Creatinine Calculator

FeNa is the percentage of filtered sodium that is excreted in the urine. It helps differentiate prerenal azotemia from intrinsic acute kidney injury (ATN). Formula: FeNa = (UNa × PCr) / (PNa × UCr) × 100.

Normal FeNa in a euvolemic patient with normal kidney function is approximately 0.5–1%. Values < 1% suggest prerenal causes, while > 2% suggest intrinsic renal failure.

FeNa(%) = (Urine Sodium × Plasma Creatinine) / (Plasma Sodium × Urine Creatinine) × 100. Both sodium and creatinine must be in consistent units.

FeNa < 1% indicates prerenal azotemia. The kidneys are avidly retaining sodium in response to decreased effective circulating volume (dehydration, heart failure, cirrhosis).

FeNa > 2% suggests intrinsic renal failure, most commonly acute tubular necrosis (ATN). The damaged tubules lose the ability to reabsorb sodium appropriately.

FeNa in the 1–2% range is indeterminate. It can be seen in both prerenal and intrinsic causes. Clinical correlation and additional tests (FeUrea, urine microscopy) are needed.

FeUrea is the percentage of filtered urea that is excreted in the urine. It is more reliable than FeNa in patients receiving diuretics. Formula: FeUrea = (UUN × PCr) / (PUN × UCr) × 100.

FeUrea is less affected by diuretics than FeNa. Loop diuretics increase sodium excretion, falsely elevating FeNa. Urea handling is not directly affected by diuretics, making FeUrea more reliable in these patients.

Normal FeUrea is approximately 50–65% in healthy individuals. In AKI, FeUrea < 35% suggests prerenal cause, while > 50% suggests intrinsic ATN.

AKI is a sudden decrease in kidney function over hours to days, resulting in accumulation of waste products (creatinine, BUN) and electrolyte abnormalities. It is classified by severity using KDIGO criteria.

Prerenal AKI results from decreased renal perfusion. Causes include hypovolemia (dehydration, hemorrhage, burns), reduced cardiac output (heart failure, MI), systemic vasodilation (sepsis, anaphylaxis), and renal vasoconstriction (NSAIDs, ACE inhibitors).

Intrinsic AKI involves damage to the renal parenchyma. Causes include ATN (ischemic, nephrotoxic), acute interstitial nephritis (drug-induced, infection), glomerulonephritis, and vascular causes (vasculitis, HUS).

ATN is the most common cause of intrinsic AKI. It involves necrosis of tubular epithelial cells due to ischemia or nephrotoxins (aminoglycosides, contrast dye, rhabdomyolysis). Urine sediment shows muddy brown granular casts.

KDIGO staging: Stage 1: Cr 1.5–1.9× baseline or urine output < 0.5 mL/kg/hr for 6–12h. Stage 2: Cr 2.0–2.9× baseline or urine output < 0.5 mL/kg/hr for ≥12h. Stage 3: Cr > 3× baseline or Cr ≥ 4 mg/dL or RRT initiation.

The BUN/Cr ratio is the ratio of blood urea nitrogen to serum creatinine. Normal ratio is 10:1 to 20:1. Ratio > 20:1 suggests prerenal azotemia due to increased urea reabsorption. Ratio < 10:1 can be seen in liver disease or malnutrition.

Postrenal AKI is caused by obstruction of the urinary tract (bladder outlet, ureters). Common causes include BPH, prostate cancer, nephrolithiasis, and retroperitoneal fibrosis. Relief of obstruction typically reverses the AKI.

FeNa is less reliable in CKD because the kidneys have impaired concentrating ability. In CKD, FeNa may be > 1% even without AKI. Clinical context and comparison to baseline are essential.

Urine microscopy helps differentiate causes of AKI. Muddy brown granular casts and renal tubular epithelial cells suggest ATN. White cell casts suggest interstitial nephritis. Red cell casts suggest glomerulonephritis.

Common nephrotoxins include aminoglycosides, vancomycin, amphotericin B, contrast dye, NSAIDs, ACE inhibitors/ARBs, cisplatin, ifosfamide, tenofovir, and myoglobin (rhabdomyolysis).

Rhabdomyolysis releases myoglobin from damaged muscle cells. Myoglobin is nephrotoxic and causes tubular obstruction, direct cytotoxicity, and renal vasoconstriction. Treatment includes aggressive IV fluids and alkalinization of urine.

CIN is AKI occurring within 48–72 hours of intravascular contrast administration. Risk factors include CKD, diabetes, dehydration, older age, and high contrast volume. Prevention includes hydration and minimizing contrast dose.

Management includes identifying and treating the underlying cause, optimizing hemodynamics, avoiding nephrotoxins, adjusting medication doses, maintaining fluid and electrolyte balance, and initiating RRT if indicated (severe hyperkalemia, acidosis, volume overload, uremia).

AEIOU: A — Acidosis (severe metabolic), E — Electrolytes (refractory hyperkalemia), I — Intoxications (methanol, ethylene glycol, lithium), O — Overload (volume overload unresponsive to diuretics), U — Uremia (pericarditis, encephalopathy).

Loop diuretics inhibit Na-K-2Cl cotransport in the loop of Henle, increasing sodium excretion and falsely elevating FeNa. Urea excretion is not directly affected by diuretics, so FeUrea remains reliable in patients on diuretics.

Yes. FeNa can be < 1% in some intrinsic renal diseases such as acute glomerulonephritis, vasculitis, and acute interstitial nephritis (early stage) because the tubules can still reabsorb sodium.

FeNa has approximately 85–90% sensitivity and 80–85% specificity for differentiating prerenal from intrinsic AKI. FeUrea has similar sensitivity but better specificity in patients on diuretics.

A random (spot) urine sample is sufficient for FeNa calculation. Both urine sodium and urine creatinine are measured from the same sample, paired with a simultaneous plasma sample for plasma sodium and creatinine.

Novel biomarkers like NGAL (neutrophil gelatinase-associated lipocalin), KIM-1 (kidney injury molecule-1), and L-FABP (liver-type fatty acid-binding protein) allow earlier detection of AKI (within hours) compared to creatinine (24–48h delay).

AIN is an inflammatory condition of the renal interstitium, most commonly caused by drug hypersensitivity (penicillins, cephalosporins, NSAIDs, PPIs, allopurinol). Urine shows white cell casts and eosinophiluria.

In CKD, FeNa > 1% may be normal due to reduced tubular function. In AKI, FeNa is used dynamically to distinguish prerenal from intrinsic causes. Always compare to recent or baseline values.