Renal vascular hyperresponsiveness to elevated ionized calcium in spontaneously hypertensive rat kidneys

Abstract

First, renal vascular responses to high [Ca+2] in SHR are exaggerated. At the upper end of the hypercalcemia range the observed changes in renal flow at constant perfusion pressure were modest, however, and with lesser degrees of hypercalcemia they may be anticipated to be even less pronounced. Second, effects of high [Ca+2] were abolished after verapamil. If these findings are clinically applicable, they are of interest when calcium is infused in patients with hypertension.

Acute kidney injury in the patient with cancer

“…In some scenarios, such as with multiple myeloma, the presence of hypercalcemia may potentiate other AKI etiologies. Hypercalcemia promotes direct afferent arteriolar vasoconstriction and also leads to volume depletion from excessive renal sodium and water loss [101]. Hypercalcemia causes sodium wasting at the loop of Henle by activating the calcium-sensing receptor, and also leads to renal water losses by blocking arginine vasopressin activity in the distal nephrons [2].…”

Acute Kidney Injury in the Patient with Cancer

“…Hypercalcemia leads to severe volume depletion via the activation of the calcium sensor located in the thick ascending loop of Henle, causing a furosemide-like effect [20]. Hypercalcemia leads to the vasoconstriction of the afferent arteriole, decreasing intra-glomerular pressure [21]. Finally, the precipitation of calcium phosphate crystals and clogging of the tubules have been described [22].…”