PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Hyperphosphatemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1991

[Spurious hyperphosphatemia in multiple myeloma].

We present a 68-year-old woman with Ig A-K multiple myeloma and a laboratory report of extreme hyperphosphatemia (29 mg/dl), but no clinical manifestations attributable to such a high serum phosphorus. The hyperphosphatemia was demonstrated to be spurious and due to interference of monoclonal immunoglobulin with the phosphomolybdate calorimetric assay for phosphorus of some automated systems. In this case, after removal of serum proteins phosphorus values were normal. Normal values of phosphorus were also obtained with the phosphomolybdate calorimetric assay after reduction of paraprotein levels in this patient by chemotherapy. Knowledge of this phenomenon may obviate unnecessary testing and treatment. It may also suggest the presence of dysproteinemia.

Aged↗
PubMed1989

Spurious hyperphosphatemia in patients with dysglobulinemia.

Following the introduction of the ASTRA automated chemical analyzer to the Brooklyn VA Hospital, we identified 14 patients with normal renal function and marked hyperphosphatemia (9.1 +/- 3.1 mg/dl). Reanalysis of these samples by standard SMA-II autoanalyzer demonstrated normal phosphate concentration (3.5 +/- 0.7 mg/dl). All patients had a dysglobulinemic syndrome and further examination indicated that ASTRA reagents produced significant optical turbidity in these sera. We conclude that chemical analysis of inorganic phosphorus by methods which do not deproteinate sera prior to colorimetric analysis are subject to nephelometry in the presence of dysglobulinemic samples and may result in spurious hyperphosphatemia.

Aged↗
PubMed1988

[Hyperphosphatemia and transient renal insufficiency following chemotherapy of acute lymphoblastic leukemia].

Acute renal failure during treatment of lymphoblastic malignancies is usually due to drug toxicity or acute uric nephropathy. Observations were recently reported where extreme hyperphosphatemia may represent another pathophysiological mechanism. We describe 2 cases, in 36- and 77-year-old women, with acute lymphoblastic leukemia. Acute renal failure was observed 2 days after cytotoxic treatment. Maximal blood creatinine values were 860 and 550 mumol/l respectively, and for phosphate 6.3 and 7.5 mmol/l. With oral phosphate binders, and after four peritoneal exchanges for the second patient, renal function gradually returned to normal values within 4 weeks. Tumor lysis syndrome with associated hyperphosphatemia is described exclusively in lymphoblastic malignancies and renal failure is probably a consequence of intratubular calcium phosphate precipitation. In this situation prophylactic administration of phosphate binders and attentive monitoring of phosphatemia are necessary.

Acute Kidney Injury↗
PubMed1987

[Magnesium hydroxide treatment of hyperphosphatemia in chronic hemodialysis patients with an aluminum overload].

The control of hyperphosphatemia in dialysis patients is frequently achieved using aluminium hydroxide (A1(OH)3) and/or calcium carbonate (Ca CO3). However, this effect is counterbalanced by risk of aluminium intoxication and hypercalcemia. An alternative to the use of these phosphate binders is the prescription of magnesium hydroxide (Mg(OH)2) in association with a magnesium free dialysate. 19 patients with subtoxic plasma aluminium concentration received such a therapy. 9 months after starting the essay 4 patients had been excluded for digestive intolerance (3 cases) and neuro-psychic symptoms related to hypermagnesemia (1 case) after therapy with maximal doses of 6 to 12 g/d. Plasma inorganic phosphorus was decreased from 2.47 +/- 0.32 to 1.86 +/- 0.40 mmol/l (P less than 0.05) and plasma aluminium from 3.03 +/- 0.93 to 1.52 +/- 0.15 mumol/l (P less than 0.05). The results have been obtained without any significant increase in plasma and red cell magnesium levels. Metabolic alkalosis has been observed in association with the increase of ion exchange resin (sodium polystyrene sulfonate: Kayexalate) to treat progressive hyperkalemia. With the exception of possible metabolic effects occurring on a long term basis, Mg(OH)2 in association with magnesium-free dialysate seems of value to treat dialysis hyperphosphatemia.

Adult↗
PubMed1985

Spurious hyperphosphatemia due to hyperlipidemia.

A patient had hyperlipidemia associated with apparent hyperphosphatemia. Further tests on his serum and on the lipemic sera from 15 additional patients revealed a method-dependent overestimation of inorganic phosphorus values. The degree of overestimation was found to correlate positively with the serum triglyceride concentration. Unexplained elevation of the serum phosphorus level should alert the physician to the possibility of spurious hyperphosphatemia due to hyperlipidemia.

Aged↗
PubMed1983

[Tumor-like bursal calcifications due to uncontrollable hyperphosphatemia in chronic hemodialysis. Case report].

The most important factor that appears to be associated with soft-tissue calcifications in uremics is the increase of serum-phosphate levels, especially if the calcium-phosphate product exceeds the value of 75 (concentrations in mg/dl) [6]. In contrast to previous years tumoral paraarticular calcinosis is now rarely seen because much more attention has been paid to the prevention of hyperphosphatemia and because of pharmacological improvement of phosphate binding agents. Therefore, the level of serum phosphate in hemodialysed patients primarily depends on the patients adherence to the low phosphate diet and compliance with the phosphate binding therapy [4, 8]. We want to report of a patient on chronic intermittent hemodialysis who developed tremendous paraarticular soft tissue calcifications during a short period of time due to uncontrolled hyperphosphatemia despite correct intake of phosphate binding compounds.

Bursa, Synovial↗
PubMed1993

Fatal hyperphosphatemia following Fleet Phospo-Soda in a patient with colonic ileus.

A fatal case of hyperphosphatemia secondary to enteral administration of Fleet Phospo-Soda is presented. A 64-yr-old male admitted for theophylline toxicity was treated with activated charcoal and sorbitol, but subsequently developed colonic ileus. Two sequential doses of Phospo-Soda were administered to facilitate clearance of the charcoal; however, this resulted in marked hyperphosphatemia, hypocalcemia, acidemia, and other electrolyte abnormalities, followed by the patient's demise. This case is added to several other reports about the risks of injudicious use of sodium phosphate cathartics.

Charcoal↗
PubMed1977

Hyperphosphatemia.

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.

Acromegaly↗
PubMed1999

A randomized trial of sevelamer hydrochloride (RenaGel) with and without supplemental calcium. Strategies for the control of hyperphosphatemia and hyperparathyroidism in hemodialysis patients.

OBJECTIVE: We have previously shown sevelamer hydrochloride (RenaGel) to be an effective and well-tolerated treatment for hyperphosphatemia in hemodialysis patients. PATIENTS AND METHODS: We performed a randomized clinical trial to compare the efficacy of RenaGel alone and RenaGel with calcium, using the serum phosphorus concentration and intact parathyroid hormone (PTH) as the principal outcomes of interest. Calcium (900 mg elemental) was provided as a once-nightly dose on an empty stomach. 71 patients were randomized and included in the intent-to-treat population; 55 completed the 16-week study period (2 weeks washout, 12 weeks treatment, 2 weeks washout). 49% of subjects were taking vitamin D metabolites. RESULTS: Serum phosphorus and PTH rose significantly when patients stopped their phosphate binders during both washout periods. RenaGel and RenaGel with calcium were equally effective at reducing serum phosphorus (mean change -2.4 mg/dL vs. -2.3 mg/dL). RenaGel with calcium was associated with a small increase in serum calcium (mean change 0.3 mg/dL vs. 0.0 mg/dL in RenaGel group, P = 0.09) that was not statistically significant. During the treatment phase, the reduction in PTH tended to be greater in the RenaGel with calcium group (median change -67.0 vs. -22.5 pg/mL in RenaGel group, P = 0.07). Non-users of vitamin D metabolites treated with RenaGel with calcium experienced a significant decrease in PTH (median change -114.5 vs. -22 pg/mL in RenaGel group, P = 0.006). Adverse events were seen with equal frequency in both groups, being generally mild in intensity, and rarely attributable to the drugs. CONCLUSION: We conclude that RenaGel and RenaGel with calcium are similarly effective in the treatment of ESRD-related hyperphosphatemia. Provision of supplemental calcium or metabolites of vitamin D with RenaGel may enhance control of hyperparathyroidism.

Calcium↗
PubMed2006

Left ventricular hypertrophy: is hyperphosphatemia among dialysis patients a risk factor?

Cardiovascular disease occurs in ESRD patients at rates that are far higher than is seen in the general population, and cardiovascular deaths account for the majority of deaths among dialysis patients. Abnormal mineral metabolism is a novel cardiovascular risk factor among dialysis patients. Recently published results demonstrated that even with good control of BP and anemia, conventional hemodialysis is associated with significant left ventricular hypertrophy (LVH); however, daily hemodialysis was associated with a significant reduction in LV mass index (LVMI). Furthermore, it was shown that control of serum phosphorus correlates with the reduction in LVMI. These data suggest a novel mechanism for the deleterious effect of elevated serum phosphorus on cardiovascular outcomes among hemodialysis patients: LVH. Other investigators have noted an association of hyperphosphatemia and LVH; however, this study was the first to demonstrate that improvement in serum phosphorus is associated with reduction in LVM. In addition, it is shown that daily hemodialysis is an effective modality in improving serum phosphorus through significantly improved phosphorus removal. Elevated serum phosphorus leads to vascular calcification, which can lead to LVH by decreasing vascular compliance. However, our study showed an improvement in LVMI during a 12-mo period. Because vascular calcification is unlikely to remit over this time period, it is proposed that serum phosphorus has a reversible, cardiotoxic effect that leads to LVH that can be reversed successfully with good control of serum phosphorus.

Humans↗
PubMed1984

Acute renal failure caused by extreme hyperphosphatemia after chemotherapy of an acute lymphoblastic leukemia.

The authors report a documented case of hyperphosphatemia-induced nephrocalcinosis after chemotherapy of an acute lymphoblastic leukemia (ALL). Microscopic examination of the kidney showed numerous calcium deposits with concentric structure in the calyces and in the tubules. Electronic microsound analysis proved the deposits to be composed of calcium phosphate. The nephropathy mechanism is studied, and a review of the 34 similar cases of this acute tumor lysis syndrome is made. Some suggestions are put forward to present the consequences of this therapy-induced syndrome.

Acute Kidney Injury↗
PubMed1991

Hyperphosphatemia in multiple myeloma due to a phosphate-binding immunoglobulin.

Hyperphosphatemia (HP) is usually seen in patients with hypoparathyroidism, renal failure, and tumor lysis. The authors described a patient with HP due to a phosphate-binding immunoglobulin (Ig). An 86-year-old woman had serum phosphate levels as high as 4.75 mmol/l, (normal, 0.77 to 1.45 mmol/l). Serum ionized calcium, blood urea nitrogen (BUN), creatinine, and N-terminal parathyroid hormone (PTH) levels were normal, but serum 1,25-dihydroxyvitamin D level was subnormal at less than 12 pmol/l (normal, 36 to 146 pmol/l). Serum total protein was elevated at 105 g/l (normal, 60 to 80 g/l), and additional studies confirmed a diagnosis of immunoglobulin G (IgG) multiple myeloma. Results of in vitro studies using anti-human IgG antibodies showed that the IgG of the patient bound inorganic phosphate. Several isolated case reports have documented spurious HP due to interference of the paraprotein in the routine serum phosphate assay. In only one patient, however, has actual binding of phosphate to a myeloma protein been documented. The studies of the authors document phosphate binding by an IgG paraprotein and suggest that in this setting HP may be of physiologic significance as evidenced by depressed serum levels of 1,25-dihydroxyvitamin D.

Aged↗
PubMed1995

Severe hyperphosphatemia following acute tumor lysis syndrome.

We report on a 14-year-old boy with acute lymphoblastic leukemia (lymphoma-leukemia) who had two episodes of acute tumor lysis syndrome during induction of remission with oral prednisolone alone and oral prednisolone, intravenous vincristine, and doxorubicin, respectively. Subsequently he had severe hyperphosphatemia (29.3 and 14.1 mg/dl; 9.46 and 4.55 mmol/L), hypocalcemia, hyperuricemia, hyperkalemia, and azotemia. Multiple stones and tumor cells infiltration were demonstrated in both kidney. He responded favorably to hemodialysis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Oral Fleet Phospho-Soda laxative-induced hyperphosphatemia and hypocalcemic tetany in an adult: report of a case.

PURPOSE: This study was undertaken to report an adverse outcome of the routine use of Fleets Phospho-Soda for bowel cleansing and to review the available literature. METHOD: Report of a case and review of the literature is presented. RESULT: Administration of Fleets Phospho-Soda for bowel preparation in an adult resulted in hyperphosphatemia and hypocalcemic tetany. Review of the literature shows this to be the first such report. Further evaluation suggests a role for partial bowel obstruction and renal failure in this complication. CONCLUSION: Although Fleet Phospho-Soda solution continues to be a safe bowel preparation, caution should be used in adults with bowel obstruction and renal failure.

Acute Kidney Injury↗
PubMed2005

Tumoral calcinosis with hyperphosphatemia.

Tumoral calcinosis is a rare disorder of mineral metabolism among adolescents and young adults characterized by deposition of calcific masses around large joints. It is less commonly reported in pediatric population and commonly mistaken for bone tumors. Typical lab parameters include hyperphosphatemia with normal levels of serum calcium, parathyroid hormone (PTH) and alkaline phosphatase. A ten-year-old boy with typical features of tumoral calcinosis is presented.

Alkaline Phosphatase↗
PubMed2004

Identification of a recurrent mutation in GALNT3 demonstrates that hyperostosis-hyperphosphatemia syndrome and familial tumoral calcinosis are allelic disorders.

Hyperphosphatemia-hyperostosis syndrome (HHS) is a rare autosomal recessive metabolic disorder characterized by elevated serum phosphate levels and repeated attacks of acute, painful swellings of the long bones with radiological evidence of periosteal reaction and cortical hyperostosis. HHS shares several clinical and metabolic features with hyperphosphatemic familial tumoral calcinosis (HFTC), which is caused by mutations in GALNT3 encoding a glycosyltransferase responsible for initiating O-glycosylation. To determine whether GALNT3 is involved in the pathogenesis of HHS we screened two unrelated Arab-Israeli HHS families for pathogenic mutations in this gene. All affected individuals harbored a homozygous splice site mutation (1524+1G-->A) in GALNT3. This mutation was previously described in a large Druze HFTC kindred and has been shown to alter GALNT3 expression and result in ppGalNAc-T3 deficiency. Genotype analysis of six microsatellite markers across the GALNT3 region on 2q24-q31 revealed that the HHS and HFTC families share a common haplotype spanning approximately 0.14 Mb. Our results demonstrate that HHS and HFTC are allelic disorders despite their phenotypic differences and suggest a common origin of the 1524+1G-->A mutation in the Middle East (founder effect). The heterogeneous phenotypic expression of the identified splice site mutation implies the existence of inherited or epigenetic modifying factors of importance in the regulation of ppGalNAc-T3 activity.

Calcinosis↗