Hyperparathyroidism Hypertension

The pathogenesis of hypertension in patients with CKD is multifactorial and includes fluid retention, increased sympathetic activity, an endogenous digitalis-like substance, elevated levels of endothelin-1, erythropoietin use, hyperparathyroidism, and structural arterial changes. 

Blum M, Kirsten M, Worth MH Jr. Reversible hypertension. Caused by the hypercalcemia of hyperparathyroidism, vitamin D toxicity, and calcium infusion. JAMA 1977 237(3) 262-3. 

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... 

Congestive heart failure is common and is related to fluid overload, hypertension, or atherosclerosis. Some workers have postulated a uremic cardiomyopathy. The enhancement by parathormone of cellular calcium uptake may contribute to myocardial calcification, degeneration, and fibrosis (M26). There is a higher incidence of calcification of the aortic and mitral valves, as well as of visceral and peripheral arteries in association with uremic hyperparathyroidism (M13). In addition to PTH, middle molecules (B19), phenols (L3), guanidino-succinic acid (K5), or cobalt (P6) may contribute to the observed cardiotoxicity in vitro of uremic serum. 

The patient s plasma PTH should be measured and, if increased, a diagnosis of primary hyperparathyroidism can be made. However, hyperparathyroidism with a serum calcium of 2.8 mmol/1 is usually asymptomatic and thus another cause for his hypertension, headaches and anxiety should be sought. If the symptoms were episodic this would suggest the possibility of a phaeochromocytoma which is associated with hyperparathyroidism in families with MEN. The patient should have his urinary catecholamines measured and, if the diagnosis is made, it is important that other members of his family be screened for hyperparathyroidism and phaeochromocytoma. 

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