Acute Kidney Injury for Internal Medicine Residents

1. ACUTE KIDNEY INJURY (AKI)
APPROACH TO DIAGNOSIS AND TREATMENT
July 2022
Rajeev Raghavan MD M.Ed FASN

2. Objectives
1. Define acute kidney injury (AKI) and differentiate how abnormal kidney
function (as measured clinically) occurs in anatomically normal kidneys
2. Recognize which laboratory and diagnostic markers are commonly used to
diagnose AKI
3. Discuss how the management of AKI varies by the underlying pathology and
patient presentation

3. Adapted from: United States Renal Data System. USRDS annual
data report: epidemiology of kidney disease in the US. Bethesda,
MD: National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases; 2017
Glomerular Filtration
Rate (mL/min/1.73m2)
Normal to Mildly
Increased Albuminuria
Moderately
Increased
Albuminuria
Severely
Increased
Albuminuria
1 Normal or High
>90
Low risk
Moderately
increased risk
High risk
2 Mildly decreased
60-89
Low risk
Moderately
increased risk
High risk
3a
Mildly to moderately
decreased
45-59
Moderately increased
risk
High risk Very high risk
3b
Moderately to severely
decreased
30-44
High risk Very high risk Very high risk
4 Severely decreased
15-29
Very high risk Very high risk Very high risk
5 Kidney failure
<15
Very high risk Very high risk Very high risk
CKD - Staging

4. Adapted from KDIGO AKI – page 8
https://kdigo.org/guidelines/acute-kidney-injury/

5. Examples
A healthy 54-year-old with a sCr increase from 1.1 to 1.5
mg/dl within 3 months. Stage 1 AKI.
A 63-year-old with diabetic kidney disease and a
baseline sCr of 1.8 mg/dl four months ago presents with
a sCr of 2.9 mg/dl. Stage 1 AKI.

6. Acute Kidney Disease (AKD)
Acute Kidney Injury (AKI)
• Acute change in kidney function (< 3 months) by markers
• Anatomic damage may not be present!
• AKI and AKD are terms used interchangeably: AKI: < 7 days | AKD 7-90 days
• AKI/AKD is associated with a 6.5-fold increase in the odds of death and a 3.5-
day increase in LOS
• AKI may be reversible but CKD occurs in 30% of individuals
• Diagnosis of AKI hampered by its relative asymptomatic nature in early stages

7. Grams KI 81:942, 2011
Organ Damage is a
SYSTEMIC PROBLEM

8. ATI or AIN

9. Urinalysis includes visual inspection, dipstick, and microscopy
Dipstick

10. Note that the urinalysis by the laboratory
is excellent for cell count!
Example of the cell count screen from the Iris™ instrument Example of images of RBC’s

11. Microscopic hematuria is
not defined by the
dipstick… it is defined by
urine microscopy
>3 RBC/hpf of a single
properly collected urine
specimen
WBC
RBC

12. The urine sediment provides additional clues about AKI…
1) Casts
2) Crystals
3) Cells: WBC or RBC
4) Bacteria
Dysmorphic RBC with
bleb
RBC cast
Muddy brown casts
Many WBCs
WBC Cast

13. Case 1
Answer: Atheroembolic Disease.
1) Why are the other choices incorrect?

14. Choleresterol-Induced Embolic Disease
Patient: Older, heart disease, smoker, diabetic, male
Timing: following a cardiac procedure
Clinical: Systemic disorder; 100% hematuria,
hypocomplementemia, reduction in eGFR proportional
to burden of emboli
Diagnosis: History and physical examination
Treatment: Supportive Care

15. Contrast Associated AKI
• Utilize the Mehran calculator to estimate risk of CA-AKI
• Most cases of CA-AKI do not result in tubular cell injury
• Reduce risk of CA-AKI with isotonic crystalloids (1 - 3 cc/kg/hr, before & after)
• Do NOT withhold necessary imaging

16. Case 2
Answer: Intravenous Crystalloid
Why are the other choices incorrect?

17. Intravenous Fluids: Which? How much? What target?
• Isotonic
• Lactated Ringers
• Isotonic (Normal) Saline
• Indicated for volume (ECF) expansion
• 2 liters is sufficient to raise MAP
• Hypotonic
• D5W
• Indicated for hypernatremia or dehydration (ICF >> ECF)
1831, Cholera Epidemic
“…has lost a large portion of its water… a great
proportion of its neutral saline ingredients and
the free alkali in healthy serum”

18. FENa (>1%) had a specificity of just 54% in detecting intrinsic kidney injury.
FENa of <1% may still provide value in patients on diuretics (negative predictive value of 82%). Diuretics may
not have full effectiveness at the time of FENa calculation
Fractional excretion of urea is not widely used in clinical settings.
FENa not as useful in kidney injuries that spare tubular function, such as GN, interstitial nephritis, or vasculitis,
and those that produce more vasoconstriction than tubular dysfunction, such as intravenous contrast
administration
Pigment-induced injuries, like rhabdomyolysis or hemoglobinopathies, can also mimic a prerenal state, yet
there is indeed intrinsic AKI present
FENa is purely a marker for evaluating renal perfusion and tubular sodium handling and cannot fundamentally
differentiate between “prerenal” and “renal” causes of AKI.
Harish Seethapathy and Andrew Z. Fenves
CJASN June 2022, 17 (6) 777-778

19. Case 3
Answer: Diuretic Challenge
Convert that Oliguric AKI to a Non-Oliguric AKI!!!
Sepsis-AKI secondary is cytokine-mediated
Why are the other choices incorrect?

20. A positive response to furosemide does not
accelerate recovery of injured tubular cells
But… it may avoid dialysis

21. >10% gain from
admission
associated with
inc. mortality

23. Bottom Line
• iHD (5-6 x per week) vs CRRT
• No difference in mortality
• Post cardiac surgery (ELAIN)
• Early RRT may be of benefit, likely due to better control of volume
• Most cases with AKI Stage 3 … okay to delay dialysis until absolute
indication because prognosis tied to patient’s comorbidities

24. 1. Acute Kidney Injury Stage 3 secondary to acute tubular injury from sepsis.
Improving multi-organ failure.
Severity: sCr 1.1 to 3.9 over 5 days; oliguric in past 24h
Tests: bladder scan daily; no additional tests needed
Volume: >10% gain since admission; 70 mg Furosemide IV now. Assess urine output in
2 hours. Target net negative balance and MAP > 65 mm
Electrolyte/Acid-Base: Metabolic acidosis, improving; hyperK – reassess with AM lab
or this PM if oliguric
Dialysis / Access: None. Recommend temporary catheter and initiate HD today if no
response to diuretic
Medications: I have reviewed all medications. Vanc trough before next dose
BP: Hold Ace-I until ATI resolves

25. Case 4
Answer: Acute Interstitial Nephritis (70% are drug-induced)
Why are the other choices incorrect?

26. MECHANISM OF INJURY
PATHOGENESIS of AIN
1
2
3

27. Case 5
Answer: Decompression if > 25 mm Hg
Hepatorenal physiology vs syndrome
Albumin + vasoconstriction x 2 weeks

30. Pre-renal AKI / AKD
A pre-renal cause of elevated sCr does not mean
volume contraction
THINK: WHAT IS THE EFFECTIVE ARTERIAL BLOOD VOLUME?
You may or may not need to volume expand the patient

31. Case 6
Answer: Obstruction… perc neph!
Discuss with IR and Urology