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Renin

SI UNITS (recommended)

CONVENTIONAL UNITS

(Key Enzyme in Renin–Angiotensin–Aldosterone System – Essential for Evaluating Hypertension, Primary Aldosteronism & Volume Status)

Synonyms

  • Renin
  • Plasma Renin Concentration (PRC)
  • Plasma Renin Activity (PRA) (biological activity; different test)
  • Active Renin
  • Direct Renin
  • Renin enzyme
  • Aspartyl protease renin

Important:
 Renin is measured either as concentration (PRC) or activity (PRA).
This article focuses on renin concentration (PRC) since your requested units correspond to PRC.

Units of Measurement

  • pmol/L
  • ng/L
  • ng/dL
  • ng/100 mL
  • ng%
  • pg/mL
  • µIU/mL
  • mIU/L

Unit Conversions

Renin molecular weight ≈ 37,000 Da (37 kDa)

pmol/L ↔ pg/mL

1 pmol/L≈37 pg/mL1\ \text{pmol/L} \approx 37\ \text{pg/mL}1 pmol/L≈37 pg/mL 1 pg/mL≈0.027 pmol/L1\ \text{pg/mL} \approx 0.027\ \text{pmol/L}1 pg/mL≈0.027 pmol/L

ng/L ↔ pg/mL

1 ng/L=1 pg/mL1\ \text{ng/L} = 1\ \text{pg/mL}1 ng/L=1 pg/mL

ng/dL → ng/L

1 ng/dL=10 ng/L1\ \text{ng/dL} = 10\ \text{ng/L}1 ng/dL=10 ng/L

ng% = ng/100 mL

1\ \text{ng%} = 1\ \text{ng/100 mL} = 10\ \text{ng/L}

µIU/mL ↔ mIU/L

1 μIU/mL=1 mIU/L1\ \mu IU/mL = 1\ mIU/L1 μIU/mL=1 mIU/L

(Values depend on assay calibration.)

Description

Renin is an aspartyl protease enzyme, synthesized and stored by juxtaglomerular (JG) cells in the kidney.

Its major role:

  • Cleaves angiotensinogen → angiotensin I
  • Initiates the renin–angiotensin–aldosterone system (RAAS)

Renin secretion is stimulated by:

  • Low renal perfusion
  • Low sodium delivery to macula densa
  • Sympathetic activation (β₁ receptors)

Renin is critical for evaluating:

  • Hypertension
  • Aldosterone disorders
  • Volume depletion or overload
  • Renovascular disease

Physiological Role

  • Regulates blood pressure
  • Controls sodium/potassium balance
  • Maintains intravascular volume
  • Stimulates aldosterone secretion from adrenal cortex
  • Part of RAAS

Clinical Significance

HIGH RENIN

Seen in:

1. Secondary Hyperaldosteronism

  • Renal artery stenosis
  • Renin-secreting tumor (rare)
  • Malignant hypertension
  • Congestive heart failure
  • Cirrhosis
  • Nephrotic syndrome

2. Diuretic Use

Especially loop diuretics (furosemide).

3. Sodium Depletion

Dehydration, low-salt diet.

4. Adrenal Insufficiency

Low aldosterone → feedback increase in renin.

5. Pregnancy

Physiologic rise.

LOW RENIN

Seen in:

1. Primary Aldosteronism

Low renin + high aldosterone → ARR elevated

2. Low-renin Hypertension

  • Elderly
  • African ancestry
  • Metabolic syndrome
  • Volume overload states

3. Cushing’s Syndrome

Glucocorticoid excess suppresses renin.

4. High Salt Intake

5. Genetic Disorders

  • Liddle syndrome
  • Apparent mineralocorticoid excess

Reference Intervals

(Tietz 8E + Endocrine Society + Mayo + ARUP; vary by posture & sodium status)

Plasma Renin Concentration

Supine

  • 2.8 – 39.9 pg/mL
     (= 0.08 – 1.1 pmol/L)

Upright

  • 5.3 – 60 pg/mL
     (= 0.14 – 1.6 pmol/L)

Plasma Renin Activity

For reference only:

  • 1–3 ng/mL/hr (upright)
    (Not the same test; different units.)

Diagnostic Uses

1. Primary Aldosteronism Screening

Renin part of ARR (Aldosterone : Renin Ratio)

  • Low renin + high aldosterone → high ARR → primary aldosteronism

2. Hypertension Workup

Classifies:

  • Low-renin HTN
  • High-renin HTN
  • Secondary causes

3. Renovascular Hypertension

  • Renin ↑ in unilateral renal artery stenosis
  • Captopril renin test may help

4. Volume Status Assessment

Renin rises with:

  • Dehydration
  • Diuretics
  • Hypotension
    Renin falls with:
  • High salt intake
  • Volume overload
  • Edematous states

5. Adrenal Disorders

Differentiates:

  • Primary vs secondary hyperaldosteronism
  • Addison disease
  • Congenital adrenal hyperplasia (salt-wasting forms)

Analytical Notes

  • Measure in morning, after 2 hours upright unless otherwise specified.
  • Many drugs interfere:
    • ACE inhibitors ↑ renin
    • ARBs ↑ renin
    • Beta-blockers ↓ renin
    • Diuretics ↑ renin
    • NSAIDs ↓ renin
  • Paired measurement with aldosterone is essential.
  • Sodium intake must be stable.
  • Renin is unstable; special handling may be required (chilled EDTA plasma).

Clinical Pearls

  • Renin low + aldosterone high = primary aldosteronism (most important use).
  • RAAS drugs dramatically affect results; medication washout improves interpretation.
  • High renin does not always imply high aldosterone (e.g., renal artery stenosis).
  • Renin helps distinguish primary vs secondary hypertension causes.

Interesting Fact

Renin was discovered in 1898 by Tigerstedt & Bergman, making it one of the earliest identified endocrine regulators of blood pressure-far earlier than the rest of the RAAS components.

References

  1. Tietz Clinical Chemistry & Molecular Diagnostics, 8th Edition - Renin/Aldosterone
  2. Endocrine Society Clinical Practice Guideline - Primary Aldosteronism
  3. Mayo Clinic Laboratories - Renin
  4. ARUP Consult - Aldosterone/Renin Testing
  5. European Society of Hypertension - RAAS Physiology
  6. MedlinePlus / NIH - Renin Test

Last updated: January 27, 2026

Reviewed by : Medical Review Board

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