic – Pericarditis, Encephalopathy etc)

If any of these factors are apparent on clinical/biochemical findings – discuss the possibility of RRT urgently.


 

In summary:

The assessment of these 7 steps can be done easily in <30 minutes in a patient who has developed a decreasing urine output or had an unexpected jump in creatinine. These 7 steps  may provide you with a good, memorable structure with which to conquer acute kidney injury.

For further reading on how poorly AKI is typically managed in the hospital setting – and what we can do better – here is a link to the NCEPOD report – aptly named – “AKI adding insult to injury”

Credit to Dr. Sam Kant for providing the base material for this post in the Irish Medical Times (Link)

 

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One Comment Add yours

  1. Ciaran Ryan says:

    Very informative article. Covers all the bases without being superfluous.

    Like

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