It has traditionally been defined as having a daily calcium excretion of greater than 4 mg/kg body weight. Hypercalciuria is often considered the most frequent metabolic risk factor of calcium nephrolithiasis. It also has a role in osteopenia and osteoporosis.
Its importance stems mainly from two clinical entities: bone resorption and nephrolithiasis. Hypercalciuric calcium stone formers have a lower bone mineral density on average compared to individuals with neither stone nor hypercalciuric.
Epidemiology
Hypercalciuria affects 5-10% of the adult population and accounts for roughly one-third of all calcium stone formation. Close relatives of hypercalciuric patients are more likely to develop hypercalciuria themselves. It also has a 20% likelihood in postmenopausal women with osteoporosis and no history of kidney stones.
Hypercalciuria affects up to 40% of first and second-degree relatives of hypercalciuric recurrent stone formers. In the United States, over thirty million kidney stone patients and 1.2 million new kidney stone cases are reported annually.
There is an increased risk of hypercalciuria in children with severe vesicoureteral reflux. The most typical stone constitution in children is calcium phosphate and oxalate; however, obesity and nephrolithiasis do not appear to be linked in children, unlike in adults who develop kidney stones.
Anatomy
Pathophysiology
Enhanced gastrointestinal calcium absorption elevates serum calcium levels while decreasing serum levels of Vitamin D and parathyroid hormone. Only 20% of the calcium consumed is absorbed, which generally occurs in the duodenum. Renal calcium elimination is about 5-10% of all hypercalciuric stone formers have hypercalciuria.
It is caused by a renal malfunction that results in mandatory calcium loss in the urine, irrespective of dietary calcium intake or serum calcium levels. It is generally accompanied by hypocalcemia and increased PTH levels in the blood. The calcium/creatinine ratio is elevated, and there is a correlation to the medullary sponge kidney.
Hypophosphatemia is caused by increased urine phosphate excretion caused by renal impairment. It causes increased Vitamin D activation in the kidney, which enhances intestinal phosphate absorption to compensate for the low serum phosphate. Unfortunately, the additional Vitamin D boosts intestinal calcium absorption. The additional calcium absorbed is eliminated in the urine, causing hypercalciuria.
This kind of hypercalciuria is vitamin D dependent and resistant to thiazides. Pregnancy causes an increase in hypercalciuria in all three trimesters. Still, it does not seem to increase the incidence of the new stone disease since there is an elevation in kidney stone inhibitors. In patients with nephrolithiasis, bone mineral density is inversely associated with hypercalciuria.
There is an association between recurring stomach pain and hypercalciuria in children. A recent study indicates hypercalciuric pediatric kidney stone patients increase lipid metabolism/transport-related protein urine excretion. This shows that problems in lipid metabolism may be responsible for or linked to pediatric hypercalciuria and nephrolithiasis.
Etiology
The proximal tubule absorbs more than 60% of the serum calcium filtered by the glomerulus. A paracellular system involving the tight junction proteins claudins-2 and -12 accomplishes this. Water, specifically sodium reabsorption, drives this process. A similar mechanism is used to resorb about 20% to 25% of the residual calcium in the thick ascending limb of Henle. Several chemical pathways are used by the distal convoluted tubule and the collecting ducts to maintain the remaining calcium excretion and reabsorption.
The most common cause of typical idiopathic hypercalciuria is a genetic mutation or alteration within one of the calcium reabsorption mechanisms. The recommended normal limits for calcium or creatinine ratios vary by age since young children and newborns often have higher urine calcium excretion and lesser urinary creatinine levels.
Milk-alkali syndrome, Paget disease, sarcoidosis, paraneoplastic syndrome, glucocorticoid excess, multiple myeloma, Addison disease, metastatic cancers involving bone, and hypervitaminosis D are other causes of hypercalciuria. A diet rich in animal protein will result in an acid loading that emits calcium from the bones and inhibits calcium reabsorption in the renal tubules, leading to hypercalciuria.
It has traditionally been defined as having a daily calcium excretion of greater than 4 mg/kg body weight. Hypercalciuria is often considered the most frequent metabolic risk factor of calcium nephrolithiasis. It also has a role in osteopenia and osteoporosis.
Its importance stems mainly from two clinical entities: bone resorption and nephrolithiasis. Hypercalciuric calcium stone formers have a lower bone mineral density on average compared to individuals with neither stone nor hypercalciuric.
Hypercalciuria affects 5-10% of the adult population and accounts for roughly one-third of all calcium stone formation. Close relatives of hypercalciuric patients are more likely to develop hypercalciuria themselves. It also has a 20% likelihood in postmenopausal women with osteoporosis and no history of kidney stones.
Hypercalciuria affects up to 40% of first and second-degree relatives of hypercalciuric recurrent stone formers. In the United States, over thirty million kidney stone patients and 1.2 million new kidney stone cases are reported annually.
There is an increased risk of hypercalciuria in children with severe vesicoureteral reflux. The most typical stone constitution in children is calcium phosphate and oxalate; however, obesity and nephrolithiasis do not appear to be linked in children, unlike in adults who develop kidney stones.
Enhanced gastrointestinal calcium absorption elevates serum calcium levels while decreasing serum levels of Vitamin D and parathyroid hormone. Only 20% of the calcium consumed is absorbed, which generally occurs in the duodenum. Renal calcium elimination is about 5-10% of all hypercalciuric stone formers have hypercalciuria.
It is caused by a renal malfunction that results in mandatory calcium loss in the urine, irrespective of dietary calcium intake or serum calcium levels. It is generally accompanied by hypocalcemia and increased PTH levels in the blood. The calcium/creatinine ratio is elevated, and there is a correlation to the medullary sponge kidney.
Hypophosphatemia is caused by increased urine phosphate excretion caused by renal impairment. It causes increased Vitamin D activation in the kidney, which enhances intestinal phosphate absorption to compensate for the low serum phosphate. Unfortunately, the additional Vitamin D boosts intestinal calcium absorption. The additional calcium absorbed is eliminated in the urine, causing hypercalciuria.
This kind of hypercalciuria is vitamin D dependent and resistant to thiazides. Pregnancy causes an increase in hypercalciuria in all three trimesters. Still, it does not seem to increase the incidence of the new stone disease since there is an elevation in kidney stone inhibitors. In patients with nephrolithiasis, bone mineral density is inversely associated with hypercalciuria.
There is an association between recurring stomach pain and hypercalciuria in children. A recent study indicates hypercalciuric pediatric kidney stone patients increase lipid metabolism/transport-related protein urine excretion. This shows that problems in lipid metabolism may be responsible for or linked to pediatric hypercalciuria and nephrolithiasis.
The proximal tubule absorbs more than 60% of the serum calcium filtered by the glomerulus. A paracellular system involving the tight junction proteins claudins-2 and -12 accomplishes this. Water, specifically sodium reabsorption, drives this process. A similar mechanism is used to resorb about 20% to 25% of the residual calcium in the thick ascending limb of Henle. Several chemical pathways are used by the distal convoluted tubule and the collecting ducts to maintain the remaining calcium excretion and reabsorption.
The most common cause of typical idiopathic hypercalciuria is a genetic mutation or alteration within one of the calcium reabsorption mechanisms. The recommended normal limits for calcium or creatinine ratios vary by age since young children and newborns often have higher urine calcium excretion and lesser urinary creatinine levels.
Milk-alkali syndrome, Paget disease, sarcoidosis, paraneoplastic syndrome, glucocorticoid excess, multiple myeloma, Addison disease, metastatic cancers involving bone, and hypervitaminosis D are other causes of hypercalciuria. A diet rich in animal protein will result in an acid loading that emits calcium from the bones and inhibits calcium reabsorption in the renal tubules, leading to hypercalciuria.
It has traditionally been defined as having a daily calcium excretion of greater than 4 mg/kg body weight. Hypercalciuria is often considered the most frequent metabolic risk factor of calcium nephrolithiasis. It also has a role in osteopenia and osteoporosis.
Its importance stems mainly from two clinical entities: bone resorption and nephrolithiasis. Hypercalciuric calcium stone formers have a lower bone mineral density on average compared to individuals with neither stone nor hypercalciuric.
Hypercalciuria affects 5-10% of the adult population and accounts for roughly one-third of all calcium stone formation. Close relatives of hypercalciuric patients are more likely to develop hypercalciuria themselves. It also has a 20% likelihood in postmenopausal women with osteoporosis and no history of kidney stones.
Hypercalciuria affects up to 40% of first and second-degree relatives of hypercalciuric recurrent stone formers. In the United States, over thirty million kidney stone patients and 1.2 million new kidney stone cases are reported annually.
There is an increased risk of hypercalciuria in children with severe vesicoureteral reflux. The most typical stone constitution in children is calcium phosphate and oxalate; however, obesity and nephrolithiasis do not appear to be linked in children, unlike in adults who develop kidney stones.
Enhanced gastrointestinal calcium absorption elevates serum calcium levels while decreasing serum levels of Vitamin D and parathyroid hormone. Only 20% of the calcium consumed is absorbed, which generally occurs in the duodenum. Renal calcium elimination is about 5-10% of all hypercalciuric stone formers have hypercalciuria.
It is caused by a renal malfunction that results in mandatory calcium loss in the urine, irrespective of dietary calcium intake or serum calcium levels. It is generally accompanied by hypocalcemia and increased PTH levels in the blood. The calcium/creatinine ratio is elevated, and there is a correlation to the medullary sponge kidney.
Hypophosphatemia is caused by increased urine phosphate excretion caused by renal impairment. It causes increased Vitamin D activation in the kidney, which enhances intestinal phosphate absorption to compensate for the low serum phosphate. Unfortunately, the additional Vitamin D boosts intestinal calcium absorption. The additional calcium absorbed is eliminated in the urine, causing hypercalciuria.
This kind of hypercalciuria is vitamin D dependent and resistant to thiazides. Pregnancy causes an increase in hypercalciuria in all three trimesters. Still, it does not seem to increase the incidence of the new stone disease since there is an elevation in kidney stone inhibitors. In patients with nephrolithiasis, bone mineral density is inversely associated with hypercalciuria.
There is an association between recurring stomach pain and hypercalciuria in children. A recent study indicates hypercalciuric pediatric kidney stone patients increase lipid metabolism/transport-related protein urine excretion. This shows that problems in lipid metabolism may be responsible for or linked to pediatric hypercalciuria and nephrolithiasis.
The proximal tubule absorbs more than 60% of the serum calcium filtered by the glomerulus. A paracellular system involving the tight junction proteins claudins-2 and -12 accomplishes this. Water, specifically sodium reabsorption, drives this process. A similar mechanism is used to resorb about 20% to 25% of the residual calcium in the thick ascending limb of Henle. Several chemical pathways are used by the distal convoluted tubule and the collecting ducts to maintain the remaining calcium excretion and reabsorption.
The most common cause of typical idiopathic hypercalciuria is a genetic mutation or alteration within one of the calcium reabsorption mechanisms. The recommended normal limits for calcium or creatinine ratios vary by age since young children and newborns often have higher urine calcium excretion and lesser urinary creatinine levels.
Milk-alkali syndrome, Paget disease, sarcoidosis, paraneoplastic syndrome, glucocorticoid excess, multiple myeloma, Addison disease, metastatic cancers involving bone, and hypervitaminosis D are other causes of hypercalciuria. A diet rich in animal protein will result in an acid loading that emits calcium from the bones and inhibits calcium reabsorption in the renal tubules, leading to hypercalciuria.
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