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PubMed2000

[Renal osteodystrophy (3); its treatment in dialysis patients].

The prevalence and the clinical gravity of the various histopathological varieties of renal osteodystrophy in dialysis patients depends on the severity of both the aluminium intoxication and that of hyperparathyroidism. The prevalence of bone pains, fractures and hypercalcemias are the highest in adynamic bone diseases (ABD) with severe aluminium intoxication, then in osteitis fibrosa and mixed osteopathy, in the ABD with moderate aluminium intoxication and rare in the mild lesion in spite of similar moderate aluminium intoxication. In the absence of aluminium intoxication, hypercalcemia and hyperphosphatemia prevalence is higher only when intact PTH is more that 4 times the upper limit of normal. When PTH is between 1 and 2 folds the ULN this prevalence is null and bone mineral density is the highest. 2. The low turnover aluminic bone diseases (osteomalacic or adynamic) will be cured by long term deferoxamine treatment. The hazards of such treatment justify the performance of a bone biopsy to ensure the diagnosis. Their prevention relies on adequate treatment of tapwater and definitive exclusion of long term administration of aluminum phosphate binders. 3. Non aluminic osteomalacia will be treated according to the same guidelines given for the uremic patients before dialysis. 4. Non aluminic adynamic bone disease will be cured by means aiming at stimulating PTH secretion as discontinuing 1 alpha hydroxylated vitamin D derivatives, and, if there is no hyperphosphatemia by discontinuation of calcium supplement. In case of hyperphosphatemia in dialysis patients CaCO3 doses have to be nevertheless increased after the dialysate calcium concentration (DCa) has been decreased in order to induce a negative perdialytic calcium balance for PTH secretion stimulation. In the near future substitution of CaCO3 by non calcemic non aluminic phosphate binders will suffice. 5. Osteitis fibrosa due to hyperparathyroidism will be treated first by securing an optimal vitamin D repletion (bringing plasma 25OH vitamin D around 30 and 60 ng/ml or 75-150 nmol/l) and by correcting hypocalcemia and hyperphosphatemia by CaCO3 at high doses (3-12 g/day) taken with the meals. In case of hypercalcemia dialysate calcium concentration will be decreased to correct it or, in a near future, CaCO3 will be decreased to 3 g/day and hyperphosphatemia will be controlled by non calcemic, non aluminic phosphate binders. When hyperphosphatemia is controlled whereas plasma calcium is normal or low, 1 alpha hydroxylated vitamin D derivatives can be administered. 6. Instrumental parathyroidectomy should be considered when plasma levels of intact PTH remain above 7 folds the upper limit of normal whereas hyperphosphatemia persists and hypercalcemia occurs in order to prevent thining of the corticals and subsequent fracture risk. In case of previous exposition to aluminum, a deferoxamine test and/or a bone biopsy will be performed to decide a long term DFO treatment before the parathyroidectomy in order to prevent the transformation of a mixed osteopathy into an aluminic adynamic bone disease. 7. The difficulty of hyperparathyroidism control in dialysis patients is due to poor compliance to phosphate binders and to irreversible parathyroid hyperplasia with occured before the dialysis stage. This stress the primary importance if its early prevention without iatrogenia by first CaCO3 and vitamin D repletion, as soon as the creatinine clearance decreases below 60 ml/min/1.73 m2.

Aluminum↗

PubMed2005

Connections between vascular calcification and progression of chronic kidney disease: therapeutic alternatives.

We have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreases the serum phosphate. Most recently, these observations were rediscovered in low-density lipoprotein receptor null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance). We had demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial type. We have shown that VC is worsened by CKD and ameliorated by bone morphogenetic protein -7 (BMP-7). The finding that high-fat-fed low-density lipoprotein receptor null animals without CKD have hyperphosphatemia led us to examine the skeletons of these mice. We found significant reductions in bone formation rates, associated with increased VC and superimposing CKD results in the adynamic bone disorder (ABD), while VC was worsened and hyperphosphatemia persisted. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. BMP-7 treatment corrected the ABD and corrected hyperphosphatemia, compatible with BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. Thus, in the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to ABD producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through increased bone formation and skeletal deposition of phosphate, and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury before demonstrable hyperphosphatemia, and they are preventable and treatable. Therefore, early intervention in CKD is warranted and may affect mortality of the disease.

Animals↗

PubMed1995

Effect of iron as a new type of phosphate binder in hemodialysis patients.

Hyperphosphatemia is one of the major problems requiring management in the majority of hemodialysis patients and they require phosphate-binding agents to control the hyperphosphatemia. Aluminum hydroxide and calcium compounds are used currently as phosphate-binding agents to treat hyperphosphatemia, but these compounds can cause undesirable side effects. Therefore, the development of new phosphate-binding agents is imperative. It is well known that oral and intravenous administration of iron causes hypophosphatemia. We hypothesized that this side effect of iron may be beneficial for the treatment of hyperphosphatemia in hemodialysis patients. Consequently, we conducted a fundamental and clinical investigation of the effects of iron administration. Membrane permeability of phosphorus in a mixture of sodium ferrous citrate and dessicated aluminium hydroxide in the presence of hydrogenated lecithin as a phosporic compound was examined. Fifteen patients undergoing hemodialysis were treated with 150 mg of sodium ferrous citrate given orally for eight weeks. The permeability of the filtering membrane to phosphorus decreased in accordance with the dosage of sodium ferrous citrate and dessicated aluminum hydroxide. The degree of phosphate-binding effect of sodium ferrous citrate was larger than that of dessicated aluminum hydroxide. Serum phosphorus decreased significantly during the experiment. These results suggest that the oral administration of sodium ferrous citrate as a new phosphate binder is a useful therapeutic method for hemodialysis in patients with hyperphosphatemia.

Administration, Oral↗

PubMed1980

Acute tumor lysis syndrome. A review of 37 patients with Burkitt's lymphoma.

Renal and metabolic complications of tumor lysis during 46 episodes of remission induction chemotherapy were reviewed in 37 patients with American Burkitt's lymphoma. Azotemia occurred in 14 patients, preceding chemotherapy in eight. All of these patients had abdominal tumors. Pretreatment azotemia was associated with elevated lactic dehydrogenase (LDH) and uric acid levels, and sometimes extrinsic ureteral obstruction by tumor. Two patients required dialysis for uric acid nephropathy before chemotherapy was initiated. Following chemotherapy, major complications of tumor lysis (hyperuricemia, hyperkalemia and hyperphosphatemia) were associated with very large tumors, high LDH levels and inadequate urinary output. In patients undergoing diuresis and receiving allopurinol, hyperkalemia or hyperuricemia developed infrequently unless concomitant renal failure ensued. Hyperphosphatemia, which occurred only after chemotherapy, developed in 10 of 32 (31 per cent) nonazotemic and in all azotemic patients. Hemodialysis was required in three post-treatment patients for control of azotemia, hyperuricemia, hyperphosphatemia and/or hyperkalemia. Because of the potential for renal failure caused by precipitation of phosphate, severe hyperphosphatemia is an additional criterion for dialysis in patients with acute tumor lysis syndrome.

Adolescent↗

PubMed1998

Renal osteodystrophy in dialysis patients: diagnosis and treatment.

This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.

Adult↗

PubMed1981

Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas.

The early metabolic events in 33 patients with non-Hodgkin lymphoma were analyzed in the present study. Twenty-three patients had Burkitt lymphoma, 3 had non-Burkitt undifferentiated lymphoma and 7 had lymphoblastic lymphoma. Eight patients developed azotemia prior to starting chemotherapy while five did so during the first treatment week. All the patients but two who developed azotemia had stage C or D disease. Serum LDH prior to chemotherapy correlated well with the stage of disease and predicted the serum levels of creatinine, uric acid and phosphorus in the post-treatment period. Surgical excision of the main tumor mass was associated with a low incidence of azotemia and other metabolic derangements. Hyperuricemia and occasionally obstruction were encountered as the causes of azotemia in the pre-treatment period. Hyperuricemia and/or hyperphosphatemia were presumed responsible for the development of azotemia in the post-chemotherapy period. Two patients were dialyzed for renal failure due to hyperuricemia and one for renal failure due to hyperphosphatemia which developed shortly after starting chemotherapy. The patterns of renal and metabolic disturbances observed during treatment of these patients were characterized by the following profiles: 1. Azotemia due to hyperuricemia prior to treatment. 2. Hyperuricemia without azotemia in the pre-treatment period with azotemia due to hyperphosphatemia in the post-treatment period. 3. Azotemia due to combined hyperphosphatemia and hyperuricemia developing gradually in post-treatment period. 4. Increased urine phosphorus excretion in both non-azotemic and azotemic patients.

Adolescent↗

PubMed2006

Function and effect of bone morphogenetic protein-7 in kidney bone and the bone-vascular links in chronic kidney disease.

In two independent and separate studies, we have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreased the serum phosphate. In the first study, the serum Ca PO(4), parathyroid hormone (PTH), and calcitriol were maintained normal after renal ablation in mice, and even mild renal injury equivalent to stage 3 CKD decreased bone formation rates. More recently, these observations were rediscovered in low-density lipoprotein receptor null (LDLR-/-) mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia and insulin resistance). We demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial calcification. We have also shown that VC is made worse by CKD and ameliorated by bone morphogenetic protein-7 (BMP-7). The finding that high-fat fed LDLR-/- animals with CKD had hyperphosphatemia which was prevented in BMP-7-treated animals lead us to examine the skeletons of these mice. It was found that significant reductions in bone formation rates were associated with high-fat feeding, and superimposing CKD resulted in the adynamic bone disorder (ABD), while VC was made worse. The effect of CKD to decrease skeletal anabolism (decreased bone formation rates and reduced number of bone modelling units) occurred despite secondary hyperparathyroidism. The BMP-7 treatment corrected the ABD and hyperphosphatemia, owing to BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in the metabolic syndrome with CKD, a reduction in bone forming potential of osteogenic cells leads to the ABD producing hyperphosphatemia and VC, processes ameliorated by BMP-7, in part through increased bone formation and skeletal deposition of phosphate and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury affecting the skeleton before demonstrable hyperphosphatemia and that they are preventable and treatable. Therefore, early intervention in the skeletal disorder associated with CKD is warranted and may affect mortality of the disease.

Animals↗

PubMed2005

Low turnover osteodystrophy and vascular calcification are amenable to skeletal anabolism in an animal model of chronic kidney disease and the metabolic syndrome.

LDL receptor (LDLR)-null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome, have vascular calcification (VC) worsened by chronic kidney disease (CKD) and ameliorated by bone morphogenetic protein-7 (BMP-7), an efficacious agent in treating animal models of renal osteodystrophy. Here, LDLR-/- high-fat-fed mice without CKD were shown to have significant reductions in bone formation rates, associated with increased VC and hyperphosphatemia. Superimposing CKD resulted in a low turnover osteodystrophy, whereas VC worsened and hyperphosphatemia persisted. BMP-7 treatment corrected the hyperphosphatemia, corrected the osteodystrophy, and prevented VC, compatible with skeletal phosphate deposition leading to reduced plasma phosphate and removal of a major stimulus to VC. A pathologic link between abnormal bone mineralization and VC through the serum phosphorus was supported by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in this model of the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to low bone turnover rates, producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through deposition of phosphate and increased bone formation.

Animals↗

PubMedDate not supplied

Some clues and pitfalls in the diagnosis of acromegaly.

OBJECTIVE: To describe a case of acromegaly in a young woman using oral contraceptives who had nonspecific symptoms and persistent hyperphosphatemia and to analyze the reasons for delay in diagnosis. METHODS: A 31-year-old woman underwent evaluation for failure of menstrual flow to resume after discontinued use of oral contraceptives. Clinical and laboratory findings are summarized, and atypical manifestations of acromegaly are discussed. RESULTS: The patient complained of weight gain, acne, and increased facial hair growth, and laboratory tests showed a low estradiol level and hyperinsulinemia. "Post-pill amenorrhea" and polycystic ovary syndrome were considered possible diagnoses. During subsequent endocrinology consultation, hyperphosphatemia was present on three occasions during a 7-month period. Hormonal studies for evaluation of pituitary function revealed increased insulin-like growth factor-I and growth hormone (GH) levels. Acromegaly was suspected, and the increased GH level failed to suppress after a glucose load. Magnetic resonance imaging revealed a pituitary macro-adenoma with suprasellar extension. Visual field testing showed bitemporal abnormalities. Transsphenoidal resection successfully removed the GH-producing tumor, and hormone replacement therapy was initiated postoperatively. CONCLUSION: The textbook presentation of GH excess is a late feature of acromegaly. The diagnosis in a young woman can be easily missed when clinicopathologic findings are not classic and the picture is further clouded by factors such as oral contraceptive use. Features may also resemble polycystic ovary syndrome, a more common condition in women of childbearing age. This case also illustrates that hyperphosphatemia, overlooked in this patient, can precede the full-blown clinical manifestations of acromegaly and serve as a subtle clue to the underlying disease. Awareness of these situations and screening for high GH levels in patients with unexplained, persistent hyperphosphatemia are advisable for making an early correct diagnosis and providing appropriate therapy.

Acromegaly↗

PubMed1999

Evolutive aortic stenosis in hemodialysis patients: analysis of risk factors.

Cardiovascular diseases represent the major cause of death in hemodialysis patients. However, little information is available about the repercussion of uremia on cardiac valves. We retrospectively investigated the incidence rate of aortic stenosis (AS), from 1991 to 1996, in 110 hemodialysis patients followed by Doppler-echocardiography. Progressive AS was diagnosed in 16 patients who had a decrease in their indexed aortic valve area from 1.24 +/- 0.09 to 0.66 +/- 0.21 cm2/m2 of BSA in 16.8 +/- 1.9 months. The mean incidence of AS per year was of 3.3%, ranging from 1.5 to 8.0%. Eight patients died in less than 3 years after the diagnosis of AS with a mean survival time of 23.0 +/- 9.5 months. Survival curves using Kaplan-Meier estimates showed a statistically significant decrease in the survival rate of patients with AS compared with patients without valvulopathy (p < 0.001). They were older than patients with normal valve, 68.6 +/- 11.1 versus 56.7 +/- 16.0 years, respectively. Men were 4 times more affected than women and showed a significantly more rapid progression to AS than women. The calcium-phosphorus product was higher in AS patients, 5.43 +/- 0.98 than in patients without AS, 3.95 +/- 0.50 mM. It was mainly due to hyperphosphatemia without hypercalcemia and the hyperphosphatemia was associated with biological signs of hypoparathyroidism or adynamic bone disease in 62% of the cases. Plasma vitamin D3 was also higher in patients with AS, 20.5 +/- 13.5 ng/ml than in those with normal valves, 9.6 +/- 6.3 ng/ml. Logistic regression showed that age, vitamin D3 and hyperphosphatemia correctly predicted 56% of the AS cases. In conclusion, AS is frequent and of poor outcome in hemodialysis patients. Age, relatively high plasma vitamin D3 levels, and hyperphosphatemia, mostly due to hypoparathyroidism, must be considered as risk factors.

Adult↗

PubMed1998

The acidosis of exogenous phosphate intoxication.

BACKGROUND: Severe hyperphosphatemia resulting from the use of laxatives and enemas with high levels of phosphate has been the subject of many case reports. These have generally focused on the hypernatremia and hypocalcemia that develop and become life-threatening. Less attention has been paid to the metabolic acidosis of phosphate intoxication. METHODS: In-depth analysis of a case of severe hyperphosphatemia and review of the literature for cases with sufficient data to permit correlation between the phosphate concentration, acidosis, and anion gap. RESULTS: Marked metabolic acidosis with a large increase in the anion gap was present in our patient. The correlation between these parameters and the plasma phosphate concentration was highly significant. Despite a paucity of data in most case reports, we did uncover other cases of anion gap-positive metabolic acidosis in patients with hyperphosphatemia. CONCLUSIONS: Among high-risk patients, including the elderly and debilitated, the presence of metabolic acidosis, hypernatremia, an increased anion gap, and low plasma calcium levels or a prolonged QT interval on the electrocardiogram should raise suspicion of phosphate intoxication.

Acidosis↗

PubMed1996

Calcium acetate versus calcium carbonate as oral phosphate binder in pediatric and adolescent hemodialysis patients.

Calcium carbonate is widely used as an oral phosphorus binder to control hyperphosphatemia in children on maintenance hemodialysis. Intestinal calcium absorption may induce hypercalcemia, particularly if calcitriol is given simultaneously. In adults, calcium acetate binds phosphorus more effectively than calcium carbonate, while reducing the frequency of hypercalcemic events. We therefore compared calcium acetate with calcium carbonate in nine pediatric patients on long-term maintenance hemodialysis. Following a 1-week withdrawal of phosphorus binders, calcium carbonate was administered for 7 weeks; after a second withdrawal, calcium acetate was given for another 7 weeks. All patients received calcitriol regularly. Both agents lowered the serum phosphorus concentration significantly (calcium carbonate 5.7 +/- 1.4 vs. 7.7 +/- 2.1 mg/ dl, P < 0.005; calcium acetate 5.8 +/- 1.4 vs. 7.8 +/- 2.0 mg/dl, P < 0.005). Significantly less elementary calcium was ingested with calcium acetate than with calcium carbonate: 750 (375-1,500) vs. 1,200 (0-3,000) mg calcium/day, P < 0.0001. Wit calcium carbonate serum calcium increased significantly. The number of episodes of hyperphosphatemia or hypercalcemia did not differ between treatments. Intact plasma parathyroid hormone (PTH) decreased significantly with both phosphate binders, and serum 25-hydroxyvitamin D3 increased. There was a close relationship between serum phosphorus and PTH in prepubertal but not in pubertal patients. We conclude that hyperphosphatemia can be controlled effectively by both calcium acetate and calcium carbonate in pediatric hemodialysis patients. The oral load of elementary calcium is reduced significantly by binding phosphorus with calcium acetate instead of calcium carbonate; nevertheless, hypercalcemic episodes remain equally frequent with both phosphate binders.

Acetic Acid↗

PubMed1984

Effect of various vitamin D analogs on plasma calcium and phosphorus and intestinal calcium absorption in fed and unfed American eels, Anguilla rostrata.

Injection of about 1 ng/g body wt per day of either vitamin D3 or 1,25-(OH)2-vitamin D3 for 7 days induces hypercalcemia and hyperphosphatemia in fed American eels, Anguilla rostrata, but only hyperphosphatemia in unfed eels. These same analogs also stimulated the uptake of 45Ca from intestinal sacs in situ. The vitamin D3 appeared to be relatively more effective than the 1,25-(OH)2D3 metabolite and chlorpromazine inhibited the effect of vitamin D3 on intestinal calcium uptake. 7-Dehydrocholesterol, vitamin D2, and 24,25-(OH)2D3 did not stimulate hypercalcemia, hyperphosphatemia, or intestinal calcium uptake.

24,25-Dihydroxyvitamin D 3↗

PubMed2006

Management of vascular calcification in CKD patients.

Vascular calcification is common in patients with chronic kidney disease (CKD) and it may affect almost every artery. It is associated with a significant increase in morbidity and mortality. Therefore, the detection, prevention and treatment of vascular calcification in CKD patients are critical for the overall approach for the management of these patients. Hyperphosphatemia, especially when the blood levels of serum phosphorus are above 5.5 mg/dl, plays a major role in the development of vascular calcification. Hyperphosphatemia induces vascular calcification by both passive and active processes. By increasing calcium-phosphate product, hyperphosphatemia results in direct deposition of calcium salts in the arteries and in cardiac valves. The active process involves the uptake of phosphate by the smooth muscle cells of the arteries by a Na-P co-transporter. This increase in cell phosphate then induces phenotypic changes of these cells, rendering them into osteoblasts which in turn, begin laying calcium salts in the arterial walls. Therefore, it is critical that the blood levels of serum phosphorus be maintained below 5.5 mg/dl in CKD patients. Inflammation and the production of C-reactive protein (CRP) and interleukin 6 are also risk factors for vascular injury and vascular calcification. In a study of 254 dialysis patients with elevated blood levels of CRP (>1.0 mg/l) and 258 patients with CRP levels equal to or less than 1.0 mg/l, it was found that higher levels of CRP are significantly associated with the presence of both atheromatous and medial calcification of the aorta and hand arteries. Also, it was reported that a significant association between CRP levels and cardiac valves calcification in patients undergoing continuous ambulatory peritoneal dialysis. The reasons for the elevation in CRP in dialysis patients are not clear, but certainly, is more evident in those with obvious inflammatory processes. Therefore, any inflammation that is detected should be treated appropriately.

Calcinosis↗

PubMed2004

The secondary dyslipidemia and deranged serum phosphate concentration in thyroid disorders.

Hyperlipidemia is a secondary disorder associated with many metabolic disorders including hypothyroidism. The occurrence of dyslipidemia in subclinical hypothyroidism is controversial. Hyperphosphatemia may accompany the dyslipidemia in some metabolic disorders. Both hyperlipidemia and hyperphosphatemia are considered to be risk factors for the coronary heart diseases. In the present study, we investigated the occurrence of dyslipidemia and altered serum phosphate concentrations in patients with thyroid disorders. The results indicated a significantly elevated serum cholesterol and triglyceride concentrations in the hypothyroid patients. The dyslipidemia was accompanied with significantly elevated serum phosphate level. On the other hand, no significant difference was evident in the serum lipid or phosphate concentrations of subclinical hypothyroid patients compared to euthyroid subjects. A significantly reduced serum phosphate level was shown in hyperthyroid patients with unaltered serum lipid levels. Significant correlations were evident between TSH and T(4) levels as independent parameters and the serum concentrations of triglyceride, cholesterol and phosphate. The results indicate in hypothyroidism that a secondary hyperphosphatemia may aggravate myocardial and arterial abnormalities induced by the secondary hyperlipidemia, which may need correction.

Cholesterol↗

PubMed2002

Serum phosphate abnormalities in the emergency department.

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.

Blood Chemical Analysis↗

PubMed2003

Spuriously elevated inorganic phosphate level in a multiple myeloma patient.

We report the case of a patient with IgG multiple myeloma and pseudohyperphosphatemia. The patient had no clinical features of hyperphosphatemia. Subsequent investigations demonstrated that this hyperphosphatemia was spurious and was caused by a high concentration of the paraprotein. Deproteinization of the serum samples by sulfosalicylic acid resulted in normalization of the elevated phosphate values. This pseudohyperphosphatemia resulted from an increase in optic density because of interference between monoclonal immunoglobulin and the molybdic reagent used to determine phosphate in serum. These data indicate that the finding of marked hyperphosphatemia in multiple myeloma patients should always prompt an assay carried out on a deproteinized sample. In addition, knowledge of this phenomenon may avoid confusion, unnecessary testing and obviate confusion in the clinical evaluation of patients with multiple myeloma.

Chemical Precipitation↗

PubMed2003

Deficiencies of calcium-regulatory proteins in dialysis patients: a novel concept of cardiovascular calcification in uremia.

Dialysis patients suffer a manifold increase in cardiovascular mortality when compared to a nonuremic population, while this phenomenon is not sufficiently explained by an increased prevalence of traditional risk factors, such as hypercholesterolemia and hypertension. The presence of hyperphosphatemia, of an increased calcium x phosphate product, as well as the magnitude of vascular and valvular calcifications, were recently identified as specific major risk factors of cardiovascular mortality in the uremic population. Furthermore, hyperphosphatemia and an increased calcium x phosphate product could be quantitatively linked to the burden of coronary artery calcification in young dialysis patients, suggesting the correction of hyperphosphatemia as the central target for preventive therapeutic intervention. Recent studies in knockout mice, however, point to the alternative possibility that deficiencies in calcium-regulatory proteins may represent important pathomechanisms leading to extraosseous calcifications. alpha 2-Heremans Schmid glycoprotein (Ahsg/fetuin) and matrix Gla protein (MGP) are strong inhibitors of calcification in vivo. Novel evidence that deficiencies of such proteins may be involved in the pathogenesis of cardiovascular calcifications in dialysis patients will be discussed.

Animals↗