Secondary Hyperparathyroidism and Hypertension: An Intriguing Couple

Abstract

Secondary hyperparathyroidism (SHPTH) is a major complication in patients on maintenance hemodialysis burdened with high cardiovascular risk. Hypertension is also a high prevalence complication contributing to an increase in the mortality rate in hemodialysis patients. A possible association between SHPTH and hypertension has been widely reported in the literature and several pathogenetic mechanisms have been described. There is evidence that the decrease of plasma iPTH levels are correlated with hypertension correction in hemodialysis patients undergoing parathyroidectomy and oral calcimimetics administration. We have observed a similar behaviour also in a patient on chronic hemodialysis treated with Etelcalcetide. Even if this is an isolated observation, it could stimulate future investigation, possibly in dedicated clinical trials.

Elevated parathyroid hormone one year after kidney transplantation is an independent risk factor for graft loss even without hypercalcemia

“…Since GFR reduction is a direct cause of PTH elevation, it is difficult to determine whether high PTH after KTx is mainly due to low GFR or to parathyroid gland hyperplasia [26]. In addition, hyperparathyroidism is also associated with hypertension [27]. Therefore, although adjusted by mulitivariate analysis and PS-based methods in this study, the inferior graft survival in the NC-HPT group may have been influenced by low GFR or hypertension.…”

Hypertension in Chronic Kidney Disease: An Update on Diagnosis and Management

“…Even before the anemia is corrected, these agents may cause vasoconstriction, and HTN may occur independently of an increase in hemoglobin 30 . The increase in intracellular calcium secondary to hyperparathyroidism also causes vasoconstriction 31 . Vessel wall calcification also occurs frequently in advanced renal failure and often is responsible for resistant isolated systolic HTN 32 …”

“…30 The increase in intracellular calcium secondary to hyperparathyroidism also causes vasoconstriction. 31 Vessel wall calcification also occurs frequently in advanced renal failure and often is responsible for resistant isolated systolic HTN. 32…”

A Review of Current Evidence on the Relationship between Phosphate Metabolism and Metabolic Syndrome

“…The dysregulation of RAAS has been suggested as the molecular link between these hormonal changes and hypertension. The mechanistic actions of PTH to hypertension include the increase in renin secretion as well as its direct effects on arteries and myocytes to promote arterial stiffness and left ventricular hypertrophy [ 51 , 62 ]. The upregulation of FGF-23 contributes to vascular calcium deposition and sodium reabsorption in sodium chloride cotransporter, resulting in blood volume expansion and hypertension [ 62 ].…”

“…The mechanistic actions of PTH to hypertension include the increase in renin secretion as well as its direct effects on arteries and myocytes to promote arterial stiffness and left ventricular hypertrophy [ 51 , 62 ]. The upregulation of FGF-23 contributes to vascular calcium deposition and sodium reabsorption in sodium chloride cotransporter, resulting in blood volume expansion and hypertension [ 62 ]. FGF-23 also inhibits the activation of 1,25-dihydroxyvitamin D, a potent suppressor for renin synthesis [ 63 ].…”