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BACKGROUND Kidney transplantation (KTx) reverses most abnormalities related to chronic kidney disease (CKD), but sedentary lifestyle persists in most kidney graft recipients. Physical inactivity has been associated with altered adipokine profile and inflammation in CKD. We postulated that increased physical activity achieved through an individually-tailored program can reverse these changes. MATERIAL AND METHODS We included 25 clinically stable KTx recipients at least 12 months after transplantation and with eGFR &gt;30 mL/min and 15 age-matched non-dialysis patients with CKD stage 3. Body composition, pattern of daily physical activity, and serum concentrations of leptin, adiponectin, NT-proBNP, and hsCRP were assessed at baseline. All patients in both groups participated in a 12-week supervised exercise program with short cell phone text reminders. All measurements were repeated after 3 months. RESULTS Active energy expenditure increased significantly during the 3 months in both the KTx and CKD patients, compared with baseline by 47% (p&lt;0.001) and 20% (p=0.01), respectively. Time spent daily on physical activity was also increased (129±83 vs. 194±142 and 81±56 vs. 124±57 min, respectively, p&lt;0.001). Adipose tissue mass decreased significantly in the KTx group (from 40.8±11 to 38.5±10.3 kg, p=0.01). Serum leptin decreased significantly in both KTx and CKD patients (from 11.5±7.0 to 10.0±5.6, p=0.03 and from 14.1±8.3 to 12.2±6.1 ng/mL, p=0.01, respectively). Serum adiponectin increased only in the KTx group (from 1900±953 to 2015±1133 ng/L, p=0.004). Serum CRP decreased in both groups (from 15.1±5.2 to 14.0±5.6 mg/L, p=0.01 in the KTx group and from 16.5±3.9 to 15.4±4.3 mg/L in the CKD group p=0.05). NTpro-BNP was unchanged during the study. CONCLUSIONS Increased physical activity induces beneficial effects on adipokine profile and inflammation but does not seem to affect volume overload in kidney transplant recipients and CKD patients.

Effects of a Structured Physical Activity Program on Serum Adipokines and Markers of Inflammation and Volume Overload in Kidney Transplant Recipients