Cross-talk between renal lithogenesis and atherosclerosis: an unveiled link between kidney stone formation and cardiovascular diseases

Abstract

The prevalence of kidney stones and cardiovascular diseases (CVDs) are increasing throughout the world. Both diseases are chronic and characterized by accumulation of oxidized proteins and lipids in the renal tissue and arterial wall, respectively. Emerging studies have revealed a positive association between nephrolithiasis and CVDs. Based on preclinical and clinical evidences, this review discusses: (i) stone forming risk factors, crystal nucleation, aggregation, injury-induced crystal retention, and stone formation, (ii) CVD risk factors such as dyslipidemia, perturbation of gut microbiome, obesity, free radical-induced lipoprotein oxidation, and retention in the arterial wall, subsequent foam cell formation, and atherosclerosis, (iii) mechanism by which stone forming risk factors such as oxalate, calcium, uric acid, and infection contribute toward CVDs, and (iv) how CVD risk factors, such as cholesterol, phospholipids, and uric acid, contribute to kidney stone formation are described.

Excretion of urine extracellular vesicles bearing markers of activated immune cells and calcium/phosphorus physiology differ between calcium kidney stone formers and non-stone formers

“…Differences in the urinary biochemical pro le of the CSF versus NSF group in the current study were not surprising, including lower urine pH and greater calcium and phosphorous excretion and uric acid SS (Table 1) in CSF [4,16,27,44]. Urine calcium and phosphorus excretion in high RP participants were markedly higher compared with NSFs, however those of low RP were not signi cantly different.…”

Lipidomics Reveals the Therapeutic Effects of EtOAc Extract of Orthosiphon stamineus Benth. on Nephrolithiasis

“…In addition, NF-kB upregulates the expression of pro-inflammatory cytokines and adhesion molecules to promote leukocyte adhesion, increase the release of oxygen free radicals and aggravate tissue damage (Holthe et al, 2004). In damaged cells and kidney tissues, crystals preferentially attach and aggregate into the nucleus, and the attached crystals can destroy the cells and form new tissue damage (Devarajan, 2018). From the aforementioned words, this study suggests that a potential mechanism of EEOS extracts in the treatment of stones may be through the regulation of fatty acid composition on glycerophospholipids to mediate oxidative stress and inflammation.…”

A Short Review on the Relationships Between Nephrolithiasis and Myocardial Infarction

“…Based on the normal secretion of oxalate and morphology of the nephrons, the particle should not reach a size to tangle up in the nephrons. The assumption of damages to the urothelium leads to the tangling of the crystal in the nephrons giving rise to nucleation followed by cellular damage and completion of stone formation cycle [30]. [54].The nucleus of this plaque is separately located in the interstitial tissue, which is interconnected in the basal membrane, near to which hyaline crystals deposit.…”