[Experience with active vitamin D metabolites in phosphorus-calcium metabolic disorders in patients with predialysis chronic kidney disease].

AIM: To evaluate the efficacy and safety of alfacalcidol and paracalcitol used to correct impaired phosphorus-calcium metabolism (PCM) in patients with predialysis chronic kidney disease (CKD). SUBJECTS AND METHODS: Examinations were made in 128 patients with Stages III-V CKD, including 89 (69.5%) patients with chronic glomerulonephritis, 30 (23.4%) with chronic tubulointerstitial nephritis, and 9 (7.1%) with hypertensive nephrosclerosis. Impaired PCM was detected in 90 (70.3%) of the examined patients. According to the pattern of the previous therapy, all the 90 CKD patients with PCM disorders were divided into 3 groups: 1) 32 patients with Stages IIIB-V CKD who had taken oral alfacalcidol 0.25 microg/day; 2) 28 patients with Stages IIIB-V CKD who had used oral paricalcitol 1 microg/day; 3) 30 patients with Stages IIIB-V CKD who had not received, as self- motivated, active vitamin D metabolites at the predialysis stage. RESULTS: Alfacalcidol and paricalcitol were quite satisfactorily tolerated by the patients. After 3 months of initiation of the use of these agents, Groups 1 and 2 patients with predialysis CKD and baseline elevated blood intact parathyroid hormone (iPTH) levels could not only achieve, but also maintain target blood iPTH levels. In the patients taking paricalcitol, the urinary protein level decreased more promptly; moreover, by the end of month 6 the reduction in blood pressure (BP) was more significant than in those using alfacalcidol (p < 0.05). Comparison of the effects of angiotensin-converting enzyme inhibitors in combination with alfacalcidol or paricalcitol on BP changes and left ventricular mass index indicated that the most pronounced positive changes occurred when angiotensin-converting enzyme inhibitors were used in combination with paricalcitol. CONCLUSION: The use of paricalcitol in predialysis CKD with PTH hyperproduction results in not only normalization of the levels of both PTH and osseous isoenzyme of alkaline phosphatase, but also in significantly reduced daily proteinuria and regression of left ventricular hypertrophy and chronic heart failure.

Phosphorus metabolic disorder of Guizhou semi-fine wool sheep.

Guizhou semi-fine wool sheep are affected by a disease, characterized by emaciation, lameness, stiffness in the gait, enlargement of the costochondral junctions, and abnormal curvature in the long bones. The objective of this study was to determine possible relationships between the disease and mineral deficiencies. Samples of tissue and blood were collected from affected and unaffected sheep. Samples of soil and forage were collected from affected and unaffected areas. The samples were used for biochemical analyses and mineral nutrient measurements. Results showed that phosphorus (P) concentrations in forage samples from affected areas were significantly lower than those from unaffected areas (P < 0.01) and the mean ratio of calcium (Ca) to P in the affected forage was 12:1. Meanwhile, P concentrations of blood, bone, tooth, and wool from the affected sheep were also significantly lower than those from the unaffected group (P < 0.01). Serum P levels of the affected animals were much lower than those of the unaffected ones, whereas serum alkaline phosphatase levels from the affected were significantly higher than those from the unaffected (P < 0.01). Inorganic P levels of the affected sheep were about half of those in the control group. Oral administration of disodium hydrogen phosphate prevented and cured the disease. The study clearly demonstrated that the disease of Guizhou semi-fine wool sheep was mainly caused by the P deficiency in forage, as a result of fenced pasture and animal habitat fragmentation.

Disorders of phosphorus homeostasis.

PURPOSE OF REVIEW: The study of phosphorus physiology and investigations into clinical disorders of phosphorus metabolism has blossomed over the past decade. Recent work has confirmed and further extended our knowledge of basic mechanisms of phosphorus metabolism. RECENT FINDINGS: This review will focus on FGF-23 and Klotho, and on the recent further dissection of their roles in phosphorus and skeletal metabolism. Additionally, this review will detail recent studies that implicate a role for these phosphaturic and vitamin D regulating factors in extraskeletal calcification, including that occurring in soft tissue and vascular beds. SUMMARY: These findings in total provide fertile ground for investigations into the cause and treatment of abnormal skeletal and extraskeletal calcification in patients with inherited hypophosphatemic disorders. More importantly, and certainly with wider potential clinical application, these studies likewise imply a role for these factors in the pathogenesis of accelerated cardiovascular disease that occurs in patients with the most common hyperphosphatemic disorder, chronic kidney disease. Future studies are needed to confirm a harmful or possibly even beneficial role for FGF-23 and other factors in these disease states, and to determine whether therapeutic manipulation of these factors does truly affect clinical outcomes in patients with hypophosphatemia and hyperphosphatemia.

Epidemiología de la enfermedad renal crónicano terminal en la población pediátrica española. Proyecto REPIR II / Epidemiology of chronic kidney disease in the Spanish paediatric population. REPIR II Project

Objetivo: Describir el funcionamiento del Registro Español Pediátrico de Insuficiencia Renal (REPIR II), dar a conocer la epidemiología de la enfermedad y estudiar aquellos factores que puedan influir en el curso de ésta. Material y métodos: En el REPIR II participan 46 centros distribuidos por toda la geografía española. Para la clasificación y la valoración de la comorbilidad de la enfermedad, hemos utilizado los criterios de las Guías de Práctica Clínica K/DOQI. Cada centro aporta, con una periodicidad anual, los datos evolutivos de cada paciente, que quedan registrados en una base de datos on-line. Criterios de inclusión: Pacientes diagnosticados de enfermedad renal crónica (ERC) que se encuentren entre el estadio 2 y 5 en predialisis y con una edad igual o inferior a 18 años. Resultados: En el año 2008 se habían incluido 605 pacientes de 37 centros; la incidencia de la ERC no terminal era de 8,66 por millón de población (ppm) menores 18 años y la prevalencia de 71,06. La patología estructural era la primera causa de ERC (59% de casos). El porcentaje de glomerulopatías fue muy reducido (3%). Había un claro predominio de hombres (66%) y de la raza caucásica (88%). El valor medio del GFR era de 52 ± 2 ml/min/1,73 m2, con un 82% de pacientes en estadios 2 y 3. La prevalencia de la anemia era del 30%. Solamente el 19% de nuestros pacientes presentaban HTA y únicamente el 17% de ellos cumplían las cuatro recomendaciones de las Guías K/DOQI sobre el metabolismo calcio-fósforo. El valor medio global del Z-Score de la talla era del —1,03 ± 2. Había 136 pacientes (25%) que tenían un Z-Score de la talla ≤1,88. En un análisis de regresión logística multivariante, sólo se detectó una relación significativa entre la edad y la talla baja. Los menores de 2 años tenían una probabilidad un 40% mayor de tener una talla baja (OR = 1,40; p <0,01). El porcentaje de malnutrición (Z-Score de IMC ≤1,88) era del 7%, la mayoría en el grupo de edad de 0-2 años. Conclusiones: Presentamos el primer estudio que realiza un análisis prospectivo sobre la incidencia, prevalencia, etiología y comorbilidad de la ERC en la población pediátrica del estado español. Teniendo en cuenta la corta vida de este registro, los datos presentados son provisionales, y pueden estar sometidos a cambios importantes en los próximos años (AU)

Objective: A national registry of children with Chronic Kidney Disease (CKD) was started in 2007. We analize it to know the incidence, prevalence, demography, etiology, clinical and metabolic state of the children with CKD, in stages 2-5 pre-dialysis, and complying with the K/DOQI guidelines. Material and methods: In the REPIR II 46 centers distributed throughout the Spanish geography are involved. To classify and evaluate comorbidity of the disease, the Clinical Practice Guidelines K/DOQI criteria are used. Each center provides an annual developmental data of each patient which is recorded in a On-line database. Inclusion criteria: patients with CKD who are between stage 2 and 5 in predialysis and which are 18 years old or less. Results: In 2008 there were 605 patients with CKD, the incidence was 8.66 per million of pediatric population (pmpp) and the prevalence was 71.06 pmpp. Structural anomalies was the primary cause of CKD (59% of the cases). The percentage of glomerular diseases was very low (3%). There was a clear predominance of males (66%) and Caucasian race (88%). Mean GFR was 52 ± 2 ml/min/1.73 m2 with 82% of them in stage 2 and 3. The prevalence of anaemia was 30%. Only 19% of our patients had hypertension and only 17% of them fulfilled the 4 recommendations for calcium-phosphorus metabolism of K/DOQI Guidelines. Mean height Z-Score was —1.03 ± 2. There were 136 patients (25%) who had a mean height Z-Score of size < —1.88. In a multivariate logistic regression analysis only a meaningful relationship between age and height was identified. All the children under 2 years old had a 40% higher probability of having a short height (OR = 1.40; P <0.01). The percentage of malnutrition (BMI Z-Score < 1.88) was 7%, mostly in the 0-2 years old group. Conclusions: We report the first study that performs a prospective analysis of incidence, prevalence, etiology and comorbidity of CKD in the pediatric population of the Spanish State. Given the short life of this record the data presented is provisional and may suffer meanful changes in coming years (AU)

Disturbance of inorganic phosphate metabolism in diabetes mellitus: its impact on the development of diabetic late complications.

The pathogenesis of diabetic late complications (DLC) is multifactorial. Studies of mechanisms leading to early functional microvascular changes in retina and kidneys point towards a disturbance in the metabolism of inorganic phosphate (Pi) in diabetes. Since tissue hypoxia and reduced high energy phosphates may be important factors in the development of DLC, the influence of Pi concentration on the metabolism and function of the erythrocytes and renal tubular cells, as well as the relationship of the concentration of Pi to total oxygen consumption, have been reviewed. While extensive research data in non-diabetic conditions support the suggestion, that the Pi concentration is a determining factor in regulation of metabolism and rate of oxygen consumption, diabetes shows the opposite behavior. In diabetes, the highest oxygen consumption is associated with the lowest concentration of Pi. Many conventionally-treated juvenile diabetic patients respond as if their tissues were in a state of chronic hypoxia. A disturbance in phosphate handling occurs in the kidney tubules, where the excessive sodium-dependent glucose entry in diabetics depolarizes the electrochemical sodium gradient and consequently impairs inorganic phosphate reabsorption. Similar changes may occur in other cells and tissues in which glucose entry is not controlled by insulin, and particularly in poorly-regulated diabetic patients in whom long-term vascular complications are more likely.

[Prevalence and quality of control of calcium and phosphorus metabolism disorders among Lithuanian hemodialysis patients in 2004 and 2005]. / Kalcio ir fosforo apykaitos sutrikimu paplitimas, pobudis bei kontroles kokybe tarp Lietuvos hemodializuojamu ligoniu (2004-2005 metu duomenimis).

UNLABELLED: The aim of the study was to determine the prevalence and quality of control of disorders of calcium and phosphorus metabolism among patients on hemodialysis in Lithuania during the period of 2004-2005 and to assess rarely used methods of treatment such as parathyroidectomy and administration of calcimimetics. MATERIAL AND METHODS: All Lithuanian hemodialysis centers were visited, and data on disorders of calcium-phosphorus metabolism were collected in December 2004 and 2005. The quality of control was evaluated according to Kidney Disease Outcome Quality Initiative recommendations. RESULTS: According to Kidney Disease Outcome Quality Initiative guidelines, normal parathyroid hormone levels were found in 20.4% of hemodialysis patients in 2004 and 18.8% of hemodialysis patients in 2005; normal levels of phosphate were in 41.9% and 39.4%, respectively; normal levels of calcium were observed in 44.7% of patients in 2004 and in 42.3% of patients in 2005. In 2005 as compared to 2004, there were statistically significantly more patients with low parathyroid hormone level (39.9% and 45.8%, respectively, P<0.05). Only in 5.6% of patients in 2004 and 3.9% of patients in 2005, all four parameters of calcium-phosphate metabolism (calcium, phosphate, and of parathyroid hormone levels and calcium-phosphate product) were within the normal range. No parameters in the normal range were found in 17-20% of patients. The use of alfacalcidol significantly increased: 316 (30.8%) patients in 2004 and 388 (35.7%) patients in 2005 were treated with alfacalcidol (P<0.05). Alfacalcidol was prescribed for 16.5% of patients in 2004 and for 17% of patients in 2005, in whom parathyroid hormone level was below the normal range in the presence of hypercalcemia and hyperphosphatemia. The use of calcimimetics was considered rational in 142 (13.8%) patients in 2004 and 119 (10.9%) patients in 2005. According to the data of our study, parathyroidectomy was indicated in 19 (1.85%) patients in 2004 and 17 (1.56%) patients in 2005. CONCLUSIONS: According to Kidney Disease Outcome Quality Initiative recommendations, the control of disorders of calcium-phosphate metabolism in Lithuanian hemodialysis patients was insufficient in 2004 and 2005. One-third of the patients were treated with alfacalcidol when parathyroid hormone level was low and hypercalcemia and hyperphosphatemia persisted. Calcimimetics for the treatment of secondary hyperparathyroidism were administered in about 10% of patients.

The cost-effectiveness of lanthanum carbonate in the treatment of hyperphosphatemia in patients with end-stage renal disease.

OBJECTIVE: To assess the cost-effectiveness of lanthanum carbonate (LC) as a second-line therapy for hyperphosphatemia in end-stage renal disease (ESRD) patients not achieving target phosphorus levels. METHODS: A cohort of ESRD patients not adequately maintained on calcium carbonate (CC) and three subgroups of patients with baseline phosphorus levels of 5.6 to 6.5 mg/dl, 6.6 to 7.8 mg/dl, and more than 7.9 mg/dl were modeled. The following policy options were considered: continued CC (Policy 1); LC trial-if successful continue LC, if unsuccessful switch to CC (Policy 2). The survival benefit of using second-line LC to improve phosphorus control has been extrapolated from the relationship between hyperphosphatemia and mortality. Lifetime UK National Health Service drug and monitoring costs, expected survival, and quality-adjusted life-years (QALYs) were examined (discounting at 3.5% per annum). RESULTS: Policy 2 had a cost-effectiveness ratio (cost/QALY) of pound25,033 relative to Policy 1. The results show it is particularly cost-effective to treat patients with phosphorus levels above 6.6 mg/dl. The outcomes did not vary significantly during the one-way sensitivity analysis carried out on important model parameters and assumptions except when the utility value for ESRD was decreased by more than 30%. CONCLUSIONS: Applying a cost-effectiveness threshold of pound30,000 per QALY, the model shows it is cost-effective to follow current treatment guidelines and treat all patients who are not adequately maintained on CC (serum phosphorus above 5.6 mg/dl) with second-line LC. This is particularly the case for patients with serum phosphorus above 6.6 mg/dl. Our estimates are probably conservative as the possible compliance difference in favor of LC and the reduced number of hypercalcemic events with LC relative to CC was not considered.

Hyperphosphatemia among end-stage renal disease patients in developing countries: a forgotten issue?

The prevalence of hyperphosphatemia and increased calcium-phosphorus product has never been evaluated in a large multicenter study in a developing country. Our aim is to study the prevalence of hyperphosphatemia in 38 HD centers in Egypt (as an example of a developing country) and to correlate it with different co-morbid conditions and the patient's demographic data. This is a cross-sectional study conducted on 1005 chronic kidney disease stage 5 patients (CKD-stage 5) on HD for a period of more than 1 year in 38 dialysis centers in Egypt. All patients were receiving calcium-based salts as a phosphate binder. Hyperphosphatemia and increased calcium-phosphorus product were evaluated and correlated with different parameters including age, sex, knowledge by diet parameters, HD session duration, the frequency of HD per week, the type of dialysis membrane, the surface area of the dialyzer, dialyzer phosphorus clearance (phosphorus KoA), and the type of dialysate. Other co-morbid medical conditions and evidence of IHD were also investigated. Hyperphosphatemia was present in 69.1% of cases and a high calcium-phosphorus product was present in 30.2%. A higher calcium-phosphorus product was found among males. 83.2% of those with a poor knowledge by diet parameters had hyperphosphatemia compared with 67.6% in patients with a satisfactory knowledge by diet parameters. 72.3% of patients using a membrane with low-to-medium clearance had hyperphosphatemia, compared with 67.2% using a membrane with a high clearance. Seventy-two percent of patients with IHD were hyperphosphatemic compared with 67.6% of the non-ischemic patients. Hyperphosphatemia is a major problem in dialysis patients in developing countries, reflecting differences from developed countries regarding dietary habits, ethnic factors, dialysis quality, types of dialysis membranes, as well as economic factors hampering the use of the more expensive phosphate binders. Extended dialysis hours may be a good alternative solution in developing countries.

[Study of calcium-phosphorous metabolism and intact parathyroid hormone levels in end stage renal disease patients].

OBJECTIVE: To investigate the state of calcium-phosphorus metabolism and serum intact parathyroid hormone (iPTH) levels in end stage renal disease (ESRD) patients, to analyze clinical characters, and to provide scientific basis for clinical treatment. METHODS: The data of 100 ESRD patients who received hemodialysis in Peking University First Hospital from January 2000 to July 2003 were analyzed retrospectively. RESULTS: (1) The levels of serum total calcium were adjusted by serum albumin. There were 15 patients with hypocalcemia and 85 patients with normocalcemia or hypercalcemia. 31.8% of the latter took calcium-containing phosphate binders or/and vitamin D. In the 14 patients with hypocalcemia and 58 patients without low serum calcium who did not take calcium-containing phosphate binders or/and vitamin D, we found the levels of carbon dioxide combining power (CO(2)CP) were lower in the group of hypocalcemia (P<0.05), at the same time, there were no significant differences in age and the levels of serum phosphorous, creatinine and iPTH between the two groups. (2) Hyperphosphataemia occurred in 81 patients (81%). (3) The levels of serum iPTH were lower than 100 ng/L in 18 patients (18%) and higher than 300 ng/L in 46 patients (46%), the most common cause of the former was chronic tubular-interstitial nephropathy and that of the latter was chronic glomerulonephritis, excluding the patients who took calcium-containing phosphate binders or/and vitamin D. There were no significant differences in age and the levels of serum calcium, phosphorous and CO(2)CP between the two groups. Multiple regression analyses indicated the levels of serum calcium were in negative correlation with the levels of serum iPTH (r=-0.275, P=0.006). CONCLUSION: Hyperphosphataemia is one of the outstanding characters in ESRD patients and nearly 50% of all the patients develop secondary hyperparathyroidism. The serum calcium levels are correlative with acidosis besides calcium-containing phosphate binders or/and vitamin D.

Management of hyperphosphataemia in dialysis patients: role of phosphate binders in the elderly.

Phosphorus control remains a relevant clinical problem in dialysis patients. With age, however, serum phosphorus level decreases significantly because of a spontaneous decrease in protein intake. Older patients usually need lower doses of phosphorus binders. Nevertheless, hyperphosphataemia is observed in a quarter of patients aged >65 years. Phosphorus retention is related to an imbalance between phosphorus intake and removal by dialysis, and is usually aggravated when vitamin D analogues are employed. Hyperphosphataemia induces secondary hyperparathyroidism and the development of osteitis fibrosa. Recent publications describe an association between phosphorus retention and increased calcium and phosphorus product (Ca2+ x P), with significant progression of tissue calcification and higher mortality risk. Dietary intervention, phosphorus removal during dialysis and phosphorus binders are current methods for the management of hyperphosphataemia. However, the phosphorus removed by standard haemodialysis is insufficient to achieve a neutral phosphorus balance when protein intake is >50 g/day. Additional protein restriction may impose the risk of a negative protein balance. More frequent dialysis may help to control resistant hyperphosphataemia. Phosphorus binders constitute the mainstay of serum phosphorus level control in end-stage renal disease patients. Aluminium-based phosphorus binders, associated with toxic effects, have largely been substituted by calcium-based phosphorus binders. However, widespread use of calcium-based phosphorus binders has evidenced the frequent appearance of hypercalcaemia and long-term progressive cardiovascular calcification. Sevelamer, a relatively new phosphorus binder, has proved efficacious in lowering serum phosphorus and parathyroid hormone (PTH) levels without inducing hypercalcaemia. Furthermore, several investigators have reported that sevelamer may prevent progression of coronary calcification. However, its efficacy in severe cases of hyperphosphataemia remains to be confirmed in large series. There are no specific guidelines for phosphorus control in the elderly. Until more information is available, levels of mineral metabolites should be targeted in the same range as those recommended for the general population on dialysis (calcium 8.7-10.2 mg/dL, phosphorus 3.5-5.5 mg/dL and Ca2+ x P 50-55 mg2/dL2). PTH values over 120 ng/L help to avoid adynamic bone disease. Since elderly patients have a higher incidence of adynamic bone (which buffers less calcium) and vascular calcification, sevelamer should be the phosphorus binder of choice in this population; but sevelamer is costly and its long-term efficacy has not been definitively validated. Patients with low normal levels of calcium may receive calcium-based phosphorus binders with little risk. Patients with low values of PTH and high normal calcium should receive sevelamer. Tailored combinations of calcium-based phosphorus binders and sevelamer should be considered, and calcium dialysate concentration adjusted accordingly.

[Prevalence of anemia, calcium-phosphorus abnormalities and metabolic acidosis in different stages of chronic renal failure]. / Stopien niewydolnosci nerek a czestosc wystepowania niedokrwistosci, zaburzen gospodarki wapniowo-fosforanowej oraz kwasicy metabolicznej.

BACKGROUND: Chronic kidney disease (CKD) is associated with the reduction of haemoglobin concentration and a variety of biochemical abnormalities including changes in serum concentration of sodium, potassium, calcium, phosphate, bicarbonate, and hydrogen ions. However, data concerning epidemiology of these abnormalities are rare and incomplete, especially among subjects with mild to moderate CKD. PATIENTS AND METHODS: Patients with a serum creatinine concentration > 110 micromol/l hospitalized in the Department of Nephrology, Endocrinology and Metabolic Diseases Medical University of Silesia from 1998 to 2002 were analyzed. Patients with acute renal failure or chronic renal failure treated with renal replacement therapy were excluded from this study. A total of 653 patients (262F and 391M) were divided into 9 subgroups differing from each other by progressive decline of glomerular filtration rate (GFR). RESULTS: A statistically significant decrease in haemoglobin concentration and increase in the prevalence of anaemia were found in patients with GFR < 50 ml/min. In a large number of patients with a GFR < 80 but > 50 ml/min, Hb concentration <11 g/dl was observed. Mean MCV, MCH and serum iron concentration were similar in all studied subgroups. A progressive increase in serum phosphorus concentration and decrease of calcaemia was found in patients with GFR < 30 ml/min. The elevated Ca x P product (> 4.44 mmol2/12) was noticed almost exclusively in patients with GFR< 30 ml/min. A decompensated metabolic acidosis was observed in 29.8% of patients with GFR <30 ml/min. CONCLUSIONS: Anaemia is an early symptom of chronic kidney disease preceding disturbances of calcium, phosphate and hydrogen ions metabolism. These abnormalities seem to be of therapeutic relevance.

Serum phosphate abnormalities in the emergency department.

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.

[Is respiratory syncytial virus one of the causative agents for transient hyperphosphatasemia?].

OBJECTIVE: In the winter of 2001, we found several cases of transient hyperphosphatasemia (TH) in patients with respiratory syncytial virus (RSV) infection. Therefore, we tried to verify that RSV was one of the causative agents for TH. RESULTS: From November 2001 to January 2002, we diagnosed 94 cases of RSV infection with the detection of virus antigens in the nasal mucus. Among these cases, we found six cases (6.4%) of TH, and all six patients were over one year of age. There were 55 cases of RSV infection in patients over one year of age, and the rate of TH with RSV infection was estimated to be 10.9% in this age group. This rate of TH (6.4%) was significantly higher than rates reported in previous studies (0.33% to 1.5%, p = 0.0145 to p < 0.0001). CONCLUSION: We conclude that RSV is one of the causative agents for TH.

Benign familial hyperphosphatasemia: a report of two families and review of the literature.

Benign familial hyperphosphatasemia is a rare biochemical abnormality of hereditary nature, characterized by the presence of persistently elevated levels of serum alkaline phosphatase in several members of the same family, in the absence of disease or any known cause of hyperphosphatasemia. To date, there have been 29 pedigrees reported in the literature. Another two families affected with hyperphosphatasemia, originating in an increase in the bone isoenzyme, are described. The epidemiology, inheritance, isoenzymatic patterns, postulated mechanisms and clinical significance of this entity are discussed.

[The characteristics of histocompatibility antigen distribution in urolithiasis patients with a phosphorus metabolic disorder]. / Osobennosti raspredeleniia antigenov gistosovmestimosti u bol'nykh urolitiazom s narusheniem fosfornogo obmena.

Phosphorus metabolic disturbances play a great role in the occurrence of urolithiasis. This study covered 150 patients with urolithiasis to establish correlations between the frequency of histocompatibility antigens and the increase in blood and urinary phosphorus levels. The HLA antigens were identified by the routine microlymphocytotoxic method involving a histotyping serum panel. The ABO antigens and rhesus were determined by the agglutination method by using reference sera. The study revealed specific distribution of histocompatibility antigens in urolithiasis patients with disturbed phosphorus metabolism. Hyperphosphatemia correlated with the higher frequency of HLA-B35 (chi 2 = 9.89) and E/E system rhesus (chi 2 = 8.63); hyperphosphaturia showed a negative association with the HLA-A28 antigens (chi 2 = 9.7), as well as with E/e (chi 2 = 14.69) and e/e (chi 2 = 39.36) and a positive association with HLA-B13 (chi 2 = 5.98) and B35 (chi 2 = 36.58). The highest relative risk for hyperphosphatemia associated with the B27 and B35 antigens was observed with genetic predisposition, being 3.63 and 7.13, respectively. B12- and B35-positive individuals were at higher risk for hyperphosphaturia up to 11.25. There were significant differences in antigen frequency, and sex, genetic predisposition to urolithiasis, association of phosphorus metabolic disturbances with other metabolic disorders, and their effects of parathyroid lesions, etc. The findings reveal the immunogenetically induced risk for the occurrence and development of urolithiasis with disturbed phosphorus metabolism to make goal-oriented prophylactic measures.

[Hypophosphatemia. A review (author's transl)]. / Les hypophosphorémies.

Hypophosphatemia with or without phosphorus depletion can be observed in various diseases--particularly diabetic ketoacidosis, respiratory alkalosis, alcoholism, parenteral nutrition and hyperalimentation--and may cause serious neurologic, muscular, and hematologic disorders. This review summarizes the knowledges about hypophosphatemia--etiological mechanisms, pathophysiology and therapeutic modalities--and suggests that some place be reserved for serum phosphate in systematic and emergency panels of blood tests.