Transient Proteinuria Induced by High-Dose Rosuvastatin

This case describes a 70-year-old woman who developed transient proteinuria after starting high-dose rosuvastatin following a non-ST elevation myocardial infarction. The objective of this report is to describe the development of proteinuria in a patient after high-dose rosuvastatin therapy and discuss the subsequent resolution with a medication switch.

A 70-year-old woman with a history of type 2 diabetes, primary hypertension, hypothyroidism, and hyperlipidemia, developed proteinuria after receiving high-dose rosuvastatin following an episode of non-ST elevation myocardial infarction. Prior to therapy, her low-density lipoprotein cholesterol was 123 mg/dL, coronary calcium score was 270, and urine albumin-to-creatinine ratios were 7.6 mg/g and 6.7 mg/g (normal albumin-to-creatinine ratio <30 mg/g). After 3 months of rosuvastatin therapy, proteinuria (albumin-to-creatinine ratio of 344.1) and muscle cramps developed, though her renal function remained stable (glomerular filtration rate >70 mL/min/1.73 m²). After discontinuing rosuvastatin and switching to atorvastatin (20 mg/d) and ezetimibe (10 mg/d), proteinuria resolved, and low-density lipoprotein cholesterol was maintained at 45 mg/dL.

Statin-induced proteinuria is a dose-dependent and typically reversible condition, more likely to occur with higher statin doses, such as rosuvastatin. Although proteinuria is generally transient, careful monitoring and dose adjustments are critical to optimizing statin therapy and patient adherence.

This case highlights the importance of individualized statin therapy, emphasizing monitoring for dose-dependent side effects such as proteinuria.