CRP-Werte: C-reaktives Protein Normalbereich
A comprehensive reference on C-reactive protein (CRP) and high-sensitivity CRP (hs-CRP) — normal ranges, causes of elevation, cardiovascular risk categories, and clinical interpretation.
Normal CRP Range — Quick Reference
<1.0 mg/L = Low risk · 1.0–3.0 mg/L = Moderate risk · >3.0 mg/L = High risk
What Is C-Reactive Protein (CRP)?
C-reactive protein (CRP) is an acute-phase reactant produced primarily by hepatocytes in response to interleukin-6 (IL-6) stimulation. It is one of the most widely used laboratory markers of systemic inflammation. CRP levels rise rapidly — often within 6–8 hours of an inflammatory stimulus — and can increase up to 1,000-fold during severe infections or tissue injury.1
CRP was first identified in 1930 by Tillett and Francis, who discovered a substance in the serum of patients with pneumococcal pneumonia that reacted with the C-polysaccharide of Streptococcus pneumoniae. Since then, it has become a cornerstone of inflammatory assessment in clinical medicine, used to detect and monitor infections, autoimmune diseases, and post-surgical recovery.2
The development of high-sensitivity CRP (hs-CRP) assays expanded the clinical utility of CRP measurement. While standard CRP tests are designed to detect the marked elevations seen in acute illness, hs-CRP can detect the low-grade chronic inflammation associated with atherosclerosis and cardiovascular risk.3
CRP Normal Range
CRP reference ranges differ depending on whether a standard or high-sensitivity assay is used and the clinical context:
Standard CRP
| CRP Level | Conventional (mg/L) | SI (mg/L) | Interpretation |
|---|---|---|---|
| Normal | <10 | <10 | No significant inflammation |
| Moderate elevation | 10–100 | 10–100 | Active inflammation — infection, autoimmune flare, tissue injury |
| Marked elevation | >100 | >100 | Severe infection (often bacterial), major tissue damage |
hs-CRP (Cardiovascular Risk Stratification)
| hs-CRP Level | mg/L | Cardiovascular Risk |
|---|---|---|
| Low risk | <1.0 | Lower relative cardiovascular risk |
| Moderate risk | 1.0–3.0 | Average cardiovascular risk |
| High risk | >3.0 | Higher relative cardiovascular risk |
| Acute inflammation | >10 | Not useful for CV risk — investigate acute cause |
CRP is measured in the same units (mg/L) in both conventional and SI systems. Some labs report CRP in mg/dL — multiply by 10 to convert to mg/L.
What Does a High CRP Level Mean?
Elevated CRP indicates systemic inflammation but is nonspecific — it does not identify the source. The degree of elevation can help narrow the differential:
Common Causes of Elevated CRP
- Bacterial infection — CRP typically >100 mg/L in serious bacterial infections (pneumonia, pyelonephritis, sepsis). Bacterial infections generally produce higher CRP than viral infections.4
- Viral infection — Usually CRP 10–50 mg/L, though severe viral illnesses (e.g., COVID-19 pneumonia) can cause marked elevation
- Autoimmune disease — Rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease (especially Crohn's disease), and vasculitis
- Tissue injury or surgery — CRP peaks 2–3 days post-operatively and should decline thereafter; persistent elevation suggests complications (e.g., infection)
- Malignancy — Particularly lymphomas, renal cell carcinoma, and advanced solid tumors
- Obesity — Chronic low-grade inflammation with mildly elevated hs-CRP (typically 3–10 mg/L), mediated by adipose tissue IL-6 production5
- Smoking — Associated with mildly elevated hs-CRP levels
Symptoms Associated with High CRP
CRP itself does not cause symptoms. Clinical features depend on the underlying cause:
- Fever, chills, malaise (infection)
- Joint pain and swelling (autoimmune arthritis)
- Abdominal pain, diarrhea (IBD flare)
- Chest pain, dyspnea (pneumonia, PE)
- Wound erythema or drainage (surgical site infection)
What Does a Low CRP Level Mean?
Low or undetectable CRP levels are generally not clinically significant and indicate an absence of systemic inflammation. There is no established pathologic condition associated with an abnormally low CRP.
In the context of hs-CRP cardiovascular risk stratification, a very low hs-CRP (<1.0 mg/L) is favorable and associated with a lower relative risk of future cardiovascular events.3
Some medications — particularly statins — can reduce hs-CRP levels by 15–30%, independent of their effects on LDL cholesterol. The JUPITER trial demonstrated that statin therapy reduced cardiovascular events in patients with elevated hs-CRP even with normal LDL cholesterol.6
Verwandte Tests & Rechner
CRP is frequently ordered alongside other tests in the evaluation of inflammation and cardiovascular risk:
- ASCVD Risk Calculator — 10-year atherosclerotic cardiovascular disease risk using the Pooled Cohort Equations. hs-CRP can be used as a risk enhancer when ASCVD risk is borderline.
- Framingham Risk Score — Classic coronary heart disease risk calculator. Consider hs-CRP as an adjunct in intermediate-risk patients.
- HEART Score — Risk stratification for acute chest pain in the emergency department.
- Erythrocyte sedimentation rate (ESR) — Another acute-phase marker, often ordered with CRP. ESR rises and falls more slowly than CRP.
- Procalcitonin — More specific for bacterial infection than CRP; useful for distinguishing bacterial from viral causes.
Über diesen Test
Klinische Praxistipps
🔑 Wichtige Hinweise
- CRP >100 mg/L has roughly an 80–85% positive predictive value for bacterial infection, though autoimmune flares and major tissue injury can also reach this level.4
- CRP has a short half-life (~19 hours), making it useful for monitoring treatment response. A declining CRP is reassuring; a rising or plateaued CRP after 3–4 days of antibiotics should prompt re-evaluation.
- hs-CRP for cardiovascular risk should be measured twice (at least 2 weeks apart) in a non-inflamed state. A single hs-CRP >10 mg/L should be repeated after the acute process resolves.
- CRP is minimally affected by anemia, polycythemia, red cell morphology, or protein levels — unlike ESR, which is affected by all of these.
- Liver failure can blunt CRP production. In patients with severe hepatic dysfunction, a "normal" CRP does not exclude infection.
- CRP does not cross the blood-brain barrier. It is not reliably elevated in isolated CNS infections (e.g., meningitis may show only modest CRP elevation early).
- The 2019 ACC/AHA guidelines list hs-CRP ≥2.0 mg/L as a "risk-enhancing factor" that can guide statin initiation in borderline-risk patients (5–7.5% 10-year ASCVD risk).7
Test Methodology
CRP is measured by immunoassay (immunoturbidimetry or immunonephelometry). Standard CRP assays have a detection limit of approximately 3–8 mg/L. High-sensitivity assays detect concentrations as low as 0.1–0.3 mg/L, enabling cardiovascular risk stratification in the low mg/L range.
Specimen Requirements
CRP is measured on serum or plasma. No fasting is required. The sample is stable for several days refrigerated. Results are typically available within 1–2 hours in most hospital laboratories.
Referenzen
- Burtis CA, Ashwood ER, Bruns DE, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018.
- Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest. 2003;111(12):1805–1812. doi:10.1172/JCI200318921
- Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003;107(3):363–369. doi:10.1161/01.CIR.0000053730.47739.3C
- Hofer N, Zacharias E, Müller W, Resch B. An update on the use of C-reactive protein in early-onset neonatal sepsis: current insights and new tasks. Neonatology. 2012;102(1):25–36. doi:10.1159/000336629
- Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999;282(22):2131–2135. doi:10.1001/jama.282.22.2131
- Ridker PM, Danielson E, Fonseca FAH, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (JUPITER). N Engl J Med. 2008;359(21):2195–2207. doi:10.1056/NEJMoa0807646
- Arnett DK, Blumenthal RS, Gerber B, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease. Circulation. 2019;140(11):e596–e646. doi:10.1161/CIR.0000000000000678
- Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice (AHA/CDC scientific statement). Circulation. 2003;107(3):499–511. doi:10.1161/01.CIR.0000052939.59093.45
Referenzen zuletzt überprüft: Februar 2026