Short-term aerobic exercise and vascular function in CKD stage 3: a randomized controlled trial.

BACKGROUND: The present study was designed to determine the effect of short-term moderate-intensity exercise training on arterial stiffness in patients with chronic kidney disease (CKD) stage 3. STUDY DESIGN: Randomized controlled trial with a parallel-group design. SETTING & PARTICIPANTS: Testing and training sessions were performed at Springfield College. 46 (treatment group, n=25; control group, n=21) patients with CKD with diabetes and/or hypertension completed the study. INTERVENTION: The aerobic training program consisted of 16 weeks of supervised exercise training at 50%-60% peak oxygen uptake (Vo2peak) 3 times per week, while the control group remained sedentary. Identical testing procedures were performed following the 16-week intervention. OUTCOMES: The primary outcome was arterial stiffness. Secondary outcomes were aerobic capacity, various blood parameters (endothelin 1, nitrate/nitrite, and high-sensitivity C-reactive protein), and health-related quality of life. MEASUREMENTS: Arterial stiffness was assessed with aortic pulse wave velocity (PWV), aerobic capacity by Vo2peak, blood parameters by enzyme-linked immunosorbent assays, and health-related quality of life by the 36-Item Short Form Health Survey (SF-36). Participants attended 4 sessions before being randomly assigned to either the treatment or control group. Participants gave consent during the first session, whereas a graded exercise test with measurement of Vo2peak was completed during the second session. During sessions 3 and 4, aortic PWV was measured at rest prior to 40 minutes of either moderate-intensity exercise training or seated rest. A venous blood sample was obtained prior to exercise or rest and participants completed the SF-36 questionnaire. RESULTS: 16 weeks of training led to an 8.2% increase in Vo2peak for the treatment group (P=0.05), but no changes in aortic PWV . LIMITATIONS: Randomization was not concealed and was violated on one occasion; also, use of an indirect measurement of endothelial function and the short duration of the intervention. CONCLUSIONS: Short-term moderate-intensity exercise training does not alter arterial stiffness in patients with CKD, but seems to reduce endothelin 1 levels.

Serum C-reactive protein and leptin as predictors of kidney disease progression in the Modification of Diet in Renal Disease Study.

BACKGROUND: In vitro and in vivo data suggest that markers of inflammation and nutritional status may be risk factors for the progression of chronic kidney disease. METHODS: We investigated whether higher levels of C-reactive protein (CRP) and leptin were risk factors for progression of chronic kidney disease in the Modification of Diet in Renal Disease (MDRD) Study. Frozen samples were assayed for high sensitivity C-reactive protein (CRP) or leptin in 804 patients. CRP and leptin were then evaluated as risk factors for glomerular filtration rate (GFR) decline using univariate and multivariable analyses. RESULTS: At baseline, the mean (median) CRP in Study A (GFR between 25 and 55 mL/min/1.73 m2) and Study B (GFR between 13 and 24 mL/min/1.73 m2) were 0.48 (0.25) and 0.46 (0.20) mg/dL, respectively, while the mean (median) leptin in Study A and Study B were 15.2 (9.80) and 15.1 (7.80) ng/mL, respectively. Mean follow-up time was 2.2 years. The mean GFR decline was -4.33 and -3.65 mL/min/year in Study A and B, respectively. There was no significant association between the rate of GFR decline with the level of CRP or leptin in multivariable analysis in Study A [0.08 (-0.14, 0.30) mL/min/year slower GFR decline per twofold increase in CRP level; and 0.14 (-0.13, 0.40) mL/min/year slower GFR decline per twofold increase in leptin level], or in multivariable analysis in Study B [-0.05 (-0.28, 0.18) mL/min/year faster GFR decline per twofold increase in CRP level; and -0.12 (-0.42, 0.19) mL/min/year faster GFR decline per twofold increase in leptin level]. CONCLUSIONS: Higher serum levels of CRP and leptin are not independent risk factors for progression of non-diabetic kidney disease.