Reference — Renal
Renal Laboratory Values Reference
Key renal lab values for nurses — BUN, creatinine, eGFR, urine specific gravity, urine output, FENa, and electrolytes: normal ranges, elevated and decreased causes, and clinical interpretation notes.
Educational use only. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Reference ranges vary by lab.Always confirm with your institution's reference ranges and clinical context. These values reflect typical adult ranges from common clinical references.
Serum Renal Markers
| Lab Test | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| Blood Urea Nitrogen (BUN) | 7–20 mg/dL | AKI, CKD, prerenal azotemia (dehydration, HF, shock), GI bleeding (hemoglobin catabolized to urea), high-protein diet, corticosteroid use, catabolic states (sepsis, burns) | Liver failure (urea synthesis impaired), malnutrition, overhydration, pregnancy |
| Serum Creatinine | 0.6–1.2 mg/dL (males); 0.5–1.1 mg/dL (females) | AKI, CKD, rhabdomyolysis (muscle creatinine release), high meat diet, medications that block tubular secretion (trimethoprim, cimetidine) | Low muscle mass (elderly, malnutrition, cachexia), pregnancy, amputees |
| BUN:Creatinine Ratio | 10:1 to 20:1 | >20:1 indicates prerenal cause (dehydration, HF, hemorrhage, shock) — kidneys concentrate urine and retain urea. Also elevated in: GI bleeding, high-protein diet, steroids. | <10:1 indicates intrarenal (tubular) damage — damaged tubules cannot reabsorb urea normally. Also low in: liver disease (↓ BUN synthesis), malnutrition. |
| eGFR (Estimated GFR) | ≥60 mL/min/1.73m² (normal kidney function); ≥90 is ideal | Not clinically significant when elevated (may indicate hyperfiltration in early diabetes/obesity) | CKD staging: G3a (45–59), G3b (30–44), G4 (15–29), G5 (<15). Any acute fall in eGFR = AKI until proven otherwise. |
Blood Urea Nitrogen (BUN) — Interpretation note:
BUN is less specific than creatinine for GFR. Elevated BUN with normal creatinine suggests prerenal or extra-renal causes (bleeding, diet, steroids). Always interpret with creatinine.
Serum Creatinine — Interpretation note:
Creatinine is a better marker of GFR than BUN alone. Serum creatinine DOUBLES when GFR decreases by ~50%. Does not rise significantly until 50% of nephron function is lost — early kidney disease may be missed with creatinine alone.
BUN:Creatinine Ratio — Interpretation note:
A BUN:Cr ratio >20:1 is the classic prerenal AKI pattern on NCLEX. The ratio helps differentiate prerenal (volume/perfusion problem) from intrinsic kidney damage.
eGFR (Estimated GFR) — Interpretation note:
eGFR is calculated from creatinine, age, and sex (2021 CKD-EPI equation — race was removed in 2021). Better than creatinine alone. <60 for ≥3 months = CKD definition. Acute fall = AKI.
Urine Studies
| Lab Test | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| Urine Specific Gravity | 1.003–1.030 | >1.030: concentrated urine — fluid volume deficit (dehydration), SIADH, adrenal insufficiency, contrast exposure | <1.003: dilute urine — excessive hydration, diabetes insipidus (unable to concentrate), renal tubular damage (ATN — loses concentrating ability) |
| Urine Output | 0.5–1.0 mL/kg/hr (adults); minimum 30 mL/hr | Polyuria (>3 L/day): diabetes insipidus, hyperglycemia (osmotic diuresis), diuretics, post-obstructive diuresis, recovery phase of ATN | Oliguria (<0.5 mL/kg/hr): prerenal AKI, intrarenal AKI, postrenal obstruction, cardiogenic shock, septic shock. Anuria (<50 mL/day) = severe AKI or bilateral obstruction. |
| Fractional Excretion of Sodium (FENa) | Not applicable — used to differentiate AKI types | >2%: intrarenal AKI (damaged tubules cannot reabsorb sodium — sodium spills into urine). Also elevated in: diuretic use (must be interpreted cautiously), chronic kidney disease. | <1%: prerenal AKI (kidneys maximally conserving sodium — avid reabsorption in tubules) or hepatorenal syndrome |
| Urine Osmolality | 300–900 mOsm/kg (varies with hydration) | >900 mOsm/kg: concentrated urine in dehydration, SIADH. In prerenal AKI: kidneys concentrate urine (>500 mOsm/kg). | <300 mOsm/kg: dilute urine in overhydration, diabetes insipidus, ATN (fixed dilute urine ~300 mOsm/kg — isosthenuric) |
Urine Specific Gravity — Interpretation note:
Urine specific gravity measures urine concentration. Fixed 1.010 (isosthenuria) = severe tubular damage — kidneys can neither concentrate nor dilute urine. This is seen in severe AKI/ATN.
Urine Output — Interpretation note:
Urine output is a real-time kidney perfusion indicator. Monitor hourly in unstable patients. A sudden drop in urine output is an early warning of hemodynamic compromise or AKI.
Fractional Excretion of Sodium (FENa) — Interpretation note:
FENa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100. Requires spot urine sodium and creatinine simultaneously with serum Na and Cr. INVALID if diuretics given (use FEUrea instead).
Urine Osmolality — Interpretation note:
In prerenal AKI: urine osmolality >500 mOsm/kg (kidneys trying to conserve fluid). In intrarenal ATN: urine osmolality ~300 mOsm/kg (isosthenuria — tubular damage prevents concentration).
Electrolytes Affected by Kidney Function
| Lab Test | Normal Range | Elevated Causes | Decreased Causes |
|---|---|---|---|
| Serum Potassium | 3.5–5.0 mEq/L | Hyperkalemia: AKI, CKD (kidneys cannot excrete K⁺), acidosis (H⁺ drives K⁺ out of cells), tissue necrosis, rhabdomyolysis, potassium-sparing diuretics, ACE inhibitors/ARBs | Hypokalemia: loop diuretics (furosemide), vomiting, diarrhea, alkalosis, insufficient intake |
| Serum Phosphorus | 2.5–4.5 mg/dL | Hyperphosphatemia: AKI/CKD (kidneys cannot excrete phosphate), hypoparathyroidism, rhabdomyolysis, excessive intake | Hypophosphatemia: malnutrition, refeeding syndrome, antacid use (binds phosphate), hyperparathyroidism |
| Serum Calcium | 8.5–10.5 mg/dL (total); ionized 4.6–5.3 mg/dL | Hypercalcemia: hyperparathyroidism, malignancy, immobility, thiazide diuretics, excess vitamin D, Paget disease | Hypocalcemia: AKI/CKD (↑ phosphorus binds Ca²⁺; ↓ active vitamin D production), hypoparathyroidism, pancreatitis, hypomagnesemia |
Serum Potassium — Interpretation note:
Hyperkalemia is the most life-threatening complication of AKI/CKD. ECG changes: peaked T waves → widened QRS → sine wave → V-fib. K⁺ >6.0 = emergency. Treat immediately: calcium gluconate, insulin/dextrose, sodium bicarbonate, Kayexalate, dialysis.
Serum Phosphorus — Interpretation note:
In CKD: hyperphosphatemia + hypocalcemia + elevated PTH = renal osteodystrophy. Treat with phosphate binders (calcium acetate, sevelamer) taken WITH meals to bind dietary phosphate.
Serum Calcium — Interpretation note:
In CKD: failing kidneys cannot activate vitamin D → low Ca²⁺ → elevated PTH. Treat with active vitamin D (calcitriol) and calcium supplementation.
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with KDIGO Clinical Practice Guidelines · National Kidney Foundation (NKF). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →