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Epidemiological data suggest an association between kidney stones and some features of metabolic syndrome such as an overweight condition, arterial hypertension or glucose intolerance. However, mechanisms remain to be elucidated. This study aimed to evaluate insulin resistance, as assessed by homeostasis model assessment (HOMA-IR), and urine composition analysis in patients affected by calcium nephrolithiasis. A cohort of 61 (38 male, 29-57 years of age) non-diabetic calcium stone formers was studied. Data about body mass index, arterial blood pressure, serum biochemistry including parathyroid hormone and calcitriol were recorded in all the patients; fasting glucose and insulin were determined to calculate HOMA-IR value and accordingly the patients were grouped into tertiles. Urine pH and urinary excretion of calcium, citrate, phosphate, oxalate, uric acid, urea and creatinine were measured on 24h urine samples. Patients of the highest HOMA-IR tertile showed lower urine citrate levels than patients of the lowest HOMA-IR tertile (475+/-243 vs. 630+/-187 mg/24h, p<0.05), whereas no difference was detected as far as urinary oxalate, calcium, uric acid, phosphate, and urine pH and urine volume output were concerned. HOMA-IR values were positively related to uric acid serum levels (r=0.31, p<0.05) and negatively to urinary citrate excretion (r=-0.26, p<0.05). Hypocitraturic patients showed higher levels of HOMA-IR than normocitraturic ones (3.03+/-0.92 vs. 2.25+/-1.19, p<0.05). This study shows that a higher level of insulin resistance is associated with lower urinary citrate excretion, and that hypocitraturic patients show a greater insulin resistance than normocitraturic calcium stone formers. This may be related to changes in citrate, Na(+)-K(+) and H(+) renal tubule transports, which have been described in insulin resistance. In conclusion, insulin resistance may contribute to an increased risk of calcium stone formation by lowering urinary citrate excretion. This finding suggests the need for a careful metabolic assessment in patients known to form calcium stones in order to ensure stone recurrence prevention and cardiovascular protection.
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PMID:Insulin resistance and low urinary citrate excretion in calcium stone formers. 1718 67

In recent years stone disease has become more widespread in developed countries. At present the prevalence is 5.2 and 15% of men and 6% of women are affected. The increase is linked to changes in lifestyle, eating patterns and obesity which has become very common. The 'metabolic syndrome' includes all the diseases, e.g. hypertension, lipid imbalances, type 2 diabetes mellitus, gout and cardiovascular disease, which are concomitant in the majority of stone formers. Dietary patterns, besides leading to stone formation, also determine stone chemistry. With a diet that is rich in oxalates, calcium oxalate will constitute 75% of stones, struvite 10-20%, uric acid 5-6% and cystine 1%. As approximately 50% of patients with stones suffer recurrences, metabolic and/or pharmacological prophylaxis is recommended.
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PMID:Prevention of stone disease. 1772 51

In our societies, the increase of the frequency of the diseases of overweight, in particular obesity, diabetes type 2 and metabolic syndrome, coincides with that of the urinary lithiasis. Like the lithiasic disease, the metabolic syndrome or syndrome X is multi-factor. Several epidemiological studies were interested in research of a physiopathological relation between the various components of this syndrome (obesity, arterial hypertension, diabetes, dyslipemy) and lithogenesis. During the metabolic syndrome, resistance to insulin and the defect of renal ammoniogenesis constitute the principal disorders supporting lithogenesis. The defect of renal ammoniogenesis armature by the resistance of the renal cells to insulin involves a urinary hyperacidity which supports the crystallization of the uric acid responsible for the formation of uric or mixed uric acid/oxalate stones.
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PMID:[Metabolic syndrome: pathophysiology and impact on lithogenesis]. 1822

Over the past 10 years, major progress has been made in the pathogenesis of uric acid and calcium stones. These advances have led to our further understanding of a pathogenetic link between uric acid nephrolithiasis and the metabolic syndrome, the role of Oxalobacter formigenes in calcium oxalate stone formation, oxalate transport in Slc26a6-null mice, the potential pathogenetic role of Randall's plaque as a precursor for calcium oxalate nephrolithiasis, and the role of renal tubular crystal retention. With these advances, we may target the development of novel drugs including (1) insulin sensitizers; (2) probiotic therapy with O. formigenes, recombinant enzymes, or engineered bacteria; (3) treatments that involve the upregulation of intestinal luminal oxalate secretion by increasing anion transporter activity (Slc26a6), luminally active nonabsorbed agents, or oxalate binders; and (4) drugs that prevent the formation of Randall's plaque and/or renal tubular crystal adhesions.
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PMID:Recent advances in the pathophysiology of nephrolithiasis. 1964 81

The current obesity epidemic in the United States has deleterious effects on the health of the population. Temporally related to the increase in obesity is an increase in the prevalence of urolithiasis. Epidemiologic studies have shown that the incident stone risk increases with body mass index. Obesity can increase stone risk in multiple ways. Excess nutritional intake increases traffic of lithogenic substances such as calcium, oxalate, and uric acid. Metabolic syndrome, commonly associated with obesity, alters renal acid-base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. The low urine pH is caused by deficient ammonia production, which appears to be related to insulin resistance. Even weight-loss programs to combat obesity can influence stone risk. Contemporary bariatric surgery has been shown to frequently cause hyperoxaluria with associated stone formation and even oxalate nephropathy. Commonly used low-carbohydrate diets increase the risk of both calcium and uric acid stones. Certainly, the many health risks of obesity, including urolithiasis, necessitate weight loss, but recognition of the potential complications of such therapies is required to prevent induction of new and equally severe medical problems. The optimal approach to weight control that minimizes stone risk needs to be determined.
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PMID:Obesity and urolithiasis. 1909 1

Management of obesity-associated comorbidities costs about $60 billion/year, about 5% of total US healthcare expenditure. Bariatric surgery is the only proven effective weight loss therapy for severely obese patients with a BMI > or =35 kg/m2. Bariatric surgery produces long-term weight loss, improves quality of life, and reduces the number of sick days and medication costs. Surgery has a profound effect on the metabolic milieu and nutritional status from the first few days after surgery, even before significant weight loss has been achieved. Metabolic effects of bariatric surgery reduce obesity-related comorbidities like type 2 diabetes, hypertension, metabolic syndrome, and cardiovascular disease risk. Improvement in renal function is seen, but adverse effects like oxalate nephropathy can lead to chronic kidney disease or end-stage renal disease (CKD/ESRD). Surgery can also lead to micronutrient deficiencies, making dietary supplementation necessary. Reduction in insulin resistance and hypertension after surgery makes medication adjustment imperative. Improvement in comorbidities and nutritional deficiencies after bariatric surgery has important clinical implications.
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PMID:Metabolic, renal, and nutritional consequences of bariatric surgery: implications for the clinician. 2129 38

A nationwide survey of urolithiasis in Japan conducted in 2005 disclosed its steady increase in incidence and the life-long risk was estimated to be 15% in men and 6% in women. The recurrence rate has also increased, to 70 -80% in the extracorporeal shock wave lithotripsy (ESWL) era from around 50% previously. Although urolithiasis is very common and highly recurrent, the impact and concern of stone disease are not necessarily as high as expected either medically or socially, because of its benign nature and easy accessibility to treatments by ESWL and/or endourological procedures. Dramatic progress is taking place both experimentally and clinically in this field, such as development of a simple method of measuring metastable limits using a microplate, clarifying altered oxalate metabolism due to insulin resistance and close relationship between stone disease and metabolic syndrome, elucidating the exact role of osteopontin in an experimental model at a molecular level, prophylaxis of stone disease by angiotensin II type I receptor blocker, and addition of a new modality of fiberscopic transurethral lithotripsy (f-TUL) to the conventional endourological treatments. We hope that "change and future perspective" in the field of urolithiasis will be discussed and clarified in this symposium.
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PMID:[Change in concepts of urolithiasis: recent advances in pathogenesis, assessment, treatment and prophylaxis]. 2130 58

Recent epidemiological studies revealed an association of obesity, diabetes mellitus, hypertension and metabolic syndrome (MetS) with kidney stone disease. We examined how these disorders cause kidney stones. A clinical study on 467 patients with nephrolithiasis at our institution revealed that clustering of MetS traits increased the risk of uric acid stone formation by decreasing urinary pH. A subsequent study analyzing detailed data from 30,448 patients enrolled in the 6th Nationwide Survey on Urolithiasis in Japan showed that clustering of MetS traits were associated with an increased severity of the kidney stone disease and elevated urinary excretion of calcium, uric acid and oxalate. Finally, the OLETF rats, an animal model of MetS, showed lower urinary pH, decreased citrate excretion, and increased uric acid and calcium excretion. In addition, the administration of pioglitazone, an agent that improves insulin resistance, significantly increased the urinary pH. These results indicate that MetS causes changes in urinary constituents, leading to an increased risk of both uric acid and calcium oxalate stone formation. We suggest that kidney stone disease should be considered as a component of MetS and that the improvement in insulin resistance by means of diet and lifestyle changes and medical therapy might help to prevent this disorder.
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PMID:[Metabolic syndrome and nephrolithiasis]. 2130 61

Epidemiologically, there are many same characteristics among patients with urolithiasis, life-style related diseases and metabolic syndrome. In a comparison with the major urological diseases, the patients with stone disease have the largest amount of visceral fat on computerized tomography. The patients who finally had a diagnosis of metabolic syndrome in urolithiasis were 43% of men and female 31%. The clinical features of the patients include increased urinary oxalate excretion, abnormal uric acid metabolism, and acidic urine. The basic studies by the animal experiments suggest that there is a close relationship between urolithiasis and metabolic syndrome. After the treatment of the urinary stone, it is very important to make a long-term follow-up by not only the prevention of recurrent stone episode but also life style management and medical treatment for metabolic syndrome.
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PMID:[Relationship between metabolic syndrome and urinary stone disease]. 2196 Feb 34

Epidemiological studies have provided the evidence for association between nephrolithiasis and a number of cardiovascular diseases including hypertension, diabetes, chronic kidney disease, metabolic syndrome. Many of the co-morbidities may not only lead to stone disease but also be triggered by it. Nephrolithiasis is a risk factor for development of hypertension and have higher prevalence of diabetes mellitus and some hypertensive and diabetic patients are at greater risk for stone formation. An analysis of the association between stone disease and other simultaneously appearing disorders, as well as factors involved in their pathogenesis, may provide an insight into stone formation and improved therapies for stone recurrence and prevention. It is our hypothesis that association between stone formation and development of co-morbidities is a result of certain common pathological features. Review of the recent literature indicates that production of reactive oxygen species (ROS) and development of oxidative stress (OS) may be such a common pathway. OS is a common feature of all cardiovascular diseases (CVD) including hypertension, diabetes mellitus, atherosclerosis and myocardial infarct. There is increasing evidence that ROS are also produced during idiopathic calcium oxalate (CaOx) nephrolithiasis. Both tissue culture and animal model studies demonstrate that ROS are produced during interaction between CaOx/calcium phosphate (CaP) crystals and renal epithelial cells. Clinical studies have also provided evidence for the development of oxidative stress in the kidneys of stone forming patients. Renal disorders which lead to OS appear to be a continuum. Stress produced by one disorder may trigger the other under the right circumstances.
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PMID:Is oxidative stress, a link between nephrolithiasis and obesity, hypertension, diabetes, chronic kidney disease, metabolic syndrome? 2221 19


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