Background. Metabolic syndrome is a risk factor for nephrolithiasis. This study was performed to evaluate the clinical and biochemical profile of calcium-oxalate nephrolithiasis in stone formers with metabolic syndrome. Methods. A total of 526 recurrent stone formers, 184 of them with metabolic syndrome, and 214 controls were examined on a free diet and after a sodium-restricted diet (sodium intake <100 mmol/24 h). Results. On free diet, stone formers with metabolic syndrome showed higher sodium excretion [mean (95% confidence interval), 196 (176218) vs 160 (150168)mmol/24 h; P < 0.01] and lower citrate excretion [2.23 (1.992.58) vs 2.84 (2.513.17)mmol/24 h; P < 0.01] compared to controls, whereas stone formers without metabolic syndrome showed higher calcium and oxalate excretion [5.43 (5.015.82) vs 3.58 (2.844.19) and 0.34 (0.320.36) vs 0.26 (0.200.31)mmol/24 h for calcium and oxalate, respectively; P < 0.01] and lower citrate excretion [2.18 (1.982.38) vs 2.84 (2.513.17)mmol/24 h; P < 0.01] compared to controls. The ion activity product of urinary calcium-oxalate salts was similar between stone formers with and without metabolic syndrome [1.41 (1.311.59) vs 1.40 (1.351.45); P > 0.05]. After the test diet, this index was lower in diet-compliant stone formers with metabolic syndrome compared to diet-compliant stone formers without metabolic syndrome [1.15 (1.101.21) vs 1.39 (1.311.45); P < 0.01]. Conclusions. The biochemical profiles and responses to the sodium-restricted diet were significantly different between stone formers with metabolic syndrome and those without. Dietary habits play a central role in the pathogenesis of nephrolithiasis in stone formers with metabolic syndrome.
The melatonin receptor 1a (MTNR1A) gene is associated with recurrent and idiopathic calcium nephrolithiasis
Esposito T;Magliocca S;Gianfrancesco F;
2012
Abstract
Background. Metabolic syndrome is a risk factor for nephrolithiasis. This study was performed to evaluate the clinical and biochemical profile of calcium-oxalate nephrolithiasis in stone formers with metabolic syndrome. Methods. A total of 526 recurrent stone formers, 184 of them with metabolic syndrome, and 214 controls were examined on a free diet and after a sodium-restricted diet (sodium intake <100 mmol/24 h). Results. On free diet, stone formers with metabolic syndrome showed higher sodium excretion [mean (95% confidence interval), 196 (176218) vs 160 (150168)mmol/24 h; P < 0.01] and lower citrate excretion [2.23 (1.992.58) vs 2.84 (2.513.17)mmol/24 h; P < 0.01] compared to controls, whereas stone formers without metabolic syndrome showed higher calcium and oxalate excretion [5.43 (5.015.82) vs 3.58 (2.844.19) and 0.34 (0.320.36) vs 0.26 (0.200.31)mmol/24 h for calcium and oxalate, respectively; P < 0.01] and lower citrate excretion [2.18 (1.982.38) vs 2.84 (2.513.17)mmol/24 h; P < 0.01] compared to controls. The ion activity product of urinary calcium-oxalate salts was similar between stone formers with and without metabolic syndrome [1.41 (1.311.59) vs 1.40 (1.351.45); P > 0.05]. After the test diet, this index was lower in diet-compliant stone formers with metabolic syndrome compared to diet-compliant stone formers without metabolic syndrome [1.15 (1.101.21) vs 1.39 (1.311.45); P < 0.01]. Conclusions. The biochemical profiles and responses to the sodium-restricted diet were significantly different between stone formers with metabolic syndrome and those without. Dietary habits play a central role in the pathogenesis of nephrolithiasis in stone formers with metabolic syndrome.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.