2025 Volume 68 Issue 2 Pages 40-45
The patient was a 57-year-old man who was hospitalized for a myocardial infarction. On arrival, he was diagnosed with diabetes based on an HbA1c level of 8.8 %, postprandial blood glucose level of 281 mg/dL, and urine ketone level of 3+. His fasting serum C-peptide immunoreactivity (CPR) concentration was 3.1 ng/mL (with a corresponding fasting blood glucose level of 164 mg/dL), and his CPR index was 1.89, which was not abnormally high. Notably, his urinary CPR level was abnormally high at 659 μg/day, and remained consistent during repeat testing (491 μg/day). It is possible that the discrepancy between the urine and serum results was due to the recent initiation of sacubitril/valsartan hydrate, a neprilysin inhibitor. After switching the antihypertensive drug from sacubitril/valsartan to olmesartan, the patient's urinary CPR level decreased to 86.9 μg/gCre. However, when sacubitril/valsartan was resumed, his urinary CPR became abnormally high again, increasing to 304.5 μg/gCre. Neprilysin, which is predominantly localized in the brush border of renal tubular cells, has been implicated as a potential modulator of C-peptide degradation. Sacubitril/valsartan, which has a neprilysin inhibitory effect, is likely to contribute to increased urinary CPR.
