Andrew J Cohen1, Melanie A Adamsky2, Charles U Nottingham1, Jaclyn Pruitt3, Brittany Lapin3, Chi H Wang3, Sangtae Park3. 1. Department of Surgery, Section of Urology, University of Chicago, Chicago, IL. 2. Department of Surgery, Section of Urology, University of Chicago, Chicago, IL. Electronic address: Melanie.adamsky@uchospitals.edu. 3. Division of Urology, NorthShore University Health System, Evanston, IL.
Abstract
OBJECTIVE: To determine whether statin intake affects nephrolithiasis risk, and whether higher lipid levels correlate with stone risk. Dyslipidemia is a known independent risk factor for urolithiasis, and emerging evidence suggests common biological pathways. Previous work has suggested that statins protect against new stone formation, but these findings have not been verified by other investigators. METHODS: We queried our Institution's Electronic Data Warehouse for all patients who were newly diagnosed with hyperlipidemia between 2009 and 2011, and had never taken a statin drug. These patients' clinical outcomes were followed until 2015, to assess whether they had been newly prescribed statins and whether they had developed symptomatic urolithiasis. Patient demographics, stone risk factors, prescription data, and serum lipid values were collected. RESULTS: A total of 101,259 patients met inclusion criteria, 47.8% of whom received a statin prescription during the study period. Patients prescribed statins were significantly older, had a greater likelihood of osteoporosis, hemiplegia, immobility, and more likely to take a thiazide diuretic. Patients without a history of urolithiasis who were started on statin therapy were significantly less likely to develop new stones than patients not taking statins. This protective effect was even greater in patients with a history of stone disease. Lipid parameters (low-density lipoprotein, triglyceride, cholesterol) were lower in the statin-treated group, suggesting overall compliance with these medications. CONCLUSION: Our data confirm previous work that statins protect against urinary stone formation; however, the underlying mechanism seems to be distinct from statins' lipid-lowering effect.
OBJECTIVE: To determine whether statin intake affects nephrolithiasis risk, and whether higher lipid levels correlate with stone risk. Dyslipidemia is a known independent risk factor for urolithiasis, and emerging evidence suggests common biological pathways. Previous work has suggested that statins protect against new stone formation, but these findings have not been verified by other investigators. METHODS: We queried our Institution's Electronic Data Warehouse for all patients who were newly diagnosed with hyperlipidemia between 2009 and 2011, and had never taken a statin drug. These patients' clinical outcomes were followed until 2015, to assess whether they had been newly prescribed statins and whether they had developed symptomatic urolithiasis. Patient demographics, stone risk factors, prescription data, and serum lipid values were collected. RESULTS: A total of 101,259 patients met inclusion criteria, 47.8% of whom received a statin prescription during the study period. Patients prescribed statins were significantly older, had a greater likelihood of osteoporosis, hemiplegia, immobility, and more likely to take a thiazide diuretic. Patients without a history of urolithiasis who were started on statin therapy were significantly less likely to develop new stones than patients not taking statins. This protective effect was even greater in patients with a history of stone disease. Lipid parameters (low-density lipoprotein, triglyceride, cholesterol) were lower in the statin-treated group, suggesting overall compliance with these medications. CONCLUSION: Our data confirm previous work that statins protect against urinary stone formation; however, the underlying mechanism seems to be distinct from statins' lipid-lowering effect.