Diuretics and Disorders of Calcium Homeostasis
Section snippets
Use of Diuretics in Nephrolithiasis
Nephrolithiasis is a common disorder, affecting as many as 12% of men living in industrialized nations.1, 2 Approximately 70% to 80% of all kidney stones contain calcium, usually in the form of calcium oxalate or calcium phosphate, and hypercalciuria is found in 40% to 50% of these calcium stone formers. The precise etiology of hypercalciuria in these stone formers is generally not known and is termed idiopathic hypercalciuria. Without treatment, 40% to 50% of stone formers will pass a second
Association of Thiazides With Bone Health
Osteoporosis is the most prevalent metabolic bone disorder in developed countries. It is characterized by low bone mass and abnormal bone architecture, which predisposes to fractures. Risk factors for osteoporosis include age; genetic factors including sex, ethnicity, and family history; as well as environmental characteristics including nutrition and calcium intake. Many hypercalciuric patients have decreased bone density whether or not they form stones.22 Thiazides reduce urine calcium
Thiazide-Induced Hypercalcemia
Thiazide diuretics are associated with and presumably cause hypercalcemia in some patients. The hypercalcemia is typically mild and in the absence of other causes of hypercalcemia is promptly reversible on discontinuation of the thiazide. Wermers et al30 investigated the incidence of thiazide-associated hypercalcemia in Olmsted County, Minnesota. They found that the incidence was 7.7 per 100,000, with the highest rate of 55.3 per 100,000 in women aged 70 to 79 years. The average of the highest
Use of Loop Diuretics in the Treatment of Hypercalcemia
The serum calcium level represents a balance between gastrointestinal absorption of calcium, calcium flux into and out of the skeleton, as well as urinary excretion of calcium. The most common causes of hypercalcemia include primary hyperparathyroidism and malignant disease. In primary hyperparathyroidism, parathyroid hormone (PTH) will increase the serum 1,25-dihydroxycholecalciferol, resulting in increased intestinal calcium absorption. In addition, both parathyroid hormone and
Loop Diuretics and Osteoporosis
Loop diuretics increase renal calcium excretion. Treatment with loop diuretics is associated with a decrease in bone mineral density. In one cohort study including 348 postmenopausal women, use of a loop diuretic was associated with an increased risk of osteoporotic fractures.44 Rejnmark et al,45 in a randomized controlled study with bumetanide in postmenopausal women, showed that treatment with this loop diuretic for 1 year resulted in a decrease in bone mineral density measured from: the
Loop Diuretics, Nephrolithiasis, and Nephrocalcinosis
Furosemide-related nephrocalcinosis was first reported by Hufnagle et al47 in low-birth-weight premature infants in 1982. These calcifications generally resolve on discontinuation of the diuretic. The nephrocalcinosis caused by furosemide appears related to hypercalciuria, but has been reported even in infants who are not hypercalciuric.48 Resolution of the nephrocalcinosis occurs more often if the hypercalciuria resolves after stopping furosemide.
In adults, Kim et al49 reported medullary
Carbonic Anhydrase Inhibitors and Nephrocalcinosis
Carbonic anhydrase inhibitors act in the proximal tubule to inhibit bicarbonate reabsorption and can cause metabolic acidosis. Hypocitraturia, hypercalciuria, nephrocalcinosis, and nephrolithiasis have been reported with acetazolamide.50, 51 It is likely that both hypocitraturia and hypercalciuria lead to nephrocalcinosis and nephrolithiasis owing to the carbonic anhydrase inhibitors. Metabolic acidosis will decrease urinary citrate, which is an important inhibitor of nephrolithiasis because it
Conclusions
Although diuretics commonly are administered to increase sodium excretion, they do have significant effects on calcium balance. The effects often can be explained physiologically by the site of action of these diuretics in the nephron. Thiazides can be used therapeutically in nephrolithiasis whereas loop diuretics can be used as an adjunct to the treatment of hypercalcemia. Both thiazides and loop diuretics appear to have effects on bone. In the case of acetazolamide, secondary metabolic
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2018, Best Practice and Research: Clinical Endocrinology and MetabolismCitation Excerpt :PTH-secretion is not believed to be directly stimulated, but PTH is often inappropriately high and this makes differentiation towards primary hyperparathyroidism challenging [122,123]. Thiazide induced hypercalcemia is normally mild and non-progressive (equilibrium) [124,125]. Hypercalcemia normally resolves within months after discontinuation of medication.
The evidence and rationale for the perioperative use of loop diuretics during kidney transplantation: A comprehensive review
2018, Transplantation ReviewsCitation Excerpt :This causes inactivation of calcium dependent proteases and mitochondrial dysfunction [72,86–88]. LD increase calcium excretion via multiple mechanisms [89]. In rat hearts, LD use significantly improved the mechanical recovery and the coronary flow of the hearts preserved for 8 h [88].
Primary Hyperparathyroidism and the Kidney
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