Cystatin C in chronic kidney disease: enhancing diagnostic accuracy and patient outcomes.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, epidemiologic, and clinical literature without systematic review methodology
PubMed 41733278 · doi:10.1080/00325481.2026.2634426
What was done
The authors reviewed epidemiologic, mechanistic, and clinical studies examining cystatin C biology, assay methodology, and its clinical performance for estimating glomerular filtration rate (GFR). The review synthesized comparative evidence evaluating creatinine-based, cystatin C-based, and combined creatinine–cystatin C eGFR equations for detecting chronic kidney disease (CKD) and predicting clinical outcomes.
What was found
The abstract reports no numerical estimates or statistical effect sizes. Qualitatively, cystatin C is less dependent on muscle mass and diet than creatinine. Both cystatin C-based and combined creatinine–cystatin C equations improve accuracy for early CKD identification and more reliably predict CKD progression, cardiovascular events, and mortality. However, cystatin C levels are influenced by non-renal factors, including thyroid dysfunction, corticosteroid therapy, systemic inflammation, obesity, smoking, and malignancy.
Why it matters
Incorporating cystatin C alongside creatinine refines GFR estimation and improves cardiovascular and mortality risk stratification, particularly in clinical populations where creatinine alone is unreliable due to altered muscle mass or diet.
Limits
The abstract describes a narrative review without specified systematic search criteria or meta-analytic pooling. Key non-GFR determinants (such as inflammation, obesity, corticosteroid use, and thyroid disease) can confound cystatin C interpretation.
Cited by
- supports Cystatin C-based estimated GFR is not influenced by muscle mass or creatine intake, unlike creatinine-based eGFR.