Dietary Acid Reduction With Fruits and Vegetables or Bicarbonate Attenuates Kidney Injury in Patients With a Moderately Reduced Glomerular Filtration Rate Due to Hypertensive Nephropathy

Nimrit Goraya; Jan Simoni; Chanhee Jo; Donald E Wesson

Disclosures

Kidney Int. 2012;81(1):86-93. 

In This Article

Results

Table 1 shows general subject characteristics by group at baseline. There was no significant difference in age, weight, systolic BP (Sys BP), or gender proportion among groups. Subjects with metabolic acidosis were excluded (Materials and Methods), but P-value for venous plasma total CO2 (TCO2), across all groups, supports slightly, but significantly, lower plasma TCO2 in CKD 2 than in CKD 1. Nevertheless, there were no differences in potential renal acid load, a measure of dietary acid intake,[9] or in urine 8 h net acid excretion (8 h NAE) between CKD 1 and CKD 2. Urine albumin excretion (Ualb), a general index of the course and level of kidney injury,[10] was not significantly different among groups. Urine N-acetyl β-D-glucosaminidase excretion (UNAG), an index of tubulo-interstitial injury,[11] was not different among groups, but CKD 2 had higher urine excretion of transforming growth factor-β (UTGF), a possible mediator of hypertensive nephropathy activity,[12] than CKD 1.

Table 2 shows net changes in acid–base parameters at 30 days after HCO3, F+V, or no intervention (Time Control). Venous plasma TCO2 did not change significantly in any group. Although potential renal acid load did not decrease in either HCO3 group, potential renal acid load decreased in CKD 1 F+V and CKD 2 F+V. Each intervention to reduce dietary acid decreased 8 h NAE in both CKD 1 and CKD 2, and the net decrease was not significantly different between respective F+V and HCO3 groups of CKD 1 and CKD 2.

Figure 1 shows box plots for net Ualb change (post–pre) in the three CKD 1 and CKD 2 groups. Net Ualb change was not different among the three CKD 1 groups (P=0.201). Net Ualb for CKD 2 Time Control (9.0±29 mg/g Creatinine (Cr)) was not significantly different from zero (P=0.0564), but Ualb significantly decreased in CKD 2 HCO3 (−14.7±22.2 mg/g Cr, P<0.001 versus zero) and CKD 2 F+V (−34.3±46.9 mg/g Cr, P<0.001 versus zero). Figure 1 also shows that the net Ualb decrease was significantly more than Time Control in CKD 2 HCO3 (P=0.003) and CKD 2 F+V (P<0.001), and that the net decrease in CKD 2 F+V was significantly greater than CKD 2 HCO3 (P=0.012).

Figure 1.

Box plots of change of urine albumin (mg)-to-creatinine (g) ratio (Ualb) for the three groups of subjects with estimated glomerular filtration rate (eGFR) >90 ml/min (CKD 1) and eGFR 60–90 ml/min (CKD 2). CKD, chronic kidney disease; F+V, subjects given fruits+vegetables for 30 days; HCO3, subjects given oral NaHCO3 daily for 30 days; Time Control, subjects followed up for 30 days with no further intervention. * P<0.05 versus Time Control; + P<0.05 versus HCO3.

Figure 2 shows box plots of the net UNAG change (post–pre) in the three groups of CKD 1 and CKD 2. After 30 days, net UNAG change was not significantly different among the three CKD 1 groups (P=0.994). On the other hand, net UNAG significantly increased for CKD 2 Time Control (0.062±0.136 U/g Cr, P=0.006) but significantly decreased for CKD 2 HCO3 (−0.088±0.134 U/g Cr, P<0.001) and CKD F+V (−0.080±0.080 U/g Cr, P<0.001). Figure 2 shows that the net UNAG decrease was significantly greater than CKD 2 Time Control in CKD 2 HCO3 (P<0.001) and CKD 2 F+V (P<0.001), but the net decrease was not significantly different between CKD 2 HCO3 and CKD 2 F+V (P=0.081).

Figure 2.

Box plots of change of urine N-acetyl-β-D-glucosaminidase (U)-to-creatinine (g) ratio (UNAG) for the three groups of subjects with eGFR >90 ml/min (CKD 1) and eGFR 60–90 ml/min (CKD 2). CKD, chronic kidney disease; F+V, subjects given fruits+vegetables for 30 days; HCO3, subjects given oral NaHCO3 daily for 30 days; Time Control, subjects followed up for 30 days with no further intervention. * P<0.05 versus Time Control.

Figure 3 shows box plots of the net change (post–pre) of UTGF. After 30 days, UTGF significantly decreased in CKD 1 Time Control (−1.819±3.106 ng/g Cr, P=0.005), HCO3 (−2.223±2.721 ng/g Cr, P<0.001), and F+V (−2.397±3.403 n/g Cr, P=0.001), but net UTGF decrease was not significantly different among the three CKD 1 groups (P=0.783). By contrast, UTGF significantly increased in CKD 2 Time Control (2.298±6.994 ng/g Cr, P=0.044) but decreased in HCO3 (−6.888±4.953 ng/g Cr, P<0.001) and F+V (−6.483±4.908 ng/g Cr, P<0.001). Figure 3 shows that net UTGF decrease was significantly greater than CKD 2 Time Control in CKD 2 HCO3 (P<0.001) and CKD 2 F+V (P<0.001), but the net decrease was not significantly different between HCO3 and F+V (P=0.751).

Figure 3.

Box plots of change of urine transforming growth factor-β (ng)-to-creatinine (g) ratio (UTGF) for the three groups of subjects with estimated glomerular filtration rate (eGFR) >90 ml/min (CKD 1) and eGFR 60–90 ml/min (CKD 2). CKD, chronic kidney disease; F+V, subjects given fruits+vegetables for 30 days; HCO3, subjects given oral NaHCO3 daily for 30 days; Time Control, subjects followed up for 30 days with no further intervention. * P<0.05 versus Time Control.

Table 3 shows the net change in body weight, Sys BP, and selected plasma and urine parameters. Body weight did not change significantly in Time Control and HCO3 groups of both CKD 1 and CKD 2, but it decreased significantly in both CKD 1 and CKD 2 groups given F+V. The net body weight decrease was not significantly different between CKD 1 and CKD 2 groups given F+V (P=0.062). Similarly, Sys BP did not change significantly in any Time Control or HCO3 group, but decreased significantly in both CKD 1 and CKD 2 given F+V. In contrast to body weight, the net Sys BP decrease was significantly greater in CKD 2 F+V than in CKD 1 F+V (P=0.001).

In addition, Table 3 shows the net change in plasma levels and urine excretion of Na+ (UNaV) and K+ (UKV). Plasma Na+ did not change significantly in any group and plasma K+ did not change significantly in any CKD 1 group. Although plasma K+ did not significantly change in CKD 2 Time Control and CKD 2 F+V, plasma K+ decreased slightly but significantly in CKD 2 group given HCO3, and the net decrease was greater than CKD 2 Time Control and F+V. Both UNaV and UKV increased significantly in CKD 1 and CKD 2 groups given HCO3, and the net increase in CKD 1 and CKD 2 was significantly greater than their respective Time Control. UNaV decreased significantly and UKV increased significantly in both CKD 1 and CKD 2 groups given F+V, and the net UNaV decrease and the net UKV increase in both CKD 1 and CKD 2 groups given F+V were significantly different from their respective Time Control. The UKV increase was greater in the respective F+V than in the HCO3 group for CKD 1 (P<0.001) and CKD 2 (P<0.001).

Table 3 also shows the net change in plasma levels and urine excretion of endothelin (ET)-1 and aldosterone. Urine ET-1 excretion (UET), a surrogate of kidney ET-1 levels,[13] did not decrease in any CKD 1 group or in CKD Time Control. By contrast, UET decreased significantly in both intervention groups of CKD 2, and the net decrease was significantly greater than CKD 2 Time Control in both CKD 2 intervention groups. Urine aldosterone excretion (Ualdo), a surrogate of kidney aldosterone levels,[7] significantly decreased in both the intervention groups of CKD 1 and CKD 2. The net decrease in Ualdo was significantly greater in both the intervention groups than the respective Time Controls in both CKD 1 and CKD 2. Although the net Ualdo decrease was not significantly different between the two CKD 1 intervention groups, the net Ualdo decrease was greater in CKD 2 HCO3 than in CKD 2 F+V.

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