Primary hyperparathyroidism (PHPT) is usually characterized by fasting hypercalcemia associated with inappropriately high PTH concentration. Nevertheless, cases of proven PHPT have been reported in normocalcemic patients. The purpose of the study was to investigate the mechanism(s) of persistent normocalcemia in PHPT. One hundred seventy-eight patients with PHPT were studied after exclusion of any evident cause of masked hypercalcemia. Patients were separated into normocalcemic (n = 34) and hypercalcemic (n = 144) subgroups on the basis of their fasting serum ionized calcium value. Patients with normocalcemic PHPT had, on average, a milder excess in PTH secretion assessed by a lower serum PTH concentration. Because of a clear overlap in PTH values between the two groups, normocalcemic and hypercalcemic patients were matched on the basis of serum PTH concentration, age, and sex. Patients with normocalcemic PHPT had lower fasting urine calcium excretion and renal tubular calcium reabsorption. In addition, normocalcemic patients differed from hypercalcemic patients by lower values of markers of bone turnover and plasma 1,25 dihydroxyvitamin D and higher values of renal phosphate threshold. In conclusion, a significant proportion of patients with PHPT are truly normocalcemic, and in addition to a milder increase in PTH secretion, the normocalcemic patients appear to display resistance to PTH action on bone and kidney.

Chronic kidney disease, even at moderate stages, is characterized by a high incidence of cardiovascular events. Subclinical damage to large arteries, such as increased arterial stiffness and outward remodeling, is a classical hallmark of patients with chronic kidney disease. Whether large artery stiffness and remodeling influence the occurrence of cardiovascular events and the mortality of patients with chronic kidney disease (stages 2–5) is still debated. This prospective study included 439 patients with chronic kidney disease (mean age, 59.8±14.5 years) with a mean measured glomerular filtration rate of 37 mL/min per 1.73 m 2 . Baseline aortic stiffness was estimated through carotid-femoral pulse wave velocity measurements; carotid stiffness, diameter, and intima-media thickness were measured with a high-resolution echotracking system. For the overall group of patients, the 5-year estimated survival and cumulative incidence of cardiovascular events were 87% and 16%, respectively. In regression analyses adjusted on classical cardiovascular and renal risk factors, aortic stiffness remained significantly associated with all-cause mortality (for 1 SD, Cox model–derived relative risk [95% CI], 1.48 [1.09–2.02]) and with fatal and nonfatal cardiovascular events (for 1 SD, Fine and Gray competing risks model–derived relative risk [95% CI], 1.35 [1.05–1.75]). Net reclassification improvement index was significant (29.0% [2.3–42.0%]). Carotid internal diameter was also independently associated with all-cause mortality. This study shows that increased aortic stiffness and carotid internal diameter are independent predictors of mortality in patients with stages 2 to 5 chronic kidney disease and that aortic stiffness improves the prediction of the risk.