Step 2 CK · Internal Medicine · Nephrology

Acute Kidney Injury

Name: Acute Kidney Injury
Creator: Veli Bakalov, MD

Localize it, read the sediment, protect the nephrons

Nephrology·Acute Kidney Injury & Renal Diagnostics·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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AKI (KDIGO): creatinine up ≥0.3 mg/dL within 48 h, or ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for 6 h.
Prerenal (most common): BUN:Cr >20, urine Na <20, FENa <1%, urine osm >500, bland or hyaline sediment → isotonic IV fluids.
On diuretics, FENa is unreliable: use FEurea (<35% = prerenal).
ATN (most common intrinsic, ischemic or nephrotoxic): FENa >2%, urine osm ~300, muddy brown granular casts; the oliguric maintenance phase is the hyperkalemia danger window.
AIN: NSAIDs, PPIs, β-lactams, sulfonamides, allopurinol → fever, rash, eosinophilia (often absent), sterile pyuria, WBC casts → stop the drug, steroids if severe.
Contrast-associated AKI: creatinine rises at 24–48 h, peaks at 3–5 days, low FENa; prevent with periprocedural isotonic saline.
Postrenal AKI needs bilateral obstruction (or a solitary kidney): bladder catheter plus renal ultrasound; watch for postobstructive diuresis.
Casts: muddy brown = ATN, WBC = AIN/pyelonephritis, RBC = glomerulonephritis, fatty = nephrotic, broad waxy = advanced CKD.
Urgent dialysis (AEIOU): refractory Acidosis, Electrolytes (hyperkalemia), Intoxication (salicylate, lithium, methanol, ethylene glycol), Overload, Uremia (pericarditis, encephalopathy, bleeding).

Definition and framework

Small bumps count. By KDIGO criteria, AKI is any one of the following. Even small, rapid creatinine changes qualify and predict worse outcomes, and because creatinine lags behind the fall in GFR, the true injury is usually worse than the first value suggests.

≥0.3 mg/dLcreatinine rise within 48 hours

≥1.5×baseline creatinine within 7 days

<0.5 mL/kg/hurine output for 6 hours

Staging. KDIGO stage 1 is 1.5–1.9× baseline (or the 0.3 mg/dL rise), stage 2 is 2.0–2.9×, and stage 3 is ≥3× baseline, a creatinine ≥4.0 mg/dL, or the need for dialysis.

Three buckets. Localize every AKI as prerenal (hypoperfusion, the most common), intrinsic (tubular, interstitial, glomerular, or vascular), or postrenal (obstruction). The category drives urine studies, imaging, and treatment.

PrerenalHypoperfusion; FENa <1%; responds to restoring perfusion.
IntrinsicATN, AIN, glomerulonephritis, vascular disease.
PostrenalObstruction; hydronephrosis on ultrasound.

Localize the AKI

Prerenal azotemia and urine indices

Intact but underperfused. In prerenal azotemia the kidneys are structurally normal but underperfused, so they avidly retain sodium and water. Causes include hypovolemia, heart failure, cirrhosis (including hepatorenal physiology), NSAIDs (afferent constriction), ACE inhibitors (loss of efferent tone), and renal artery stenosis. Isotonic IV fluids reverse the volume-depleted form.

FENa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100. Under 1% indicates prerenal azotemia because the tubules are reabsorbing sodium avidly; over 2% indicates ATN. Diuretics raise FENa, so on diuretics use the fractional excretion of urea instead (FEurea <35% = prerenal).

Prerenal azotemia vs acute tubular necrosis

Index	Prerenal	ATN
BUN:Cr	>20:1	~10–15:1
Urine sodium	<20 mEq/L	>40 mEq/L
FENa	<1%	>2%
Urine osmolality	>500 mOsm/kg (concentrated)	~300 (isosthenuria)
Sediment	Bland or hyaline casts	Muddy brown granular casts

Intrinsic AKI: ATN, AIN, and contrast

Acute tubular necrosis is the most common intrinsic AKI. It is ischemic (prolonged hypoperfusion, sepsis) or nephrotoxic (aminoglycosides, contrast, cisplatin, myoglobin). Treatment is supportive while the tubules regenerate. In rhabdomyolysis, the dipstick is positive for blood but microscopy shows few or no RBCs; aggressive IV fluids are protective.

InitiationThe ischemic or toxic insult.
Maintenance (oliguric)Lasts 1–3 weeks; hyperkalemia, acidosis, and uremia threaten. This is the danger window for fatal hyperkalemia.
Recovery (polyuric)Brisk diuresis risks hypokalemia and volume depletion.

Phases of ATN: watch potassium throughout

Three intrinsic patterns

Feature	ATN	Acute interstitial nephritis	Contrast-associated AKI
Trigger	Hypoperfusion, sepsis, aminoglycosides, cisplatin, myoglobin	Hypersensitivity to NSAIDs, PPIs, β-lactams, sulfonamides, allopurinol	Iodinated contrast
Clues	FENa >2%, isosthenuria	Fever, rash, arthralgia, peripheral eosinophilia	Creatinine rises at 24–48 h, peaks at 3–5 days, resolves in 1–2 weeks
Urine	Muddy brown granular casts	Sterile pyuria, WBC casts; urine eosinophils are unreliable and not recommended as a test	Often a low FENa
Management	Supportive care	Stop the drug; steroids if severe	Prevent: IV isotonic saline, least contrast, hold nephrotoxins

The fever-rash-eosinophilia triad appears in only a minority of AIN cases, so its absence does not exclude AIN; NSAID-related AIN is especially likely to lack it. Biopsy is definitive when the diagnosis is uncertain.

Contrast prevention. Periprocedural isotonic saline is the mainstay; sodium bicarbonate and N-acetylcysteine add no benefit over saline.

Glomerular and vascular causes. Glomerulonephritis announces itself with RBC casts, proteinuria, and hypertension and calls for serologies and often biopsy. Vascular causes include cholesterol atheroemboli after catheterization (livedo reticularis, eosinophilia, low complement) and thrombotic microangiopathy (schistocytes, thrombocytopenia).

Postrenal AKI and the urine sediment

Both sides must be blocked. Postrenal AKI requires bilateral obstruction, or unilateral obstruction of a solitary kidney: BPH, pelvic malignancy, bilateral stones, neurogenic bladder, retroperitoneal fibrosis. A bladder catheter is both diagnostic and therapeutic for outlet obstruction, and renal ultrasound shows hydronephrosis. Relieving the obstruction can trigger a postobstructive diuresis, so monitor volume and electrolytes.

Urine microscopy localizes the lesion

Finding	Points to
Hyaline casts	Prerenal state or normal urine
Muddy brown granular casts	Acute tubular necrosis
WBC casts	Acute interstitial nephritis or pyelonephritis
RBC casts	Glomerulonephritis or vasculitis
Fatty casts, Maltese crosses	Nephrotic syndrome
Broad waxy casts	Advanced CKD

Management and dialysis

Fix the cause, stop the toxins. Treat the underlying cause, restore euvolemia, and stop or dose-adjust nephrotoxins (NSAIDs, aminoglycosides, contrast, and ACE inhibitors or ARBs as appropriate). Monitor potassium and acid-base status closely. Loop diuretics relieve volume overload and may convert oliguric to nonoliguric AKI, but they do not speed renal recovery or improve survival.

Hyperkalemia with ECG changes. Give IV calcium to stabilize the myocardium, shift potassium into cells with insulin plus glucose and albuterol, then remove it with binders, loop diuretics, or dialysis.

Urgent dialysis (AEIOU). Indications are refractory complications, not a number alone:

Acidosis refractory to medical therapy
Electrolytes: refractory hyperkalemia
Intoxication with a dialyzable toxin (salicylate, lithium, methanol, ethylene glycol)
Overload of fluid refractory to diuretics
Uremia: pericarditis, encephalopathy, or bleeding

An isolated BUN, creatinine, or oliguria without a refractory complication is not by itself an indication for urgent dialysis.