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Department of Medicine, Queen Mary Hospital, University of Hong Kong, 102 Pok Fu Lam Road, Hong Kong, E-mail: aymwang{at}hku.hk
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, New Territories, Hong Kong
Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, New Territories, Hong Kong
Dear Sir:
The daily ultrafiltration volume of patients with 25-hydroxyvitamin D [25(OH)D] 
45.7 nmol/L and those with 25(OH)D concentrations > 45.7 nmol/L was 7.49 ± 1.36 and 7.45 ± 1.33 L, respectively (P = 0.85). The need for hypertonic (glucose: 3.86%) peritoneal dialysis (PD) solution did not differ between patients with 25(OH)D concentrations 45.7 nmol/L and those with concentrations > 45.7nmol/L. Only one patient from either group used 2 L of 3.86% PD solution daily and one patient from either group used 4 L of 3.86% PD solution daily (P = 1.0). These results suggested that the use of hypertonic glucose solution and the daily ultrafiltration volume had no relation with serum 25(OH)D in PD patients. However, we cautioned that this did not rule out a possible relation between volume status and 25(OH)D because daily ultrafiltration volume did not necessarily relate to the volume status of patients. Volume status was also partly determined by the fluid intake of these patients.
Our additional analysis showed that 89 of the 230 PD patients had experienced previous complications with heart failure. Those with previous history of heart failure had significantly lower serum 25(OH)D concentrations than those with no history of heart failure (45.4 ± 18.5 compared with 53.2 ± 21.8 nmol/L; P = 0.006). The exact mechanism of this association is currently not clear but may suggest that either patients with previous history of heart failure were at increased risk of 25(OH)D deficiency or that patients with 25(OH)D deficiency had increased risk of heart failure. A previous study reported similar findings of a lower serum 25(OH)D concentration in patients with heart failure compared with control subjects (1). Further study will be needed to determine the exact interrelation between 25(OH)D deficiency and heart failure.
The association between residual renal function (RRF) and serum 25(OH)D concentrations in PD patients suggested that 25(OH)D deficiency may partly be the culprit link between loss of RRF and increased cardiovascular mortality in PD patients. In this study we did not record the calcium content of the PD fluids in our PD patients. Thirty-seven percent of our PD patients received oral active vitamin D as a treatment of secondary hyperparathyroidism.
It is of interest to note that serum 25(OH)D concentrations showed a differential relationship with the cardiovascular outcomes of PD patients depending on the severity of left ventricular (LV) systolic dysfunction and hypertrophy. Among patients with well-preserved LV systolic function and among patients with less severe LV hypertrophy, those with a higher serum 25(OH)D concentration had better cardiovascular event–free survival compared with those with lower serum 25(OH)D concentrations. The significance of serum 25(OH)D was retained when adjusting for different clinical, biochemical, and dialysis parameters, including RRF. On the other hand, a low serum 25(OH)D concentration had no significant impact on the cardiovascular outcomes of patients with established LV systolic dysfunction and more severe LV hypertrophy. This observation is novel and intriguing. The explanation is not clear but suggests that serum 25(OH)D may be more involved in early but not advanced cardiac disease in end-stage renal disease. It raises the possibility that correction of serum 25(OH)D deficiency may be of value in improving the cardiovascular outcomes of patients with less established or less severe cardiac disease but not those in patients with severe and advanced cardiac disease and will require further testing in future studies. A causal relationship has yet to be proven by intervention trials with vitamin D. There is experimental evidence that 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is a negative endocrine regulator of the renin-angiotensin system (2). In vitamin D receptor knockout mice, cardiac hypertrophy developed as a consequence of activation of both the systemic and cardiac renin-angiotensin system. These data suggest that 1,25(OH)2D3 regulates cardiac function, at least in part, through the renin-angiotensin system (3). Activated vitamin D has also been shown to attenuate LV abnormalities induced by dietary sodium in Dahl salt-sensitive rats (4). The involvement of 25(OH)D in cardiac function is also evident from a recent clinical study showing that low concentrations of 25(OH)D and 1,25(OH)2D were associated with prevalent myocardial dysfunction, deaths due to heart failure, and sudden cardiac death in the general population (5). Our data are in keeping with the study by Wolf et al, which reported an association between 25(OH)D deficiency and early mortality in incident hemodialysis patients. Furthermore, a significant interaction was observed between vitamin D levels, subsequent active vitamin D therapy, and survival in that untreated, 25(OH)D-deficient patients showed an even greater risk of early mortality (6). Another recent study also confirmed that the use of oral active vitamin D was associated with improved survival in hemodialysis patients (7).
We agree that it will be interesting to include volume status indices as a confounder in the survival analysis. However, there is currently no gold standard marker for assessing volume status in PD patients. The bioelectric impedance analysis provides information on total body water but does not provide an absolute cutoff above which patients are considered to be volume overloaded. Serum cardiac biomarkers such as N-terminal pro-brain natriuretic peptide may become elevated with extracellular volume overload but their interpretations are confounded by RRF and preexisting cardiac disease (8). The use of inferior vena cava diameter also has its limitations because it varies with respiration. We believe that further prospective studies will be needed to evaluate the efficacy of oral active vitamin D in lowering mortality and cardiovascular death in dialysis patients, taking into account the baseline cardiac status of these patients.
ACKNOWLEDGMENTS
No conflicts of interest were reported.
REFERENCES
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