The objective of this meta-analysis was to evaluate the associations between consumption of sugar-sweetened

and artificially sweetened soda and CKD. A literature search was performed using MEDLINE, EMBASE and the Cochrane Database of Systematic Reviews from inception until 30 June 2014. Studies that reported odds ratios or hazard ratios comparing the risk of CKD in patients consuming significant amounts of either sugar-sweetened or artificially sweetened soda versus those who did not consume soda were included. Pooled risk ratios (RR) and 95% confidence intervals (CI) were calculated using a random-effects, generic inverse variance method. Five studies were included in our analysis of the association between consumption of sugar-sweetened soda and CKD. The pooled RR of CKD in patients consuming sugar-sweetened soda was 1.58 (95% CI 1.00–2.49). Four studies were selected to assess the association between Akt inhibitor consumption of artificially sweetened soda and CKD. The pooled RR of CKD in patients consuming artificially sweetened soda was 1.33 (95% CI 0.82–2.15). Our study demonstrates statistically significant increased AZD0530 risks of CKD in

patients consuming sugar-sweetened soda, but not in patients consuming artificially sweetened soda. This finding suggests that sugar-sweetened soda consumption is associated with CKD and may impact clinical management and primary prevention of CKD in high-risk patients. “
“The

intrarenal renin-angiotensin system (RAS) has been reported to be activated in chronic proteinuria patients. This study aimed to compare intrarenal RAS activity between diabetic nephropathy (DN) and non-diabetic nephropathy (NDN) patients with overt proteinuria. A multicenter, cross-sectional study was conducted in 116 patients with overt proteinuria (urinary protein/creatinine ratio [uPCR] > 1 mg/mg Cr). To estimate intrarenal RAS activity we measured urinary excretion of angiotensinogen (uAGT) and renin (uRenin) in patients with DN (n = 38) and NDN (n = 78). Both natural logarithms of uAGT/urinary second creatinine (ln[uAGT/uCr]) and uRenin (ln[uRenin/uCr]) levels were significantly higher in patients with DN compared with those with NDN (ln[uAGT/uCr]: 4.16 ± 1.13 vs. 3.52 ± 1.21 in NDN, P = 0.007; ln[uRenin/uCr]: 5.66 ± 1.60 vs. 4.29 ± 1.48 in NDN, P < 0.001), when estimated glomerular filtration rate (eGFR) and uPCR showed no significant difference between the two groups (P > 0.05). In a subgroup analysis, according to amount of proteinuria, both uAGT and uRenin were higher in DN in patients with subnephrotic-range proteinuria (uPCR < 3.5 mg/mg Cr), as expected. However, in patients with nephrotic-range proteinuria (uPCR ≥ 3.5 mg/mg Cr), only uRenin was higher in DN compared to NDN. In a multiple regression analysis, diabetes maintained independent association with uRenin excretion.