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Unmasking artifactual increases in creatine kinase isoenzymes in patients with renal failure
Insights
Creatine kinase isoenzymes, including MB and BB, show minor elevations in chronic renal failure patients on dialysis. These modest increases are unlikely to cause diagnostic confusion for chest pain evaluation.
Area of Science:
- Clinical Chemistry
- Nephrology
- Cardiology
Background:
- Elevated creatine kinase isoenzymes in chronic renal failure (CRF) may limit their diagnostic utility for chest pain.
- Previous reports suggest total creatine kinase is elevated in CRF patients.
Purpose of the Study:
- To evaluate the clinical significance of creatine kinase isoenzyme elevations (CK-MB and CK-BB) in patients with chronic renal failure undergoing maintenance dialysis.
- To determine if these elevations cause diagnostic confusion in assessing chest pain.
Main Methods:
- Analyzed plasma creatine kinase (total, MB, and BB) levels in 88 patients with CRF on maintenance dialysis.
- Utilized the glass bead method for measuring CK-MB to prevent interference from non-specific fluorescence.
- Compared patient values to established normal ranges and assessed statistical and biological significance.
Main Results:
- Total plasma creatine kinase was elevated as expected in CRF patients.
- CK-MB and CK-BB showed statistically significant but biologically unimpressive elevations.
- 92% of CRF patients had normal CK-MB levels (<13 IU/L); only 8% had mildly elevated values (highest 20 IU/L).
Conclusions:
- Infrequent and modest increases in plasma CK-MB in CRF patients are unlikely to cause diagnostic confusion.
- Substantial CK-MB elevations are still indicative of acute myocardial infarction, differentiating it from CRF-related changes.
Abstract:
Previous reports have suggested that creatine kinase isoenzymes are elevated in patients with chronic renal failure and thus are less useful in the evaluation of chest pain in such patients. Our data in 88 patients with chronic renal failure receiving maintenance dialysis confirm this observation for total plasma creatine kinase. However, elevations in MB and BB creatine kinase, although statistically significant, were biologically unimpressive (5.9 +/- 0.05 [SEM] IU/L compared with 4.8 +/- 0.04 IU/L for MB creatine kinase [p less than 0.02], and 5.5 +/- 0.08 ng/ml compared with 3.2 +/- 0.05 ng/ml for BB creatine kinase [p less than 0.0002] ), and were unlikely to cause diagnostic confusion. In 92% of patients with chronic renal failure, plasma MB creatine kinase activity was within the normal range (less than 13 IU/L). Eight percent of patients manifested abnormal MB creatine kinase values; the highest was 20 IU/L. The glass bead method for measuring MB creatine kinase was used to avoid the potential confusion induced by non-creatine kinase-mediated fluorescence, which occurs in the region of MB and BB creatine kinase on electrophoresis. The infrequent and modest increases in plasma MB creatine kinase observed in patients with chronic renal failure should be appreciated, but it should not cause diagnostic confusion, because acute myocardial infarction usually results in more substantial elevations of MB creatine kinase.