Procalcitonin and the inflammatory response to salt in essential hypertension: A randomized cross-over clinical trial

Objectives: Inflammation is considered as a major effector of arterial damage brought about by salt excess in animal models. In a randomized, single masked, cross-over study in 32 uncomplicated essential hypertensive patients, we assessed the effect of a short-term low-salt diet on biomarkers of innate immunity [procalcitonin (PCT), interleukin-6, C-reactive protein, and tumor necrosis factor-A (TNF-A)], adiponectin (ADPN, an anti-inflammatory cytokine), and leptin. Methods: Patients were randomized to either a 10-20 mmol sodium diet and sodium tablets (180 mEq/day) to achieve a 200 mmol intake per day or the same diet and identical placebo tablets, each for 2 weeks. At the end of each of these periods, all patients underwent a 24-h urine collection, a fasting blood sampling, and a 24 h ambulatory blood pressure monitoring. Results: In parallel with expected increase in plasma renin activity and aldosterone (P<0.001), both PCT (R33%) and TNF-A (9%) rose at low salt intake (P<0.007) while ADPN underwent an opposite change (-17%, P<0.001). In a linear regression analysis for repeated measurements, PCT was significantly and inversely related to urinary salt (weighted r=-0.27, P=0.03). Changes in inflammation biomarkers did not differ in salt-sensitive (n=7) and salt-resistant (n=25) patients. Conclusion: In essential hypertensive patients, a very low salt diet generates a pro-inflammatory phenotype characterized by an increase in PCT and TNF-A and an opposite effect on an anti-inflammatory cytokine like ADPN. © Lippincott Williams and Wilkins.