Kidney calcium excretion

Since this increased calcium loss, the quality of dietary protein may be important in conserving body calcium in the bone reservoir via the kidney. Human renal studies have corroborated animal data in-so-far as calcium excretion as influenced by urinary acidity is concerned. This was emphasized by Marone et al. (15) who reported increased excretion of calcium in the acidotic dog and by Zemel, et al. (27) who studied calcium filtration by the kidney. They fed subjects low or high-protein (50 or 150 g/d) diets, then compared... 

The suppression of PTH secretion from the parathyroid gland that accompanies the constitutive activation of the CASR makes the disorder difficult to recognize and treat. In some cases, it has been reported that seizures can be intractable. The abnormal set point of calcium regulation complicates treatment with calcitriol and dietary calcium supplementation because the CASR expressed in the kidney controls calcium excretion. The constitutively activated CASR mutant induces hypercalciuria, which may compound the hypocalcemia (42). 

Kidney Decreased calcium excretion, increased phosphate excretion Calcium and phosphate excretion may be decreased by 25(OH)D and l,25(OH)2D1 Increased phosphate excretion... 

Certain foreign compounds may cause the retention or excretion of water. Some compounds, such as the drug furosemide, are used therapeutically as diuretics. Other compounds causing diuresis are ethanol, caffeine, and certain mercury compounds such as mersalyl. Diuresis can be the result of a direct effect on the kidney, as with mercury compounds, which inhibit the reabsorption of chloride, whereas other diuretics such as ethanol influence the production of antidiuretic hormone by the pituitary. Changes in electrolyte balance may occur as a result of excessive excretion of an anion or cation. For example, salicylate-induced alkalosis leads to excretion of Na+, and ethylene glycol causes the depletion of calcium, excreted as calcium oxalate. 

Parathyroid hormone (PTH) is an 84-amino acid peptide secreted by the parathyroid glands, and is the principal regulator of extracellular calcium levels [44, 45]. The effects of PTH on extracellular calcium are mediated directly or indirectly through effects on bone, kidney, and intestine. A decrease in extracellular calcium causes an increase in PTH secretion. As a consequence, the rise in PTH levels causes increased bone resorption and the release of calcium from bone, decreased calcium excretion by the kidney, and increased intestinal calcium absorption. The therapeutic application of PTH has centered on the bone effects as an anabolic treatment for osteoporosis. PTH increases the activity of both osteoblasts (which form bone) and osteoclasts (which mediate bone resorption). The desirable anabolic effects of PTH on osteoblasts appear to be highly dependent on dose schedule and the duration of daily exposure. 

Q2 The hormones that are normally involved in the control of calcium balance are parathyroid hormone (PTH) from the parathyroid gland calcitonin, which is secreted by the thyroid gland and 1,25-dihydroxycholecalciferol (1,25-DHCC, or calcitriol), which is produced in the kidneys. Calcitonin reduces the level of plasma calcium by attenuating its release from bone and by increasing its excretion. The PTH and 1,25-DHCC increase the level of plasma calcium by two mechanisms (1) a combination of an increase in calcium absorption by the gut and an increase in the release of calcium from bone and (2) a reduction in both bone formation and calcium excretion. The three hormones act together to maintain the physiological level of calcium and normal bone turnover. Over 95% of body calcium is located in bone as hydroxyapatite. 

When plasma calcium level falls the major sites of action of calcitriol and PTH are bone where they stimulate bone resorption and the kidneys where they inhibit calcium excretion by stimulating reabsorption by the distal tubules. 

Hyperphosphatemia is much more commonly produced by chronic renal failure, and by other problems of kidney function, than by phosphate poisoning. Chronic renal failure, hypoparathyroidism low parathyroid hormone), and pseudoparathyroidism (failure of kidneys to respond to parathyroid hormone) all involve the failure of the kidneys to excrete phosphate into the urine at a normal rate. The danger of long-term hyperphosphatemia is the deposit of calcium phosphate crystals into the so/t tissues of the body (Knochel, 1994 Holick, 1996). 

Hypercalcemia can result from an excessive intake of vitamin D. Prolonged immobilization can also result in hypercalcemia, as bone resorption increases with this immobilization, especially where there is concurrent renal failure (where the kidneys cannot excrete the excess calcium). Sudden, severe hypercalcemia results in vomiting, coma, and possibly death. Prolonged hypercalcemia can result in the formation of kidney stones and in the calcification of soft tissues, such as the eye. Stone formation and caiciheahon are more likely to occur with concurrent hyperphosphatemia. 

Since unresolved nephrocalcinosis may lead to residual abnormalities in the kidney including microscopic hematuria, hypercalcemia, and impaired tubular function [100,104,105], renal ultrasonography within a few months of initiating loop diuretics may be warranted [100 104]. If long-term diuretic therapy is needed, a thiazide diuretic alone or in combination with furosemide may reduce the risk of renal calcifications by decreasing urinary calcium and oxalate excretion [100,102,104,107,108]. However, two studies of premature infants failed to show a reduction in either urinary oxalate or calcium excretion when thiazides were added to furosemide therapy [107,109]. 

Your kidneys will excrete some of this excess acidity. But if there is more than they can handle, another mechanism kicks in to put the brakes on and try to keep the blood at 7.365. This process centers around the bones, which the body uses as a sort of bank account system to maintain acid-alkaline balance. Whenever your body becomes excessively acidic, it makes a withdrawal of calcium from the bones, the primary storehouse of this very alkaline mineral, to neutralize the acidity. In... 

Calcium withdrawn from our bones to combat acidity is dumped into our urine along with the acid expelled by our kidneys. A 2001 study by Dr. David Bushinsky proved that chronic acidity causes an increase in calcium excretion through the urine however, no change in intestinal calcium absorption was observed (we absorb most nutrients, including calcium, through the walls of our intestines).5 Because bone contains most of the body s calcium, it is widely regarded as the source of the increased calcium excretion in urine. This net loss of calcium is rarely reversed on the Standard American Diet. Nor can it be resolved simply by popping calcium pills. Unless we address the cause of the calcium loss—acidity—it is a lost battle. 

The milder ( classic, type III) Bartter s syndrome is due to defects in tire basolateral pump CLC-Kb. Although the phenotype is extremely variable (neonatal, life-threatening presentations do occur), these patients typically present in the first year of hfe with weakness and hypovolemia and normal urinary calcium excretion. Nephrocalcinosis and kidney stone formation are not normally features. 

Hypercalcemia is commonly encountered in clinical prac-results when the flux of calcium into the extracellular fluid compartment from the skeleton, intestine, or Iddney is greater than the efflux. For example, when excessive resorption of bone mineral occurs in malignancy, hy-percalciuria develops. When the capacity of the kidney to excrete filtered calcium is exceeded, hypercalcemia develops. Hypercalcemia can be caused by increased intestinal absorption (vitamin D intoxication), increased renal retention (thiazide diuretics), increased skeletal resorption (immobilization), or a combination of mechanisms (primary hyperparathyroidism). 

Excessive urinary losses of magnesium from the kidneys are important causes of magnesium deficiency. Clinically important causes include alcohol, diabetes meUitus (osmotic diuresis), loop diuretics (furosemide), and aminoglycoside antibiotics. Increased sodium excretion (parenteral fluid therapy) and increased calcium excretion (hypercalcemic states) also result in renal magnesium wasting. 

Bones are constantly dissolved by osteoclasts and remineralized by osteoblasts in response to mechanical forces. Osteoclasts possess an acidic compartment and pass demineralized bone products to the periosteum (Sect. 1). They develop in stress-induced bony microcracks and are activated by differentiation factors secreted by osteoblasts, especially after menopause. Menopausal osteoporosis is controlled by drugs that are a stable form of pyrophosphate (bisphosphonate) or cathepsin K inhibitors (Sect. 2). The calcium ion concentration of blood is raised by parathyroid hormone and a vitamin D derivative called calcitriol. Parathyroid hormone causes kidneys to excrete phosphate, retain calcium, and activate calcitriol production (Sect. 3). Calcitriol induces calcium transporter proteins in osteoclasts and intestinal epithelium, where they move calcium from bone or diet into blood (Sect. 4). The chapter concludes with a discussion of calcitonin which lowers blood calcium concentrations by reversing parathyroid hormone effects on the kidney and inhibiting osteoclast activity (Sect. 5). 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

Calcium excretion in the kidney also is highly regulated. About 9 g of Ca + is fdtered in the glomeruli, of which >98% is reabsorbed in the tubules. The efficiency of tubular reabsorption is tightly regulated by parathyroid hormone (PTH) but also is influenced by filtered Na, the presence of non-reabsorbed anions, and diuretics. 

PTH increases serum calcium levels by two other mechanisms. PTH increases the synthesis of the active form of vitamin D, 1,25-dihyroxycholecalciferol, in the kidney, which in turn stimulates production of calcium binding protein. Calcium binding protein enhances calcium phosphate absorption from the gut lumen. PTH also inhibits renal calcium excretion, while promoting phosphate excretion, causing a small increase in serum calcium levels. 

Uncertain. Mild osteomalacia induced by antiepileptics is a recognised phenomenon (see also Vitamin D substances + Phenytoin and Barbiturates , p.l291). It seems that this is exaggerated by acetazolamide, which increases urinary calcium excretion, possibly by causing systemic acidosis, which results from the reduced absorption of bicarbonate by the kidney. The changes in the antiepileptic levels are not understood. 

In view of the above it is no surprise to note that Jones (1944) found that supplying only one I.U. of vitamin D per day to rats on a high Ca, very low P diet increased the blood calcium considerably. This net result is due only to the fact that no new bone can be laid down in the absence of phosphate, and that more calcium is absorbed than the kidney can excrete without increased calcium load. Under such circumstances the toxic dose might be found to be very low. Actually, kidney stones are a practically constant occurrence on a diet containing more than 1 per cent calcium (Polak, 1934). 

The average daily intake of calcium is about 1250 mg, although there is a considerable variation between different parts of the world. Fifteen to forty percent is absorbed from the intestine. The intestine also secrets calcium, and the net calcium absorbed each day approximates 200 mg. At calcium balance, the kidneys therefore excrete slightly less than this amount. In case of low calcium intake a greater fraction is absorbed than at a higher calcium intake. This adaptation to the calcium content of the food is a slow process, which is connected to complex changes in the concentrations of the calcium-transporting mechanisms in the mucosa cells [2]. 

The kidneys regulate mineral metabolism directly through excretion and indirectly through the formation of the active form of vitamin D, l,25(OH)2D3. No active secretion of calcium has been proven and therefore calcium excretion is determined by the amount of filtration and the degree of reabsorption. This reabsorption of calcium takes place mainly in the proximal tubuli but... 

In a normal adult the kidney has to excrete nearly the same amount of calcium as is absorbed by the intestine. However, studies of the relationship between dietary calcium intake and calcium excretion have revealed that only 6% of an oral calcium load appears in the urine, i.e., other dietary factors modulate intestinal calcium absorption. Indeed, proteins and carbohydrates increase the intestinal absorption, and oxalate, phosphate, and phytic acid decrease it. 

The homeostasis of calcium in the blood is partly maintained by calcium excretion. Calcium is excreted in bile, urine, feces, and milk. Except during lactation, the kidney and intestine provide the main excretory paths for calcium. The exact amount of calcium that is excreted by way of the intestine is difficult to evaluate because of the large amounts of unabsorbed calcium normally present in the feces (6.5-8 mg/100 ml). Under normal conditions, it seems that little calcium is excreted through the intestine. The renal threshold for calcium is below the minimal levels of calciuni in the blood, so the glomeruli constantly remove calcium from the circulating blood. Most of the excreted calcium is reabsorbed in the tubules. In chronic renal failure, excessive amounts of calcium are lost in the urine, leading to decalcification of the bones and a form of secondary hyperparathyroidism. 

---