Abstract
Calcium oxalate (CaOx) is the major constituent of kidney stones. Growing evidence shows a close connection between hyperlipidemia, cardiovascular disease (CVD), and the formation of kidney stones. Owing to their antioxidant properties, statins control hyperlipidemia and may ameliorate CaOx stone formation. The present study was designed to investigate the suppressive effects of statins on CaOx urolithiasis and their potential mechanism. We used rats fed a high-fat diet (HFD) to achieve hyperlipidemia (HL) and hydroxyproline (HP) water to establish a hyperoxaluric CaOx nephrolithiasis model; the animals were administered statins (A) for 28 days. The rats were divided into eight groups treated or not with A, i.e., Control, HP, HL, HL + HP. HL aggravated urinary calcium crystallization compared to the control. Due to increased expression of renal osteopontin (OPN), a key anti-lithic protein, and reduced free radical production, the calcium crystals in the urinary bladder increased as renal calcium deposition decreased. The levels of the ion activity product of CaOx (AP(CaOx)) decreased after statins administration, and AP(Calcium phosphate) (CaP) increased, which suggested the dominant calcium crystal composition changed from CaOx to CaP after statin administration. In conclusion, atorvastatin decreases renal CaOx stone deposits by restoring OPN expression in hyperoxaluric rats fed a HFD.
Highlights
Urinary tract stone disease, known as urolithiasis, is one of the most common urologic diseases worldwide with increasing prevalence
The composition of electrolytes was generally similar in all groups, except for Pi, whose level was mildly higher in the HL + HP group
To determine the effects of statins on calcium stone formation, we used the results from the 24 h urine analysis to calculate the urinary supersaturation with respect to Calcium oxalate (CaOx) and calcium phosphate (CaP), which was assessed using the index proposed by Tiselius et al, as the ion activity product of CaOx and CaP (AP(CaOx) and AP (CaP)) [18]
Summary
Known as urolithiasis, is one of the most common urologic diseases worldwide with increasing prevalence. Accumulating evidence suggests that metabolic syndrome is closely associated with urolithiasis [3]. Several studies have suggested that renal stone formers carry a higher risk of atherosclerosis than controls without stones [4]. Numerous epidemiological studies have reported an association between metabolic syndrome and urolithiasis in recent years, the mechanism underlying this association is still unclear [5]. Dyslipidemia, the hallmark of metabolic syndrome, is linked to atherosclerosis. Oxidized low-density lipoprotein (oxLDL) is a key factor contributing to atherosclerosis [6]. Macrophages can be stimulated by oxLDL to increase reactive oxygen species (ROS) production and enhance oxidative stress (OS), and these changes are closely related to CaOx kidney stone formation [8,9]. Some studies have reported that oxLDL may represent the connection between atherosclerosis, CVD risk, and urolithiasis, these studies have yielded conflicting results [10]
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