Association of inflammation and malnutrition with cardiac valve calcification in continuous ambulatory peritoneal dialysis patients

Cardiac valve calcification (VC) has long been regarded as a consequence of aging and abnormal calcium-phosphate metabolism in uremic patients, In vie w of the recent recognition of association among inflammation, malnutrition , and atherosclerosis, the possible role of inflammation and malnutrition i n VC was investigated. Inflammatory markers (including C-reactive protein [ CRP], fibrinogen, and basal metabolic rate) and nutritional status (assesse d using serum albumin, subjective global nutrition assessment, and handgrip strength) were examined, in addition to calcium phosphate parameters and o ther traditional cardiovascular risk factors, including gender, smoking hab its, BP, and lipid profile. in relation to VC in 137 patients who were on c ontinuous ambulatory peritoneal dialysis. Compared with patients with no VC , patients with VC not only were older (60 [10] versus 54 [12] yr; P=0.005) , had higher plasma phosphate (1.89 [0.52] versus 1.64 [0.41] mmol/L; P=0.0 03), and had higher parathyroid hormone (83 [40, 145] versus 38 [16, 71] pm ol/L; P=0.001) but also had higher CRP (4.5 [0.1, 13.4] versus 0.2 [0.1, 4. 4] mg/L; P=0.004), had higher fibrinogen (6.6 [1.9] versus 5.7 [1.3] g/L; P = 0.002), and had lower serum albumin (26 [4] versus 29 [3] g/L; P = 0004) . Twenty-three percent of patients with VC versus 17% of patients with no V C were moderately to severely malnourished according to subjective global n utrition assessment (P = 0.05). Even after adjustment for patients' age, du ration of continuous ambulatory peritoneal dialysis, diabetes, and calcium x phosphate product, cardiac VC remained strongly associated with CRP (odds ratio, 1.05; P=0.026) and albumin (odds ratio, 0.85; P = 0.01). The data s uggest that VC not only is a passive degenerative process but also involves active inflammation, similar to that seen in atherosclerosis. The presence of uncontrolled hyperphosphatemia and hyperparathyroidism further accelera tes the progression of calcification. The data also indicate that VC and at herosclerosis should be considered as associated syndromes, sharing similar pathogenic mechanisms, namely active inflammation.