AKI

AKI Phenotype Calculator

Calculates KDIGO stage, urine output, FeNa, FeUrea, BUN/Cr ratio, and the most likely AKI pattern using labs and clinical context.

Core Inputs

Serum + Urine Studies

Clinical Context

Advanced inputs

Electrolytes / Dialysis Flags

AKI can be oliguric or non-oliguric.

Oliguric AKI: urine output <0.5 mL/kg/hr
Isolated oliguria: low urine output with stable creatinine
Non-oliguric AKI: elevated creatinine with preserved urine output

KDIGO Criteria

AKI is defined by any of the following:

  • Increase in serum creatinine by ≥0.3 mg/dL within 48 hr
  • Increase in serum creatinine to ≥1.5x baseline within 7 days
  • Urine output <0.5 mL/kg/hr for 6 hr

AKI Staging

Stage 1 AKI

  • Cr 1.5-1.9x baseline
  • Cr increase ≥0.3 mg/dL
  • Urine output <0.5 mL/kg/hr for 6-12 hr

Stage 2 AKI

  • Cr 2.0-2.9x baseline
  • Urine output <0.5 mL/kg/hr for ≥12 hr

Stage 3 AKI

  • Cr ≥3x baseline
  • Cr ≥4.0 mg/dL
  • Initiation of dialysis/RRT
  • Urine output <0.3 mL/kg/hr for ≥24 hr
  • Anuria ≥12 hr

Initial Approach

First decide whether this is true AKI, isolated oliguria, or a pseudo-creatinine rise.

Review:

  • Baseline Cr
  • Timing of Cr rise
  • Urine output trend
  • Hemodynamics
  • Volume status
  • Recent hypotension, sepsis, surgery, contrast, or nephrotoxins
  • Medication list
  • UA and urine sediment

Pseudo-AKI or non-GFR creatinine rise can occur with:

  • Trimethoprim
  • Cimetidine
  • Dolutegravir/cobicistat
  • Creatine supplementation
  • High meat intake
  • Lab variation

Initial Workup

Basic labs:

  • BMP
  • Mg, Phos, Ca
  • CBC
  • UA with microscopy
  • CK if rhabdo possible

Imaging:

  • Bladder scan if oliguria/anuria
  • Renal/bladder ultrasound if obstruction possible, severe AKI, solitary kidney, transplant kidney, unclear cause, or no improvement

Additional workup if clinically indicated:

  • Urine protein/Cr if proteinuria
  • Urine Na, Cr, urea if volume status unclear
  • LDH, haptoglobin, smear if TMA/hemolysis concern
  • ANA, ANCA, anti-GBM, complements, hepatitis/HIV testing if nephritic picture
  • SPEP/UPEP/free light chains if myeloma concern

Causes of AKI

Pre-renal / Low Effective Arterial Blood Volume

The kidney is structurally intact but underperfused.

Common causes:

  • Hypovolemia
  • Sepsis
  • Hemorrhage
  • Overdiuresis
  • Poor PO intake
  • Cardiogenic shock
  • Hepatorenal physiology
  • Nephrotic syndrome
  • Severe venous congestion/cardiorenal syndrome

Intrinsic Renal

Kidney parenchymal injury.

Common causes:

  • ATN from ischemia, sepsis, or shock
  • ATN from nephrotoxins
  • AIN
  • Glomerulonephritis
  • TMA
  • Pigment nephropathy from rhabdo or hemolysis
  • Tumor lysis syndrome
  • Myeloma cast nephropathy

Common nephrotoxins:

  • NSAIDs
  • ACEi/ARB in the wrong context
  • Vancomycin
  • Aminoglycosides
  • Amphotericin
  • Acyclovir/valacyclovir
  • TMP-SMX
  • IV contrast
  • Cisplatin and other chemo agents
  • Calcineurin inhibitors
  • PPIs, beta-lactams, and NSAIDs as AIN triggers

Post-renal

Obstruction until proven otherwise.

Common causes:

  • BPH
  • Occluded or malpositioned foley
  • Nephrolithiasis
  • Pelvic/retroperitoneal malignancy
  • Neurogenic bladder
  • Urethral stricture
  • Bilateral ureteral obstruction
  • Solitary kidney obstruction

In oliguria/anuria, first check the foley, bladder scan, and evaluate for obstruction.

UA Clues

Bland UA, hyaline casts: pre-renal, cardiorenal, hepatorenal
Muddy brown granular casts: ATN
WBCs/WBC casts: AIN, pyelo, GN
RBC casts/dysmorphic RBCs: glomerulonephritis
Heavy proteinuria: glomerular disease, nephrotic syndrome
Heme positive with few RBCs: rhabdo or hemolysis
Crystals: stones, uric acid, acyclovir, ethylene glycol, TLS

Urine Electrolyte Calculators

Separate FeNa and FeUrea calculators for AKI evaluation.

FeNa Calculator

FeNa = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100

Reliability Flags

FeUrea Calculator

FeUrea = (Urine Urea × Serum Cr) / (Serum Urea/BUN × Urine Cr) × 100

Reliability Flags

FeNa

FeNa can support the diagnosis, but it should not be used alone to classify AKI.

Formula:

FeNa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100

Traditional interpretation:

  • FeNa <1%: suggests pre-renal physiology
  • FeNa >2%: suggests intrinsic renal injury

FeNa is most useful in oliguric patients who are not on diuretics and do not have CKD, sepsis, contrast injury, rhabdo, GN, or obstruction.

FeUrea

FeUrea was historically taught as more useful than FeNa in patients taking diuretics.

Formula:

FeUrea = (Urine Urea × Plasma Cr) / (Plasma Urea × Urine Cr) × 100

Traditional interpretation:

  • FeUrea <35%: suggests pre-renal physiology
  • FeUrea >50%: suggests intrinsic renal injury

Approach to Oliguria

Oliguria = urine output <0.5 mL/kg/hr.

1. Confirm it is real

  • Check I/O accuracy
  • Check foley position
  • Flush or replace foley if needed
  • Bladder scan

2. Exclude obstruction

  • Bladder scan
  • Renal/bladder ultrasound if persistent, severe, or unexplained

3. Assess perfusion

Review:

  • MAP trend
  • Shock/sepsis
  • Bleeding
  • Recent diuresis
  • Poor PO intake
  • Cardiac function
  • Venous congestion
  • Abdominal compartment physiology

4. Decide if fluid helps or hurts

Give fluid only if hypovolemic or fluid responsive.

Avoid blind fluid boluses in patients with CHF, cirrhosis, ESRD, pulmonary edema, or obvious congestion.

5. If hypotensive

  • Target MAP ≥65 mmHg for most patients
  • Consider higher MAP target in chronic severe HTN
  • Use pressors instead of repeated fluids if not fluid responsive

6. If congested

  • Diurese if volume overloaded
  • Escalate early if diuretic resistant, worsening hypoxia, worsening acidosis, or refractory electrolyte abnormalities

Furosemide Stress Test

Use only if the patient is euvolemic or hypervolemic and does not already clearly need dialysis.

Dose:

  • Loop-naive: furosemide 1 mg/kg IV
  • Prior loop exposure: furosemide 1.5 mg/kg IV

Interpretation:

  • Urine output >200 mL in 2 hr: lower risk of progression
  • Urine output <200 mL in 2 hr: higher risk of progression to severe AKI/RRT

Treatment

There is no specific AKI medication. Treat the cause and prevent secondary injury.

Hemodynamics

  • Maintain renal perfusion
  • Avoid hypotension
  • Avoid unnecessary fluid overload
  • Treat shock early
  • Decongest if cardiorenal/venous congestion physiology

Medication Management

Hold or reduce:

  • NSAIDs
  • ACEi/ARB if hypotensive, hyperkalemic, or rapidly worsening AKI
  • SGLT2 inhibitors during acute illness
  • Metformin in significant AKI
  • Diuretics if hypovolemic
  • Nephrotoxic antibiotics if alternatives exist
  • Renally dose all medications

Volume Management

Hypovolemic:

  • Use balanced crystalloid such as LR or Plasma-Lyte
  • Consider isotonic bicarbonate if significant metabolic acidosis

Euvolemic:

  • Avoid maintenance fluid creep
  • Match intake to clinical need

Hypervolemic:

  • Sodium restriction
  • Loop diuretics if responsive
  • Add thiazide-type diuretic if loop resistant
  • Dialysis/UF if refractory pulmonary edema or severe volume overload

Electrolytes and Acidosis

Monitor:

  • K
  • Bicarb/pH
  • Phos
  • Ca
  • Mg

Hyperkalemia management:

  • Calcium if ECG changes or severe hyperkalemia
  • Insulin/dextrose
  • Albuterol
  • Bicarbonate if acidemic
  • Potassium binder if appropriate
  • Diuresis if making urine
  • Dialysis if refractory or severe

For severe metabolic acidosis, consider bicarbonate if not immediately dialyzing.

Common strategy:

  • D5W + 150 mEq sodium bicarbonate/L
  • Target pH >7.2 rather than normalizing bicarbonate

Watch for hypernatremia, hypocalcemia, volume overload, and CO2 generation.

Hyperphosphatemia

Treat the underlying AKI and restrict phosphate if severe.

Consider phosphate binders if persistent/severe hyperphosphatemia, especially in advanced AKI/CKD or dialysis-level renal failure.

Options:

  • Calcium acetate 1334 mg PO TID with meals
  • Sevelamer 800 mg PO TID with meals

Avoid calcium-based binders if hypercalcemic.

Dialysis Indications

A: Acidosis
Severe or refractory metabolic acidosis

E: Electrolytes
Severe or refractory hyperkalemia

I: Intoxications
Dialyzable toxins

O: Overload
Pulmonary edema or volume overload refractory to diuretics

U: Uremia
Encephalopathy, pericarditis, bleeding, seizures, severe symptoms

Dialysis Disequilibrium Syndrome

Dialysis disequilibrium syndrome occurs when very high BUN is reduced too quickly during initial dialysis, causing osmotic shifts and cerebral edema.

Risk factors:

  • Very high BUN
  • First dialysis session
  • Severe uremia
  • Metabolic acidosis
  • CNS disease

Symptoms:

  • Headache
  • Nausea
  • Restlessness
  • Confusion
  • Seizures
  • Cerebral edema in severe cases

Prevention/management:

  • Slower initial dialysis
  • Shorter first session
  • Lower blood flow rate
  • Higher dialysate sodium in selected patients
  • Hypertonic saline or mannitol if severe cerebral edema suspected

References

  1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1–138. https://doi.org/10.1038/kisup.2012.1
  2. Moore, P. K., Hsu, R. K., & Liu, K. D. (2018). Management of acute kidney injury: Core Curriculum 2018. American Journal of Kidney Diseases, 72(1), 136–148. https://doi.org/10.1053/j.ajkd.2017.11.021
  3. Mercado, M. G., Smith, D. K., & Guard, E. L. (2019). Acute kidney injury: Diagnosis and management. American Family Physician, 100(11), 687–694.
  4. Espinel, C. H. (1976). The FeNa test: Use in the differential diagnosis of acute renal failure. JAMA, 236(6), 579–581. https://doi.org/10.1001/jama.1976.03270060029022
  5. Carvounis, C. P., Nisar, S., & Guro-Razuman, S. (2002). Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney International, 62(6), 2223–2229. https://doi.org/10.1046/j.1523-1755.2002.00683.x
  6. Chawla, L. S., Davison, D. L., Brasha-Mitchell, E., Koyner, J. L., Arthur, J. M., Shaw, A. D., Tumlin, J. A., Trevino, S. A., Kimmel, P. L., & Seneff, M. G. (2013). Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Critical Care, 17(5), R207. https://doi.org/10.1186/cc13015
  7. Semler, M. W., Self, W. H., Wanderer, J. P., Ehrenfeld, J. M., Wang, L., Byrne, D. W., Stollings, J. L., Kumar, A. B., Hughes, C. G., Hernandez, A., Guillamondegui, O. D., May, A. K., Weavind, L., Casey, J. D., Siew, E. D., Shaw, A. D., Bernard, G. R., & Rice, T. W. (2018). Balanced crystalloids versus saline in critically ill adults. The New England Journal of Medicine, 378(9), 829–839. https://doi.org/10.1056/NEJMoa1711584
  8. Self, W. H., Semler, M. W., Wanderer, J. P., Wang, L., Byrne, D. W., Collins, S. P., Slovis, C. M., Lindsell, C. J., Ehrenfeld, J. M., Siew, E. D., Shaw, A. D., Bernard, G. R., & Rice, T. W. (2018). Balanced crystalloids versus saline in noncritically ill adults. The New England Journal of Medicine, 378(9), 819–828. https://doi.org/10.1056/NEJMoa1711586
  9. Jaber, S., Paugam, C., Futier, E., Lefrant, J. Y., Lasocki, S., Lescot, T., Pottecher, J., Demoule, A., Ferrandiere, M., Asehnoune, K., Dellamonica, J., Velly, L., Abback, P. S., de Jong, A., Brunot, V., Belafia, F., Roquilly, A., Chanques, G., Muller, L., ... Constantin, J. M. (2018). Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit: A multicentre, open-label, randomised controlled, phase 3 trial. The Lancet, 392(10141), 31–40. https://doi.org/10.1016/S0140-6736(18)31080-8
  10. Perazella, M. A. (2010). Drug-induced acute interstitial nephritis. Nature Reviews Nephrology, 6(8), 461–470. https://doi.org/10.1038/nrneph.2010.71
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