Perirenal fat differs in patients with chronic kidney disease receiving different vitamin D-based treatments: a...

Chronic kidney disease (CKD) patients show high rates of cardiovascular disease (CVD) and mortality. In the general population, obesity, hypertension, and diabetes are known as the classical CVD risk factors. However, CKD patients have other predisposing CVD factors more associated with bone and mineral metabolism disorders (BMD). BMD originates from reduced 1,25-dihydroxy vitamin D and hypocalcemia, which lead to secondary hyperparathyroidism, with increased parathyroid hormone (PTH) levels and hyperphosphatemia as the progression of renal damage. Due to their pleiotropic effects, vitamin D and its analogs, such as cholecalciferol, calcitriol, or paricalcitol, have proven effective in controlling BMD and CVD. On the other hand, visceral adiposity has been shown to increase the risk for CVD in both the general and CKD populations via complex autocrine and paracrine hormonal mechanisms. This seems to be the case with fat surrounding the epicardium. Although it has not been widely evaluated, the fat surrounding the kidneys, or the perirenal adipose tissue (PAT), could also share similarities with the epicardial in terms of its potential contribution to the CVD risk observed in these patients. We conducted a preliminary study to assess differences in PAT on a sample of patients with CKD presenting diverse CVD history and who were receiving different vitamin D-receptor activators.

An observational study was performed at UNIRENAL Center (Venezuela), from January to November 2015. Analytical and clinical parameters were evaluated. The PAT thickness was measured in centimeters through a B-mode ultrasound. Thus, we included 83 CKD patients treated with vitamin D or analogs (mean age 58.3 ± 16y); 57.83% were females. Nearly half of the sample was classified as CKD-G3 (n = 40). Prior history of CVD was present in 55.4% (N = 46) of participants. Must of the patients (n = 46;55.42%) receiving oral cholecalciferol (1000 IU/day) as part of the treatment for lower levels of vitamin D or BMD related to CKD (mainly elevated PTH), followed by those under calcitriol at 0.5 mcg/day (n = 27;32.53%), and around 12% (n = 10;12.05%) on paricalcitol (1 mcg/day). The mean treatment vintage was 20 ± 6 months for cholecalciferol, 18 ± 4 months for calcitriol, and 16 ± 2 months for paricalcitol. Those with a history of CVD (n = 46) showed higher levels of urea (mean 62.0vs45.2 mg/dl, p < 0.05), uric acid (mean 5.5vs4.3 mg/dl; p < 0.03), and iPTH (mean 186.2vs65.2pcg/dl; p < 0.05) than patients free of CVD events (n = 37). These findings were also in parallel with decreased renal function in the group with previous CVD history, as evidenced by a significantly lower eGFR (mean 53.55vs89.00 ml/min/1.73 m²,p < 0.001). Similarly, the mean PAT thickness was elevated in the group with a history of CVD in relation to those with no previous CVD events (0.99vs0.80 cm; SD ± 0.30;p ~ 0.05). The comparative analysis for the patients with prior cardiovascular events between the three treatments revealed that those on paricalcitol had lesser PAT accumulation than those treated with cholecalciferol or calcitriol (p < 0.05). In conclusion, our study shows that PAT thickness in CKD may be influenced by vitamin D analog-based treatment. Further research is needed to better understand the mechanistic links between PAT, BMD, and CVD in this population.