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At least 469 records · Page 26Linked to original sources
PubMed2004

[Association of brain computed tomography images of intracranial calcifications in three different cases of hypoparathyroidism].

The problem of intracranial calcifications in children has not been widely discussed in the literature yet. The aim of this study is to emphasise different clinical aspects of intracranial calcifications found in subcortical nuclei and cerebellum in children with disturbed calcium metabolism. We report three different cases of hypoparathyroidism in children in whom similar radiological changes on computed tomography (CT) of the brain were found. An 11-year-old boy was referred to us after episode of tetany. We confirmed the diagnosis of idiopatic hypoparathyroidism (presence of Chvostek and Trousseau signs, hypocalcemia, hyperphosphatemia, low parathormone serum concentration). On brain CT small, symmetric calcifications in the subcortical nuclei and frontal lobes were imaged. A diagnosis of pseudohypoparathyroidism type Ib in 10-year-old girl was established on the basis of clinical symptoms (syncope with seizures, recurrent carpopedal spasms in the past) and laboratory investigations (hypocalcemia, hyperphosphatemia, high parathormone serum concentration). In 11-year-old girl autoimmune polyglandular syndrome type I was diagnosed (hypoparathyroidism with chronic mucocutaneous candidiasis and nail dystrophy from the age of 2). CT of the brain showed multiple irregular symmetric calcifications in cerebellar hemispheres, internal capsula and subcortical nuclei on the border of white and grey matter in both frontal lobes.

Brain Diseases↗
PubMed2004

[Mechanism of intracerebral calcification in hypoparathyroidism].

The mechanism of intracranial calcification in hypoparathyroidism, more frequently seen in pseudo--than idiopathic hypoparathyroidism, has not been completely elucidated, but may be related more to the duration of hypocalcaemia and hyperphosphatemia than parathyroid hormone itself. Hyperphosphatemia promotes ectopic calcification, especially in blood vessel and periarticular tissue in renal failure, but in brain tissue in hypoparathyroidism. Participation of PTH receptor2 in the brain and superoxide production by mitochondria in hypoparathyroidism should be explored with reference to intracerebral calcification and neurodegenerative diseases.

Brain↗
PubMed2002

[Ectopic calcification in dialysis patients].

Vascular calcification is the most important type of the ectopic calcinosis in dialysis patients. Hyperphosphatemia is an independent risk factor for the vascular calcification. A sodium-dependent phosphate co-transporter is associated with an increase in the intracellular phosphate concentration in vascular cells. After degeneration and/or apoptosis of smooth muscle cells in the vascular walls, macrophage infiltration into the calcified tissues followed by production of bone matrix protein leads to the vascular calcification. Uremic conditions such as hyperphosphatemia may enhance the vascular calcification. Therefore, we should treat the vascular calcification in association with bone remodeling in dialysis patients.

English Abstract↗
PubMed2005

[Cardiovascular calcification and accelerated atherosclerosis in chronic kidney disease].

Cardiovascular disease is the first cause of morbidity and mortality in dialysis patients. Hyperphosphatemia and elevated serum calcium-phosphate levels have recently been investigated as inducing factors on extraskeletal calcification in this population. In vitro studies demonstrated that human aortic smooth muscle cells calcify when incubated in a high phosphate medium, where calcium and calcitriol are not changed. Furthermore, the lack of inhibitory proteins, such as fetuin and matrix Gla protein, is a possible main determinant of calcium-phosphate deposition in soft tissues. The classical treatment of hyperphosphatemia and secondary hyperparathyroidism in dialysis patients consists of calcium-based phosphate binders and calcitriol administration. Unfortunately, this "first-generation" therapy is not free of dramatic side effects. New free-calcium and -aluminum phosphate binders, new vitamin D metabolites, and calcimimetics are examples of "second-generation" therapies that may prevent vascular calcification and possibly prevent some of the burden of cardiovascular disease in uremia.

Animals↗
PubMed2005

[Changes of control of disorders of calcium and phosphorus metabolism in Lithuanian hemodialysis centers 1996-2003].

The aim of the study was to evaluate the changes of the rate of disorders of calcium and phosphorus metabolism and their control in patients on hemodialysis (HD) in Lithuania in 1996-2003. Every December during this period we visited all HD centers of Lithuania and collected data on calcium-phosphorus metabolism in HD patients. 51.8% of HD patients in 1999 and 44.6% in 2003 had hyperphosphatemia (>1.8 mmol/l) (p<0.05). The mean phosphate concentration was 1.82+/-0.56 mmol/l in 2003 (p<0.05, comparing with 1.95+/-0.72 mmol/l in 1999 and 1.9+/-0.72 mmol/l in 2001). 7.1% of HD patients had hypocalcemia in 2003 and 7.8% hypercalcemia. Serum parathyroid hormone level was investigated only in 27.3% of HD patients in 1999 and 84.8% in 2003 (p<0.05). Use of alfacalcidol significantly decreased from 77.5% in 1998 to 29.4% in 2003, when the evaluation of serum parathyroid hormone increased (r=-0.911, p=0.03). Serum parathyroid hormone level was not analyzed for 59.8% of patients who used alfacalcidol and 59.4% of them had hyperphosphatemia in 1999 (6.3% and 32.9% in 2003, respectively; p<0.05). 10.7% of these patients had hypercalcemia in 2003. In summary, the correction of disorders of calcium and phosphorus metabolism in HD patients was insufficient but ameliorative. Monitoring of serum parathyroid hormone increased significantly during 1997-2003. The percentage of the precarious use of alfacalcidol decreased significantly when the evaluation of serum parathyroid hormone level became regular.

Calcium↗
PubMed2005

[Fibroblast growth factor (FGF)-23 in patients with hypoparathyroidism].

Hypoparathyroidism is a well-described cause of hyperphosphatemia. We aimed to clarify the physiological role of FGF-23 in serum phosphate homeostasis in hypoparathyroidism after thyroidectomy. Increased serum FGF-23 levels were found in patients with hyperphosphatemia and hypocalcemia, caused by hypoparathyroidism after thyroidectomy. After the recovery of parathyroid function, the serum level of calcium, phosphate, and FGF-23 was normalized. Serum FGF-23 levels were significantly higher in patients with permanent hypoparathyroidism than in healthy controls. These results indicate that FGF-23 may play an important role in serum phosphate homeostasis by its up-regulation in the hyperphosphatemic condition.

Female↗
PubMed1991

Renal osteodystrophy.

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Assessment of activity of care of a nutritional support multidisciplinary team in the follow-up of total parenteral nutrition].

INTRODUCTION: In total parenteral nutrition (TPN) nutritional support multidisciplinary teams (NSMT) must provide a high quality nutritional assistance based on evidence and daily follow-up of patients with TPN. OBJECTIVES: To assess the degree of adherence to quality standards of care provided to patients on TPN by the NSMT in two consecutive annual periods, according to structure, procedure, and outcomes indicators, previously defined in the team working protocol. PATIENTS AND METHODS: Prospective study of all patients that received TPN at our Center (421-bed general teaching hospital) during the years 2002 and 2003, using the data introduced in NUTRIDATA by daily follow-up of clinical and analytical conditions, and nutritional and non-nutritional complications, comparing both periods and considering an statistical significance level of p < 0.05. RESULTS: One hundred and sixty-three patients and 145 patients received TPN during 2002 and 2003(65.9% male), respectively, with similar parameters of gender, age, indications for TPN, baseline nutritional status, mean nutritional supply, and non-nutritional complications. As to the different quality indicators established in the comparative study, we found a significant improvement in 2003 vs. 2002 in relation to initial anthropometrical assessment (71.03% vs 51.53%; p < 0.001), initial biochemical assessment (97.93% vs. 92.63%; p < 0.04), performance of systematic monitoring analysis (84.83% vs. 71.78%; p < 0.01), hypernatremia incidence (8.27% vs. 15.34%; p = 0.05) and moderate hyperphosphatemia (26.89% vs. 40.49%; p < 0.02), TPN ending for clinical improve- ment (76.60% vs. 64.40%; p = 0.04), and reduction of days on TPN (15.74 +/- 20.43 vs. 11.88 +/- 8.34; p < 0.02), the impaired electrolyte levels significantly improving as a whole. We also observed a non-significant trend towards an improvement of adequacy of TPN indications, hyperphosphatemia, severe hypophosphatemia, total stay, and post-surgical stay, in 2003 vs. 2002. CONCLUSIONS: The NSMT experience shows that analysis of indicators based on quality standards, in two successive annual periods allows assessing the improvement of efficiency of nutritional intervention in hospital-admitted patients with TPN with regards to indication, assessment, follow-up, and course.

Aged↗
PubMedDate not supplied

Sevelamer hydrochloride versus aluminum hydroxide: effect on serum phosphorus and lipids in CAPD patients.

BACKGROUND: Dietary phosphorus restriction, oral administration of phosphorus binders, and dialysis are the main strategies to control hyperphosphatemia in patients with stage 5 chronic kidney disease. Aluminum hydroxide (AH) and calcium carbonate, the most commonly used phosphorus binders, have serious disadvantages, such as aluminum toxicity and hypercalcemia. Sevelamer hydrochloride (SH) is a relatively new nonabsorbed calcium- and aluminum-free phosphorus binder. The present study was designed to evaluate the efficacy of SH in the control of hyperphosphatemia and its effect, compared to AH, on serum lipid parameters in patients on continuous ambulatory peritoneal dialysis (CAPD). METHODS: 30 stable patients on CAPD were included in an open-label, randomized crossover study. After a 2-week phosphorus binder washout period, 15 patients (group I) were administered SH for 8 weeks and in the remaining patients (group II), AH was introduced (phase A). After a new 2-week washout period, patients crossed over to the alternate agent for another 8 weeks (phase B). RESULTS: There were similar reductions in serum phosphorus levels over the course of the study with both agents: by 1.18 +/- 0.07 mg/dL (0.38 +/- 0.03 mmol/L) with SH and by 1.25 +/- 0.15 mg/dL (0.40 +/- 0.05 mmol/L) with AH in phase A (p = NS), and by 1.35 +/- 0.25 mg/dL (0.43 +/- 0.08 mmol/L) with AH and by 1.23 +/- 0.80 mg/dL (0.39 +/- 0.25 mmol/L) with SH in phase B (p = NS). Moreover, SH administration was associated with a 10.5% +/- 9.4% and a 20.1% +/- 6.8% fall in total cholesterol (p < 0.05) and low-density Lipoprotein cholesterol (p < 0.001) in phase A, and 11.9% +/- 7.2% (p < 0.05) and 21.5% +/- 2.4% (p < 0.001), respectively, in phase B. In both phases of the study, AH administration was not followed by a significant change in serum lipid parameters. CONCLUSION: Sevelamer hydrochloride is a well-tolerated alternative to calcium- or aluminum-containing phosphorus binder in the control of serum phosphorus in CAPD patients. Furthermore, SH improves the lipid profile in these patients.

Adult↗
PubMed2006

Renal osteodystrophy: review of the disease and its treatment.

Renal osteodystrophy (ROD), which is most evident in patients on renal replacement therapy (RRT), usually begins when the kidney function starts to deteriorate. The spectrum of skeletal abnormalities seen in ROD is classified according to the state of bone turnover. In the past two decades, the prevalence of high turnover ROD has decreased while low bone turnover has become increasingly recognized. Secondary hyperparathyroidism represents a common disorder in patients with chronic kidney disease (CKD); it develops as a result of hyperphosphatemia, hypocalcemia and impaired synthesis of renal vitamin D with reduction in serum calcitriol levels. Patients with secondary hyperparathyroidism have a range of symptoms that affect their quality of life. The aim of treatment of ROD is to reduce the incidence of uremic bone disease as well as cardiovascular morbidity and mortality caused by elevated serum levels of parathormone (PTH) and calcium X phosphorus product. Treatment measures include control of phosphorus retention and prevent hyperphosphatemia, maintaining serum calcium concentrations within the normal range and prevent excess PTH secretion.

Biomarkers↗
PubMed1990

Tendinitis and tendon ruptures in successful renal transplant recipients.

The musculoskeletal system of 167 successful renal transplant recipients was examined for locomotor complications. Apart from avascular necrosis and spontaneous fractures, two new clinical entities were identified: tendinitis and spontaneous tendon ruptures. Tendinitis was found in the supraspinatus and calcaneal tendons in 12 patients (7.2%). Pretransplant hyperphosphatemia and posttransplant hypercalcemia were seen in patients developing tendinitis. Spontaneous tendon ruptures were observed in the calcaneal tendons in four patients (2.4%). Pretransplant hyperphosphatemia was observed in this group of patients. The cumulative dose of prednisolone was not significantly different than in asymptomatic patients.

Adolescent↗
PubMed1989

Calcium carbonate as a phosphate binder: is there a need to adjust peritoneal dialysate calcium concentrations for patients using CaCO3?

The widespread use of calcium carbonate as a phosphate binder is limited by its tendency to develop hypercalcemia in some patients using effective dosages needed to control hyperphosphatemia. Most common continuous ambulatory peritoneal dialysis (CAPD) regimens using dialysis solutions containing 3.5 mEq/L of calcium result in net absorption of calcium from the dialysis solution and, hence limit the amount of oral calcium that can be administered. Peritoneal dialysis solutions with reduced calcium levels are needed for effective use of CaCO3 to control hyperphosphatemia in some dialysis patients.

Calcium↗
PubMed1989

[Progression of chronic renal failure. Pathogenesis and therapeutic aspects].

Once established, chronic renal failure does not progress only when the specific triggering metabolic, immunological or vascular-renal underlying disease persists. Unspecific factors also cause progression of chronic renal failure when the underlying renal disease is no longer active or has been successfully treated. Today, such unspecific progression factors are considered to be glomerular capillary hyperfiltration/hyperperfusion, the effects of angiotensin II, uremic-associated lipid metabolic disorder, hyperphosphatemia or secondary hyperparathyroidism, as also the effect of glucocorticoids. For therapy, apart from adequate antihypertensive management, a low-protein diet and treatment of the lipid metabolic disorder and the secondary hyperphosphatemia, is recommended in the patient with chronic renal disease.

Animals↗
PubMed1989

[Disorders of fluid and electrolyte metabolism in elderly diabetics].

Disorders of fluid and electrolyte metabolism in elderly diabetics were studied. High frequency of hyperkalemia (20.8%), hypomagnesemia (14.6%), hypocalcemia (13.7%), hyperphosphatemia (8.6%), hyponatremia (8.1%) and hyperchloremia (7.2%) was observed among 332 elderly diabetics. Furthermore, hyperkalemia, hyperphosphatemia, hyponatremia, hyperchloremia, hypercalcemia and hypermagnesemia were more frequent in diabetics with renal insufficiency (serum Cr greater than or equal to 1.5 mg/dl) than in diabetics with normal renal function (serum Cr less than or equal to 1.4 mg/dl). In addition, statistically significant negative correlation were observed between plasma glucose levels and serum levels of sodium and chloride in diabetics with normal renal function. These results clearly demonstrated that the most important causal factor of electrolyte disorders in elderly diabetics might be the renal dysfunction due to diabetic nephropathy and/or nephrosclerosis. Moreover, glucose intolerance is also one of the causal factors for hyponatremia and hypochloremia. Disorders of fluid and electrolyte metabolism were manifest in 31 diabetic patients with hyperosmolar non-ketotic coma. The frequency of patients with abnormally elevated serum levels of sodium, potassium and chloride, and patients with abnormally lowered serum levels of calcium was high in this morbid state. Water and sodium deficit, examined in 11 cases of hyperosmolar non-ketotic coma, was 4780 +/- 2100 ml (107 +/- 43 ml/kg body weight) and 290 +/- 170 mEq (6.8 +/- 4.2 mEq/kg body weight), respectively. However, no significant deficit of potassium was observed in the patients. Statistically significant positive correlations between water deficit and serum Cr levels and with serum effective osmolarity were observed. However, there were no significant correlations between water deficit and plasma glucose levels, serum sodium levels and serum osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia.

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.

Adult↗
PubMed1986

[Iatrogenic aluminum osteopathy in a uremic infant].

An infant with uremia due to congenital renal hypoplasia was treated with oral aluminum hydroxide for 9 months in an attempt to reduce hyperphosphatemia. An increasingly painful osteopathy with pathological fractures ensued with loss of thoracic wall stability and respiratory failure. Increased serum aluminium levels and histochemically proved deposits of aluminium at the mineralisation front between calcified and noncalcified osteoid were demonstrated. In the context of recent findings concerning aluminium bone toxicity it is beyond doubt that this phosphate binding agent was detrimental for this child. Though a low phosphate diet normalized hyperphosphatemia after aluminium hydroxide treatment had been stopped, no effect on the progressive osteopathy was observed. Since aluminium hydroxide as a phosphate binder can be replaced by calcium carbonate or a low phosphate diet at least in young children, it should not be further recommended in this age group. This seems especially important in nondialyzed patients.

Aluminum↗
PubMed1986

Paraprotein interference with colorimetry of phosphate in serum of some patients with multiple myeloma.

In untreated serum of three patients with multiple myeloma, concentrations of inorganic phosphate ranged from 130 to 270 mg/L as measured with a chromogenic assay based on the interaction of phosphate ion with ammonium molybdate in the presence of ferrous sulfate. There were no clinical features of hyperphosphatemia, and values for total calcium concentration in serum remained within normal limits throughout. Subsequent investigations demonstrated that this hyperphosphatemia was spurious and was caused by high concentrations of the paraprotein interfering with the chromogenic assay. Because this type of assay, adapted for automated systems, is now widely used in clinical laboratories, we call attention to this limitation to avoid confusion in clinical evaluations of patients with multiple myeloma.

Aged↗