Urinary calcium excretion in treated and untreated essential hypertension.

Abstract

A high prevalence of hypercalciuria has been reported in patients with essential hypertension. Nevertheless, the clinical and therapeutic implications of this finding have scarcely been studied. This study was designed to determine the prevalence of hypercalciuria in an unselected population with essential hypertension and to analyze the relationship between the urinary calcium and the clinical and therapeutic status of these patients. This article presents a prospective study of 112 patients with essential hypertension and 49 healthy normotensive control subjects. Urinary excretion rates of calcium, sodium, chloride, potassium, urinary calcium/creatinine index, the fractional excretion of sodium, potassium and uric acid, the creatinine clearance and serum values of creatinine, urea, uric acid, electrolytes, total proteins, parathormone (intact molecule), plasma renin activity, aldosterone, glucose, and insulin (fasting and after an oral glucose load) were performed in every patient and control subject. Untreated hypertensive patients had a higher prevalence of hypercalciuria (35% had a urinary calcium/creatinine ratio > 0.20 versus 20% of treated hypertensives and 2% of control subjects; P < 0.001). Patients on thiazide or beta-blocker monotherapy had lower urinary excretion rates of calcium and urate than patients on calcium-antagonist monotherapy or untreated patients. Urinary calcium, sodium, and urate correlated positively both in treated and untreated essential hypertension patients. Patients with the higher urinary calcium levels also had higher excretion rates of sodium and urate, higher creatinine clearance rates, and lower serum creatinine and serum uric acid levels. It was concluded that hypercalciuria is a frequent finding of untreated essential hypertension. The association of high urinary calcium levels with high urinary urate excretion rates in the same patient may predispose to development of lithiasis in patients with essential hypertension. Antihypertensive drugs have a variable effect on calciuria-uricosuria, which may constitute an additional criterion in the selection and individualization of therapy. Thiazides and beta-blockers can decrease calciuria and uricosuria and, therefore, the lithogenic risk in these patients.

Investigating the effect of history of fractures and hypertension on the risk of all-cause death from osteoporosis: A retrospective cohort study

“…Generally speaking, patients with osteoporosis who have history of fractures often met the diagnosis of severe osteoporosis, if the patients also accompanied by hypertension, which would mediate a common pathway to significantly raise the death risk of osteoporosis. The possible mechanisms are as follows: hypertension could increase the loss of calcium in urine for patients with osteoporosis who have history of fractures, leading to a negative calcium balance for bone remodeling and further reducing BMD [ 20 ] ; epidemiological studies have found that with the enhancement of blood pressure, the rate of mineral loss in bone increases, thus further reducing BMD in osteoporosis patients with history of fractures; hypertension is associated with high concentrations of parathyroid hormone and accelerates bone conversion, which causing the reducing in bone quality and bone mass [ 21 ] ; hypertension may damage brain structures associated with gait control and balance, leading to falls and subsequent fractures. [ 22 ]…”

“…Model have history of fractures, leading to a negative calcium balance for bone remodeling and further reducing BMD [20] ; epidemiological studies have found that with the enhancement of blood pressure, the rate of mineral loss in bone increases, thus further reducing BMD in osteoporosis patients with history of fractures; hypertension is associated with high concentrations of parathyroid hormone and accelerates bone conversion, which causing the reducing in bone quality and bone mass [21] ; hypertension may damage brain structures associated with gait control and balance, leading to falls and subsequent fractures. [22] The strength of our study should be pointed.…”

The Effect of Extracellular Calcium Metabolism on Aldosterone Biosynthesis in Physiological and Pathological Status

“…For instance, urinary Ca excretion levels were elevated in patients with hypertension. In addition, patients with EH were also reported to harbor a higher prevalence of hypercalciuria with significantly positive correlation between urinary Ca levels and blood pressure 7 . Increased levels of parathyroid hormones and activated vitamin D were also reported in EH patients in response to the increased urinary excretion of calcium 8 9 .…”

“…Under these regulatory mechanisms above, serum calcium level is considered to be maintained within normal ranges in these patients [10]. However, the detailed mechanisms of calcium metabolic disorders in EH patients have still remained in dispute [7,8,[11][12][13].…”