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Familial association of pseudohypoparathyroidism and psoriasis: case report.

CONTEXT: The association between psoriasis and hypoparathyroidism has been reported by several authors, and it has been suggested that abnormalities in calcium homeostasis may be involved in the development or exacerbation of psoriasis. However, so far there have only been two reports of pseudohypoparathyroidism associated with psoriasis. OBJECTIVE: To describe the familial occurrence of this association for the first time. CASE REPORTS: Two siblings with psoriasis associated with pseudohypoparathyroidism were presented. The first patient was a 24-year-old white male with disseminated erythrodermic pustular psoriasis that began 2 months before admission. He had had a history of mental retardation, recurrent otitis, seizures and arthralgia from the age of 11 years onwards. He presented the characteristic phenotype of Albright osteodystrophy: short stature, obesity, round facies, broad forehead, short neck and brachydactylia. He adopted a position of flexed limbs and showed proximal muscle weakness and a positive Trousseau sign. He had clinical signs of hypocalcemia (0.69 mmol/l ionized calcium and 3.2 mg/dl total calcium), hyperphosphatemia (6.6 mg/dl), hypomagnesemia (1.0 mEq/l), hypoalbuminemia (3.1 g/dl), normal serum intact PTH levels (45.1 pg/ml), primary hypothyroidism (13.2 mU/ml TSH, and 4.7 mg/dl total T(4)), hypergonadotrophic hypogonadism (116.0 ng/ml LH, 13.2 mU/ml FSH and 325.0 ng/dl testosterone), osteoporosis, and diffuse calcifications in soft tissues and in the central nervous system. The second case was a 14-year-old white girl with a history of psoriasis vulgaris from the age of five years onwards, and antecedents of mental retardation. She presented signs of Albright osteodystrophy (short stature, round facies, obesity, short neck, brachydactylia), hypocalcemia (ionized calcium of 1.08 mmol/l and total calcium of 6.7 mg/dl) hyperphosphatemia (9.4 mg/dl), elevated serum PTH levels (223.0 pg/ml), osteoporosis, and hypergonadotrophic hypogonadism (7.0 mU/ml LH, 9.3 mU/ml FSH and undetectable estradiol levels).

Abnormalities, Multiple↗

Sevelamer therapy for pediatric end-stage renal disease.

Sevelamer, a non-calcium-containing, non-aluminum-containing phosphate binder, is frequently prescribed for treatment in adults with hyperphosphatemia secondary to end-stage renal disease (ESRD). However, published information regarding sevelamer use in children younger than 11 years is lacking. We report the use of sevelamer as a phosphate binder in a 19-month-old girl with ESRD who was receiving calcium carbonate 1250 mg 3 times/day for hyperphosphatemia. The patient's initial serum phosphorus concentration was 8.6 mg/dl, and the calcium-phosphorus product was 75 mg(2)/dl(2). This was well above the level that places patients at risk for complications such as joint, vessel, and soft-tissue calcification. An aluminum-containing phosphate binder was not an option given the patient's renal disease and the concern for neurotoxicity. Sevelamer was considered, but a MEDLINE search revealed no pediatric dosing information. An initial dosage of 100 mg/kg/day divided every 8 hours was administered, as extrapolated from adult data, and then titrated to 130 mg/kg/day divided every 8 hours based on the patient's response. The child's dietary phosphorus intake remained constant throughout her hospital stay. During sevelamer therapy, her serum phosphorus concentration dropped as low as 5.2 mg/dl; at discharge it was 6.5 mg/dl, with a corresponding calcium-phosphorus product in the upper 50s. No adverse effects associated with sevelamer were observed. In the dosages we used, sevelamer resulted in an acceptable calcium-phosphorus product and returned the patient's serum phosphorus concentration to near normal. Sevelamer appears to be a viable option as a phosphate binder in children with ESRD.

Calcium↗

Levels of serum 1,25(OH)2D in patients with pre-dialysis chronic renal failure.

One hundred and ninety-five outpatients in pre-dialysis period served as subjects. The mean age of subjects was 58.0 +/- 11.2 (range: 29-82) years. The subjects were divided into 8 groups according to their serum creatinine (Cr) levels (Cr < or = 1.0, 1.0 < Cr < or = 2.0, 2.0 < Cr < or = 3.0, 3.0 < Cr < or = 4.0, 4.0 < Cr < or = 5.0, 5.0 < Cr < or = 6.0, 6.0 < Cr < or = 8.0, and Cr > 8.0 mg/100 ml). The level of 1,25-dihydroxyvitamin D (1,25(OH)2D) decreased in accordance with the progression of chronic renal failure (CRF). Even in subjects with 1.0 < Cr < or = 2.0 mg/100 ml, the levels of 1,25(OH)2D were significantly lower than those in subjects with Cr < or = 1.0 mg/100 ml. The levels of calcium adjusted by serum albumin levels (adjusted Ca) were relatively maintained within the normal range until Cr > 8.0 mg/100 ml. The levels of inorganic phosphate (IP) were significantly lower in subjects with 1.0 < Cr < or = 2.0 mg/100 ml, but significantly higher in subjects with Cr > 4.0 mg/100 ml than those in subjects with Cr < or = 1.0 mg/100 ml. The levels of immunoreactive high-sensitive parathyroid hormone (HS-PTH) were greatly increased and the levels of intact PTH were significantly increased even in subjects with 1.0 < Cr < or = 2.0 mg/100 ml, in association with a decrease in levels of 1,25(OH)2D suggesting that a decline in 1,25(OH)2D production due to a decrease in renal mass contributes to the acceleration of secondary hyperparathyroidism. When the levels of adjusted Ca, intact PTH and 1,25(OH)2D of subjects with hypophosphatemia (IP < 2.8 mg/100 ml), normophosphatemia and hyperphosphatemia (IP > 4.4 mg/100 ml) were compared, there were not any significant differences in the levels of adjusted Ca among these subjects in each group. But, the levels of 1,25(OH)2D in subjects with hypophosphatemia were significantly higher than those with normophosphatemia in groups with Cr < or = 2.0 mg/100 ml, and those with hyperphosphatemia were significantly lower than those with normophosphatemia in groups with 3.0 < Cr < or = 4.0, 5.0 < Cr < or = 6.0 and Cr > 8.0 mg/100 ml. These results suggest that increased secretion of PTH might compensate the decreased production of 1,25(OH)2D3 by lowering phosphate in the early phase of CRF, and phosphate retention inhibits the activity of 1 alpha-hydroxylase and contributes to the decrease in 1,25(OH)2D3 in the advanced stage of CRF. Monitoring of 1,25(OH)2D is considered to be vitally important for diagnosing the 1,25(OH)2D3 deficiency in CRF.

Adult↗

Influence of infecting serogroup on clinical features of leptospirosis in dogs.

The purpose of this study was to review recent cases of leptospirosis seen at referral centers in New York State and to identify differences in clinical or clinicopathologic aspects of the disease among different suspected infecting serogroups. Medical records at the Cornell University Hospital for Animals and the Animal Medical Center in New York City were reviewed to identify dogs diagnosed with leptospirosis from September 1996 to August 2002. Records of 55 dogs met the inclusion criteria for the study. The suspected infecting serogroups included 21 occurrences of Grippotyphosa, 12 of Pomona, 6 of Autumnalis, 5 of Bratislava, 2 of Hardjo, and 1 of Canicola. Five dogs had equal titers to serogroups Grippotyphosa and Pomona, and 3 had equal titers to 2 other serogroups. Common clinical signs included lethargy, anorexia, and vomiting. Common clinicopathologic findings included anemia, thrombocytopenia, azotemia, hyperphosphatemia, high liver enzyme activity, and hyperbilirubinemia. Forty-three of 55 dogs were discharged from the hospital. Serogroup-specific analysis indicated that dogs with suspected serogroup Pomona infection were more likely to suffer from vomiting (P = .01), thrombocytopenia (P = .009), severe azotemia (P = .04), and hyperphosphatemia (P = .006) than dogs with other serogroups and were less likely to be discharged alive from the hospital (P = .03). This study suggests that only minor clinically relevant differences exist among serogroups. Leptospira serogroup Pomona caused more severe renal disease and was associated with a worse outcome compared with disease caused by other serogroups.

Animals↗

Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in cats with ureteral calculi: 163 cases (1984-2002).

OBJECTIVE: To determine clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in cats with ureteral calculi. DESIGN: Retrospective study. ANIMALS: 163 client-owned cats. PROCEDURE: Medical records were reviewed, and information on signalment, history, clinical signs, and results of clinicopathologic testing and diagnostic imaging was obtained. RESULTS: The number of cats in which ureterolithiasis was diagnosed each year increased progressively during the study period. Clinical signs tended to be non-specific and included inappetence, vomiting, lethargy, and weight loss. A combination of survey radiography and abdominal ultrasonography revealed ureteral calculi in 66 of 73 (90%) cats in which the diagnosis was confirmed at surgery or necropsy. Ultrasonography revealed that ureteral calculi were causing ureteral obstruction in 143 of 155 (92%) cats. One hundred thirty-four of 162 (83%) cats had azotemia, 84 of 156 (54%) had hyperphosphatemia, and 22 of 152 (14%) had hypercalcemia. Urinary tract infection was documented in 10 of 119 (8%). Fifty-eight of 76 (76%) cats with unilateral ureterolithiasis had azotemia and 33 (43%) had hyperphosphatemia, indicating impairment of renal function in the contralateral kidney or prerenal azotemia. Ultrasonographic imaging of the contralateral kidney in cats with unilateral ureteral calculi suggested that preexisting renal parenchymal disease was common in cats with ureterolithiasis. Ninety-one of 93 (98%) ureteral calculi contained calcium oxalate. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that abdominal imaging should be performed in all cats with chronic nonspecific signs or with acute or chronic renal failure to rule out ureterolithiasis. Preexisting renal disease may be common in cats with ureteral calculi.

Animals↗

Cardiac and pulmonary calcification in a hemodialysis patient: partial regression 4 years after parathyroidectomy.

AIMS: The reversibility of extraskeletal calcifications in dialysis patients is an important and unresolved issue. Although periarticular calcifications have been shown to be reversible, little data are available on vascular or parenchymal calcifications. CASE HISTORY: A patient on maintenance hemodialysis with severe hyperparathyroidism, hypercalcemia and hyperphosphatemia was admitted to undergo parathyroidectomy. A preoperative total body bone scintigraphy was performed to better evaluate a lytic lesion in the pelvis, the histology of which proved to be a "brown tumor". The scan showed the typical findings of renal osteodystrophy, but also a diffuse extra-skeletal uptake of bone tracer in the lungs, kidneys, femoral arteries and myocardium. After surgery, good control of serum calcium, phosphate (Ca x P product < 50 mg2/dl2) and PTH levels was maintained during 4 years of follow-up. Bone scans were repeated after 2 and 4 years, showing marked improvement of periarticular uptake at the ends of long bones. Extraosseous calcium deposition was still markedly evident, but progressively decreased (at 4 years: heart -36%, lungs -18%). CONCLUSION: In this dialysis patient, extraskeletal calcification of visceral organs (particularly in the heart and the lungs) due to prolonged hypercalcemia and hyperphosphatemia was partially reversible by parathyroidectomy followed by good long-term control of serum phosphate and calcium.

Adult↗

Increasing blood flow increases kt/V(urea) and potassium removal but fails to improve phosphate removal.

BACKGROUND: Hyperphosphatemia and hyperkalemia are major determinants of morbidity and mortality in hemodialysis patients. Half of the dialysis population suffers from hyperphosphatemia which is now recognized as an important cardiovascular disease risk factor. It is, therefore, necessary to improve the removal of these molecules. In this study, we investigated the effect of enhancing blood flow on Kt/V for urea (Kt/Vu), potassium and phosphate removal. METHODS: Thirteen patients were investigated in a randomized, cross-over, prospective study using 3 blood flows (Qb) of 200,250 and 300 ml/min which gave 39 standardized high-flux hemodialysis treatments. Effective blood flows were measured by ultrasonic flow meter. Quantification of delivered dialysis dose was performed by partial dialysate and ultrafiltrate collection for the determination of potassium and phosphate removal and by blood urea concentrations for determination of Kt/Vu. RESULTS: Kt/Vu rose significantly from 1.10 +/- 0.14 to 1.22 +/- 0.14 and finally to 1.39 +/- 0.16 (p = 0.0001) with increasing Qb similar to the increase in potassium removal from 53.0 +/- 2.4 to 63.4 +/- 2.6 and to 74.2 +/- 3.8 mMol (p = 0.01). Phosphate removal only improved from 28.1 +/- 1.3 to 31.4 +/- 1.5 (p = 0.050) when Qb was increased from 200 to 250 ml/min but remained unchanged at 31.2 +/- 1.5 mMol (NS compared to phosphate removal at Qb = 250 ml/min) when Qb was increased to 300 ml/min. CONCLUSIONS: Increasing delivered Kt/Vu and potassium removal with higher Qb fails to produce the same desired effect with phosphate removal during high-flux hemodialysis.

Adult↗

Efficacy and safety of lanthanum carbonate for reduction of serum phosphorus in patients with chronic renal failure receiving hemodialysis.

BACKGROUND: Lanthanum carbonate is a highly effective phosphate binder with significant potential as a treatment for hyperphosphatemia in patients with end-stage renal disease (ESRD). Here, the results of a placebo-controlled, dose-ranging study are presented. METHODS: 196 patients (> or = 18 years) receiving hemodialysis for at least 6 months entered a 1- to 3-week, single-blind, placebo run-in phase. Of these, 145 patients were randomized to a double-blind phase in which they received placebo or lanthanum carbonate in daily lanthanum doses of 225, 675, 1,350 or 2,250 mg for 6 weeks. Serum levels of phosphorus, calcium and parathyroid hormone, and adverse events were monitored throughout the study. RESULTS: The intent-to-treat analysis (n = 144) showed significant dose-related reductions in serum phosphorus at lanthanum doses of 675, 1,350 and 2,250 mg. After 6 weeks of treatment, phosphorus levels were significantly lower in the lanthanum groups receiving 1,350 mg/day and 2,250 mg/day, compared with the placebo group (respective changes from randomization: -0.95 +/- 1.39 mg/dl (-0.31 +/- 0.45 mmol/l), -1.13 +/- 2.01 mg/dl (-0.36 +/- 0.65 mmol/l), 0.75 +/- 1.47 mg/dl (0.24 +/- 0.47 mmol/l), p < 0.001). Significant reductions in serum phosphorus, compared with placebo, occurred in the lanthanum 1,350 mg/day group from the second week of treatment and in the 2,250 mg/day group from the first week of treatment. Adverse events were mainly gastrointestinal (e.g. nausea and vomiting). Treatment-related adverse events occurred in 39% of patients treated with lanthanum carbonate and 44% of the placebo group. CONCLUSION: Lanthanum carbonate is an effective and well-tolerated agent for the short-term treatment of hyperphosphatemia in patients with ESRD.

Calcium↗

Lanthanum carbonate (Fosrenol) efficacy and tolerability in the treatment of hyperphosphatemic patients with end-stage renal disease.

AIMS: High serum phosphorus levels are a common problem in patients receiving long-term dialysis treatment. Lanthanum carbonate (Fosrenol) is a new non-aluminum, non-calcium phosphate binder developed for the treatment of hyperphosphatemia in patients with end-stage renal disease (ESRD). We report data from a recent trial, which, for the first time, assessed the efficacy and tolerability of lanthanum carbonate treatment, compared with placebo, in Chinese patients with ESRD. PATIENTS AND METHODS: Following a one- to three-week washout phase and a four-week, open-label lanthanum carbonate dose-titration phase, male and female hemodialysis patients were randomized (1:1) to receive either lanthanum carbonate or placebo for four weeks. The primary efficacy parameter of the study was the control of serum phosphorus levels (< or =1.8 mmol/l [< or = 5.6 mg/dl]). Secondary endpoints included the profile of serum phosphorus during titration and parathyroid hormone, calcium, and calcium x phosphorus (Ca x P) product levels. The safety and tolerability of lanthanum carbonate were assessed by monitoring adverse events throughout the study. RESULTS: Mean serum phosphorus level at the end of washout was 2.5 +/- 0.5 mmol/l (7.7 +/- 1.5 mg/dl; n=73), and there was no evidence of a difference in levels between the treatment groups pre-randomization. At the end of the study, lanthanum carbonate-treated patients had significantly lower phosphorus levels (1.6 +/- 0.5 mmol/l [5.1 +/- 1.5 mg/dl]; n=30) than those receiving placebo (2.3 +/- 0.4 mmol/l [7.2 +/- 1.3 mg/dl]; n=31; p < 0.001). In addition, a significantly higher proportion of patients receiving lanthanum carbonate had controlled serum phosphorus levels (60%) compared with the placebo group (10%; p < 0.001). Ca x P product levels were also significantly lower in the lanthanum carbonate group at the end of randomized treatment (p < 0.001). Lanthanum carbonate was well tolerated; only one serious adverse event was reported, which was unrelated to treatment. CONCLUSIONS: Lanthanum carbonate was shown to be an effective and well-tolerated phosphate binder for the treatment of hyperphosphatemia in Chinese patients with ESRD. This finding supports the results of previous US and European studies, which have also shown that lanthanum carbonate treatment effectively controls serum phosphorus levels.

Adult↗

[Metabolic changes in critically ill children].

OBJECTIVE: Our aim was to analyze the incidence of metabolic disturbances in critically ill children and to evaluate their correlation with severity of illness, complications, mortality and length of hospital stay. PATIENTS AND METHODS: We retrospectively studied 360 children who were admitted into a Pediatric Intensive Care Unit (PICU) between January 1995 and May 1996. We analyzed age, sex, initial diagnosis, complications, length of hospital stay and initial and final concentrations of serum glucose, calcium, phosphorus, magnesium and alkaline phosphatase. RESULTS: The incidence of different metabolic disturbances at admission to the PICU was: hyperglycemia 51.9%, hypoglycemia 1.9%, hypocalcemia 24.5%, hypercalcemia 5.8%, hyperphosphatemia 7.3%, hypophosphatemia 7.9%, hypomagnesemia 47.4% and hypermagnesemia 3%. Patients with shock had lower concentrations of calcium and higher phosphorus levels, while children with sepsis had lower magnesium concentrations. Patients who died had a higher incidence of hyperphosphatemia and higher values of serum glucose and magnesium at admission, while patients who survived had lower concentrations of calcium and higher incidence of hypomagnesemia. We did not find any correlation between the initial values for metabolites and length of stay in the PICU. CONCLUSIONS: Metabolic disturbances in critically ill children are frequent findings, correlate with important complications and can be prognostic markers. Thus, regular controls of different metabolites must be performed so we can precociously detect these disturbances and correct them.

Adolescent↗

High prevalence of hyperparathyroidism among peritoneal dialysis patients: a review of 176 patients.

OBJECTIVES: Parathyroid dysfunction continues to produce significant morbidity in dialysis patients. Since the introduction of low calcium dialysate for peritoneal dialysis (PD), no large studies have been done to determine the prevalence of parathyroid dysfunction in these patients. This study was done to assess the prevalence of parathyroid disease in the PD population and to determine the risk factors associated with this dysfunction. DESIGN: We analyzed data on 176 patients who received PD at a single center between August 1998 and February 1999. Clinical data, laboratory variables related to parathyroid function, and data pertaining to dialysis treatment and weekly drug dosing were obtained for each patient on two different occasions, approximately 3 months apart. Variables predictive of the development of parathyroid dysfunction were calculated by univariate and multivariate logistic regression analysis. RESULTS: Two-thirds of the patients surveyed had an abnormal intact parathyroid hormone (iPTH) level: 47% had an iPTH level more than three times normal, the mean was 54.6+/-35.4 pmol/L; 23% had an iPTH value below the upper limit of normal, here the mean was 3.6+/-1.8 pmol/L. Diabetic patients had lower iPTH levels (22.2+/-28.4 pmol/L) than nondiabetics (33.9+/-34.8 pmol/L) (p = 0.02). On multivariate regression analysis, we found that age, duration of dialysis, Kt/V, serum bicarbonate, and serum ionized calcium levels did not significantly affect parathyroid function. Hyperphosphatemia was the only factor that was associated with the development of secondary hyperparathyroidism in this study population (p = 0.029). CONCLUSION: There is a high prevalence of hyperparathyroidism in the current PD population. Phosphate control is suboptimal and hyperphosphatemia is an independent risk factor for the development of hyperparathyroidism.

Adult↗

Pseudohypoparathyroidism type IA and II with severe neuropsychic manifestations.

Pseudohypoparathyroidism (PHP) is characterized by unresponsiveness of target tissues to the biological actions of the parathyroid hormone (PTH), with resulting hypocalcemia and hyperphosphatemia, despite the elevated serum levels of PTH. PHP is divided into types Ia, b, c and II, depending on the presence of Albright's hereditary osteodystrophy (AHO), defective urinary excretion of phosphate (U-P) and response in urinary excretion of cyclic adenosine monophosphate (U-cAMP) after the administration of exogenous PTH. Patients with PHP might exhibit various manifestations of neuropsychic disturbances. We present two boys, aged 14 and 16 years, both with paresthesia, anxiety and epilepsy; the former patient also suffered from mild mental retardation. In both patients, hypocalcemia and hyperphosphatemia together with increased serum levels of PTH suggested the diagnosis of PHP. After administration of exogenous PTH (Ellsworth-Howard test), there was a drop in U-P in both patients, while U-cAMP was decreased in the first patient and increased in the second one, thus confirming the diagnoses of PHP Ia and II, respectively. Neuropsychic disturbances and epilepsy resolved completely in both patients after treatment with calcium and dihydrotachysterol. Evaluation of calcemia and phosphatemia should be mandatory in all patients with neuropsychic disorders. Ellsworth-Howard test remains a useful tool in the differential diagnosis of PHP.

Adolescent↗

A preference study: calcium acetate tablets versus gelcaps in hemodialysis patients.

End stage renal disease (ESRD) patients are frequently noncompliant with phosphate binder therapy. This noncompliance may lead to uncontrolled hyperphosphatemia, resulting in an increased risk of mortality via the development of serious comorbid conditions. A new gelcap form of calcium acetate has been introduced for control of hyperphosphatemia. This single center, unblinded study compared calcium acetate tablets versus calcium acetate gelcaps with regards to patient preference and ease of swallowing. Twenty-two patients were randomized to receive 1 day of treatment with calcium acetate tablets, followed by 1 day of treatment with calcium acetate gelcaps, or vice versa. Following completion of the treatment period, the patients were given a questionnaire to complete that asked them to compare their experience with both treatments. Twenty patients completed the study. Eighteen patients preferred the gelcap to the tablet in all preference categories. The same 18 patients responded that the gelcap was easier to swallow than the tablet. Because of the evidence documenting the noncompliant behavior of ESRD patients with respect to their binder therapy, efforts made to give the patients a more satisfying alternative can aid in improving compliance.

Acetates↗

Derman necrosis due to thrombosis in severe secondary hyperparathyroidism.

Two patients had gangrenous dermal necrosis associated with chronic renal disease and secondary hyperparathyroidism. Thromobosed and heavily calcified small arteries were underlying the infarcted areas. One patient had severe hypotension secondary to hemorrhage, which immediately preceded the appearance of dermal lesions. Both patients had notably elevated serum parathyroid hormone and serum alkaline phosphatase levels, as well as severe hyperphosphatemia. Therapy with phosphate binders and calcium and vitamin D supplementation corrected the hyperphosphatemia and reduced serum alkaline phosphatase levels. One patient died; the other patient's dermal lesions healed completely. Localized thrombosis, rather than obliterative intimal proliferation, represents a unique cause of dermal necrosis in this condition.

Arteriosclerosis↗

[Role of diet in the management of osteodystrophy during progressive renal insufficiency].

Secondary hyperparathyrodism (SH) is an early manifestation of chronic renal failure (CRF), which has serious complications. Moreover, treating SH is not a risk-free process. Once in its advanced state, it is extremely difficult to reverse and therefore it is critical an early intervention and prevention. An excess of phosphorus and a deficit of calcium and calcitriol are key factors in the evolution of SH. Despite the fact that plasma phosphorus levels remain normal until an extremely advanced stage of CRF, and even apparent hyperphosphatemia in mild CRF, it has been shown that restricting dietary levels of protein and phosphorus impedes the progression of SH. A decrease of protein in the diet also decreases the amount of calcium, thus the calcium levels must be supplemented in order to prevent their deficit. In addition to that slightly diminished levels of calcitriol can be observed in the early stages of CRF, thus it is logical to provide this hormone. However, administering calcitriol may induce hypercalcemia and hyperphosphatemia, which in turn risks the onset of cardiovascular calcifications and complications. Therefore, the calcitriol dosage should be small and then adjusted according to the degree of SH. Neither the PTH levels nor alterations in the phospho-calcium metabolism follow a linear increase appropriate to the decrease in renal function, therefore we propose a treatment strategy which adapts to the different degrees of renal failure.

Calcinosis↗

Low calcium (2.5 mEq/l) and high calcium (3.5 mEq/l) dialysate in peritoneal dialysis patients.

STUDY OBJECTIVE: To compare the effects of low-calcium and high-calcium dialysate in stable ESRD patients on peritoneal dialysis (PD). DESIGN: Dialysate containing 2.5 mEq/l and 3.5 mEq/l calcium in combination with oral calcium salts as phosphate binders were evaluated. SETTING: Tertiary-referral university hospital. PATIENTS AND METHODS: Fifteen patients (6 male, 9 female) on low-calcium (2.5 mEq/l) and 15 patients (6 male, 9 female) on high-calcium (3.5 mEq/l) dialysate were studied for 6 months. All patients received calcium acetate or calcium carbonate to control hyperphosphatemia before the study. RESULTS: Serum calcium, phosphorus and albumin did not differ before and after between the two groups. Three patients in low-calcium and five in high-calcium group developed hypercalcemia. Three in low-calcium group and four in high-calcium group required sucralfate to control hyperphosphatemia and hypercalcemia. Mean dose of elemental calcium was 1152 mg/day in low-calcium group and 790 mg/day in high-calcium group. A negative correlation (r = -0.82, p < 0.005) was observed between serum calcium and PTH at the end of study period in the low-calcium group. No such relationship was observed in the high-calcium group. CONCLUSIONS: Degree and frequency of hypercalcemia appeared similar with low-calcium and high-calcium dialysate in peritoneal dialysis patients.

Calcium↗

High doses of intravenous calcitriol in the treatment of severe secondary hyperparathyroidism.

BACKGROUND: In hemodialysis (HD) patients, secondary hyperparathyroidism (HPTH) is a severe common disease. Calcitriol administration has been demonstrated as an effective therapy. In this prospective study, our aim was to determine the necessary calcitriol dose required to control severe HPTH preventing hypercalcemia or hyperphosphatemia and avoiding parathyroidectomy. METHODS: Eighteen dialysis patients suffering from severe HPTH during a 12-month period received intravenous (i.v.) calcitriol pulse doses (2-8 mcg/3x/week). Multislice helical computed tomography (CT) cardiac imaging was performed to measure coronary artery calcifications. RESULTS: Fourteen patients showed an improvement (parathyroid hormone (PTH) level < 400 pcg/mL), one patient an incomplete reduction, and three patients starting from PTH levels between 1100 and 2386 pcg/mL did not appear to benefit from the therapy. After a 6-month therapy in 15/18 patients PTH levels were significantly lower (p<0.05). In a large portion of the group, as well as in the control group, coronary calcification values were high when compared to the normal range. CONCLUSIONS: According to our data, we concluded that severe HPTH could be treated successfully by i.v. calcitriol pulse doses reaching high doses (up to 8 mcg/3x/week) and for a prolonged period of time (6 months). In such cases, close monitoring is necessary to prevent hyperphosphatemia and hypercalcemia episodes.

Aged↗

Total parathyroidectomy reduces elevated circulating fibroblast growth factor 23 in advanced secondary hyperparathyroidism.

BACKGROUND: Secondary hyperparathyroidism is a common complication in patients with stage 5 chronic kidney disease (CKD), accelerated by hyperphosphatemia. Fibroblast growth factor 23 (FGF-23), a phosphorus-regulating protein, has key roles in several phosphate-wasting disorders. The aim of this study is to examine the association of advanced secondary hyperparathyroidism with circulating FGF-23 levels. METHODS: Fifteen patients with marked secondary hyperparathyroidism (parathyroid hormone [PTH], 990 +/- 118 pg/mL [ng/L]) were enrolled. All underwent parathyroidectomy with forearm autotransplantation (PTX), and their FGF-23 levels were measured before and after PTX (days 1, 3, 7, and 10) by means of sandwich enzyme-linked immunosorbent assay. RESULTS: Preoperative FGF-23 levels correlated positively with phosphorus (P < 0.05), calcium-phosphorus product (Ca x P; P < 0.0005), and PTH values (P < 0.05). Serum FGF-23 levels decreased time dependently after PTX (P < 0.0005). Both serum phosphorus and Ca x P values decreased similarly after PTX ( P = 0.0001). Furthermore, FGF-23 levels days 1 and 3 correlated linearly with serum phosphorus (P < 0.05; P < 0.005, respectively) and Ca x P values (P < 0.01; P < 0.0001, respectively). CONCLUSION: FGF-23 levels correlate positively with serum phosphorus, Ca x P, and PTH values in patients with advanced secondary hyperparathyroidism. Complete ablation of progressive parathyroid glands reduces circulating FGF-23 levels, simultaneously decreasing serum phosphorus and Ca x P values. These findings suggest that hyperplastic parathyroid glands, together with hyperphosphatemia, affect abnormal FGF-23 metabolism in patients with stage 5 CKD with advanced secondary hyperparathyroidism.

Chronic Disease↗