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PubMed2006

Prognostic significance of the serum phosphorus level and its relationship with other prognostic factors in multiple myeloma.

We studied the serum phosphorus (P) level of 110 patients with multiple myeloma (MM) (age range 42-83 years, median 62 years) and evaluated the relationship between that and other prognostic factors. Serum P level significantly correlated with the prognostic factors that are relevant to renal dysfunction: serum creatinine (P<0.00000001), serum beta2-microglobulin (P=0.00000088), serum uric acid (P=0.0000014), and corrected serum calcium (cCa P=0.000067). Although it also correlated with the percentage of plasma cells in bone marrow nucleated cells (BMPC%) and the hemoglobin (Hb) and leukocyte counts, the significance was less than for the other four prognostic factors. Serum creatinine, BMPC%, leukocyte count, serum uric acid, bone lesions, beta2-microglobulin, and serum cCa were all significantly higher and Hb significantly was lower in the MM patients with hyperphosphatemia (serum P>3.8 mg/dl). The survival time was significantly shorter in these patients (P=0.000087). Multivariate analysis (Cox's proportional hazards regression model) showed that the serum P level is a significant negative prognostic factor in MM patients.

Adult↗

PubMed2003

Acute tumor lysis syndrome in solid tumors--a case report and review of the literature.

PURPOSE: Tumor lysis syndrome (TLS) is a potential complication in cancer therapy. It may occur in highly sensitive tumors, especially in childhood cancers and acute leukemias, whereas it is rare in the treatment of adult solid tumors. TLS is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia following massive lysis of malignant cells. Complications include acute renal failure and metabolic acidosis. We report the first case of TLS during chemotherapy in a patient with metastatic medulloblastoma, together with a review of the literature regarding the occurrence of TLS in patients with solid tumors. METHODS: Data regarding clinical and biochemical parameters were extracted from the actual patients' files. Reports of TLS in the English language literature up to 2002 were identified by searching Medline. RESULTS: A 23-year old male with metastatic medulloblastoma received chemotherapy with cisplatin and etoposide due to massive extracerebral manifestations including metastases to the liver, mediastinal lymph nodes and bone marrow metastases. The patient developed classical signs of TLS on the second day of chemotherapy, including acute renal failure. A 17-fold increase in plasma LDH up to 87608 U/l was observed together with a 4-fold increase in plasma creatinine. The patient was treated with aggressive hydration, allopurinol and repeated hemodialysis. During the following days the patient improved and the biochemical markers all returned to normal. REVIEW. Reviewing the literature, a total of 45 patients with solid tumors who developed TLS have been reported. Most of the patients presented with metastatic, therapy-sensitive disease. Although preventable in practically 100% of patients, TLS is a potentially fatal complication, and in this material the mortality rate was one in three. Risk factors included increased LDH, hyperuricemia and pretreatment azotemia. CONCLUSIONS: TLS is only rarely associated with treatment of solid tumors. Precautions should be taken to avoid this potentially fatal complication in (chemo)therapy of solid tumors, especially in therapy-sensitive tumors presenting with bulky, metastatic disease and preexisting risk factors, including azotemia, elevated LDH and hyperuricemia. Prophylactic treatment to avoid TLS includes allopurinol, hydration prior to treatment and alkalization of the urine. Urate oxidase (rasburicase) is now beginning to replace allopurinol as a more effective way of reducing hyperuricemia and thereby the risk of TLS.

Adult↗

PubMed2000

Recent experience with Moyamoya disease in Turkey.

A series of moyamoya patients is presented. Angiographic findings, outcome of revascularization surgery and a young case with moyamoya disease and hyperphosphatemia are reported. Thirteen patients (6 males and 7 females; age range 2-50 years) were included in the study group. Findings of the patients at presentation were intracranial haemorrhage in two adult cases and sequelae of cerebral ischemia in the rest of the group. One young girl had hyperphosphataemia. Angiography showed distal internal carotid or proximal anterior and middle cerebral artery stenosis, unique collaterals, microaneurysm of the posterior lateral choroidal artery and flow-related changes in the posterior circulation. In 3 patients, encephalo-duro-arterio-synangiosis (EDAS) and burrholes were performed at surgery. Follow-up angiograms of these patients showed revascularization. Moyamoya, a rare but potentially devastating disease, must be addressed as a cause of haemorrhagic and ischaemic cerebral events.

Adolescent↗

PubMed2000

Renal disease as a risk factor for cardiovascular disease.

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.

Calcinosis↗

PubMed2004

A case of familial tumoral calcinosis in a neonate and review of the literature.

BACKGROUND: Tumoral calcinosis occurs in two distinct clinical forms. The sporadic form is secondary to chronic renal failure, hyperparathyroidism, milky-alkali syndrome, hypervitaminosis D and other systemic disorders. The familial form is extremely rare (around 100 cases worldwide) and affects patients in the first or second decade of life. It is believed to be transmitted in a dominant autosomal manner with variable clinical expressivity and is manifested as hyperphosphatemia, elevated serum 1,25-dihydroxyvitamin D with juxta-articular tumorous calcifications. Moreover, the theory of a unique dental malformation serving as a screening marker for clinically non-apparent affected individuals is revisited and reconfirmed. CASE REPORT: We present a case of a Caucasian male newborn, as well as a review of the literature with differential diagnostic considerations and their therapeutical implications.

Calcinosis↗

PubMed2000

Compression of the ulnar nerve in Guyon's canal by uremic tumoral calcinosis.

We describe the case of a 70-year-old woman with chronic renal failure on haemodialysis presenting with an ulnar nerve compression in Guyon's canal secondary to uremic tumoral calcinosis. Excision of calcium deposits and external neurolysis of the ulnar nerve were successfully performed. Simultaneously, the hyperphosphatemia and hypercalcemia were corrected. The pathogenesis of this condition is different from primary tumoral calcinosis. Clinical and radiological features and therapy are discussed. Uremic tumoral calcinosis is an unusual etiology of ulnar nerve compression in Guyon's canal not previously reported in dialysis patients.

Aged↗

PubMed1996

The Ca(2+)-sensing receptor gene (PCAR1) mutation T151M in isolated autosomal dominant hypoparathyroidism.

Isolated autosomal dominant hypoparathyroidism is a heterogeneous disorder characterized by parathyroid hormone (PTH) deficiency, hypocalcemia and hyperphosphatemia. The candidate gene approach was used to study a large Norwegian family. The loci for the PTH gene, PTH receptor gene and RET protooncogene were excluded using dinucleotide markers and restriction fragment length polymorphism analysis. Complete cosegregation of this trait was found with the chromosomal region 3q13, using the short tandem repeat markers D3S1267, D3S1269, D3S1303, D3S1518, and RHO. This region contains the candidate locus for the Ca(2+)-sensing receptor (PCAR1). By single-strand conformation polymorphism (SSCP) analysis of all PCAR1 exons followed by automated sequencing, we identified a C to T transition in exon 2 (cDNA position 452) on the mutant allele in the family. The mutation predicts a substitution of Thr to Met in amino acid position 151 (T151M). A StyI restriction site created by the nucleotide substitution was used to confirm the mutation on all alleles, as well as to exclude it among 100 normal alleles (blood donors). SSCP analysis also identified a novel polymorphism of PCAR1 intron 4 (1609-88t --> c) on normal alleles. The T151M mutation is located in the extracellular N-terminal domain of PCAR1, which belongs to the superfamily of G protein-coupled receptors. We suggest that this is a gain-of-function mutation that increases the sensitivity of the receptor to [Ca2+], thereby decreasing the calcium set point.

Amino Acid Sequence↗

PubMed2003

Chronic renal insufficiency in children: the 2001 Annual Report of the NAPRTCS.

End-stage renal disease (ESRD) is a major cause of morbidity in children. Besides its high cost to society, ESRD carries significant mortality. Chronic renal insufficiency (CRI) often precedes ESRD. Identifying factors that correlate with the rate of progression to ESRD is beneficial in the management of children with CRI. Since 1994 the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) has extended its registry to include children with CRI, defined as creatinine clearance ( C(Cr)) <75 ml/min per 1.73 m(2). As of January 2001, our database registered 4,666 children (<20 years of age) with CRI. Data analysis showed that at least 40% of patients entered had congenital urological anomalies; 39% of patients were followed for at least 3 years. Follow-up data showed that 31% of all registered patients progressed to ESRD by the end of the reporting period. There was a correlation between CRI and several co-morbid clinical factors: low hematocrit, hypoalbuminemia, hypocalcemia, hyperphosphatemia, and hyperparathyroidism, and the rate of progression to ESRD. Primary clinical diagnosis and the age at entry into registry were additional factors that correlated with the rate of progression to ESRD. The main cause of hospitalization in this registry was infection, which accounted for 45% of hospital admissions. Growth delay measured by standard deviation score at baseline was -1.40 at the time of registration. Our data suggest potential areas of improved care that could impact the onset of ESRD.

Acidosis↗

PubMed2004

Dietary phosphorus reduction by pretreatment of human breast milk with sevelamer.

Hyperphosphatemia leading to hyperparathyroidism and ultimately renal osteodystrophy is a well-known complication of chronic renal failure. A new hydrogel binder, sevelamer, has recently become available for use in hyperphosphatemic patients with renal failure. We had previously mixed the capsule with pumped breast milk and formula, but discovered that the hydrogel formed a viscous solution that infants were unable or unwilling to swallow. We therefore evaluated the phosphorus content of fresh and frozen breast milk before and after treating with different doses of sevelamer at different temperatures and for varying lengths of time. The hydrogel bound promptly to phosphorus, reducing the phosphorus content 78% within 5 min. The viscous hydrogel settled to the bottom of the container within 10 min allowing the supernatant to be easily decanted. We also evaluated the breast milk for changes in other electrolytes, osmolality, pH, and macronutrient content. These results show that fresh or frozen breast milk can be safely pretreated with sevelamer without significantly changing its macronutrient or ionic content, with the exception of calcium and protein. The supernatant can be fed to infants or instilled through a gastrostomy tube without difficulty since the viscous hydrogel settles rapidly to the bottom of the container.

Epoxy Compounds↗

PubMed2004

"Missing" inhibitors of calcification: general aspects and implications in renal failure.

In the recent past, it has become increasingly clear that extracellular calcium and phosphate homeostasis is a tightly regulated process. Since the physiological serum concentrations of calcium and phosphate are several orders of magnitude above their solubility product, mechanisms inhibiting precipitation must be operative to prevent extraosseous calcification. A number of local and systemic calcification inhibitors, including fetuin-A, matrix Gla protein, and osteoprotegerin, have been identified in recent years. Deficiency and dysregulation of such factors may contribute to morbidity and even mortality. Extraosseous calcifications occur with high prevalence in patients with end-stage renal disease. In particular, vascular manifestations are clearly associated with cardiovascular events and decreased survival. In addition to the well-established roles of hyperphosphatemia and an increased calcium x phosphate product, the biological and potential clinical roles of disturbances in calcification inhibition in uremia are discussed in this overview.

Blood Proteins↗

PubMed2005

The therapeutic potential of novel phosphate binders.

Hyperphosphatemia and an increased serum calcium-phosphate (CaxP) product are associated with cardiovascular mortality in adult dialysis patients. Target levels for the treatment of elevations in serum phosphorus (P) and the CaxP product have recently been redefined, but are difficult to achieve in clinical practice. This problem may be especially prevalent in children and adolescents who have a higher recommended P intake than adults and also a higher calcium (Ca) load with the intake of comparatively higher doses of Ca-containing phosphate binders. Current treatment practice with Ca-containing P binders carries the risk of hypercalcemic episodes and ectopic calcifications, including vascular calcifications, which are associated with an increased risk of cardiovascular disease. Novel P binders in the development phase include several iron-containing preparations. Clinical experience with lanthanum carbonate is limited to date and further studies are needed to establish its safety. The only available Ca-free P binder with widespread use and large-scale clinical safety data in adults is sevelamer. Preliminary data suggest that this drug can also be safely given to children.

Child↗

PubMed2005

Are new vitamin D analogues in renal bone disease superior to calcitriol?

Progression of chronic kidney disease is associated with an early reduction in serum calcitriol levels; thus, therapy with calcitriol should be initiated early in the course of chronic kidney disease to prevent the development of secondary hyperparathyroidism. Initial studies demonstrated a potential role of calcitriol in the prevention of growth retardation in children with chronic kidney disease prior to dialysis. But the optimal parathyroid hormone (PTH) levels that will maximize growth response during calcitriol treatment remain to be defined. Therapy with calcitriol has been shown to control the biochemical and skeletal manifestations of secondary hyperparathyroidism, but patients developed hypercalcemia, hyperphosphatemia and adynamic osteodystrophy. Thus, new vitamin D analogues with a lower hypercalcemic response have been developed. Although comparative studies are lacking, current evidence indicates that these new active vitamin D sterols (19-nor-paracalcitol and doxercalciferol) adequately control secondary hyperparathyroidism with minimal changes in serum calcium and phosphorus levels during treatment with calcium-containing binders. The long-term effect of such therapies on the skeleton and the process of vascular calcifications remain to be evaluated.

Calcitriol↗

PubMed2005

Intravenous calcitriol for treatment of hyperparathyroidism in children on hemodialysis.

This double-blind, placebo-controlled study evaluated the safety and efficacy of intravenous (i.v.) calcitriol (Calcijex) for treatment of secondary hyperparathyroidism (secondary HPT) in pediatric end-stage renal disease (ESRD) patients on hemodialysis (HD). After a 2 to 6-week washout period of all vitamin D compounds, patients with two consecutive PTH values > 400 pg mL(-1), calcium levels < or = 10.5 mg dL(-1) and calcium x phosphorus product values < or = 70 mg2 dL(-2) were eligible for the treatment phase. Patients received a bolus injection of calcitriol or placebo three times a week, immediately after dialysis for up to 12 weeks. Initial doses (0.5-1.5 microg) were based on the severity of secondary HPT. The dose was increased every two weeks by 0.25 microg until there was at least a 30% decrease in PTH from baseline, or Ca > 11.0 mg dL(-1), or Ca x P > 75 mg2 dL(-2). Overall, 11/21 (52%) patients in the calcitriol group had two consecutive > or = 30% decreases from baseline in serum PTH compared with 5/26 (19%) patients in the placebo group (P=0.03). The mean total alkaline phosphatase decreased from 274 to 232 IU L(-1) in the calcitriol group and increased from 547 to 669 IU L(-1) in the placebo group (P=0.002). The mean bone-specific alkaline phosphatase decreased from 72.5 to 68 microg L(-1) in the calcitriol group and increased from 105.3 to 148.5 microg L(-1) in the placebo group (P=0.03). The incidence of two consecutive occurrences of elevated calcium x phosphorus (Ca x P > 75 mg2 dL(-2)) product was higher in the calcitriol group than in the placebo group (P=0.01). Two consecutive occurrences of phosphorus > 6.5 mg dL(-1) occurred in 71% of the calcitriol group and 46% of the placebo group (P=0.14). Calcium levels > 10.5 mg dL(-1) were more common in the calcitriol group than in the placebo group (P=0.01). There was a direct relationship between serum phosphorus concentration and the percentage change in PTH from baseline in both the calcitriol group (r=0.46; P<0.0001) and the placebo group (r=0.21; P=0.0005). This study demonstrates that i.v. calcitriol, at initial doses of 0.5-1.5 microg, effectively reduces PTH levels in pediatric HD patients and that patients should be closely monitored for hyperphosphatemia and elevated Ca x P product.

Acetates↗

PubMed2005

Prevention and treatment of renal osteodystrophy in children on chronic renal failure: European guidelines.

Childhood renal osteodystrophy (ROD) is the consequence of disturbances of the calcium-regulating hormones vitamin D and parathyroid hormone (PTH) as well as of the somatotroph hormone axis associated with local modulation of bone and growth cartilage function. The resulting growth retardation and the potentially rapid onset of ROD in children are different from ROD in adults. The biochemical changes of ROD as well as its prevention and treatment affect calcium and phosphorus homeostasis and are directly associated with the development of cardiovascular disease in pediatric renal patients. The aims of the clinical and biochemical surveillance of pediatric patients with CRF or on dialysis are prevention of hyperphosphatemia, avoidance of hypercalcemia and keeping the calcium phosphorus product below 5 mmol(2)/l(2). The PTH levels should be within the normal range in chronic renal failure (CRF) and up to 2-3 times the upper limit of normal levels in dialysed children. Prevention of ROD is expected to result in improved growth and less vascular calcification.

Algorithms↗

PubMed2006

FGF23: its role in renal bone disease.

Fibroblast growth factor 23 (FGF23) is a recently characterized peptide hormone produced mainly in the bone. It is secreted in response to dietary phosphorus load, and its main function is the promotion of urinary phosphate excretion and the suppression of active vitamin D (1,25D) production in the kidney. As such, FGF23 plays an important role in the maintenance of systemic phosphate homeostasis. In the advanced stages of chronic kidney disease (CKD), the kidney cannot excrete a phosphate load even in the presence of high levels of FGF23. This results in both hyperphosphatemia and a low level of 1,25D that stimulates the secretion of parathyroid hormone (PTH), leading to the development of secondary hyperparathyroidism. In chronic dialysis patients without residual renal function, FGF23 levels become extremely high due to stimulation by vitamin D therapy as well as by high levels of serum phosphate and PTH. Recent investigations have demonstrated that serum FGF23 level can be a useful marker for the prediction of the future development of refractory hyperparathyroidism and the response to vitamin D therapy in dialysis patients. In addition, putative protective roles of FGF23 against calcification have also been speculated on. Further elucidation of the mechanisms of FGF23 action will be needed to understand the various roles of FGF23 in CKD-Mineral and Bone Disorder (CKD-MBD).

Animals↗

PubMed2000

Molecular mechanisms of secondary hyperparathyroidism.

Secondary hyperparathyroidism is a frequent complication of chronic renal failure (CRF) and a major factor in the pathogenesis of renal osteodystrophy. A high serum phosphate, decreased levels of serum 1,25(OH)2D3 and the subsequently low serum calcium are the major metabolic abnormalities in CRF, which lead to the secondary hyperparathyroidism. At the level of parathyroid hormone (PTH) secretion there is insensitivity to the ambient serum calcium. PTH mRNA levels are increased by a post-transcriptional mechanism that involves the binding of PT cytosolic proteins to the PTH mRNA 3'-untranslated region (UTR). In a dietary model of secondary hyperparathyroidism due to hypocalcemia there is increased binding of parathyroid proteins to the 3'-UTR and decreased degradation as determined by an in vitro degradation assay. Changes in serum phosphate also dramatically regulate PTH mRNA stability. There is also regulation at the level of PT cell proliferation. PT cell proliferation is increased by experimental hypocalcemia or hyperphosphatemia and decreased by hypophosphatemia and administered 1,25(OH)2D3. The understanding of the molecular mechanisms involved in the genesis of secondary hyperparathyroidism will allow the design of new effective strategies in the management of this troubling condition.

3' Untranslated Regions↗

PubMed2000

Calcitriol pulse therapy is not more effective than daily calcitriol therapy in controlling secondary hyperparathyroidism in children with chronic renal failure. European Study Group on Vitamin D in Children with Renal Failure.

Calcitriol oral pulse therapy has been suggested as the treatment of choice for secondary hyperparathyroidism, but its efficacy and safety are still under discussion. The present randomized multicenter study compares the effect of an 8-week course of daily versus intermittent (twice weekly) calcitriol therapy on parathyroid hormone (PTH) suppression in 59 children (mean age 8.4+/-4.7 years) with chronic renal insufficiency (mean Ccr 22.4+/-11.6 ml/min per 1.73 m2) and secondary hyperparathyroidism. After a 3-week washout period, the patients were randomly assigned to treatment with daily oral calcitriol (10 ng/kg per day) or intermittent oral calcitriol (35 ng/kg given twice a week). The calcitriol dose was not changed throughout the study period of 8 weeks. At start of the study, the median intact PTH (iPTH) level was 485 pg/ml (range 83-2032) in the daily group (n=29) and 315 pg/ml (range 93-1638) in the intermittent group (n=30). After 8 weeks, the respective median iPTH concentrations were 232 pg/ml (range 63-1614) and 218 pg/ml (range 2-1785) (ns). The mean iPTH decrease from baseline was 19.2+/-57.8% and 13.7+/-46.7% respectively (not significant). Calcitriol reduced the iPTH concentration in 23/29 patients in the daily group and in 21/30 in the intermittent group. One episode of hypercalcemia (>11.5 mg/dl) was observed in both groups and a single episode of hyperphosphatemia (>7.5 mg/dl) was observed in the daily group. It is concluded that oral calcitriol pulse therapy does not control secondary hyperparathyroidism more effectively than the daily administration of calcitriol in children with chronic renal failure prior to dialysis.

Acute Kidney Injury↗

PubMed1999

Phosphate binders for control of phosphate retention in chronic renal failure.

In patients with chronic renal insufficiency, phosphate retention is a major factor in the development of secondary hyperparathyroidism, renal osteodystrophy, and soft tissue calcification, and may contribute to progression of renal failure. Prevention of phosphate retention with dietary and pharmacological means, along with the administration of calcitriol, may prevent or reverse secondary hyperparathyroidism. With more-advanced renal failure, phosphate binders become necessary to maintain phosphate balance and to prevent hyperphosphatemia. Because of toxicity, aluminum-containing phosphate binders are no longer used. Currently, calcium-containing phosphate binders, such as calcium carbonate and calcium acetate, are the most widely prescribed. Although calcium salts eliminate the problems associated with aluminum toxicity, they often result in transient hypercalcemia, requiring discontinuation of calcitriol and the use of low-calcium dialysate. Several new non- aluminum- and non-calcium-containing phosphate binders are currently at various stages of development, and may provide an alternative to the currently used binders. It is unlikely, however, that the newer compounds will completely replace calcium salts, since mild hypercalcemia may be necessary in chronic renal failure patients to suppress parathyroid hormone production. Other areas of investigation must include the development of drugs to inhibit soft tissue and renal calcifications, and to enhance urinary phosphate excretion.

Aluminum↗