At a Glance

Why It's Ordered
Is kidney function falling (AKI) or chronically reduced (CKD), are K⁺ or acid-base values dangerous now, and is the patient safe for a drug or dialysis decision?
Check First
K⁺, HCO₃⁻ with the anion gap, creatinine (against baseline) and glucose: the four values that change management in minutes.
Critical Values
K⁺ <2.5 or >6.5 mEq/L · Na⁺ <120 or >160 mEq/L · Glucose <40 or >450 mg/dL · Total Ca <6.0 or >13.0 mg/dL · HCO₃⁻ <10 or >40 mEq/L
Don't Miss
Hemolysis or a delayed sample falsely raises K⁺. Repeat it, but treat now if the ECG shows peaked T waves or QRS widening.
Field & Transport
POC: i-STAT CHEM8+ or a glucometer where stocked. Send the last K⁺, creatinine, dialysis date and urine output; repeat K⁺ after shift therapy, per protocol.

Panel Overview

The Renal Panel is the standard kidney-function set: BUN, creatinine, eGFR, sodium, potassium, chloride, bicarbonate, calcium, phosphorus, glucose and albumin. It has 10 measured components. It is the basic metabolic panel (BMP, 8 analytes) plus phosphorus and albumin. It is drawn in ED triage for kidney injury or dialysis, in ICU morning labs, and before transfer. The CMP adds liver tests and total protein to the BMP.

When to Order:
  • Acute kidney injury: rising creatinine, low urine output or nephrotoxin exposure
  • Hyperkalemia or dysrhythmia: weakness, palpitations or ECG change in a patient with kidney disease
  • Acid-base or mental status change: anion gap acidosis or suspected uremia
  • Dialysis: a pre-dialysis check, or a missed or late session
  • Pre-transfer: any patient with known kidney disease before transport or procedure

Electrolytes

Sodium (Na⁺)

Normal: 135–145 mEq/L

Main extracellular cation that sets serum osmolality. Low with diuretics, SIADH, hypovolemia or hyperglycemia; high with dehydration or diabetes insipidus.

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Potassium (K⁺)

Normal: 3.5–5.0 mEq/L

Drives cardiac conduction. Kidney failure, ACE inhibitors, ARBs and acidosis raise it. Hemolysis falsely raises it.

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Chloride (Cl⁻)

Normal: 96–106 mEq/L

Main extracellular anion. Read with Na⁺ and HCO₃⁻; high in normal-gap acidosis from saline loads or diarrhea.

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Total CO₂ (HCO₃⁻)

Normal: 22–29 mEq/L

Main acid-base buffer. Low in metabolic acidosis, including uremic acidosis; high in contraction alkalosis or vomiting.

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Kidney Function

BUN

Normal: 8–23 mg/dL

Urea nitrogen from protein metabolism. High with prerenal states, kidney failure, GI bleeding and high protein intake.

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Creatinine

Normal: M 0.7–1.3 | F 0.6–1.1 mg/dL

Muscle waste product filtered by the kidney. Rise against baseline defines AKI. Low muscle mass hides injury.

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Minerals, Glucose & Albumin

Calcium (total)

Normal: 8.5–10.5 mg/dL

Correct for albumin. Low with CKD, hypoparathyroidism and massive transfusion; high with malignancy or hyperparathyroidism.

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Phosphorus

Normal: 2.5–4.5 mg/dL

Rises as GFR falls. High in advanced CKD and rhabdomyolysis; low with refeeding and some ICU states.

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Glucose

Normal: 70–99 mg/dL (fasting)

Hypoglycemia and hyperglycemia both affect kidney failure and insulin use. Hyperglycemia lowers measured sodium.

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Albumin

Normal: 3.5–5.0 g/dL

Low in inflammation, liver disease and nephrotic protein loss. Lowers total calcium.

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Calculated Values

eGFR

Normal: ≥90 mL/min/1.73 m²

Race-free CKD-EPI 2021 estimate of GFR. Valid only in stable kidney function; use it for CKD staging and drug dosing. In extreme body size, use non-indexed eGFR or the drug label.

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BUN:Cr Ratio

Normal: 10:1 to 20:1

Above 20:1 favors prerenal physiology or GI bleeding. Interpret with urine studies.

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Anion Gap

Normal: 8–12 mEq/L (without K⁺)

Na⁺ − (Cl⁻ + HCO₃⁻). Above 12 mEq/L is a high-gap acidosis, including uremia.

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Reference Ranges & Critical Values
TestAdult Normal (conventional)SI UnitsCritical LowCritical HighNotes
Sodium (Na⁺)
135–145 mEq/L
135–145 mmol/L
<120 mEq/L
>160 mEq/L
Interpret with glucose
Potassium (K⁺)
3.5–5.0 mEq/L
3.5–5.0 mmol/L
<2.5 mEq/L
>6.5 mEq/L
Hemolysis raises it; some labs call at 6.0
Chloride (Cl⁻)
96–106 mEq/L
96–106 mmol/L
—
—
Read with Na⁺ and HCO₃⁻
Total CO₂ (HCO₃⁻)
22–29 mEq/L
22–29 mmol/L
<10 mEq/L
>40 mEq/L
Venous total CO₂; arterial HCO₃⁻ 22–26
BUN
8–23 mg/dL
Urea 2.9–8.2 mmol/L
—
—
Protein load, bleeding and steroids raise it
Creatinine
M 0.7–1.3 | F 0.6–1.1 mg/dL
M 62–115 | F 53–97 µmol/L
—
—
Sex-specific; low muscle mass hides injury
eGFR
≥90 mL/min/1.73 m²
Same
—
—
2021 race-free CKD-EPI; not valid in unstable AKI
Glucose (fasting)
70–99 mg/dL
3.9–5.5 mmol/L
<40 mg/dL
>450 mg/dL
Non-fasting values run higher
Calcium (total)
8.5–10.5 mg/dL
2.1–2.6 mmol/L
<6.0 mg/dL
>13.0 mg/dL
Correct for albumin; check ionized Ca
Phosphorus
2.5–4.5 mg/dL
0.81–1.45 mmol/L
<1.0 mg/dL
—
Rises as GFR falls
Albumin
3.5–5.0 g/dL
35–50 g/L
—
—
Falls in inflammation, liver disease and nephrotic loss
Lab variation: Every lab sets its own reference intervals and critical-value lists, and they shift with the analyzer and assay. Go by your laboratory's reported interval and critical-call policy.

Systematic Interpretation
  1. Sodium and glucose: correct Na⁺ for glucose. Add about 1.6 mEq/L for every 100 mg/dL of glucose above 100 mg/dL (a factor of 2.4 is used by some labs).
  2. Potassium with the ECG: K⁺ above 6.0 mEq/L with an ECG change is a treatment decision now. Don't wait for the repeat result.
  3. Bicarbonate and anion gap: the gap is what separates one acidosis type from another.
  4. BUN, creatinine and eGFR: compare creatinine with the baseline. A BUN:Cr ratio above 20:1 favors prerenal physiology.
  5. Glucose: high glucose can cause pseudohyponatremia. It can also drive an osmotic diuresis.
  6. Calcium and phosphorus: correct total calcium for albumin, and check ionized calcium when the result is unclear.
  7. Urine studies (order with this panel): urine sodium below 20 mEq/L and fractional excretion of sodium (FENa) below 1% suggest prerenal physiology. FENa above 2% suggests tubular injury. Diuretics make FENa unreliable, so use fractional excretion of urea (FEUrea) below 35% instead.
Anion gap
Na⁺ − (Cl⁻ + HCO₃⁻)

Normal is 8–12 mEq/L and depends on the analyzer. The potassium term is left out. Above 12 mEq/L means a high-gap acidosis. Think uremia, lactate, ketones, toxic alcohols and salicylates.

Corrected calcium
Ca + 0.8 × (4.0 − albumin)

Calcium goes in mg/dL and albumin in g/dL. When albumin or acid-base status is abnormal, use ionized calcium instead.

Worked Example: Na⁺ 131 mEq/L, glucose 520 mg/dL, Cl⁻ 92 mEq/L, HCO₃⁻ 16 mEq/L, BUN 78 mg/dL, creatinine 4.6 mg/dL, K⁺ 5.9 mEq/L, total Ca 8.0 mg/dL, albumin 2.5 g/dL. The gap comes first: 131 − (92 + 16) = 23, which is high. Corrected Na⁺ is about 131 + 1.6 × 4.2 = 137.7 mEq/L. The low sodium is mostly glucose. Corrected Ca comes out at 8.0 + 0.8 × (4.0 − 2.5) = 9.2 mg/dL, which is normal. Check uremia (BUN 78, creatinine 4.6) and hyperglycemia-related ketoacidosis first.

Patterns & Differential
PatternKey FindingsCommon CausesNext Step
Prerenal AKI
BUN:Cr above 20:1; urine Na⁺ below 20 mEq/L; bland sediment
Hypovolemia, bleeding, low output; NSAID or ARB with volume loss
Volume assessment; stop nephrotoxins; trend creatinine
Intrinsic AKI (ATN)
Creatinine rise; BUN:Cr about 10–15; muddy-brown casts; FENa above 2%
Ischemia, sepsis, contrast, aminoglycosides, vancomycin with piperacillin-tazobactam
Urine microscopy; nephrology
Postrenal AKI
Anuria or oliguria with a distended bladder or flank pain
Prostate enlargement, stones, obstruction
Bladder scan; renal ultrasound; catheter
Hyperkalemia with AKI or CKD
K⁺ above 5.5 mEq/L; ECG change is variable and can occur at lower K⁺, especially when K⁺ rises quickly
Reduced GFR; ACE inhibitors, ARBs, potassium-sparing diuretics; tissue breakdown
ECG now; see Critical Findings
High-gap metabolic acidosis (uremic)
Anion gap high; BUN and creatinine high
Uremia; phosphate and sulfate retention
Dialysis indications; nephrology
Normal-gap (hyperchloremic) acidosis
Anion gap normal; HCO₃⁻ low; Cl⁻ high
Diarrhea, renal tubular acidosis, large volumes of saline
Check urine anion gap; consider balanced fluid
CKD
eGFR below 60 for more than 3 months
Diabetes, hypertension, glomerular disease
Assign G and A category (below); refer

KDIGO AKI Staging

StageSerum CreatinineUrine Output
1
1.5–1.9× baseline, or rise of 0.3 mg/dL or more within 48 hr
Below 0.5 mL/kg/hr for 6–12 hr
2
2.0–2.9× baseline
Below 0.5 mL/kg/hr for 12 hr or more
3
3.0× baseline, or creatinine 4.0 mg/dL or more with an acute rise of at least 0.3 mg/dL, or dialysis started
Below 0.3 mL/kg/hr for 24 hr, or anuria for 12 hr or more

KDIGO CKD Staging, 2024 Categories

CategoryMeasureRange
G1 to G5
eGFR (mL/min/1.73 m²)
G1 90 or more; G2 60–89; G3a 45–59; G3b 30–44; G4 15–29; G5 below 15
A1 to A3
Albumin-to-creatinine ratio (mg/g)
A1 below 30; A2 30–300; A3 above 300

Serial Testing & Kinetics
AnalyteRises or DetectablePeaksRepeat IntervalMonitoring Target
Creatinine
Lags injury by about 24–72 hr; KDIGO AKI is a rise of 0.3 mg/dL or more within 48 hr, or 1.5 times baseline within 7 days
Varies by cause; use the trend
Per clinical course and protocol
Rise against baseline; urine output
Potassium
Any time with acidosis, tissue breakdown or retained K⁺
Hours after the insult
Repeat after shift therapy, per protocol
Below 5.5 mEq/L; ECG stable
Glucose
After insulin for K⁺ shift
Can fall for hours after insulin
Every hour for several hours, per protocol
Avoid hypoglycemia
BUN
Slower than creatinine; affected by protein and bleeding
—
With each creatinine
Trend with creatinine

Critical Findings & Emergency Actions

Hyperkalemia (K⁺ above 6.0 mEq/L with ECG change, or above 6.5 mEq/L)

Recognize: peaked T waves, PR prolongation, lost P waves, QRS widening, bradycardia or sine wave. Confirm on a non-hemolyzed sample, but do not wait for the repeat when the ECG has changed.

  1. Monitor and stabilize (Paramedic/RN/CCT): continuous cardiac monitoring and 12-lead ECG. Give calcium to protect the myocardium: calcium chloride 1 g (10 mL of 10%) IV over 5–10 min, or calcium gluconate about 3 g (30 mL of 10%). Calcium chloride is a vesicant: use a large, patent vein or central or IO access, confirm placement, and watch the site for extravasation. Calcium gluconate is the safer peripheral option. The effect lasts only about 30–60 min, so repeat the dose if ECG changes persist or recur. In suspected digoxin toxicity, give calcium only with caution and medical direction. Peds: 20 mg/kg (0.2 mL/kg of 10%) IV slowly, max 1 g per dose.
  2. High-alert Shift K⁺ into cells: regular insulin 10 units IV with dextrose 25 g IV (50 mL of D50). Omit or reduce the dextrose if the starting glucose is above 250 mg/dL, per protocol. In kidney failure, low body weight, or a baseline glucose below 100 mg/dL, consider 5 units or add a dextrose infusion, because hypoglycemia risk is high. Peds: 0.1 units/kg IV (max 10 units) with dextrose 0.5 g/kg. Check glucose hourly for 4–6 hr after dosing.
  3. Bicarbonate when acidemic: sodium bicarbonate 50 mEq IV only if acidemic on blood gas and per protocol. Peds: 1 mEq/kg IV (max 50 mEq).
  4. Adjunct (off-label): nebulized albuterol 10–20 mg shifts K⁺ into cells, preferably with insulin-glucose (10 mg in ischemic heart disease, per the albuterol page).
  5. Remove K⁺: stop potassium-raising drugs and potassium-containing fluids. Loop diuretics help only when the patient makes urine. In hospital, potassium binders (sodium zirconium cyclosilicate or patiromer) are a slower option. Arrange urgent dialysis for refractory K⁺, oliguria, or ongoing tissue breakdown.

Severe hyponatremia with seizures or severe symptoms

Recognize: Na⁺ below 120 mEq/L with seizure, coma or vomiting. Confirm true hypotonic hyponatremia: check glucose and measured osmolality.

  1. High-alert 3% saline bolus: hypertonic saline 3% 100 mL IV over 10 min (US expert panel) or 150 mL over 20 min (European guideline), per protocol, repeated to raise Na⁺ by 4–6 mEq/L. Peds: 2 mL/kg IV over 10 min, max 100 mL.
  2. Correction limit: limit the rise to 10 mEq/L in the first 24 hr and 8 mEq/L per 24 hr afterward. A high-risk patient (malnutrition, alcoholism, liver disease, hypokalemia) should target 4–6 mEq/L, with an absolute limit of 8. Check Na⁺ every 1–2 hr during bolus therapy, then every 2–4 hr.
  3. Overcorrection: if Na⁺ rises faster than the limit, stop hypertonic saline and call medical direction or nephrology. A hospital team may lower Na⁺ again with D5W and/or desmopressin when urine output is brisk.

Hypoglycemia (glucose below 70 mg/dL with symptoms, or below 54 mg/dL)

Recognize: altered mental status, diaphoresis or seizure in a patient on insulin or sulfonylurea, or with kidney failure.

  1. Treat (Paramedic/RN/CCT): dextrose 25 g IV (D50 50 mL), or D10 in 10 g steps (100 mL of D10 per 10 g) until alert, per protocol. Peds: D10 2–5 mL/kg IV (0.2–0.5 g/kg), per protocol. If IV access is not available, use glucagon per protocol.
  2. Sulfonylurea-related: hypoglycemia from a sulfonylurea can recur for hours; consider octreotide per medical direction.
  3. Recheck: glucose after each dose. Kidney failure prolongs insulin and sulfonylurea effects, so recurrence is common.

Severe hypocalcemia (symptomatic, or total Ca below 6.0 mg/dL)

Recognize: tetany, seizure, prolonged QT or hypotension with a low calcium.

  1. Replace (Paramedic/RN/CCT): calcium gluconate 1–2 g IV over 10–20 min with cardiac monitoring is the usual first-line agent outside arrest, per protocol. Calcium chloride 1 g (10 mL of 10%) over 5–10 min is reserved for central access or arrest because it is more irritating. Treat when symptomatic, or when QT is prolonged or hyperkalemia is present. Asymptomatic low calcium in rhabdomyolysis or marked hyperphosphatemia is usually not replaced early, because calcium phosphate can precipitate.
  2. Follow up: a bolus needs follow-up replacement (infusion or oral calcium) and magnesium repletion. Recheck ionized calcium and magnesium, and use caution in hyperphosphatemia.

Severe metabolic acidosis (pH below 7.20) or refractory uremia

Recognize: pH below 7.20, large anion gap, altered mental status, pericardial rub or pulmonary edema in kidney failure.

  1. Stabilize: airway and ventilation support, and treat the cause (sepsis, toxic alcohol, lactate).
  2. Dialysis: nephrology for urgent dialysis when acidosis, hyperkalemia or volume overload is refractory to medical treatment.
Pitfall: calcium does not lower K⁺. It only protects the heart, and its effect lasts 30 to 60 min. Calcium chloride irritates tissue, and it precipitates with sodium bicarbonate: flush the line between them. Bicarbonate has weak evidence for lowering K⁺ alone, so give it only when acidemic or with other measures. Chloride gives about 3 times as much calcium as gluconate, so do not swap them mg-for-mg. Follow local protocols and medical direction for all doses on this page.

Prehospital & Transport Considerations

Point-of-Care Testing

DeviceAnalytesSpecimenLimitations
i-STAT CHEM8+
Na⁺, K⁺, Cl⁻, ionized Ca, glucose, BUN, creatinine, TCO₂
Whole blood (cartridge)
Cartridge storage and temperature limits; available only where stocked
Glucometer
Glucose
Capillary blood
Unreliable in shock, dehydration or vitamin C use; some strip types (for example GDH-PQQ) read falsely high with icodextrin (peritoneal dialysis) or maltose. Confirm low or high values with a lab

Interfacility Transfer & Handoff

  • Send with the patient: last K⁺, creatinine, glucose and BUN with times; date of last dialysis; urine output; current potassium-raising drugs.
  • Pending labs: list any repeat potassium, ECG or gas that is due en route.
  • Repeat en route: K⁺ and glucose after shift therapy, per protocol, with ECG monitoring.
  • Specimens in flight: do not chill a potassium sample. Cold storage of whole blood raises K⁺.

Scope Notes

  • Calcium, insulin with dextrose and bicarbonate usually fall to Paramedic, RN or critical-care transport teams under protocol. Confirm scope locally.
  • EMS-only settings may have no K⁺ measurement. Without one, treat a dialysis patient with weakness or an irregular rhythm as potentially hyperkalemic.

Special Populations

Pediatrics

During the first days of life, the neonatal creatinine reflects maternal creatinine. Pediatric ranges also shift with age and assay, so use the laboratory's pediatric interval. For dosing, see the weight-based dosing and vital signs pages.

  • Calcium chloride: 20 mg/kg (0.2 mL/kg of 10%) IV slowly; max 1 g per dose.
  • Insulin: 0.1 units/kg IV (max 10 units) with dextrose 0.5 g/kg.
  • Sodium bicarbonate: 1 mEq/kg IV (max 50 mEq).
  • 3% saline: 2 mL/kg IV over 10 min, max 100 mL per dose.

Pregnancy

A creatinine that looks normal can hide early kidney injury in pregnancy, because GFR rises by about 50%. Above 0.8 mg/dL, creatinine is abnormal in pregnancy. A rise with hypertension or proteinuria suggests preeclampsia, and it needs obstetric review.

Older Adults

Low muscle mass can hide a low GFR in older adults, so a normal creatinine does not rule one out. For drug dosing, judge by the eGFR rather than creatinine alone. Creatinine-based eGFR loses accuracy with low muscle mass, in older adults and in critical illness. KDIGO 2024 suggests adding cystatin C (eGFRcr-cys) in those cases.

CKD and Dialysis

  • Pre-dialysis K⁺: a K⁺ above 6.0 mEq/L in a dialysis patient is urgent, and more so after a missed session.
  • Access arm: do not draw blood, start an IV or take a blood pressure in an arteriovenous fistula or graft arm.

Specimen Collection & Interfering Factors
  • Specimen and tube: serum (gold or red top) or lithium heparin plasma (green top). Which tube colour applies depends on the institution.
  • Fill and tourniquet: fill to the line; release the tourniquet within 1 min.
  • Handling: separate serum or plasma promptly. Unspun blood sitting at room temperature loses glucose. Do not refrigerate a potassium sample.
  • Order of draw (CLSI GP41): blood cultures, light blue, red or gold, green, lavender, gray.
Error or InterferentEffect on ResultsPrevention
Hemolysis
Falsely high K⁺, AST and LDH
Avoid fist clenching and small-gauge needles; repeat on a clean sample
Drawing above an IV
Dilution: falsely low K⁺; dextrose raises glucose
Draw from the opposite arm, or stop the IV and flush
Prolonged tourniquet
Falsely high K⁺
Release within 1 min
Delayed processing
Falsely low glucose; K⁺ leaks from cells
Centrifuge promptly
EDTA contamination
Falsely high K⁺, low Ca
Use correct draw order; no carry-over
Lipemia or icterus
Analyzer interference; pseudohyponatremia with indirect ion-selective electrode methods
Check the lab's index; verify by direct measurement or blood gas sodium

Clinical Pearls
Trend beats one value: One creatinine is a snapshot. AKI is defined by a rise against baseline, so compare with a prior result when one exists.
BUN alone is not kidney function: A high BUN with a normal creatinine often points to protein intake, GI bleeding or steroids.
eGFR is for stable kidneys: In unstable AKI, eGFR lags behind true GFR. Lean on urine output and the creatinine trend instead.
CKD needs time: KDIGO staging needs a reduced eGFR or albuminuria that persists for more than 3 months.
Field: A dialysis patient with weakness or an irregular rhythm? Get a 12-lead ECG and a potassium check before any other step.
Nursing: Record urine output by the hour. Below 0.5 mL/kg/hr for 6 hr or more meets the KDIGO urine-output criterion, and it can come before the creatinine rises. Urine output may stay normal in non-oliguric AKI.
Critical care: The K⁺ shift is biggest in mineral (non-gap) acidosis and smaller in organic acidosis, such as lactic acidosis or ketoacidosis. K⁺ can still run high in DKA because of insulin deficiency. Measure it, and correct the acidosis and the potassium together.
Pitfall: In kidney failure, insulin for hyperkalemia keeps lowering glucose for hours. Check glucose on a schedule.
Pitfall: Don't take a normal K⁺ as reassurance when an ACE inhibitor or ARB is on board and urine output is falling. Repeat the ECG and K⁺.

Related

References
  1. KDIGO Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117–S314. https://doi.org/10.1016/j.kint.2023.10.018
  2. KDIGO Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1–138. https://kdigo.org/wp-content/uploads/2019/01/KDIGO-2012-AKI-Guideline-English.pdf
  3. Inker LA, Eneanya ND, Coresh J, et al. New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. N Engl J Med. 2021;385(19):1737–1749. https://doi.org/10.1056/NEJMoa2102953
  4. Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia with kidney diseases: conclusions from a KDIGO Controversies Conference. Kidney Int. 2020;97(1):42–61. https://doi.org/10.1016/j.kint.2019.09.018
  5. Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170(3):G1–G47. https://doi.org/10.1530/EJE-13-1020

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