Prevention Of Secondary Hyperparathyroidism Research Articles

Bariatric surgery and secondary hyperparathyroidism; a mini-review

Bariatric surgery is a type of weight loss surgery that is commonly used to treat obesity. However, this surgery can also affect the body’s calcium and PTH metabolism, leading to the development of secondary hyperparathyroidism (SHPT). Several factors contribute to the development of SHPT after bariatric surgery. Malabsorption of calcium due to reduced intestinal surface area, decreased intake of calcium-rich foods, and altered vitamin D metabolism play a significant role. The loss of weight-bearing adipose tissue can also disrupt the balance between bone formation and resorption, leading to increased bone turnover and calcium release from the skeleton. The management of SHPT after bariatric surgery involves a multidisciplinary approach. Calcium and vitamin D supplementation is essential to correct deficiency and maintain bone health. However, achieving optimal calcium and vitamin D levels can be challenging due to malabsorption issues and the need for higher supplementation doses. In some cases, pharmacological interventions such as calcimimetics or PTH analogs may be required to control PTH levels. However, these medications should be used cautiously due to limited data on their safety and efficacy in the bariatric surgery population. Prevention of SHPT is an important aspect of managing patients undergoing bariatric surgery. Nutritional counseling and regular monitoring of calcium, vitamin D, and PTH levels can help identify and address deficiencies early on. Additionally, using procedures that preserve the duodenum and proximal jejunum, such as duodenal switch or biliopancreatic diversion with duodenal switch, may reduce the risk of developing SHPT.

The Role of Diet in Bone and Mineral Metabolism and Secondary Hyperparathyroidism.

Bone disorders are a common complication of chronic kidney disease (CKD), obesity and gut malabsorption. Secondary hyperparathyroidism (SHPT) is defined as an appropriate increase in parathyroid hormone (PTH) secretion, driven by either reduced serum calcium or increased phosphate concentrations, due to an underlying condition. The available evidence on the effects of dietary advice on secondary hyperparathyroidism confirms the benefit of a diet characterized by decreased phosphate intake, avoiding low calcium and vitamin D consumption (recommended intakes 1000–1200 mg/day and 400–800 UI/day, respectively). In addition, low protein intake in CKD patients is associated with a better control of SHPT risk factors, although its strength in avoiding hyperphosphatemia and the resulting outcomes are debated, mostly for dialyzed patients. Ultimately, a consensus on the effect of dietary acid loads in the prevention of SHPT is still lacking. In conclusion, a reasonable approach for reducing the risk for secondary hyperparathyroidism is to individualize dietary manipulation based on existing risk factors and concomitant medical conditions. More studies are needed to evaluate long-term outcomes of a balanced diet on the management and prevention of secondary hyperparathyroidism in at-risk patients at.

Major Meta-Analysis, Randomized Clinical Studies, and International Consensus on Serum Levels and Importance of Supplementing Vitamin D: State of the art


 
 
 
 Introduction: Hypovitaminosis D is highly prevalent and constitutes a public health problem worldwide. It can affect more than 90% of individuals, depending on the population studied. Objective: To make a broad analysis of the world literature to compose the State of the Art on serum vitamin D levels and its adequate supplementation, to prevent and mitigate various diseases, based on randomized clinical studies, analysis, and latest international conferences and consensus. Methods: The present study followed a literary review of randomized clinical studies, meta-analysis, and the latest international consensus. Cochrane instrument was adopted to assess the quality of the included studies between 2015 and 2020. Major considerations and conclusion: Laboratory evaluation should be performed by measuring 25(OH)D, and the main groups of individuals at risk for vitamin D deficiency are the elderly, patients with osteoporosis, history of falls and fractures, obese, pregnant women, and infants. For patients with osteoporosis and increased risk of fractures, recommended that concentrations of 25(OH)D remain above 30 ng/mL for full benefits on the prevention of secondary hyperparathyroidism, decreased risk of falls. Special considerations must have taken to pregnant women and infants, in patients with chronic renal failure, obese patients, and those undergoing bariatric surgery. Several clinical studies and current meta-analysis have shown significant results with vitamin D supplementation in cardiovascular complications, diabetes, cancer, autoimmune diseases, cognitive function, among others, with doses above 30 ng/mL, reaching up to 70 ng/mL, and maintaining serum dosage at 50 ng/mL.
 
 
 

Links between Vitamin D Deficiency and Cardiovascular Diseases.

The aim of the present paper was to review the most important mechanisms explaining the possible association of vitamin D deficiency and cardiovascular diseases, focusing on recent experimental and clinical data. Low vitamin D levels favor atherosclerosis enabling vascular inflammation, endothelial dysfunction, formation of foam cells, and proliferation of smooth muscle cells. The antihypertensive properties of vitamin D include suppression of the renin-angiotensin-aldosterone system, renoprotective effects, direct effects on endothelial cells and calcium metabolism, inhibition of growth of vascular smooth muscle cells, prevention of secondary hyperparathyroidism, and beneficial effects on cardiovascular risk factors. Vitamin D is also involved in glycemic control, lipid metabolism, insulin secretion, and sensitivity, explaining the association between vitamin D deficiency and metabolic syndrome. Vitamin D deficit was associated in some studies with the number of affected coronary arteries, postinfarction complications, inflammatory cytokines and cardiac remodeling in patients with myocardial infarction, direct electromechanical effects and inflammation in atrial fibrillation, and neuroprotective effects in stroke. In peripheral arterial disease, vitamin D status was related to the decline of the functional performance, severity, atherosclerosis and inflammatory markers, arterial stiffness, vascular calcifications, and arterial aging. Vitamin D supplementation should further consider additional factors, such as phosphates, parathormone, renin, and fibroblast growth factor 23 levels.

The Relationship Between Serum 25(OH)D and Parathyroid Hormone Levels

Objective Low 25(OH)D levels are associated with increased parathyroid hormone levels leading to progressive bone loss. The serum levels of 25(OH)D sufficient to keep the parathyroid hormone level at a range that will prevent bone loss are still unclear. The current study was aimed at evaluating the relationship between 25(OH)D levels and concomitant parathyroid hormone levels. Methods The computerized laboratory database of Clalit Health Services, a not-for-profit health maintenance organization covering more than half of the Israeli population, was searched for all 25(OH)D and parathyroid hormone tests performed in 2009. Concomitant tests of parathyroid hormone and 25(OH)D were identified in 19,172 people. Results Serum parathyroid hormone levels were inversely correlated with 25(OH)D levels ( r = −0.176, P < .001); 25(OH)D levels less than 50 nmol/L were associated with a steep increase in parathyroid hormone levels and hyperparathyroidism, which decreased with increasing 25(OH)D levels and reached a plateau at 25(OH)D levels of 75 to 85 nmol/L. The quadratic fit with plateau model showed that parathyroid hormone stabilizes at 25(OH)D level of 78.9 nmol/L. However, after excluding 5449 people with hypercalcemia or renal failure, the parathyroid hormone plateau was attained at a significantly lower 25(OH)D cut point of 46.2 nmol/L. Conclusion Our data suggest that a 25(OH)D threshold of 50 nmol/L is sufficient for parathyroid hormone suppression and prevention of secondary hyperparathyroidism in persons with normal renal function. 25(OH)D levels greater than 75 nmol/L do not seem to be associated with additional change in parathyroid hormone levels.

Comment je traite les troubles phosphocalciques en cas d’insuffisance rénale chronique

Mineral metabolism abnormalities are frequently observed in patients with chronic kidney disease (CKD). The bone and cardiovascular consequences should lead to the implementation of some adapted strategies for the prevention and treatment on the basis of the physiopathology of the disease and international recommendations. Biological bone markers such as serum parathyroid hormone (PTH) and alkaline phosphatase (ALP) are necessary to classify bone diseases without the need for bone biopsy. Elevated levels of bone markers are detected in cases of secondary hyperparathyroidism (SHPT), whereas decreased levels are observed in cases of adynamic bone disease (ABD). Bone mineral density, however, is not useful for the diagnosis. Vitamin D supplementation and reducing hyperphosphataemia by dietary phosphate-intake restriction, phosphate binders, and dialysis, are the main steps for the prevention of SHPT. Calcitriol analogs and calcimimetics should be used in second line in cases of SHPT. For the treatment of ABD, excess use of calcium salts and calcitriol analogs need to be avoided. Managing these therapies adequately can help maintain the main biological values (i.e. serum PTH, calcium, phosphorus, and ALP) within their recommended ranges.

Prevention of secondary hyperparathyroidism in hemodialysis patients: The key role of native vitamin D supplementation

Secondary hyperparathyroidism (SHPT) is a frequent complication in chronic kidney disease, especially in hemodialysis (HD) patients. Treatments for SHPT include calcitriol analogues (CA), phosphate binders, cinacalcet (CC), and surgical parathyroidectomy (PTX). This study aimed to assess the incidence and prevalence of SHPT in a single center during the period when native vitamin D (N-VitD) supplementation and CC treatment became available. All incident and prevalent HD patients were prospectively recorded and compared using 3 periods from 2004 to 2005 (period 1), 2006 to 2007 (period 2), and 2008 to 2009 (period 3). SHPT was diagnosed with serum parathyroid hormone (PTH) levels >300 pg/mL or the need for CA, CC, or PTX. Between periods 1 and 3, in incident patients (n=120 and 101), N-VitD prescription increased from 11% to 68% (P<0.0001), CA prescription remained stable (40%), and patients with PTH>300 pg/mL decreased from 40% to 12% (P<0.0001). In prevalent HD patients (n=235), N-VitD treatment increased from 55% to 91% (P<0.0001), whereas treatment with CA decreased from 67% to 17% (P<0.0001). Patients with serum PTH>300 pg/mL decreased from 38% to 13% (P<0.001), whereas patients with PTH<150 pg/mL remained stable (<30%). New CC prescriptions decreased from 45 to 3 (P<0.0001). Since 2004, SHPT has decreased drastically in incident and prevalent HD patients. The preventive role of N-VitD supplementation appears to be obvious and represents one more argument for its general recommendation in CKD patients.

Statins Do Not Affect Mineral Metabolism in Chronic Kidney Disease: A Retrospective Analysis

It has recently been proposed that statins act as vitamin D analogs in binding the ubiquitously expressed vitamin D receptor, accounting for the perceived pleiotropic effects of statins (a reduction in cancer risk, prevention of organ transplant rejection and autoimmune disease). Chronic kidney disease (CKD) offers a useful test of this hypothesis: serum 25-hydroxyvitamin D levels are insufficient (<75 nmol/l) in as many as 76% of patients with advanced CKD, associated with secondary hyperparathyroidism and reduced bone mineralization. Vitamin D suppresses parathyroid hormone (PTH) secretion in part through its action on the vitamin D receptor. If statins act as vitamin D analogs, they may then be able to suppress PTH secretion in CKD. We examined data on 714 vitamin D analog naïve patients with stage 3–4 CKD. 404 patients were treated with a statin indicated almost exclusively for primary prevention of coronary heart disease, and 310 patients were not. Both groups were similar in characteristics. Statins had no effect on the intact PTH concentration, the percentage of patients achieving K/DOQI™ PTH targets, or on calcium or phosphate concentrations. In patients with stage 3–4 CKD, statins had no effect on secondary hyperparathyroidism. If the hypothesis contending that statins act as vitamin D analogs to exert pleiotropic effects is true, this is of no clinical benefit in the prevention of secondary hyperparathyroidism in CKD.

Características clínicas y analíticas de los pacientes con insuficiencia renal crónica en tratamiento con hemodiálisis en España. Proyecto ENOD (Estudio Nacional de Optimización de Diálisis)

Chronic kidney disease represents an important burden for public health systems. More than 40,000 patients suffer from chronic kidney disease in Spain, with enormous pharmacologic and health service costs. The loss of renal function requires replacement therapy, among which hemodialysis is the most frequently used while patients wait for a renal transplant.Nevertheless, patient survival in hemodialysis is markedly lower than that in the general population with the same characteristics. Especially noticeable is the high rate of cardiovascular mortality, which becomes even more important if we take into account that a substantial number of patients entering dialysis programs are previously diabetic or hypertensive, thus exponentially increasing their cardiovascular risk. There are several dialyzers, treatments, and different dialysis techniques that seem to decrease this high cardiovascular risk, together with the beneficial effects of predialysis nephrology care.The aim of this cross-sectional study was to evaluate the main cardiovascular risk factors by analyzing the characteristics of prevalent dialysis patients throughout Spain from different categories of centers. Special emphasis is placed on the presence of diabetes, previous heart disease, anemia, hypertension, and mineral-metabolism disorders to propose future potential targets to improve quality of life and decrease morbidity and mortality among this patient population.Our results demonstrate the importance of early diagnosis of diabetic nephropathy and heart disease, control of hypertension, adequate dialysis, and the prevention of secondary hyperparathyroidism. New commercially available drugs may play an important role in the near future.

Cinacalcet and the Prevention of Secondary Hyperparathyroidism in Rats With Aldosteronism

In rats receiving aldosterone/salt treatment (ALDOST), increased Ca2+ excretion leads to a fall in plasma-ionized Ca2+ and appearance of secondary hyperparathyroidism (SHPT) with parathyroid hormone (PTH)-mediated intracellular Ca2+ overloading inducing oxidative stress in diverse tissues. Parathyroidectomy prevents this scenario. Rats with ALDOST were cotreated with cinacalcet (Cina), a calcimimetic that raises the threshold of the parathyroids' Ca(2+)-sensing receptor. We monitored plasma-ionized [Ca2+]o, PTH, and total Ca2+ in heart and peripheral blood mononuclear cells (PBMC), and evidence of oxidative stress in heart, PBMC, and plasma. Cina-treated rats for 4 weeks were compared with 4 weeks of ALDOST alone and with untreated age-/gender-matched controls. In comparison to controls, ALDOST led to a fall (P < 0.05) in Ca2+ (1.16 +/- 0.01 vs 1.03 +/- 0.01 mmol/L), which was not prevented by Cina (1.01 +/- 0.03 mmol/L); a rise (P < 0.05) in plasma PTH (36 +/- 7 vs 134 +/- 19 pg/mL) that was attenuated by Cina (69 +/- 12 pg/mL); increased (P < 0.05) cardiac [Ca2+] (3.92 +/- 0.25 vs 6.78 +/- 0.35 nEq/mg FFDT) and PBMC [Ca2+]i (29.8 +/- 2.3 vs 50.2 +/- 2.3 nmol/L), each of which was prevented with Cina (3.65 +/- 0.10 nEq/mg FFDT and 32.5 +/- 6.0 nmol/L, respectively); increased cardiac MDA (0.56 +/- 0.03 vs 0.94+/-0.07 nmol/mg protein) and PBMC H2O2 production (63.5 +/- 7.5 vs 154.0 +/- 25.2 mcb) and reduced (P < 0.05) plasma alpha1-AP activity (39.8 +/- 0.6 vs 29.6 +/- 1.8 mM), each prevented by Cina (0.66 +/- 0.04 mmol/mg protein, 58.2 +/- 12.7 mcb and 37.0 +/- 1.2 mM, respectively). PTH-mediated intracellular Ca2+ overloading accounts for the induction of oxidative stress in diverse tissues in rats with aldosteronism and which can be prevented by Cina.

21 Review of Treatment with Vitamin D: Ten Month Observation

Introduction Hyperparathyroidism continues to be a major problem in patients with chronic kidney disease (CKD). Hypocalcemia and hyperphosphatemia are crucial for the development of secondary hyperparathyroidism (SHP). Preventing hyperphosphatemia ameliorates the progression of SHP. Vitamin D analogs (Alpha D3) per oral after hemodialysis (HD) could be used in the therapy of SHP. The purpose of this review in one dialysis center was to analyze the quality of such treatment.Patients and methods Patients (pts) on HD in one dialysis center were included in this analysis. Calcium (Ca) and phosphate (P) were followed during a 10 month period every 3 weeks and intact parathyroid hormone (iPTH) every three months. Vitamin D was given after HD per oral under nurse control.Results Sixty‐four pts, 34 female and 30 male, mean age 59.9 ± 11.5 (range 32–82) years, HD treatment length mean 8.8 ± 7.2 (range 0.7–30.7) years were observed. Mean Ca was 2.46 ± 0.04 mmol/L, (range from 1.06 to 2.72), mean P 1.52 ± 0.08 mmol/L (range from 0.62 to 3.53), mean iPTH 211.9 ± 36.7 ng/L (range from 1 to 699). Mean calcium concentration in dialysis fluid was 1.51 ± 0.02 mmol/L and mean dose of vitamin D was 0.35 ± 0.11 mg.Mean values of parameters during the 10 months observation are shown in Table A21. December 2003 February 2004 April 2004 June 2004 Ca (mmol/L) 2.46 2.44 2.35 2.38 P (mmol/L/ 1.52 1.56 1.71 1.53 iPTH (ng/L) 204.8 173.1 272.3 196.5 Ca in fluid (mmol/L) 1.52 1.53 1.49 1.49 Dose of vitamin D (mg) 0.47 0.28 0.21 0.43 Conclusions Regular evaluation of Ca, P, iPTH and strict correction of calcium concentration in dialysis fluid, per oral vitamin D are very helpful in prevention of SHP. Critical elevation of iPTH was in pts with low compliance in hypophosphatemic diet and therapy. If concentration of phosphate is normal, elevated iPTH could be diminished very effective by titration of vitamin D.

Treatment of secondary hyperparathyroidism of dialysis patients with calcimimetics as a valuable addition to established therapeutic means

Currently available options for the treatment of hyperparathyroidism secondary to chronic renal failure do not allow the achievement of target values for plasma calcium, phosphorus, and parathyroid hormone in the majority of patients with chronic kidney disease (CKD) stage 5. This is particularly true for CKD patients who have been referred to nephrologists late in the course of their disease and in whom prevention has not been possible. The advent of a new class of therapeutic agents, the calcimimetics, will allow an easier control of already established parathyroid overfunction, as has been demonstrated in several phase II studies and one phase III study with cinacalcet. Future studies will show whether an earlier start of treatment in patients with CKD stage 2, 3, and 4 allows the prevention of secondary hyperparathyroidism. Since all available experience has been gathered in adult patients it is also necessary to test the efficacy and safety of the calcimimetics in children with CKD.

Prevention of uremic bone disease using calcimimetic compounds.

The discovery, characterization, and cloning of the calcium-sensing receptor (CaR) in 1993 was soon followed by the creation of a new type of drug, the calcimimetics-NPS R-568 and NPS R-467-which are small phenylalkylamine derivative compounds that act as CaR agonists and increase the sensitivity of the CaR to activation by extracellular calcium (Ca2+). As expected, these compounds turned out to have a significant effect on the Ca2+/parathyroid hormone (PTH) relationship, resulting in a dramatically greater suppression of the PTH level than would otherwise occur at the actual extracellular Ca2+ levels. Renal osteodystrophy (RO) due to secondary hyperparathyroidism (HPT) in chronic renal failure was an obvious target for studying the effects of NPS R-568. In a study on experimental animals, the results clearly showed that this first generation of calcimimetics, NPS R-568, had an acute dose-dependent and short-lived suppressive effect on PTH secretion from the parathyroid glands. A similar effect was found in patients with chronic renal failure and secondary HPT. At the same time, the calcimimetics induced a slight degree of hypocalcemia. Such a significant suppressive effect on PTH secretion would be expected to result in therapeutic potential for a preventive or therapeutic effect on the RO accompanying chronic uremia. Administration would probably be in close concert with present strategies, phosphate binders and vitamin D analogs. A wide distribution of CaRs have now been demonstrated in the body, and an important question is how calcimimetics will affect the function of different tissues and organs when used for long-term treatment or prevention of secondary HPT and RO. Although relatively few experimental and clinical investigations have been completed, they clearly confirm the suppressive effect of calcimimetics on PTH secretion. In rats with experimental chronic renal failure, a significant and beneficial effect on the prevention of RO has been demonstrated. The effect of calcimimetic compounds is presently being evaluated in humans. Besides induction of hypocalcemia, the adverse effects in these mainly short-term studies have been few. Future studies with calcimimetics will further define the physiology and pathophysiology of the CaR and the long-term benefit of calcimimetic compounds in patients with chronic renal failure.

Long-Term Effects of Small Doses of Calcitriol in Hemodialysis Patients with Moderate Secondary Hyperparathyroidism

Prevention of secondary hyperparathyroidism (SHPTH) and treatment of the moderate cases by small p. os doses of Vitamin D has not been thoroughly investigated on the long term, while large doses of Vitamin D have been successful in the short term treatment of this entity.We administered calcitriol p. os 0.5–1.0 μg, according to iPTH levels, after each dialysis session, in 19 patients (group A) for 36 months. They were ten men and nine women, 63 years old (43-81), with iPTH levels

Prevention of secondary hyperparathyroidism and hip fracture in elderly women with calcium and vitamin D3 supplements.

In the next 30 years a major increase in life expectancy is expected, but will unfortunately be associated in all countries with an exponential increase in the number of hip fractures. For a 50-year-old Caucasian woman today, the risk of a hip fracture over her remaining lifetime is about 17%, and in the future the situation will clearly be worse, particularly in women but also in men [1]. Hip fractures thus represent a current and future major public health Lproblem that requires effective prevention. The preventive approach should be based on the pathophysiological mechanisms involved, which are all largely independent on ageing.

The prevention of secondary hyperparathyroidism.

It has become increasingly evident that clear-cut disturbances of bone and mineral metabolism develop early in renal failure. Among these disturbances, hyperparathyroidism is well documented and is usually asymptomatic at that early stage. It is now accepted that early therapy using phosphate restriction, through diet and calcium-containing phosphate binders, and 1 alpha-hydroxylated vitamin D analogues is an effective means of preventing or even reversing hyperparathyroidism in early renal failure. The response to these therapies is both functional (reduced parathyroid hormone secretion) and structural (prevention of parathyroid gland hyperplasia). Parathyroid hyperplasia is largely irreversible; prevention is therefore important and can be achieved initially by a combination of diet and calcium-containing phosphate binders, with later addition of calcitriol or alfacalcidol if parathyroid hormone control cannot be achieved or sustained.

Chronic Renal Failure is a State of Cellular Calcium Toxicity

Studies on the metabolic profile of many cells have shown that chronic renal failure (CRF) is associated with a significant elevation in the basal levels of cytosolic calcium ([Ca2+]i). This latter abnormality is, in major part, responsible for the organ dysfunction in CRF. The initial step leading to the eventual increase in the basal level of [Ca2+]i is parathyroid hormone (PTH)-mediated increased calcium influx into cells. This is followed by decreased extrusion of calcium out of cells due to reduced activity of the enzymes responsible for pumping calcium out of the cells. The combination of increased entry and decreased exit of calcium results in elevation of [Ca2+]i. Prevention of secondary hyperparathyroidism in CRF or blocking of the effect of PTH by a calcium channel blocker results in normalization of [Ca2+]i and restoration of cell function. Thus, the available data are consistent with the notion that CRF is a state of cellular calcium toxicity, which underlies many of the metabolic and functional derangements in CRF.

Prevention of secondary hyperparathyroidism in chronic renal failure before dialysis.

Prevention of secondary hyperparathyroidism in chronic renal failure before dialysis.

Parathyroid hormone and the regulation of acid-base balance.

Parathormone (PTH) excess limits renal bicarbonate reabsorption. This may aggravate the acidosis in patients with renal insufficiency and secondary hyperparathyroidism. Why parathormone, the primary action of which is thought to be stabilization of the inonized fraction of calcium, affects acid-base balance remains uncertain. Parathormone not only promotes the release of calcium from bone but also mobilizes salts, including bicarbonate and phosphate. Accumulation of these anions in the extracellular fluid would limit the ionization of calcium. Teleologically it is not unexpected to find that, coincident with evolution of a mechanism which permits rapid mobilization of calcium from bone, a system had to develop which removed the byproducts of bone dissolution. If this concept is valid, parathormone-induced depression of renal bicarbonate reabsorption in uremia represents an undesired side effect of an adaptive mechanism. This would extend Bricker's "trade-off" hypothesis which ascribes metabolic bone disease due to PTH-induced phosphate loss to include metabolic acidosis resulting from diminished renal bicarbonate regeneration. Parathyroidectomy or phosphate restriction have been proposed for correction of the side effects of secondary hyperparathyroidism. These therapeutic manipulations cannot be recommended for general use. A more rational apprach for prevention of secondary hyperparathyroidism is the combined use of phosphate restriction with a short-acting vitamin D derivative.

The role of phosphorus restriction in the prevention of secondary hyperparathyroidism in chronic renal disease

In normal man, the serum phosphate concentration is maintained within a narrow range, despite random and spontaneous variations in phosphorus ingestion. On an average diet in the United States, the intake of elemental phosphorus approximates one gram per day. Of this amount, about 30% is excreted through the gastrointestinal tract and 70%, or about 700mg/day, is excreted by the kidneys. To effect this rate of excretion with a normal glomerular filtration rate (GFR), some 15% of the filtered load of phosphate must be excreted; the tubular reabsorption of phosphate (TRP) thus is equal to about 85% of the filtered load. The absolute value for TRP will vary depending upon the amount of phosphate requiring excretion, and the primary effector element in the control system which governs phosphate homeostasis appears to be parathyroid hormone (PTH). Most studies indicate that the modulation of tubular reabsorption of phosphate takes place in the proximal tubule [1–3], although some investigators have presented evidence suggesting distal participation in phosphate reabsorption [4, 5].