Prerenal Causes (↓ Renal Perfusion)

Intrinsic / Renal Causes (Parenchymal Damage)

Postrenal Causes (Urinary Obstruction)

Hypovolemia – hemorrhage, dehydration, burns, third spacing (pancreatitis, bowel obstruction)

Acute Tubular Necrosis (ATN) – ischemic (shock, sepsis), nephrotoxic (aminoglycosides, contrast, amphotericin)

Bilateral ureteric obstruction– stones, malignancy, retroperitoneal fibrosis

Cardiogenic shock / Heart failure

Acute Interstitial Nephritis (AIN) – drugs (β-lactams, NSAIDs, PPIs), infections

Bladder outlet obstruction – BPH, urethral stricture

Septic shock (early phase)

Glomerulonephritis – post-infectious, IgA, lupus nephritis

Neurogenic bladder

Anaphylaxis

Vasculitis – ANCA-associated, anti-GBM

Prostate carcinoma

Cirrhosis → Hepatorenal syndrome

Thrombotic microangiopathy – HUS, TTP

Clot retention

Renal artery stenosis

Malignant hypertension

Posterior urethral valves (children)

Overdiuresis

Rhabdomyolysis (myoglobin ATN)

Pelvic tumors compressing ureters

ACE inhibitors in bilateral RAS

Contrast-induced nephropathy

Urethral calculi

Parameter

Prerenal

Logic / Reason

BUN:Cr ratio

>20:1

↓ Renal perfusion → ↑ proximal tubular water reabsorption → passive ↑ urea reabsorption. Creatinine is not reabsorbed → BUN rises disproportionately.

Urine sodium

<20 mEq/L

RAAS + sympathetic activation → ↑ sodium reabsorption in proximal tubule & collecting duct → kidney conserves sodium to restore volume.

FeNa

<1%

Intact tubular function → kidneys avidly retain sodium in response to hypoperfusion → very low fractional excretion.

Urine osmolality

>500 mOsm/kg

ADH release due to hypovolemia → maximal water reabsorption → highly concentrated urine. Tubules intact → good concentrating ability.

Urine specific gravity

>1.020

Concentrated urine due to ADH-mediated water retention → increased solute density. Reflects preserved tubular concentrating function.

Urine sediment

Bland

No structural tubular damage → no casts, no cells. Purely hemodynamic problem, not parenchymal injury.

Parameter

Intrinsic

Logic / Reason

BUN:Cr

10–15:1

Tubular damage → impaired reabsorption of urea. Creatinine and urea both accumulate proportionately → ratio remains normal or mildly elevated.

Urine sodium

>40 mEq/L

Damaged tubules cannot reabsorb sodium effectively → sodium wasting → higher urinary sodium concentration.

FeNa

>2%

Loss of tubular integrity → impaired sodium reabsorption → increased fractional excretion of sodium.

Urine osmolality

<350

Tubular concentrating mechanism impaired → inability to respond properly to ADH → dilute urine despite renal dysfunction.

Urine sediment

Muddy brown casts (ATN)

Tubular epithelial necrosis → sloughing of cells into lumen → granular “muddy brown” casts formed from necrotic debris.

Ratio

Interpretation

>20:1

Prerenal

10–15:1

Intrinsic

Variable

Postrenal

Very high (>30)

GI bleed, steroids, high protein