In renal function testing, cystatin C is considered superior to serum creatinine as an early marker of GFR decline because:
- A Cystatin C is not filtered at the glomerulus and thus accumulates when tubules are damaged
- B Cystatin C is produced at a constant rate by all nucleated cells, freely filtered, and completely reabsorbed without secretion ✓
- C Cystatin C is dependent on muscle mass and therefore more accurate in obese patients
- D Cystatin C is secreted by proximal tubules, making it a direct tubular injury marker
Explanation
Cystatin C, a cysteine protease inhibitor, is produced constitutively by all nucleated cells independent of muscle mass, sex, or age. It is freely filtered at the glomerulus and completely catabolised in proximal tubular cells without tubular secretion — ideal GFR marker behaviour. Creatinine production depends on muscle mass and is also secreted by tubules, so it overestimates GFR at lower levels. Cystatin C rises when GFR falls to 60–75 mL/min, earlier than creatinine's rise at < 50 mL/min.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.