Does Ruizhi Rosuvastatin Calcium Tablets have any effect on the liver and kidneys?

Some patients with hypertension and hyperlipidemia should know about the drug Rosuvastatin Calcium Tablets. Since the above diseases require long-term treatment, and the drug cannot be discontinued during the treatment, otherwise the disease will easily relapse. Rosuvastatin Calcium Tablets can effectively relieve many hypercholesterolemia. So does Rosuvastatin Calcium Tablets have any effect on the liver and kidneys?

First, does Rosuvastatin Calcium Tablets have any effect on the liver and kidneys ? Rosuvastatin is a selective and competitive HMG-CoA reductase inhibitor. HMG-CoA reductase is the rate-limiting enzyme in the conversion of 3-hydroxy-3-methylglutaryl-CoA to mevalonate, a precursor of cholesterol. The results of animal and cell culture experiments show that rosuvastatin is highly and selectively taken up by the liver, and the liver is the target organ for lowering cholesterol. The results of in vivo and in vitro experiments showed that rosuvastatin could increase the number of hepatic LDL receptors on the cell surface, thereby enhancing the uptake and catabolism of LDL, and inhibit the synthesis of vldl in the liver, thereby reducing the total number of vldl and LDL particles.

Second, for patients with homozygous and heterozygous familial hypercholesterolemia, non-familial hypercholesterolemia, and mixed dyslipidemia, rosuvastatin can reduce total cholesterol, LDL-C, APOB, and non-HDL-C levels. Rosuvastatin can also reduce TG and increase HDL-C levels. For patients with simple hypertriglyceridemia, rosuvastatin can reduce total cholesterol, LDL-C, VLDL-C, APOB, non-HDL-C, and TG levels, and increase HDL-C levels. The effect of rosuvastatin on cardiovascular morbidity and mortality has not been determined.

Does Rosuvastatin Calcium Tablets have any effect on the liver and kidneys ? Effect of Rosuvastatin Calcium Tablets on the kidneys: Proteinuria (test paper method) was observed in patients receiving this product, and most of the protein originated from the renal tubules. Less than 1% of patients had an increase in proteinuria from none or trace to ++ or more at some point during treatment with 10 mg and 20 mg, and this proportion was approximately 3% of patients receiving 40 mg. In the 20 mg dose treatment, proteinuria ranging from no or trace increases to mild increases of + were observed. In most cases, proteinuria decreases or disappears spontaneously with continued treatment. A causal relationship between proteinuria and acute or progressive renal disease cannot be established based on clinical trials and postmarketing data to date. Hematuria has been observed in patients taking this drug, but data from clinical trials indicate that the incidence is low.