Abstract: SA-PO0200
When Creatine Kinase (CK) Isn't Rhabdo: Persistent Asymptomatic CK and Creatinine Elevation
Session Information
- Tubular, Metabolic, and Systemic Noncystic Genetic Kidney Diseases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1202 Genetic Diseases of the Kidneys: Non-Cystic (Complex and Non-Cystic Monogenic)
Authors
- Lee, Crystal, Lenox Hill Hospital, New York, New York, United States
- Moses, Andrew A., Lenox Hill Hospital, New York, New York, United States
- Patel, Rujuta, Lenox Hill Hospital, New York, New York, United States
Introduction
Creatine kinase (CK) is an enzyme predominantly localized to skeletal and cardiac muscle, and elevations are recognized as a biomarker for muscle pathology. However, in asymptomatic individuals, increased CK levels can be attributed to a decreased rate of enzyme clearance instead of CK release from tissue damage. The following case represents where, despite initial concerns for myopathy or kidney compromise, overall workup suggested the sustained CK levels were attributed to an underlying genetic condition causing impaired CK clearance.
Case Description
A 35 year old African-American male with hyperlipidemia was referred to the nephrology clinic for four-year history of asymptomatic elevated serum creatinine (Cr) and CK. Initially, these findings were thought to be due to statin-induced myopathy or strenuous exercise. His CK values ranged from 462 to 883 U/L (reference range: 30-200 U/L) while his average Cr was 1.3 to 1.4 mg/dL (reference range: 0.50 - 1.30 mg/dL). He denied history of kidney stones, chronic NSAID use, hypertension, and diabetes. His kidney ultrasound, transthoracic echocardiogram, stress test, and autoimmune workup were unremarkable. The patient stopped his creatine and protein powder supplements for two years, discontinued his statin for two months, and avoided strenuous exercise for one month, which did not lead to reduction in CK or Cr levels. A normal urinalysis did not detect myoglobin which ruled out rhabdomyolysis. His cystatin C was 0.70 mg/L (reference range: 0.64-1.12 mg/L) which reflected preserved glomerular filtration rate (GFR). Cystatin C has demonstrated greater accuracy and less racial bias in GFR estimation. In the setting of persistent asymptomatic elevated CK levels, absence of myoglobinuria, and confirmed normal kidney function, clinical suspicion shifted to impaired CK clearance with likely genetic causes. Genetic work-up is pending at this time.
Discussion
Asymptomatic persistently elevated CK levels can be due to genetic predispositions causing impaired CK clearance such as variations in leukocyte immunoglobulin-like receptor B5. Distinguishing this phenomenon from muscle pathology is critical to prevent misdiagnosis, to avoid unnecessary invasive investigations, and to ensure appropriate clinical management. After diagnostic findings confirmed absence of kidney disease, the patient resumed statin therapy and daily exercise without rise in CK