Phosphorus Metabolism Disorders: Disorders in the processing of phosphorus in the body: its absorption, transport, storage, and utilization.Phosphorus: A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.Lipid Metabolism Disorders: Pathological conditions resulting from abnormal anabolism or catabolism of lipids in the body.Calcium Metabolism Disorders: Disorders in the processing of calcium in the body: its absorption, transport, storage, and utilization.Metabolic Diseases: Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)Parathyroid Hormone: A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.Iron Metabolism Disorders: Disorders in the processing of iron in the body: its absorption, transport, storage, and utilization. (From Mosby's Medical, Nursing, & Allied Health Dictionary, 4th ed)Phosphates: Inorganic salts of phosphoric acid.Glucose Metabolism Disorders: Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Phosphorus, Dietary: Phosphorus used in foods or obtained from food. This element is a major intracellular component which plays an important role in many biochemical pathways relating to normal physiological functions. High concentrations of dietary phosphorus can cause nephrocalcinosis which is associated with impaired kidney function. Low concentrations of dietary phosphorus cause an increase in calcitriol in the blood and osteoporosis.Phosphorus Compounds: Inorganic compounds that contain phosphorus as an integral part of the molecule.

*  Dr. Natalie Sweiss, MD - San Diego, CA - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. *Renal ...
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*  Dr. Anne Beck, MD - Saint Louis, MO - Pediatric Nephrology & Nephrology & Pediatrics | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. *Renal ...
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*  Dr. Luis Uribe, MD - Kenner, LA - Nephrology | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Phosphorus Metabolism Disorders. *Polycystic Kidney Disease ...
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*  Dr. Anita Mehrotra, MD - New York, NY - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Parathyroid (Gland) Disease. *Phosphorus ...
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*  Dr. Ronald Fischman, MD - Lakewood, CA - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Phosphorus Metabolism Disorders. *Polycystic Kidney Disease ...
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*  Dr. Jiann-Gang Luo, MD - Palo Alto, CA - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Palak Parikh, MD - Chapel Hill, NC - Nephrology | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. *Renal Artery ...
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*  Dr. Sunita Dheenan, MD - Cincinnati, OH - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. * ...
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*  Dr. Hector Santiesteban, MD - San Francisco, CA - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. *Proteinuria ... He specializes in the diagnosis and treatment of high blood pressure, kidney disease, and electrolyte disorders. He has ...
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*  Dr. Daniel Soberon, MD - Lauderdale Lakes, FL - Nephrology | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Phosphorus Metabolism Disorders ...
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*  Dr. Jack Gratch, DO - Fort Worth, TX - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Parathyroid (Gland) Disease. *Phosphorus ...
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*  Dr. Volker Haase, MD - Nashville, TN - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Phosphorus Metabolism Disorders. *Renal Hyperparathyroidism. * ...
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*  Dr. Mashood Ahmad, MD - Rockford, IL - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Peter Reese, MD - Philadelphia, PA - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Phosphorus Metabolism Disorders. *Vascular Disease. *Vitamin D ...
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*  Dr. Sharon Bartosh, MD - Madison, WI - Pediatric Nephrology & Nephrology | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Parathyroid (Gland) Disease. *Phosphorus ...
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*  Dr. Marc McKinley, DO - Westlake, OH - Nephrology | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Adetola Haastrup, MD - Grand Forks, ND - Nephrology | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Azhar Malik, MD - Victoria, TX - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ... Malik is committed to the prevention and treatment of kidney diseases, electrolyte disorders, hypertension, transplant, ...
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*  Dr. Brian Swiglo, MD - Woodbury, MN - Endocrinology, Diabetes & Metabolism & Internal Medicine | Healthgrades.com

Phosphorus Metabolism Disorders. *Polycystic Ovarian Syndrome. *Pregestational Diabetes Mellitus. *Pregnancy-Related Disorders ... Brian Swiglo, MD is an endocrinology, diabetes & metabolism doctor who practices in Woodbury, MN. He is 42 years old and has ...
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*  Dr. Andrew O'Connor, DO - Huntersville, NC - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Kenneth Choi, MD - Merrillville, IN - Nephrology & Internal Medicine | Healthgrades.com

Phosphorus Metabolism Disorders. *Polycystic Kidney Disease. *Renal Artery Arteriosclerotic Disease. *Renal Hyperparathyroidism ...
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*  Dr. Antonio Granfone, MD - Revere, MA - Endocrinology, Diabetes & Metabolism & Internal Medicine | Healthgrades.com

Phosphorus Metabolism Disorders. *Pregnancy-Related Disorders. *Proteinuria. *Retina Diseases. *Symptomatic Menopause. * ... Specializes in Endocrinology, Diabetes & Metabolism. *Board certified in Diabetes, Metabolism & Endocrinology and Internal ... Antonio Granfone, MD is an endocrinology, diabetes & metabolism doctor who practices in Revere, MA. He is 64 years old and has ... Looking for an Endocrinology, Diabetes & Metabolism Specialist? We found others matching your search, to help you compare.. ...
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*  Dr. Aditya Mattoo, MD - New York, NY - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephrotic Syndrome. *Phosphorus Metabolism Disorders. *Proteinuria. *Renal Hyperparathyroidism. ...
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*  Dr. Mary Mouracade, MD - Bonita Springs, FL - Nephrology & Internal Medicine | Healthgrades.com

Magnesium Metabolism Disorders. *Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Phosphorus ...
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*  Dr. Maria Coco, MD - Bronx, NY - Nephrology & Internal Medicine | Healthgrades.com

Mineral Metabolism Disorders. *Nephritis and Nephropathy. *Nephrotic Syndrome. *Parathyroid (Gland) Disease. *Phosphorus ...
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(1/41) Effects of partial and total colectomy on mineral and acid-base homoeostasis in the rat: magnesium deficiency, hyperphosphaturia and osteopathy, in the presence of high serum 1,25-dihydroxyvitamin D but normal parathyroid hormone.

The effects of colectomy on acid-base status, extra-osseous and bone minerals, calciotropic hormones and bone morphology have not yet been studied. To rectify this, groups of normally fed male rats were subjected to distal (n=11), proximal (n=12) or total (n=12) colectomy. Sham-operated rats (n=12) served as controls. At 112 (+/-2) days after colectomy the following changes were noted: (1) weight gain was delayed; (2) faecal excretion of calcium and phosphorus was normal, whereas that of magnesium was increased; (3) intestinal calcium secretion and absorption of calcium and phosphorus were normal, but magnesium absorption was decreased; (4) urinary excretion of magnesium was also decreased, that of phosphorus was increased, and that of pyridinium and deoxypyridinium tended to be high; (5) the serum levels of ionized magnesium, total calcium, 25-hydroxyvitamin D and parathyroid hormone were normal, while that of 1,25-dihydroxyvitamin D was markedly elevated; and (6) bone magnesium and phosphorus content were decreased, but bone calcium was normal, and thus the bone calcium/phosphorus ratio was high. These abnormalities were associated with moderate metabolic acidosis, as reflected by high urinary ammonium, low citrate and low total CO(2), but normal blood gases. Significant structural abnormalities of bone were not detectable, but trabecular bone tended to show rarefication. Distal colectomy had the least effect, whereas proximal and total colectomies had a distinct effect, on these parameters. It is concluded that colectomy in the rat causes: (1) a syndrome of magnesium deficiency of intestinal origin, compensated metabolic acidosis, urinary phosphorus loss, and high circulating 1,25-dihydroxyvitamin D levels, with the degree depending on the extent of surgical resection; and (2) brittle bones, a feature characteristic of low bone magnesium and more generalized magnesium deficiency. The mechanisms leading to this syndrome are unknown, but altered tissue levels of magnesium and phosphorus may play a key role.  (+info)

(2/41) Calcium acetate versus calcium carbonate in the control of hyperphosphatemia in hemodialysis patients.

CONTEXT: Hyperphosphatemia has an important role in the development of bone and mineral abnormalities in end-stage renal disease (ESRD). OBJECTIVE: To compare the phosphorus binding power and the hypercalcemic effect of calcium acetate and calcium carbonate in hemodialysis patients. TYPE OF STUDY: Crossover, randomized, double-blind study. PLACE: A private hospital dialysis center. PARTICIPANTS: Fifty-two patients who were undergoing regular hemodialysis three times a week ([Ca++] dialysate = 3.5 mEq/L). PROCEDURES: Half of the patients were started on 5.6 g/day of calcium acetate and, after a 2 week washout period, received 6.2 g/day of calcium carbonate. The other half followed an inverse protocol. MAIN MEASUREMENTS: Clinical interviews were conducted 3 times a week to monitor for side effects. Determinations of serum urea, calcium, phosphorus, hematocrit, Kt/V and blood gas analysis were obtained before and after each treatment. RESULTS: Twenty-three patients completed the study. A significant increase in calcium plasma levels was only observed after treatment with calcium carbonate [9.34 mg/dl (SD 0.91) vs. 9.91 mg/dl (SD 0.79), P < 0.01]. The drop in phosphorus levels was substantial and significant for both salts [5.64 mg/dl (SD 1.54) vs. 4.60 mg/dl (SD 1.32), P < 0.01 and 5.89 mg/dl (SD 1.71) vs. 4.56 mg/dl (SD 1.57), P < 0.01, for calcium acetate and calcium carbonate respectively]. The percentage reduction in serum phosphorus (at the end of the study) per milliequivalent of salt administered per day tended to be higher with calcium acetate but statistical significance was not found. CONCLUSION: Calcium acetate can be a good alternative to calcium carbonate in the handling of hyperphosphatemia in ESRD patients. When calcium acetate is used, control of hyperphosphatemia can be achieved with a lower administration of calcium, perhaps with a lower risk of hypercalcemia.  (+info)

(3/41) Management of hyperphosphataemia of chronic kidney disease: lessons from the past and future directions.

A historical look at research in hyperphosphataemia of chronic kidney disease over the last 40 years shows remarkable advances in our understanding of this abnormality and in the technology used to manage it. Phosphate binders, which have become a mainstay in the management of hyperphosphataemia, have evolved from the early use of aluminium gels to calcium salts, to novel, non-absorbed, aluminium-free, calcium-free agents such as sevelamer hydrochloride, and to magnesium-, iron-, and lanthanum-based compounds. With recent advances, clinical management of this complication of chronic renal disease is evolving from adequate care to optimal care, such that new standards in phosphorous management are being set, and various parameters of patient care are being integrated to optimize outcomes and minimize side effects. This paper provides a historical view of the clinical management of hyperphosphataemia, and looks to advances in treatment that are changing the course of renal bone disease management.  (+info)

(4/41) A prospective study of combination therapy for hyperphosphataemia with calcium-containing phosphate binders and sevelamer in hypercalcaemic haemodialysis patients.

INTRODUCTION: Hyperphosphataemia is predictive of death, in haemodialysis (HD) patients. Sevelamer is a mineral-free phosphate binder not limited by the hypercalcaemia often encountered when utilizing calcium-containing phosphate binders. Highly positive calcium balance is associated with ectopic calcification and potentially accelerated vascular disease. Unfortunately, exclusive use of sevelamer entails a large cost differential, limiting its use in many centres. We report on a strategy of partial replacement of calcium with sevelamer for the management of hyperphosphataemia in hypercalcaemic chronic HD patients. METHODS: We identified 23 HD patients with serum calcium >2.6 mmol/l. Dietary phosphate and calcium intake were assessed and baseline serum calcium, phosphate and 1alpha calcidol and elemental calcium dose recorded. Fifty per cent of this initial calcium dose was exchanged for sevelamer. Vitamin D doses were left unchanged. If serum calcium was still >2.6 mmol/l after 4 weeks a further 50% of calcium was exchanged. If serum phosphate was >2 mmol/l the sevelamer dose was increased by 25%. The patients were followed up for a further 4 weeks. RESULTS: Seven patients complained of gastrointestinal intolerance of sevelamer. Serum calcium fell from a mean value of 2.8+/-0.04 (2.64-3.54) mmol/l to 2.56+/-0.03 (2.4-2.9) mmol/l, P<0.0005. The hypercalcaemic percentage of patients fell from 100 to 26%. Mean serum phosphate was not significantly changed, 1.59+/-0.1 (0.57-2.6) mmol/l to 1.63+/-0.11 (0.55-2.68) mmol/l, 17-22% of patients having serum phosphate >2 mmol/l. Serum intact parathyroid hormone increased from 166+/-47 (12-933) ng/l to 276+/-104 (20-1013) ng/l, P=0.02. Mean sevelamer dose was 2.77+/-0.36 (0-5.6) g per day. Elemental calcium dose fell from 2.05+/-0.23 (0.5-4.5) g to 1.03+/-0.1 (0.5-2.5) g, P<0.0001. CONCLUSION: A regimen based on the combination of sevelamer and calcium is capable of effectively managing hyperphosphataemia, without hypercalcaemia, in the majority of hypercalcaemic HD patients. Such a minimally calcaemic approach might reduce the financial burden of sevelamer therapy, and enable a wider range of patients to be treated.  (+info)

(5/41) Hyperphosphataemia as a cardiovascular risk factor -- how to manage the problem.

Hyperphosphataemia is a frequent and important cardiovascular risk factor in patients with chronic kidney disease (CKD). High phosphate levels may influence vascular calcifications by two separate mechanisms: by worsening secondary hyperparathyroidism, which in turn facilitates calcification, and by promoting calcium phosphate deposition in pre-formed endothelial plaques and in the arterial wall. Recent studies have shown that hyperphosphataemia induces the proliferation and differentiation of endothelial vascular cells into osteoblast-like cells, promoting vascular calcification. High phosphate levels also increase the risk of mortality in patients with CKD. To reduce the negative impact of high phosphate, serum phosphate levels should be <5 mg/dl and serum calcium <10 mg/dl. This allows the calcium x phosphate product to be maintained at < or =50 mg(2)/dl(2), reducing the risk of vascular, valvular, and extraskeletal calcification. A multiple-factor approach can be used to reduce serum phosphate: (i). decrease bone resorption by maintaining adequate serum parathyroid hormone levels; (ii). reduce phosphorous intake in the diet, (iii). use phosphate binders efficiently; and (iv). avoid under-dialysis. The patient's diet should be high in nutrition but with the lowest possible phosphorous content. Doses of phosphate binders should be tailored to individual dietary habits and must be taken during meals in a dose proportional to the phosphorous content of the meal. Because of the risk of increased extraskeletal calcification, calcium-containing phosphate-binder intake should not exceed 2-3 g/day. Sevelamer hydrochloride, a non-calcium and non-aluminium phosphate binder with a potency similar to that of calcium salts has shown beneficial effects on lipid profiles. Better control of serum phosphate is achieved in patients on continuous ambulatory peritoneal dialysis than in those on haemodialysis. Removal of phosphate is directly correlated with duration and frequency of dialysis sessions. Thus, it is advisable not to reduce the duration of dialysis sessions to <4 h three times per week.  (+info)

(6/41) Decreased absorption of calcium, magnesium, zinc and phosphorus by humans due to increased fiber and phosphorus consumption as wheat bread.

During a 20 day period of high fiber consumption in the form of bread made partly from wheaten wholemeal, two men developed negative balances of calcium, magnesium, zinc and phosphorus due to increased fecal excretion of each element. The fecal losses correlated closely with fecal dry matter and phosphorus. Fecal dry matter, in turn, was directly proportional to fecal fiber excretion. Balances of nitrogen remained positive. Mineral elements were well-utilized by the same subjects during a 20-day period of white bread consumption.  (+info)

(7/41) Molecular targets of hyperphosphataemia in chronic renal failure.

Dietary phosphate restriction can prevent or retard the progress of chronic renal failure (CRF) and secondary hyperparathyroidism. The klotho gene is involved in the development of a syndrome resembling human ageing, and klotho mutant mice show abnormal calcium/vitamin D metabolism, developing hyperphosphataemia and vascular calcification. Phosphate retention rescues the phenotype of klotho mice. The level of expression of klotho RNA was greatly reduced in the kidneys of all CRF patients. Dietary P(i) restriction induced klotho expression, which enhances the beneficial effect of P(i) restriction in patients with CRF and/or on haemodialysis.  (+info)

(8/41) Hyperphosphataemia and treatment with sevelamer in haemodialysis patients.

More than 60% of patients on chronic haemodialysis (HD) have a serum phosphate level above 5.5 mg/dl (1.75 mmol/l), which recently has been recommended as an appropriate target in patients with end-stage renal disease (ESRD). Preventing hyperphosphataemia and elevated Ca x P product not only ameliorates the progression of secondary hyperparathyroidism and bone disease, but also appears to reduce cardio-vascular morbidity and mortality from vascular calcifications. Dietary phosphate restriction and the administration of aluminium and calcium salts have been the principal means of phosphate control over the last decade. Unfortunately, the protean disturbances of toxic aluminium accumulation in the body virtually eliminated aluminium from clinical practice. Calcium-based therapy, although well tolerated, results in frequent hypercalcaemia when administered concurrently with vitamin D analogues, despite a decrease in the concentration of dialysate calcium. Sevelamer (Renagel((R))) has been a novel, non-absorbable calcium- and aluminium-free synthetic polymer. In initial studies, sevelamer reduced serum phosphate, Ca x P product and parathyroid hormone (PTH) in a manner comparable with calcium acetate therapy. However, the effect on PTH levels may prove to be inconsistent. It seems somewhat less effective in binding phosphate than aluminium, although no direct comparisons have been made. In a recent study, it attenuated the progression of vascular calcification in HD patients. It also binds bile acids, resulting in substantially lower low-density lipo-protein cholesterol levels. The major obstacle to its current use is a substantial increase in the cost associated with sevelamer therapy.  (+info)



calcium


  • Next to calcium, phosphorus is the most abundant mineral in the body. (umm.edu)
  • Too much phosphorus is generally caused by kidney disease or by consuming too much dietary phosphorus and not enough dietary calcium. (umm.edu)
  • As the amount of phosphorus you eat rises, so does the need for calcium. (umm.edu)
  • The delicate balance between calcium and phosphorus is necessary for proper bone density and prevention of osteoporosis. (umm.edu)
  • Nutritionists recommend a balance of calcium and phosphorus in the diet. (umm.edu)
  • The typical Western diet, however, contains roughly 2 to 4 times more phosphorus than calcium. (umm.edu)
  • Meat and poultry contain 10 to 20 times as much phosphorus as calcium, and carbonated beverages can have as much as 500 mg of phosphorus in one serving. (umm.edu)
  • When there is more phosphorus than calcium in the body, the body will use calcium stored in bones. (umm.edu)
  • With increasing awareness of the key contribution of elevated serum phosphorus to vascular calcification and cardiovascular morbidity [ 3 , 4 , 7 , 9 - 11 ], more recent guidelines from the Kidney Disease: Improving Global Outcomes (KDIGO) group have highlighted the importance of tight control of serum phosphorus and calcium. (biomedcentral.com)

cardiovascular


  • Several studies suggest that higher intakes of phosphorus are associated with an increased risk of cardiovascular disease. (umm.edu)

levels


  • Some health conditions, such as diabetes, starvation, and alcoholism can cause levels of phosphorus in the body to fall. (umm.edu)
  • Some medications can cause phosphorus levels to drop, including some antacids and diuretics (water pills). (umm.edu)
  • Elevated serum phosphorus (P) levels have been linked to increased morbidity and mortality in dialysis patients with secondary hyperparathyroidism (SHPT) but may be difficult to control if parathyroid hormone (PTH) is persistently elevated. (biomedcentral.com)