The potential harmful effects of rosuvastatin on kidney function
Reviewed Dat Tien Nguyen, B.A, ScM. Posted on July 22nd, 2022
Rosuvastatin and Atorvastatin are hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibiting agents. These medications are frequently prescribed to treat hyperlipidemia, hypercholesterolemia, and to prevent cardiovascular disease. These statins are available in Vietnam in both generic and branded forms. Rosuvastatin is sold under the brand name Perosu, Crestor, Liporosa, Rostor, Robinul, etc. And Atorvastatin can be found under the brand name Lipirus, Lipistad, Lipitor, Safena, Atorlip, Shintovas, Vaslor, etc. A recent multicenter study by Dr. Jung-Im Shin, MD, PhD and colleagues found that Rosuvastatin has a higher risk of kidney damage than Atorvastatin.
The retrospective study was conducted with data collected from almost 1 million patients who were prescribed either Rosuvastatin or Atorvastatin between 2011 and 2019. The study found that Rosuvastatin and Atorvastatin have similar effectiveness at preventing myocardial infarction and stroke. However, the risk of hematuria, kidney failure, and proteinuria is 8%, 15%, and 17% higher for those who were taking Rosuvastatin. The effect Rosuvastatin has on the kidney correlates with the kidneys’ current state of function. When comparing patients with a declined kidney function (eGFR below 30 mL/min per 1.73 m2) to those with an eGFR above 60 mL/min per 1.73 m2, the former has a two-fold risk of developing hematuria and a nine-fold risk of developing proteinuria.
The mechanism behind statin damage to the kidney is not fully understood, but in vitro study might have provided a possible explanation. In human and animal kidney cell culture, the agent interferes with the activity of HMG-CoA reductase in the proximal tubule cells. As a result, the process of protein reuptake in the proximal nephron is inhibited. The different rate in renal excretion between Rosuvastatin and Atorvastatin can be a possible reason behind the difference in kidney damage. 10% of Rosuvastatin is excreted through the kidney; this is higher than the 1% of Atorvastatin. The higher passage rate of the former through the kidney might have increased the interference to the protein uptake process carried out by HMG-CoA reductase in the kidney.
It is in the current guideline of the American Cardiology Association and the American Heart Association that 40-80 mg of Atorvastatin and 20-40 mg of Rosuvastatin should be taken daily as high-intensity treatment to reduce the ratio of Low-Density Lipoprotein Cholesterol (LDL-C) by 40%. Similar recommendation is made by the Vietnamese Ministry of Health with regards to the usage and dosage of Atorvastatin and Rosuvastatin. Given the findings of the study, with similar effectiveness at preventing myocardial infarction and stroke, modifications could be made to existing guideline to prefer the usage of Atorvastatin to Rosuvastatin in patients who are at a higher risk of renal complication or are currently experiencing declined kidney function.
The retrospective study was conducted with data collected from almost 1 million patients who were prescribed either Rosuvastatin or Atorvastatin between 2011 and 2019. The study found that Rosuvastatin and Atorvastatin have similar effectiveness at preventing myocardial infarction and stroke. However, the risk of hematuria, kidney failure, and proteinuria is 8%, 15%, and 17% higher for those who were taking Rosuvastatin. The effect Rosuvastatin has on the kidney correlates with the kidneys’ current state of function. When comparing patients with a declined kidney function (eGFR below 30 mL/min per 1.73 m2) to those with an eGFR above 60 mL/min per 1.73 m2, the former has a two-fold risk of developing hematuria and a nine-fold risk of developing proteinuria.
The mechanism behind statin damage to the kidney is not fully understood, but in vitro study might have provided a possible explanation. In human and animal kidney cell culture, the agent interferes with the activity of HMG-CoA reductase in the proximal tubule cells. As a result, the process of protein reuptake in the proximal nephron is inhibited. The different rate in renal excretion between Rosuvastatin and Atorvastatin can be a possible reason behind the difference in kidney damage. 10% of Rosuvastatin is excreted through the kidney; this is higher than the 1% of Atorvastatin. The higher passage rate of the former through the kidney might have increased the interference to the protein uptake process carried out by HMG-CoA reductase in the kidney.
It is in the current guideline of the American Cardiology Association and the American Heart Association that 40-80 mg of Atorvastatin and 20-40 mg of Rosuvastatin should be taken daily as high-intensity treatment to reduce the ratio of Low-Density Lipoprotein Cholesterol (LDL-C) by 40%. Similar recommendation is made by the Vietnamese Ministry of Health with regards to the usage and dosage of Atorvastatin and Rosuvastatin. Given the findings of the study, with similar effectiveness at preventing myocardial infarction and stroke, modifications could be made to existing guideline to prefer the usage of Atorvastatin to Rosuvastatin in patients who are at a higher risk of renal complication or are currently experiencing declined kidney function.