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Results for “Hyperphosphatemia”

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At least 595 records · Page 33Linked to original sources

PubMed1989

Pathogenesis of hypocalcemia in neonatal polycythemia.

Hypocalcemia (HC) is a frequent complication of neonatal polycythemia (NP): 9.93% in the present study. Its pathogenesis is not clear. We suggest that one of the main pathogenetic explanation of HC in NP is the high level of phosphate significantly different (P less than 0.01) than serum phosphate of normal normocalcemic non-polycythemic newborns. The intense postnatal erythrocyte breakdown will increase the serum level of phosphate. This hyperphosphatemia will decrease calcium ion concentration by their combination and bone deposition, a process allowed by inadequate postnatal parathyroid gland response.

Humans↗

PubMed1988

Increases of serum phosphorus concentration and duodenal, renal and femur alkaline phosphatase (EC 3.1.3.1) activities of normal rats fed 2000 ppm aluminum diets.

In order to investigate the dietary effect of calcium on aluminum-induced hypophosphatemia, five types of diet, sucrose, lactose, milk, casein and soy protein, were prepared. These diets differed with regard to Ca concentration, and carbohydrate or protein sources which were expected to modify intestinal Ca absorption. Weanling Wistar rats were fed these diets for 67 days with the addition of Al at a concentration of 2000 ppm. Nutritional constituents had little effect on Al accumulation in the duodenum and bone. Al treatments had no effects on increases of body weight. The Al treatments significantly increased duodenum alkaline phosphatase (ALPase) activity and serum phosphorus concentration in all of the dietary groups. Slight but significant decreases of bone weight were observed. There were no significant increases in serum Al concentration but bone and kidney ALPase activities were also observed. These results suggest that Al ingestion can cause hyperphosphatemia in the intact animal. Effects of Al on nutrition should be considered even if serum Al concentration does not increase.

Alkaline Phosphatase↗

PubMed1986

Cellular phosphate metabolism in patients receiving bisphosphonate therapy.

Patients with Paget's disease of bone were treated with oral disodium dihydrogen ethylidene-1-hydroxy-1,1-bisphosphonate (EHBP), a drug that is known to stimulate renal tubular reabsorption of orthophosphate (Pi). After 2 weeks of treatment, plasma Pi rose from 1.02 to 1.67 mmol/l. No increase in Pi was observed with the related drug, dichloromethylene bisphosphonate, which also reduces bone turnover in Paget's disease. Intravenous EHBP caused a more rapid increase in plasma Pi, but maximum hyperphosphatemia was not observed until 7-11 days after treatment commenced. It is therefore unlikely that this effect is due to an immediate action of EHBP on the luminal face of the renal brush border Pi transporter. After 2 weeks of oral EHBP, the increase in the Pi concentration in patients' erythrocytes was 31% compared with 64% in plasma. In blood platelets and leukocytes, negligible changes in cellular Pi occurred. The concentrations of 2,3-diphosphoglycerate, adenosine 5'-diphosphate (ADP) and adenosine 5'-triphosphate (ATP) were unaltered, indicating that these organic phosphates were not offsetting a potential change in cellular Pi. The decrease in erythrocyte/plasma distribution ratio for Pi was also observed in patients receiving intravenous EHBP. However, no change occurred in cell/plasma distribution of chloride, suggesting that this apparent regulation of cellular Pi did not arise from changes in erythrocyte membrane potential, pH, or water content.

Administration, Oral↗

PubMed2005

Potential antiatherogenic and anti-inflammatory properties of sevelamer in maintenance hemodialysis patients.

BACKGROUND: Patients affected by end-stage renal disease (ESRD) demonstrate a very high cardiovascular risk mediated by traditional cardiovascular risk factors as well as abnormal mineral metabolism and a state of chronic inflammation. Sevelamer is a nonabsorbable non-calcium-based hydrogel with potential antiatherosclerotic properties. METHOD AND RESULTS: One hundred eight patients undergoing maintenance hemodialysis were randomized to sevelamer or calcium acetate as treatment for hyperphosphatemia. A coronary artery calcium score, as a measure of plaque burden, was calculated at baseline and 1 year, along with serial measurements of serum lipoproteins, beta2-microglobulin, and high-sensitivity C-reactive protein (hs-CRP). At 1 year, coronary artery calcium score progressed significantly from baseline in calcium acetate-treated subjects ( P < .001) but not in sevelamer-treated patients (P = NS). Total cholesterol (P < .0001), low-density lipoprotein cholesterol (P < .0001), apolipoprotein B (P < .0001), beta2-microglobulin (P = .018), and hs-CRP (P < .002) decreased, and high-density lipoprotein increased significantly (P = .036) from baseline in the sevelamer-treated subjects but not in subjects treated with calcium acetate despite the more frequent use of statins in the latter group (46% vs 22%, P < .05). The changes in total and low-density lipoprotein cholesterol, apolipoprotein B, and hs-CRP were significantly different between treatment groups (all P < .01). CONCLUSIONS: Sevelamer leads to favorable changes in lipids and inflammatory markers with potentially useful antiatherogenic effects in hemodialysis patients.

Acetates↗

PubMed2006

Increased targeting of cardiovascular risk factors in patients with chronic kidney disease does not improve atheroma burden or cardiovascular function.

BACKGROUND: Although multiple risk factor intervention (MRFI) is recommended to reduce the increased morbidity and mortality of cardiovascular disease (CVD) in chronic kidney disease (CKD), its efficacy is unknown. We studied the efficacy of a MRFI program in CKD. METHODS: This randomized controlled study of 200 patients with stage 4 or 5 CKD compared a physician-supervised, nurse-driven MRFI clinic (focused on dyslipidemia, hyperhomocysteinemia, blood pressure [BP], anemia, and hyperphosphatemia) with conventional care in CKD. One hundred eleven subjects completed 2 years of follow-up (median follow-up 674 days [interquartile range {IQR} 348-719 days]). Outcome measures were atheroma burden (carotid intimamedia thickness [IMT]) and endothelial function (brachial artery reactivity [BAR]). RESULTS: The MRFI group showed significant improvements, compared with usual care, in serum low-density lipoprotein cholesterol (-30.9 mg/dL vs -12.7 mg/dL, P = .001), homocysteine (-6.95 vs -0.67 micromol/L, P < .001), systolic BP (-6.9 vs -0.2 mm Hg, P = .049), and diastolic BP (-4.8 vs -1.0 mm of Hg, P = .043). No significant changes were seen in serum phosphate or hemoglobin level. Despite observed improvements in risk factors, no differences from baseline were demonstrated for IMT (-0.00 vs -0.01 mm, P = .533) or BAR (0.09% vs 0.22%, P = .834). Forty-two patients reached a composite end point of CVD death, acute coronary syndrome, revascularization, nonfatal stroke, and amputation and this was similar between groups (23 vs 19 events, P = .475). CONCLUSIONS: A MRFI program was not associated with improvement in vascular structure or function in stage 4 or 5 patients with CKD.

Adult↗

PubMed2004

[Renal complications of non-steroidal anti-inflammatories].

INTRODUCTION: Non-steroidal antiinflammatory drugs (NSAIDs) are known to have adverse effects on kidney function. Situations with stimulated renin-angiotensin system (RAS) like volume depletion or preexisting chronic renal failure predispose to acute renal failure (ARF) via inhibition of prostaglandin synthesis by NSAIDs. To date NSAIDs are frequently used as antipyretic drugs even in situations predisposing to ARF. PATIENTS: Within 20 months seven children presenting with diarrhea and/or vomiting and fever were treated with therapeutic doses (11.5-32 mg/kg per day) of ibuprofen for 1-3 days before developing ARF. Maximum plasma creatinine levels were 180-650 pmol/l. One patient required emergency dialysis for hyperkalemia, uremia, and hyperphosphatemia. After cessation of NSAID treatment and rehydration all patients recovered completely with a normalized creatinine level after 3-9 days. Once the acute phase is controlled long-term outcome is excellent. CONCLUSION: NSAIDs are potentially dangerous in situations with, even moderate, volume depletion.

Adolescent↗

PubMed2006

A case of oncogenic osteomalacia with preoperative secondary hyperparathyroidism: description of the biochemical response of FGF23 to octreotide therapy and surgery.

Oncogenic osteomalacia is a rare condition characterized by a low serum phosphate, reduced tubular reabsorption of phosphate and a low or inappropriately normal 1,25 dihydroxyvitamin D and is usually secondary to a phosphaturic mesenchymal tumor. Complete tumor resection results in resolution of all features. We report a patient with oncogenic osteomalacia and concurrent secondary hyperparathyroidism. Serum phosphate failed to normalize preoperatively with octreotide therapy, although this treatment did suppress serum FGF23. The postoperative course was distinguished by marked hyperphosphatemia that was associated with elevated serum 1,25 dihydroxyvitamin D concentrations.

Aged↗

PubMedDate not supplied

Dermatologic manifestations of parathyroid-related disorders.

Dermatologic manifestations of parathyroid-related disorders, although rare in sporadic cases, are not uncommon in familial syndromes. Patients with familial hyperparathyroidism have several types of skin lesions. In multiple endocrine neoplasia 1, patients commonly have angiofibromas (85%) and collagenomas (70%), lesions that show loss of one 11q13 allele, the molecular abnormality in multiple endocrine neoplasia 1. They can also present with lipomas or café-au-lait spots. Cutaneous amyloidosis, an entity that can occur sporadically, has been described in multiple endocrine neoplasia 2a and is usually localized to the interscapular area. Metastatic calcification is an entity commonly encountered in patients with hyperparathyroidism and renal failure. It can be complicated by infections and necrosis. It is best treated by controlling hypercalcemia, hyperphosphatemia, hyperparathyroidism, antibiotics, and analgesia. Parathyroidectomy is reserved for refractory cases. Hypoparathyroidism presenting in the context of polyglandular failure type 1 is characterized by mucocutaneous candidiasis. Pseudohypoparathyroidism, an inherited disorder with end-organ unresponsiveness to parathyroid hormone, is characterized by Albright hereditary osteodystrophy. Patients present with short stature, round facies, brachydactyly, and short fourth or fifth metacarpals.

Humans↗

PubMed2005

Primary hyperaldosteronism, a mediator of progressive renal disease in cats.

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.

Adrenal Glands↗

PubMed2004

Chronopharmacology of oxacalcitriol in rat model of osteoporosis.

We have previously reported the merits of chronopharmacological effect of 1-alpha(OH) vitamin D3 in aged stroke-prone spontaneously hypertensive rat (SHRSP), a model of osteoporosis [Eur. J. Pharmacol. 428 (2001) 283.]. In this study, the chronopharmacological effect of 22-oxacalcitriol, a newly developed active vitamin D3 analogue with less calcemic activity, was evaluated by a single and repeated dosing of the drug in aged SHRSP. Animals (7 months old) were kept in rooms with a 12-h light/dark cycle. Single (12.5 microg/kg, i.v.) and repeated (5 microg/kg, i.v. three times a week for 12 weeks) dosing of 22-oxacalcitriol or vehicle was given at either 2 h after lights on (2HALO) or 14 h after lights on (14HALO). The severity of adverse reactions such as the changes of body weight, hypercalcemia and hyperphosphatemia, was significantly mild when the drug was given at 14HALO. Especially, the increase of serum Ca concentration was not detected at 14HALO trial. Serum concentrations of total (protein-bound and unbound) 22-oxacalcitriol and albumin (a major binding protein of the drug) of the 2HALO and 14HALO trials did not significantly differ. The decrease of parathyroid hormone (PTH) concentration was greater in the 14HALO trial while the increase in urinary ratio of Ca to creatinine was greater in the 2HALO trial. The increase in bone density of both femurs at the end of the study was greater in the 14HALO trial. The suppression of urinary excretion of deoxypyridinoline, an index of bone resorption capacity of osteoclast, was greater in the 14HALO trial, which indicates that the efficacy of 22-oxacalcitriol for suppressing bone resorption might vary with the dosing time. This is the first study to show the dosing-time-dependent changes in the efficacy and toxicity of 22-oxacalcitriol in the animal model of osteoporosis. Chronopharmacological differences seem to be more prominent than those of other vitamin D analogues. To use 22-oxacalcitriol at an adequate timing might provide better efficacy and safety than other vitamin D3 analogues for the treatment of osteoporosis.

Absorptiometry, Photon↗

PubMed2006

A randomized prospective trial comparing different regimens of oral sodium phosphate and polyethylene glycol-based lavage solution in the preparation of patients for colonoscopy.

BACKGROUND: Regulatory agencies have warned clinicians regarding the risk of electrolyte abnormalities if more than two 45-mL bottles of oral sodium phosphate (NaP) solution are administered within a 24-hour period. OBJECTIVE: To compare the efficacy, safety, and tolerability of different regimens of oral NaP and polyethylene glycol (PEG). DESIGN: Randomized controlled trial. SETTING: Teaching hospital outpatient endoscopy clinic. PATIENTS: Two hundred outpatients without comorbidities who underwent routine colonoscopy. INTERVENTIONS: Two bottles of NaP, 6, 12, or 24 hours apart; or 4 L PEG. MAIN OUTCOME MEASUREMENTS: Bowel preparation quality, patient tolerability, and electrolyte changes. RESULTS: The 12- and 24-hour NaP achieved better cleansing than the 6-hour NaP or PEG. Only 8.5% and 8.3% of patients in the 24- and 12-hour NaP had poor preparations, respectively, compared with 15.6% and 23.4% in the 6-hour NaP and PEG, respectively. The poorer preparation scores with PEG were partly because of a greater amount of colonic fluid. There were no relevant electrolyte changes with PEG, whereas hypokalemia, hypocalcemia, or hyperphosphatemia developed in 5% to 57% of patients on NaP. All regimens were poorly tolerated by patients. LIMITATIONS: The study was likely underpowered to detect small group differences in electrolytes. CONCLUSIONS: A 24- or 12-hour NaP bowel preparation strategy was more effective than NaP 6 hours apart or PEG. PEG use is associated with more residual colonic fluid but represents an alternative to NaP in some clinical situations.

Administration, Oral↗

PubMed2004

Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing.

Nephrocalcinosis is a chronic tubulointerstitial nephropathy characterized by tubular calcium phosphate deposition and slowly progressive renal insufficiency. We report a novel association of acute nephrocalcinosis and acute renal failure (ARF) with colonoscopy preceded by a bowel-cleansing regimen consisting of oral sodium phosphate solution (OSPS). A cohort of 5 patients (mean age, 69.2 years) had normal renal function (mean serum creatininem 0.9 mg/dL) before colonoscopy and presented with ARF (mean serum creatinine, 4.9 mg/dL) from 3 days to 2 months postcolonoscopy. Past medical history included hypertension in all 5 patients. Medications included an angiotensin-converting enzyme (ACE) inhibitor (ACE-I) or angiotensin receptor blocker (ARB) in 4 patients and diuretics in 2 patients. In all patients, colonoscopy was preceded by bowel cleansing with OSPS; OSPS was contraindicated in a single patient with hyperparathyroidism and was used at excessive doses in another. Renal biopsy specimens obtained from all 5 patients revealed diffuse tubular injury and abundant tubular deposition of calcium phosphate. Although the tubular injury involved all tubular segments, lectin and immunohistochemical staining disclosed calcium phosphate deposition confined to distal tubules and collecting ducts. At a mean of 5.8 weeks of postbiopsy follow-up, renal function was unchanged in 4 patients and mildly improved in 1 patient. We conclude that acute nephrocalcinosis is a seemingly rare complication of bowel cleansing with OSPS. The pathophysiology of acute nephrocalcinosis after treatment with OSPS likely involves transient hyperphosphatemia; volume depletion exacerbated by intercurrent ACE-I, ARB, and diuretic use; and elevated distal tubular phosphate and calcium concentrations. Greater awareness of this entity is needed to identify potential risk factors.

Administration, Oral↗

PubMed2004

Calciphylaxis associated with acute, reversible renal failure in the setting of alcoholic cirrhosis.

We describe a case of calciphylaxis in a 47-year-old man with alcohol-induced end-stage liver disease and acute renal failure secondary to hepatorenal syndrome. Possible contributing factors included transiently impaired renal function, protein C and S deficiencies, elevated calcium-phosphate product, hyperphosphatemia, low serum albumin, repeated albumin infusions, and elevated alkaline phosphatase level.

Acute Kidney Injury↗

PubMed2006

Impact of chloride balance in acidosis control: the Stewart approach in hemodialysis critically ill patients.

BACKGROUND: Metabolic acidosis is highly prevalent in critically ill patients with acute renal failure. Little is known about the mechanisms by which renal replacement therapy intervenes in such cases. The objective of this study is to analyze the role of hemodialysis in acidosis correction in intensive care unit patients, with an emphasis on chloride levels in plasma and dialysate. METHODS: We studied 19 intermittent hemodialysis procedures in 17 acidotic patients. The patients were grouped by procedure type (conventional or sustained low-efficiency dialysis) and by predialysis plasma chloride level (higher or lower than the dialysate chloride concentration). Immediately before and after each procedure, blood samples were collected for biochemical analysis. The Stewart method was used to calculate the strong ion difference and strong ion gap. RESULTS: The patients presented acidosis related to hyperchloremia, hyperphosphatemia, and high unmeasured anions. Hypoalbuminemia had an alkalinizing effect. Hemodialysis corrected acidosis mainly by reducing phosphate and unmeasured anions. In the group as a whole, chloride levels did not change after dialysis. However, when analyzed according to predialysis plasma chloride, the high-chloride group presented a reduction in plasma chloride, resulting in better base excess improvement (Delta standard base excess) than in the low-chloride group. Among the determinants of acid-base status, the only factors correlating with Delta SBE were Delta strong ion gap and Delta chloride. CONCLUSION: The serum chloride/dialysate chloride relationship during hemodialysis has an important impact on acidosis control.

Acidosis↗

PubMed2004

Determination of the binding parameter constants of Renagel capsules and tablets at pH 7 by high performance capillary electrophoresis.

Sevelamer hydrochloride is a cross-linked polymeric amine; it is the active ingredient in Renagel capsules and tablets. Sevelamer hydrochloride is indicated for the control of hyperphosphatemia in patients with end-stage renal disease (ESRD). The binding parameter constants of sevelamer hydrochloride were determined using high performance capillary electrophoresis (HPCE) and the Langmuir approximation for three different dosage forms at pH 7.0. The three dosage forms were Renagel 403 mg capsules, Renagel 400 mg tablets and Renagel 800 mg tablets. The results demonstrate the in vitro bioequivalence of all three dosage forms at pH 7.0. These results are in very good agreement with previously published results obtained by ion chromatography.

Binding Sites↗

PubMed2006

Presentation and clinical progression of pseudohypoparathyroidism with multi-hormone resistance and Albright hereditary osteodystrophy: a case series.

Anthropometric and biochemical features were retrospectively evaluated in 12 patients with pseudohypoparathyroidism, Albright hereditary osteodystrophy, and multi-hormone resistance. Hypothyroidism and subcutaneous calcifications were presenting features in younger children. Temporal trends in stimulatory hormone resistance included early thyroid-stimulating hormone elevation and progression from parathyroid hormone elevation to hyperphosphatemia and hypocalcemia.

Child↗

PubMed2007

Vitamin D in patients with renal failure: a summary of observational mortality studies and steps moving forward.

Although approximately half of patients undergoing hemodialysis receive activated forms of Vitamin D, the primary reason to initiate this therapy has rested solely on the management of secondary hyperparathyroidism. Secondary hyperparathyroidism is likely one of several consequences of Vitamin D deficiency, and only now have other consequences of Vitamin D deficiency emerged. Although previously viewed as a contributor to hypercalcemia and hyperphosphatemia, recent studies suggest Vitamin D may improve cardiovascular structure and function, improve vascular compliance, and reduce pro-inflammatory cytokines, all of which may contribute to the improved survival observed in retrospective studies examining the outcome of patients treated with activated Vitamin D compared to those who were not. The current review examines two recent large-scale studies of hemodialysis patients: one that demonstrated a survival advantage of paricalcitol over calcitriol, and a second that demonstrated a significant survival advantage of any intravenous Vitamin D formulation versus none. In both studies, the findings were independent of mineral and parathyroid hormone levels, suggesting "non-traditional" actions of Vitamin D contributed to the observed survival advantage. Potential steps moving forward in light of these observational studies are subsequently discussed.

Humans↗

PubMed2007

The phosphatonins and the regulation of phosphate transport and vitamin D metabolism.

Phosphate homeostasis is preserved during variations in phosphate intake by short-term intrinsic renal and intestinal adaptations in transport processes, and by more long-term hormonal mechanisms, which regulate the efficiency of phosphate transport in the kidney and intestine. Recently, several phosphaturic peptides such as fibroblast growth factor 23 (FGF-23), secreted frizzled-related protein-4 (sFRP-4), extracellular phosphoglycoprotein (MEPE) and fibroblast growth factor 7 (FGF-7) have been shown to play a pathogenic role in several hypophosphatemic disorders such as tumor-induced osteomalacia (TIO), autosomal dominant hypophosphatemic rickets (ADHR), X-linked hypophosphatemic rickets (XLH), the McCune-Albright syndrome (MAS) and fibrous dysplasia (FD). These proteins induce phosphaturia and hypophosphatemia in vivo, and inhibit sodium-dependent renal phosphate transport in cultured renal epithelial cells. Interestingly, despite the induction of hypophosphatemia by FGF-23 and sFRP-4 in vivo, serum 1, 25-dihydroxyvitamin D (1alpha,25(OH)(2)D) concentrations are decreased or remain inappropriately normal, suggesting an inhibitory effect of these proteins on 25-hydroxyvitamin D 1alpha-hydroxylase activity. In FGF-23 knockout mice, 25-hydroxyvitamin D 1alpha-hydroxylase expression is increased and elevated serum 1alpha,25(OH)(2)D levels cause significant hypercalcemia and hyperphosphatemia. MEPE, however, increases circulating 1alpha,25(OH)(2)D. Circulating or local concentrations of these peptides/proteins may regulate 25-hydroxyvitamin D 1alpha-hydroxylase activity in renal tissues under physiologic circumstances.

Animals↗