Kidney calcium

After 12 weeks, no observable effect at 25 mg/kg diet dose- related adverse effects on liver, kidney calcium deposits, and chemistry at higher dietary levels (Knudsen etal. 1974)... 

Table XII. Kidney calcium in rats fed casein and rapeseed protein concentrates for 16 weeks (yg/g dry weight)...

Table XIV. Kidney calcium in rats fed different sources of protein for 6 weeks (mg/g dry weight)3...

Cadmium (Cd) Lung, emphysema, kidney, calcium metabolism, possible lung carcinogen Shellfish, cigarette smoke, taken up by plants, metal alloy - welding... 

Parathyroid Hormone (PTH) Increases blood calcium, kidney calcium Vitamin D synergistic with PTH m... 

Although most polypeptide hormones are unable to elicit energy-linked calcium movements in isolated mitochondrial preparations, some basic proteins share this property with parathormone. The doses of parathormone needed to affect mitochondria in vitro largely exceed the doses needed to modify kidney calcium transport in vivo. One could, however, argue that the in vitro conditions are not favorable for proper attachment of the hormone to the target, and therefore much more hormone is needed in vitro than in vivo. 

TRPV5(CaI2,CaCl) + Kidneys Calcium transport Hoenderop et al. 2001... 

Two nucleation processes important to many people (including some surface scientists ) occur in the formation of gallstones in human bile and kidney stones in urine. Cholesterol crystallization in bile causes the formation of gallstones. Cryotransmission microscopy (Chapter VIII) studies of human bile reveal vesicles, micelles, and potential early crystallites indicating that the cholesterol crystallization in bile is not cooperative and the true nucleation time may be much shorter than that found by standard clinical analysis by light microscopy [75]. Kidney stones often form from crystals of calcium oxalates in urine. Inhibitors can prevent nucleation and influence the solid phase and intercrystallite interactions [76, 77]. Citrate, for example, is an important physiological inhibitor to the formation of calcium renal stones. Electrokinetic studies (see Section V-6) have shown the effect of various inhibitors on the surface potential and colloidal stability of micrometer-sized dispersions of calcium oxalate crystals formed in synthetic urine [78, 79]. 

Blood Calcium Ion Level. In normal adults, the blood Ca " level is estabhshed by an equiUbrium between blood Ca " and the more soluble intercrystalline calcium salts of the bone. Additionally, a subtle and intricate feedback mechanism responsive to the Ca " concentration of the blood that involves the less soluble crystalline hydroxyapatite comes into play. The thyroid and parathyroid glands, the fiver, kidney, and intestine also participate in Ca " control. The salient features of this mechanism are summarized in Figure 2 (29—31). 

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. 

Parathyroid hormone, a polypeptide of 83 amino acid residues, mol wt 9500, is produced by the parathyroid glands. Release of PTH is activated by a decrease of blood Ca " to below normal levels. PTH increases blood Ca " concentration by increasing resorption of bone, renal reabsorption of calcium, and absorption of calcium from the intestine. A cAMP mechanism is also involved in the action of PTH. Parathyroid hormone induces formation of 1-hydroxylase in the kidney, requited in formation of the active metabolite of vitamin D (see Vitamins, vitamin d). 

Other Calcium Disorders. In addition to hypocalcemia, tremors, osteoporosis, and muscle spasms (tetary), calcium deficiency can lead to rickets, osteomalacia, and possibly heart disease. These, as well as Paget s disease, can also result from faulty utilization of calcium. Calcium excess can lead to excess secretion of calcitonin, possible calcification of soft tissues, and kidney stones when combined with magnesium deficiency. 

Magnesium. In the adult human, 50—70% of the magnesium is in the bones associated with calcium and phosphoms. The rest is widely distributed in the soft tissues and body duids. Most of the nonbone Mg ", like K", is located in the intracellular duid where it is the most abundant divalent cation. Magnesium ion is efftcientiy retained by the kidney when the plasma concentration of Mg fads in this respect it resembles Na". The functions of Na", K", Mg ", and Ca " are interrelated so that a deficiencv of Mg " affects the metaboHsm of the other three ions (26). Foods rich in magnesium are listed in Table 9. 

The potassium or calcium salt form of oxaUc acid is distributed widely ia the plant kingdom. Its name is derived from the Greek o>ys, meaning sharp or acidic, referring to the acidity common ia the foflage of certain plants (notably Oxalis and Mmex) from which it was first isolated. Other plants ia which oxahc acid is found are spinach, rhubarb, etc. Oxahc acid is a product of metabohsm of fungi or bacteria and also occurs ia human and animal urine the calcium salt is a principal constituent of kidney stones. 

Hydroxy vitamin D pools ia the blood and is transported on DBF to the kidney, where further hydroxylation takes place at C-1 or C-24 ia response to calcium levels. l-Hydroxylation occurs primarily ia the kidney mitochondria and is cataly2ed by a mixed-function monooxygenase with a specific cytochrome P-450 (52,179,180). 1 a- and 24-Hydroxylation of 25-hydroxycholecalciferol has also been shown to take place ia the placenta of pregnant mammals and ia bone cells, as well as ia the epidermis. Low phosphate levels also stimulate 1,25-dihydtoxycholecalciferol production, which ia turn stimulates intestinal calcium as well as phosphoms absorption. It also mobilizes these minerals from bone and decreases their kidney excretion. Together with PTH, calcitriol also stimulates renal reabsorption of the calcium and phosphoms by the proximal tubules (51,141,181—183). 

Although it is being found that vitamin D metaboUtes play a role ia many different biological functions, metaboHsm primarily occurs to maintain the calcium homeostasis of the body. When calcium semm levels fall below the normal range, 1 a,25-dihydroxy-vitainin is made when calcium levels are at or above this level, 24,25-dihydroxycholecalciferol is made, and 1 a-hydroxylase activity is discontiaued. The calcium homeostasis mechanism iavolves a hypocalcemic stimulus, which iaduces the secretion of parathyroid hormone. This causes phosphate diuresis ia the kidney, which stimulates the 1 a-hydroxylase activity and causes the hydroxylation of 25-hydroxy-vitamin D to 1 a,25-dihydroxycholecalciferol. Parathyroid hormone and 1,25-dihydroxycholecalciferol act at the bone site cooperatively to stimulate calcium mobilization from the bone (see Hormones). Calcium blood levels are also iafluenced by the effects of the metaboUte on intestinal absorption and renal resorption. 

Clinical stresses which interfere with vitamin metabohsm, can result in calcium deficiency leading to osteomalacia and osteoporosis (secondary vitamin D deficiency). These stresses include intestinal malabsorption (lack of bile salts) stomach bypass surgery obstmctive jaundice alcoholism Hver or kidney failure decreasing hydroxylation of vitamin to active forms inborn error of metabohsm and use of anticonverdiants that may lead to increased requirement. 

Three hormones regulate turnover of calcium in the body (22). 1,25-Dihydroxycholecalciferol is a steroid derivative made by the combined action of the skin, Hver, and kidneys, or furnished by dietary factors with vitamin D activity. The apparent action of this compound is to promote the transcription of genes for proteins that faciUtate transport of calcium and phosphate ions through the plasma membrane. Parathormone (PTH) is a polypeptide hormone secreted by the parathyroid gland, in response to a fall in extracellular Ca(Il). It acts on bones and kidneys in concert with 1,25-dihydroxycholecalciferol to stimulate resorption of bone and reabsorption of calcium from the glomerular filtrate. Calcitonin, the third hormone, is a polypeptide secreted by the thyroid gland in response to a rise in blood Ca(Il) concentration. Its production leads to an increase in bone deposition, increased loss of calcium and phosphate in the urine, and inhibition of the synthesis of 1,25-dihydroxycholecalciferol. 

Calcium channel blockers cause more pronounced lowering of blood pressure in hypertensive patients than in normotensive individuals. Generally, all calcium channel blockers cause an immediate increase in PRA during acute treatment in patients having hypertension but PRA is normalized during chronic treatment despite the sustained decrease in blood pressure. These agents also do not generally produce sodium and water retention, unlike the conventional vasodilators. This is because they produce diuretic effects by direct actions on the kidney. 

CP has been used as an ion-exchange material to remove radioisotopes, such as Sr, Cs (43) and U (VI) (44) from solution. CP ion-exchange resins have been used to remove calcium ions from blood (45) and calcium, magnesium, and potassium ions from wine (46). A commercial product made using CP, Calci-Bind, has been used for the treatment of kidney stones (47). 

Vitamin D is a family of closely related molecules that prevent rickets, a childhood disease characterized by inadequate intestinal absorption and kidney reabsorption of calcium and phosphate. These inadequacies eventually lead to the demineralization of bones. The symptoms of rickets include bowlegs,... 

---