Acute kidney injury — definition & workup

KDIGO: Stage 1 Cr ↑0.3 in 48 h or 1.5–1.9×; Stage 2 2–2.9×; Stage 3 3×, Cr ≥4, or RRT. Also UOP criteria.

Anishaa Sivakumar5 min6 questions1 trials

Defining AKI

Serum creatinine only approximates GFR at steady state. While Cr is still climbing you cannot trust the eGFR equation: if ΔCr >1 mg/dL/day, assume GFR <10. If the patient is anuric, assume GFR is 0 for dosing.

KDIGO AKI stages (2012)

Stage 1
Mild bump, watch UOP
Cr ↑ ≥0.3 mg/dL within 48 h, or 1.5–1.9× baseline within 7 days. UOP <0.5 mL/kg/h for ≥6 h.
Stage 2
Double-ish
Cr 2.0–2.9× baseline. UOP <0.5 mL/kg/h for ≥12 h.
Stage 3
Failure / RRT
Cr 3× baseline, Cr ≥4, ↓eGFR to <35 if <18 yo, or RRT. UOP <0.3 mL/kg/h for ≥24 h or anuria ≥12 h.

. Stage by whichever criterion is worse — creatinine or urine output.

KDIGO 2012 Guidelines.

Stage	Serum creatinine	Urine output
1	↑ ≥0.3 mg/dL within 48 h, or 1.5–1.9× baseline within 7 days	<0.5 mL/kg/h for ≥6 h
2	2–2.9× baseline	<0.5 mL/kg/h for ≥12 h
3	3× baseline, Cr ≥4, ↓eGFR to <35 (<18 yo), or RRT	<0.3 mL/kg/h for ≥24 h or anuria ≥12 h

Drugs can impair Cr excretion without ΔGFR (BUN stays stable): trimethoprim (Bactrim), H2 blockers (cimetidine), dronedarone.
↑BUN out of proportion to Cr: pre-renal, post-renal, UGIB, steroids.
↑Cr out of proportion to BUN: rhabdomyolysis, AIN, TMP-SMX, vancomycin, malnutrition.

Stepwise workup

Eight moves, in order

1
History and exam
Vitals for HTN/hypotension, volume status, exposures (contrast, meds), recent infection (IgA 1–2 days after URI; post-strep GN 10–14 days), active infection (sepsis can induce ATN independent of BP or ↓RBF — ), trauma/myalgias/found-down (rhabdomyolysis), rashes (AIN, vasculitis), B symptoms (tumor lysis: BMP, phos, uric acid).
2
Urinalysis
If AKI plus unexplained blood and protein, think GN and call renal.
3
Urine chemistries
FENa, FEUrea, Uosm, urine protein, urine creatinine. See the table below — these numbers only help if you know when they lie.
4
Urine sediment
Casts and RBC morphology. Muddy-brown = ATN. Dysmorphic RBCs / RBC casts = glomerular.
5
Skip urine eos
Eosinophiluria is a terrible AIN test. Urine eos >1% has Sn 31%, Sp 68% (). Do not use it to rule AIN in or out.
6
Renal ultrasound
Exclude hydronephrosis; often preceded by a bedside bladder scan. Without a suggestive history, <1% of renal US for AKI shows a post-renal cause; it can still show chronicity if no known CKD ().
7
Monitor the trajectory
Cr, UOP, BP, electrolytes — and whether your empiric treatment of the presumed cause is working.
8
Serologies / biopsy
If sediment or history suggests glomerular disease. Biopsy if it will change treatment.

FENa vs FEUrea is the only urine-chem pair most night-float calls actually need.

Test	Prerenal	ATN / other	When it lies
FENa	<1% (oliguric, off diuretics)	>2% c/w ATN	Only verified in oliguric AKI. Useless on diuretics or after IVF. Interpret with caution in CKD or chronic prerenal states (CHF/cirrhosis). GN, rhabdo, and IV contrast can all give FENa <1%. Limited use in hospital except to rule out HRS with ↑FENa ().
FEUrea	<35% c/w prerenal ()	Higher values argue against prerenal physiology	Use when the patient is on diuretics and pretest probability of prerenal physiology is high. Loops raise FENa; they do not wreck FEUrea the same way.
Uosm	>500 (high-ADH state)	Isosthenuria ~300 in ATN	CKD blunts concentrating ability.
Urine protein	Usually modest	APR >0.4 → glomerular > tubulointerstitial (Sn 88%, Sp 99%) (Nephro Dial Trans 2012;27:1534)	If proteinuria on UA: send serum albumin, urine total protein, urine microalbumin, and urine Cr. Low/high muscle mass will over/underestimate spot ratios.
Urine creatinine	—	12- or 24-hour collection to estimate CrCl in dynamic AKI	eGFR equations assume steady state.

FENa

FENa = (UNa/PNa) ÷ (UCr/PCr) × 100.
<1% prerenal if oliguric and off diuretics.
>2% ATN.
Do not use on loops, after IVF, in CKD, GN, rhabdo, or contrast.

FEUrea

FEUrea = (UUrea/PUrea) ÷ (UCr/PCr) × 100.
<35% prerenal even on diuretics ().
The hospital test when FENa is uninterpretable.
Still not gospel in CKD or chronic cardiorenal/hepatorenal physiology.

Pre-renal · intrinsic · post-renal

Pre-renal

↓ Absolute volume: bleeding, GI or skin loss, diuretics, osmotic diuresis, cerebral salt wasting.
↓ Effective volume: CHF/cardiorenal, cirrhosis/hepatorenal, nephrotic syndrome, sepsis/third-spacing.
Δ renal dynamics: NSAIDs/COX-2s, ACE inhibitors/ARBs, abdominal compartment syndrome.
Relative hypotension.

Intrinsic

Glomerular: anti-GBM, ANCA (MPA, GPA, EGPA, drug-induced), immune-complex.
Tubulo-interstitial: ATN, AIN, crystals, proteins.
Vascular: TTP/HUS, APLAS, HELLP/eclampsia, scleroderma, CNI/gemcitabine; RAS, dissection, renal artery/vein thrombosis, PAN.

Post-renal

Urinary retention: BPH, meds, neurogenic bladder, Foley dysfunction.
Bilateral obstruction (or obstruction of a single/transplant kidney): stones, malignancy, retroperitoneal fibrosis (radiation or IgG4), congenital anomalies.

Intrinsic bucket	Entities
Glomerular — ANCA / anti-GBM	Anti-GBM. ANCA: microscopic polyangiitis, granulomatosis with polyangiitis (GPA), eosinophilic GPA, drug-induced ANCA.
Glomerular — immune complex, low complement	PSGN, SLE, cryoglobulinemia, MPGN, MGRS.
Glomerular — immune complex, normal complement	IgA nephropathy / HSP, fibrillary, immunotactoid.
ATN	Ischemia, sepsis, toxic. Contrast, rhabdomyolysis, aminoglycosides.
AIN	Meds (NSAIDs, β-lactams, PPIs most commonly). Infectious: CMV, leptospirosis, legionella, pyelonephritis. Autoimmune/infiltrative: TINU, IgG4 disease, sarcoid, Sjögren, CLL.
Crystals	TLS (uric acid), acyclovir, sulfa antibiotics, MTX, ciprofloxacin, ethylene glycol, oxalate, bile acids.
Proteins	Myeloma, amyloid, Ig deposition, myoglobin, bilirubin.
Microvascular	TTP/HUS, APLAS, HELLP/eclampsia, scleroderma, meds (calcineurin inhibitor, gemcitabine).
Macrovascular	RAS (athero, FMD), dissection, renal artery/vein thrombosis, polyarteritis nodosa.