Granulomatous and Inflammatory Conditions

• Granulomatous Diseases:
  Elevated ACE is classically associated with sarcoidosis and may also be seen in other granulomatous conditions (e.g., berylliosis or tuberculosis‑related granulomas).
• Inflammatory States:
  In some autoimmune or inflammatory conditions, ACE might be modestly elevated.

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Medication Effects & Genetic Variability

• Medication Effect:
  Lower ACE levels can result from ACE inhibitor therapy.
• Genetic Variability:
  Some individuals naturally have lower ACE levels without clinical significance.

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Age-Related Variability and Diagnostic Considerations

• Baseline Differences:
  While baseline ACE levels may differ slightly by age.
• Clinical Implications:
  Marked changes in ACE levels in a child versus an adult can prompt further investigation for granulomatous or inflammatory diseases, depending on the overall clinical picture.

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Renin–Angiotensin–Aldosterone System (RAAS)

All these markers are components of the Renin–Angiotensin–Aldosterone System (RAAS), which regulates blood pressure, fluid balance, and electrolyte homeostasis:

• Renin is produced by the kidneys and initiates the process by converting angiotensinogen into angiotensin I.
• Angiotensin I serves as a precursor that is converted by Angiotensin Converting Enzyme (ACE) into the active Angiotensin II.
• Angiotensin II is a potent vasoconstrictor that also stimulates the adrenal cortex to secrete Aldosterone.
• Aldosterone, measured in both blood and urine, acts on the kidneys to enhance sodium and water retention, thereby increasing blood volume and pressure.

Together, these components work in a coordinated cascade to maintain cardiovascular stability and fluid balance.

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