Pharmacists see blood tests every day, often before a doctor makes a final call. Reading those reports well can prevent harm, guide dosing, and calm anxious patients. This guide explains how to interpret common lab panels with a focus on two results people ask about most: creatinine (kidney function) and bilirubin (jaundice). You will learn what high numbers mean, why they happen, and what to do next.
How to read a lab report like a pharmacist
- Confirm basics first. Check patient name, date of birth, collection date/time, and whether the sample was fasting. Mistakes here cause wrong conclusions.
- Look at units and reference ranges. Labs report in mg/dL or µmol/L and ranges vary by lab and method. Compare to the lab’s range and the patient’s baseline, not only to the “H” or “L” flag.
- Trend beats one-time values. A mild elevation that is stable over years is different from a sharp rise over days. Always compare to prior results.
- Add clinical context. Age, sex, muscle mass, hydration, pregnancy, recent exercise, and medications all shift values. Without context, you may overreact or miss risk.
- Check sample quality. Hemolysis, delays to the lab, or poor storage can distort results (for example, potassium and bilirubin). Many lab reports note if a sample was hemolyzed.
Creatinine 101: what it measures and why it matters
Creatinine comes from muscle metabolism. Healthy kidneys filter it out. Because production is fairly steady and only filtration clears it, creatinine reflects kidney function.
Typical adult reference ranges (lab methods vary):
- Men: ~0.7–1.3 mg/dL (62–115 µmol/L)
- Women: ~0.6–1.1 mg/dL (53–97 µmol/L)
We use creatinine to estimate glomerular filtration rate (eGFR). eGFR is better than raw creatinine for dosing because it adjusts for age, sex, and sometimes race. When kidney function falls, drug clearance often falls too, raising toxicity risk.
Why creatinine can be high
- Less blood flow to the kidney (pre-renal): dehydration, vomiting/diarrhea, blood loss, heart failure. Why? The kidney filters less when perfusion drops, so creatinine backs up.
- Kidney injury (intrinsic): acute interstitial nephritis (often from PPIs, penicillins), acute tubular injury (contrast dye, aminoglycosides, vancomycin, cisplatin, amphotericin B), chronic damage (diabetes, hypertension, lithium). Why? Damaged tubules cannot clear creatinine efficiently.
- Obstruction (post-renal): enlarged prostate, stones, tumors. Why? Back pressure reduces filtration.
- More creatinine made or secreted less:
- High muscle mass, recent heavy exercise, rhabdomyolysis (consider statin interactions), high meat intake, or creatine supplements increase production.
- Cimetidine, trimethoprim, cobicistat, and dolutegravir block tubular secretion of creatinine. eGFR may look worse while true GFR is unchanged.
- Cephalosporins (like cefoxitin) can falsely elevate creatinine with some lab assays (Jaffe method).
- ACE inhibitors/ARBs: a small creatinine rise (up to ~30% from baseline) can be expected after starting. Why? They relax the kidney’s efferent arteriole, slightly lowering filtration pressure. Larger increases suggest volume depletion, renal artery stenosis, or other disease.
Estimating kidney function for drug dosing
eGFR (CKD-EPI) is routine on reports and is good for staging kidney disease. Many drug labels still use creatinine clearance (CrCl) via the Cockcroft–Gault equation. Use the method the drug label specifies.
- When eGFR/CrCl is unreliable: very low muscle mass (frail or amputee), very muscular bodybuilder, pregnancy, rapidly changing kidney function. Why? Equations assume average creatinine generation and steady state.
- Do not round creatinine up to 1.0 mg/dL in older adults. That underestimates renal function and can underdose essential drugs.
Common medicines that need dose changes or caution as kidney function declines:
- Metformin: avoid if eGFR <30 mL/min/1.73m²; reduce and monitor if 30–45. Why? Lactic acidosis risk increases as clearance falls.
- Direct oral anticoagulants (DOACs): apixaban, rivaroxaban, edoxaban, dabigatran dosing depends on CrCl and age/weight. Why? Bleeding risk rises with accumulation.
- Gabapentin/pregabalin: reduce dose markedly when eGFR <60. Why? Entirely renally cleared; accumulation causes sedation and ataxia.
- Allopurinol: start low and go slow in CKD to reduce severe hypersensitivity risk.
- Nitrofurantoin: avoid when eGFR <30. Why? Low urine levels and higher toxicity risk.
- Opioids with active metabolites: morphine and codeine can accumulate; prefer alternatives or lower doses.
What to do when creatinine is high
- Verify and trend. Compare with prior values. A rise of ≥0.3 mg/dL in 48 hours or ≥50% in 7 days suggests acute kidney injury. Why? These thresholds correlate with worse outcomes and need action.
- Calculate eGFR or CrCl. Use the method relevant to the drug decisions you must make.
- Review medications. Stop or switch nephrotoxins when possible (NSAIDs, contrast, high-dose diuretics, ACEi/ARB temporarily if volume depleted). Check for recent starts of cimetidine/trimethoprim that can fake a rise.
- Assess volume and obstruction. Ask about fluid intake, vomiting/diarrhea, urinary frequency/retention, flank pain. Encourage oral rehydration if appropriate.
- Order or request follow-up tests. Urinalysis (protein, blood, casts), electrolytes (especially potassium), CK if muscle pain, and repeat creatinine in 24–72 hours depending on severity.
- Red flags for urgent care: minimal urine, rising potassium, severe dehydration, confusion, creatinine doubling from baseline, or suspected obstruction/infection.
Bilirubin 101: what it measures and why it matters
Bilirubin comes from red blood cell breakdown. The liver processes unconjugated bilirubin (water-insoluble) into conjugated bilirubin (water-soluble) and sends it into bile. High bilirubin causes jaundice (yellow skin/eyes).
Typical adult reference range for total bilirubin: ~0.2–1.2 mg/dL (3–21 µmol/L). Labs may report total and direct (conjugated) bilirubin. Indirect (unconjugated) is total minus direct.
Why it matters: the pattern of bilirubin elevation points to hemolysis, liver cell injury, or bile flow obstruction. That guides testing and urgency.
Why bilirubin can be high
- Mostly unconjugated (indirect) bilirubin:
- Increased production: hemolysis, large bruises, ineffective red cell production. Why? The liver is overwhelmed by load.
- Reduced conjugation: Gilbert syndrome (common, harmless), fasting/illness, or drugs that inhibit UGT1A1 (atazanavir, indinavir). Why? Less enzyme activity leaves more unconjugated bilirubin.
- Clues: normal AST/ALT/ALP, normal urine color (unconjugated bilirubin does not appear in urine).
- Mostly conjugated (direct) bilirubin:
- Cholestasis/obstruction: gallstones, pancreatic or biliary tumors, primary sclerosing cholangitis, pregnancy cholestasis. Why? Bile cannot flow out, so conjugated bilirubin refluxes into blood.
- Hepatocellular injury: viral hepatitis, alcohol-associated hepatitis, fatty liver (NASH), drug-induced liver injury (acetaminophen, amoxicillin–clavulanate, isoniazid, azoles, anabolic steroids). Why? Damaged hepatocytes leak conjugated bilirubin and fail to excrete it.
- Clues: dark urine (conjugated bilirubin is water-soluble), pale stools, itching, right-upper-quadrant pain.
- Benign hereditary cholestasis: Dubin–Johnson or Rotor syndrome cause mild direct hyperbilirubinemia with otherwise normal liver tests.
- Artifacts and physiology: Hemolyzed samples can distort bilirubin measurement; prolonged fasting can mildly raise unconjugated bilirubin.
Reading the liver panel: patterns that matter
- Hepatocellular pattern: AST/ALT rise more than alkaline phosphatase (ALP). Think viral hepatitis, toxins (e.g., acetaminophen), ischemia. Why? Injured hepatocytes release aminotransferases.
- Cholestatic pattern: ALP and gamma-glutamyl transferase (GGT) rise more than AST/ALT. Think bile duct obstruction, drug-induced cholestasis, or infiltrative disease. Why? Bile duct injury ramps up ALP production.
- Isolated bilirubin elevation with normal AST/ALT/ALP: often Gilbert syndrome or hemolysis. Why? The liver cells and ducts look okay; the issue is processing or load.
- ALP can come from bone. If ALP is high but GGT is normal, consider bone disease rather than liver.
What to do when bilirubin is high
- Fractionate bilirubin. If only total is reported, request direct and indirect. The split drives the differential.
- Review medications and supplements. High-dose acetaminophen, alcohol, amoxicillin–clavulanate, isoniazid, ketoconazole/azoles, anabolic steroids, chlorpromazine, rifampin, and certain herbals (e.g., kava, concentrated green tea extract) can injure liver or cause cholestasis.
- Look for symptoms. Dark urine, pale stools, itching, fever, right-upper-quadrant pain, nausea, or confusion signal urgency.
- Order or advocate for targeted tests: AST/ALT, ALP, GGT, INR, albumin; complete blood count with reticulocyte count, LDH, and haptoglobin if hemolysis suspected; abdominal ultrasound if cholestasis is likely.
- Red flags for urgent evaluation: jaundice plus fever and abdominal pain (possible cholangitis), severe abdominal pain, confusion or sleepiness (possible hepatic encephalopathy), easy bruising/bleeding, or very high AST/ALT. These can be emergencies.
Putting it together: two quick cases
- Case 1: A 68-year-old on lisinopril and furosemide starts taking ibuprofen for back pain. He has poor appetite during a heat wave. Creatinine rises from 1.1 to 1.8 mg/dL in three days.
Why: the “triple whammy” (ACEi + diuretic + NSAID) plus dehydration reduced kidney perfusion.
Action: stop NSAID, rehydrate, consider holding diuretic/ACEi short term, recheck creatinine and potassium within 48 hours, adjust any renally cleared drugs, and educate on safer pain options. - Case 2: A healthy 25-year-old has total bilirubin 2.3 mg/dL after a weekend fast; AST/ALT/ALP are normal, urine is normal.
Why: likely Gilbert syndrome with fasting-triggered unconjugated hyperbilirubinemia.
Action: repeat when fed and well; no treatment needed if pattern persists and other tests remain normal. Counsel that stress and fasting can raise levels temporarily.
Preventing problems and monitoring
- Get baseline labs before starting drugs that affect kidneys or liver (e.g., metformin, DOACs, statins, methotrexate, isoniazid, tenofovir, amiodarone).
- Time your checks. Recheck within 1–2 weeks after starting or changing doses for higher-risk drugs, sooner if symptoms arise. For ACEi/ARBs and diuretics, check creatinine and potassium after 1–2 weeks.
- Hydration and sick-day rules. Teach patients to pause nephrotoxic or dehydrating meds during vomiting/diarrhea and to maintain fluid intake.
- Avoid unnecessary NSAIDs in patients with CKD, heart failure, or on ACEi/ARB/diuretics.
- Document and communicate trends, not just snapshots. Share baseline values and percent changes with prescribers to guide safe dosing.
Common pitfalls
- Acting on a single result without context or confirmation.
- Ignoring units and lab-specific reference ranges.
- Estimating GFR in non-steady states (rapidly rising creatinine) or unusual body composition without caution.
- Rounding serum creatinine in older adults, which can lead to underdosing.
- Assuming all bilirubin is the same. Not fractionating misses key diagnoses.
- Confusing carotenemia with jaundice. Yellow skin from diet spares the sclera; bilirubin colors the eyes.
Key takeaways
- Creatinine reflects kidney filtration; always check trends, context, and eGFR/CrCl before dosing.
- Small creatinine rises can be expected with ACEi/ARB; large or rapid rises signal risk and need action.
- Bilirubin must be split into direct and indirect to narrow causes; pair with AST/ALT/ALP/GGT patterns.
- Many drugs raise creatinine or bilirubin; some by real injury, others by assay or transport effects. Know the difference to avoid wrong stops or missed harm.
- Use red flags to triage urgency: oliguria, hyperkalemia, doubling creatinine, jaundice with fever/pain, confusion, or coagulopathy.
The best lab interpretation blends numbers with clinical judgment. As pharmacists, we add value by spotting patterns early, adjusting therapy safely, and guiding timely follow-up. That keeps patients safer and treatments on target.
I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
Mail- Sachin@pharmacyfreak.com