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The association of metabolic syndrome and urolithiasis.

Wong YV, Cook P, Somani BK - Int J Endocrinol (2015)

Bottom Line: Several hypotheses have been proposed to explain the pathophysiology of urolithiasis resulting from metabolic syndrome, amongst which are the insulin resistance and Randall's plaque hypothesis.Studies have found many factors contributing to urolithiasis in patients suffering from metabolic syndrome, out of which obesity, overweight, and sedentary lifestyles have been identified as major etiological factors.Primary and secondary prevention methods therefore tend to revolve mainly around lifestyle improvements, including dietary and other preventive measures.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, University Hospital Southampton NHS Trust, Southampton SO16 6YD, UK.

ABSTRACT
There has been an increasing prevalence of kidney stones over the last 2 decades worldwide. Many studies have indicated a possible association between metabolic syndrome and kidney stone disease, particularly in overweight and obese patients. Many different definitions of metabolic syndrome have been suggested by various organizations, although the definition by the International Diabetes Federation (IDF) is universally considered as the most acceptable definition. The IDF definition revolves around 4 core components: obesity, dyslipidemia, hypertension, and diabetes mellitus. Several hypotheses have been proposed to explain the pathophysiology of urolithiasis resulting from metabolic syndrome, amongst which are the insulin resistance and Randall's plaque hypothesis. Similarly the pathophysiology of calcium and uric acid stone formation has been investigated to determine a connection between the two conditions. Studies have found many factors contributing to urolithiasis in patients suffering from metabolic syndrome, out of which obesity, overweight, and sedentary lifestyles have been identified as major etiological factors. Primary and secondary prevention methods therefore tend to revolve mainly around lifestyle improvements, including dietary and other preventive measures.

No MeSH data available.


Related in: MedlinePlus

Description of Randall's plaque and the view from a ureteroscope [57].
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fig2: Description of Randall's plaque and the view from a ureteroscope [57].

Mentions: Randall's plaque is primarily found on the thin basement membrane at the beginning of the loop of Henle which is believed to be the primary site of stone attachment [15]. Evan illustrated, in an endoscopic and histologic study, that the majority of calcium oxalate stones (75%) are formed attached to sites of Randall's plaque in idiopathic calcium oxalate stone formers [16]. Furthermore, a unified theory on pathogenesis of Randall's plaque was proposed where urinary abnormalities such as hypercalciuria, hyperoxaluria, hypocitraturia, renal stress, or trauma lead to renal epithelial injury. The nucleation of calcium phosphate crystals is then enhanced by an increased production of bone-specific proteins and reduced inhibition of crystallization inhibitors, leading to calcification of membranous cellular degradation products and other fibers until the plaque reaches the papillary epithelium (see Figure 2) [17]. The renal epithelium exposure to crystals of calcium phosphate generates reactive oxygen species (ROS), causing injury and the development of oxidation stress [18]. Randall's plaque has recently become a new prognostic factor for idiopathic calcium urolithiasis and an indicator for stone recurrence by endoscopic assessment of the papillary calcification [19].


The association of metabolic syndrome and urolithiasis.

Wong YV, Cook P, Somani BK - Int J Endocrinol (2015)

Description of Randall's plaque and the view from a ureteroscope [57].
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4385647&req=5

fig2: Description of Randall's plaque and the view from a ureteroscope [57].
Mentions: Randall's plaque is primarily found on the thin basement membrane at the beginning of the loop of Henle which is believed to be the primary site of stone attachment [15]. Evan illustrated, in an endoscopic and histologic study, that the majority of calcium oxalate stones (75%) are formed attached to sites of Randall's plaque in idiopathic calcium oxalate stone formers [16]. Furthermore, a unified theory on pathogenesis of Randall's plaque was proposed where urinary abnormalities such as hypercalciuria, hyperoxaluria, hypocitraturia, renal stress, or trauma lead to renal epithelial injury. The nucleation of calcium phosphate crystals is then enhanced by an increased production of bone-specific proteins and reduced inhibition of crystallization inhibitors, leading to calcification of membranous cellular degradation products and other fibers until the plaque reaches the papillary epithelium (see Figure 2) [17]. The renal epithelium exposure to crystals of calcium phosphate generates reactive oxygen species (ROS), causing injury and the development of oxidation stress [18]. Randall's plaque has recently become a new prognostic factor for idiopathic calcium urolithiasis and an indicator for stone recurrence by endoscopic assessment of the papillary calcification [19].

Bottom Line: Several hypotheses have been proposed to explain the pathophysiology of urolithiasis resulting from metabolic syndrome, amongst which are the insulin resistance and Randall's plaque hypothesis.Studies have found many factors contributing to urolithiasis in patients suffering from metabolic syndrome, out of which obesity, overweight, and sedentary lifestyles have been identified as major etiological factors.Primary and secondary prevention methods therefore tend to revolve mainly around lifestyle improvements, including dietary and other preventive measures.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, University Hospital Southampton NHS Trust, Southampton SO16 6YD, UK.

ABSTRACT
There has been an increasing prevalence of kidney stones over the last 2 decades worldwide. Many studies have indicated a possible association between metabolic syndrome and kidney stone disease, particularly in overweight and obese patients. Many different definitions of metabolic syndrome have been suggested by various organizations, although the definition by the International Diabetes Federation (IDF) is universally considered as the most acceptable definition. The IDF definition revolves around 4 core components: obesity, dyslipidemia, hypertension, and diabetes mellitus. Several hypotheses have been proposed to explain the pathophysiology of urolithiasis resulting from metabolic syndrome, amongst which are the insulin resistance and Randall's plaque hypothesis. Similarly the pathophysiology of calcium and uric acid stone formation has been investigated to determine a connection between the two conditions. Studies have found many factors contributing to urolithiasis in patients suffering from metabolic syndrome, out of which obesity, overweight, and sedentary lifestyles have been identified as major etiological factors. Primary and secondary prevention methods therefore tend to revolve mainly around lifestyle improvements, including dietary and other preventive measures.

No MeSH data available.


Related in: MedlinePlus