High serum calcium

A less common circumstance leading to hypercalcemia is development of a form of bone disease characterized by a profound decrease in bone cell activity and loss of the calcium buffering action of bone (adynamic bone disease). In the absence of kidney function, any calcium absorbed from the intestine accumulates in the blood. Therefore, such patients are very sensitive to the hypercalcemic action of l,25(OH)2D. These individuals generally have a high serum calcium but... 

Two analogs of calcitriol, doxercalciferol and paricalcitol, are approved for the treatment of secondary hyperparathyroidism of chronic renal failure. Their principal advantage is that they are less likely than calcitriol to induce hypercalcemia. Their biggest impact will be in patients in whom the use of calcitriol may lead to unacceptably high serum calcium levels. 

Dietary sources of calcium are dairy products, eggs, green leafy vegetables, broccoli, legumes, nuts, and whole grains. (Less than 30% of calcium in food is absorbed.) Calcium is absorbed in the small intestine. The amount of absorption depends on the serum calcium level and availability of vitamin D. There is reduced absorption of calcium if there is a high serum calcium level or a low vitamin D level. 

High serum calcium Calcitonin (produced by the thyroid gland) causes bone to absorb serum calcium and increases urine to excrete calcium. The GI tract decreases the absorption of calcium. 

High serum calcium level needs to be lowered quickly. You must ... 

Like high serum calcium levels, hypermagnesaemia can cause muscular hypotonia. Renal failure is the commonest cause of hypermagnesaemia. 

The rat has been used rather widely to study the relation between dietary protein, or acid salt feeding, and calcium loss. Barzel and Jowsey (19) showed that the rat fed a control diet supplemented with ammonium chloride excreted excessive urinary calcium, and experienced a concomitant loss of fat-free bone tissue. Draper, et al. (20) extending this work, reported an inverse relation between dietary phosphate and loss of bone calcium and dry, fat-free tissue. In subsequent studies (21), they reported that this process was accompanied by reduced serum calcium levels the high phosphorus, low calcium diet increased urinary calcium loss. Whereas, increasing the phosphorus content of the diet stopped the excessive urinary calcium loss. To test possible zinc loss that might result from this sort of acid salt feeding, Jacob and her coworkers (22) fed rats a supplement of ammonium chloride and then measured urinary zinc and calcium. The hypercalciuria occurred exclusive of an effect upon urinary zinc loss. 

Serum phosphorus levels responded more dramatically to the meals than did serum calcium. Ingestion of a high protein meal significantly reduced serum phosphorus below those levels obtained when 0 or 15 g of protein was fed. Ingestion of the basal meal elevated serum phosphorus. Therefore, the addition of 45 g of protein to the nutrients in the basal diet negated and reversed the effect on serum phosphorus. Hypophosphatemia has been shown to... 

Plasma volume and the extracellular fluid space have been observed to constrict 30% during reducing diets (300-600 calories per day) (B22). These changes can be accompanied by functional impairment of glomerular filtration and hepatic perfusion with transient increases up to 2 mg/100 ml in serum creatinine and BSP retention up to 40% (B22). In rare instances a significant fall in serum calcium, magnesium, or potassium was observed. Hyperuricemia was also observed, with concentrations as high as 9 mg/100 ml (B22). 

Osteomalacia is the condition in which bone becomes demineralised due to deficiency of vitamin D. In this condition parathyroid hormone (PTH) acts on the bone to maintain serum calcium, resulting in demineralisation. Serum calcium is usually normal or slightly low alkaline phosphatase levels are high, reflecting excessive osteoblast activity, and serum phosphate falls as an effect of PTH on the kidney. The same condition in children results in defects in long bone formation, and is termed rickets. 

Conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to l,25(OH)2D3 and 24,25(OH)2D3. Control of the latter step is exerted primarily at the level of the kidney, where low serum phosphorus, low serum calcium, and high parathyroid hormone favor the production of l,25(OH)2D3, whereas fibroblast growth factor 23 inhibits its production. The inset shows the... 

The high calcium works directly and indirectly by reducing PTH secretion. The high phosphate works directly and indirectly by increasing FGF23 levels. Since l,25(OH)2D raises serum calcium and phosphate, whereas 24,25(OH)2D has less effect,... 

Calcitonin has proved useful as ancillary treatment in a large number of patients. Calcitonin by itself seldom restores serum calcium to normal, and refractoriness frequently develops. However, its lack of toxicity permits frequent administration at high doses (200 MRC units or more). An effect on serum calcium is observed within 4-6 hours and lasts for 6-10 hours. Calcimar (salmon calcitonin) is available for parenteral and nasal administration. 

In contrast to the hypocalcemia that is more often associated with chronic kidney disease, some patients may become hypercalcemic from two other possible causes (in addition to overzealous treatment with calcium). The most common cause of hypercalcemia is the development of severe secondary (sometimes referred to as tertiary) hyperparathyroidism. In such cases, the PTH level in blood is very high. Serum alkaline phosphatase levels also tend to be high. Treatment often requires parathyroidectomy. 

Aspirin, prostaglandin, and hypercalcemia Certain solid tumors (renal cell carcinoma) cause hypercalcemia, which may be mediated by prostaglandin E2. Taking a high dose of aspirin or another nonsteroidal anti-inflammatory agent will lower the serum-calcium level. 

Renal 7 (low serum calcium and 7 (scanty urine, high levels of albumin and bile pigments in urine, increased blood urea) ... 

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