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Primary hyperoxaluria (PH) occurs due to an autosomal recessive hereditary disorder of the metabolism of glyoxylate, which causes excessive oxalate production. The most frequent and serious disorder is due to enzyme deficit of alanine-glyoxylate aminotransferase (PH type I) specific to hepatic peroxisome. As oxalate is not metabolised in humans and is excreted through the kidneys, the kidney is the first organ affected, causing recurrent lithiasis, nephrocalcinosis and early renal failure. With advance of renal failure, particularly in patients on haemodialysis (HD), calcium oxalate is massively deposited in tissues, which is known as oxalosis. Diagnosis is based on family history, the presence of urolithiasis and/or nephrocalcinosis, hyperoxaluria, oxalate deposits in tissue forming granulomas, molecular analysis of DNA and enzyme analysis if applicable. High diagnostic suspicion is required; therefore, unfortunately, in many cases it is diagnosed after its recurrence following kidney transplantation. Conservative management of this disease (high liquid intake, pyridoxine and crystallisation inhibitors) needs to be adopted early in order to delay kidney damage. Treatment by dialysis is ineffective in treating excess oxalate. After the kidney transplant, we normally observe a rapid appearance of oxalate deposits in the graft and the results of this technique are discouraging, with very few exceptions. Pre-emptive liver transplantation, or simultaneous liver and kidney transplants when there is already irreversible damage to the kidney, is the treatment of choice to treat the underlying disease and suppress oxalate overproduction. Given its condition as a rare disease and its genetic and clinical heterogeneity, it is not possible to gain evidence through randomised clinical trials. As a result, the recommendations are established by groups of experts based on publications of renowned scientific rigour. In this regard, a group of European experts (OxalEurope) has drawn up recommendations for diagnosis and treatment, which were published in 2012.

Introduction: Parathyroid hormone (PTH) shows a strong correlation with histomorphometric and biochemical parameters of bone turnover, however its measurement presents limitations due to inter-method variability. Circulating PTH is a mixture of peptides, but only on its whole form (1-84 PTH) is responsible of PTH biological activity. Carboxyl-terminal fragments exhibit antagonist actions and their proportion differs at each stage of chronic kidney disease, as consequence of differences on their renal clearance. The aim of this study is to evaluate possible differences in the proportion of these fragments according to dialysis type: haemodialysis (HD) or peritoneal dialysis (PD)., Material and Methods: Serum total (Ca) and ionized calcium (iCa), phosphate (P), carboxyl-terminal telopeptides of collagen type I (BCTx) were measured in 73 patients on PD (46 men and 27 women with an age between 22 and 82 years). PTH was quantified by six second generation assays (one isotopic and five chemiluminescence assays) and by one third generation PTH method., Results: Mean serum levels of Ca, iCa, P and BCTx were 9.03, 4.76, 4.73 mg/dl and 1181 pmol/l, respectively. Significant differences were observed in PTH values according to the method used. Adjustment of PTH results to PTH Allegro (Nichols) range of 150-300 nmol/l in PD patients showed higher values than those assessed previously for HD population. The percentage of biologically active 1-84 PTH as the 1-84 PTH/ 7-84 PTH ratio in PD were significantly lower than in HD patients, reflecting the higher proportion of 7-84 PTH circulating fragments for a given intact PTH result in PD., Conclusions: PD patients have a higher proportion of 7-84 PTH circulating fragments. Consequently, the inter-method adjustment algorithms proposed for HD patients are not useful for PD patients. This study proposes alternative algorithms for PTH inter-method adjustment to be applied in PD.

Background: The cost analysis of chronic kidney disease based on individual data for treatment methods and components has not been published in Spain., Objectives: a) To study the health costs of a year of treatment with haemodialysis (HD), deceased donor renal transplantation (RTx), renal-pancreas transplantation (RPTx), and S4 and S5 advanced chronic kidney disease (ACKD) b) Assess the potential relationship between sociocultural diversity, costs and treatment method., Methods: Observational study of: 1) 81 patients with ACKD (53 S4 and 28 S5) 2) 162 with more than 3 months on HD and 3) 173 with a Tx for more than 6 months (140 RTx and 33 RPTx). The costs were assessed in five categories: 1) HD sessions, 2) drug intake, 3) hospitalisation, 4) outpatient care and 5) transportation. We carried out a survey with socio-demographic parameters., Results: The financial impact of HD was €47,714&plusmn;18,360 (mean&plusmn;SD), that of Tx €13,988&plusmn;9970, and that of ACKD €9654&plusmn;9412. The cost of HD was the highest in all financial items. The costs were similar between RTx and RPTx. In ACKD, the greater the renal deterioration, the greater the cost is (S4 €7846&plusmn;8901 versus S5 €13,300&plusmn;9820, P<.01). Tx patients had the best sociocultural status, while HD patients had the worst profile. We did not find differences in costs between the three sociocultural groups., Conclusions: HD has the greatest financial impact in all items, five times higher than the ACKD patient cost and three times than the Tx patient cost. Optimising early prevention and Tx, if appropriate, must be priority strategies. This analysis invites us to think about whether sociocultural status can have an influence on opportunities for Tx.

Proteinuria is the main predictor of chronic kidney disease progression. Drugs that block the renin-angiotensin-aldosterone (RAA) system reduce proteinuria and slow down the progression of the disease. However, their effect is suboptimal, and residual proteinuria persists as an important predictor of renal impairment. Vitamin D has pleiotropic effects that could have an impact on these parameters. In this study, we critically review the molecular and experimental bases that suggest an antiproteinuric effect of vitamin D receptor (VDR) activation and the available evidence on its antiproteinuric effect in clinical practice. In animal models, we have observed the antiproteinuric effect of VDR activation, which could be due to direct protective action on the podocyte or other pleiotropic effects that slow down RAA system activation, inflammation and fibrosis. Clinical trials have generally been conducted in patients with a vitamin D deficiency or insufficiency and the main trial (VITAL) did not demonstrate that paricalcitol improved the study's primary endpoint (decrease in the urine albumin to creatinine ratio). In this sense, the information available is insufficient to advise the use of native vitamin D or VDR activators as renoprotective antiproteinuric drugs beyond the experimental level. Two Spanish clinical trials and one Italian trial attempted to determine the effect of paricalcitol and vitamin D on residual proteinuria in various clinical circumstances (PALIFE, NEFROVID and PROCEED).

Introduction: Plasmapheresis (PP) is a therapeutic apheresis technique used in the treatment of various renal and systemic diseases with varying degrees of proven clinical efficacy., Objective: To review our experience with PP at the Hospital Universitario de Canarias, focused on effectiveness and safety results in different disease groups., Material and Methods: A retrospective-descriptive study of patients treated with PP from 01/01/2006 to 31/12/2009 at the hospital. We analysed medical histories and demographic data (sex, age), biochemical parameters, underlying disease, volume and type of replacement used in the PP sessions (5% human albumin and/or fresh frozen plasma), complications with the technique, delay in starting PP treatment after suspected clinical diagnosis, number of PP sessions received, patient mortality, degree of renal impairment and evolution of renal function., Results: There were 51 patients studied, aged 50±18 years, of whom 60% were male; 331 PP sessions were performed. The diseases treated were grouped as: 11 vasculitis, 15 transplant immune activation, 5 haemolytic-uraemic syndrome (HUS), 7 idiopathic or thrombotic thrombocytopaenic purpura, 2 foetal Rh immunisations, 2 haematological diseases, 4 neurological diseases, among others. Overall mortality was 19.6% (n=10): 6 cases secondary to septic shock and the rest as a result of the evolution of the underlying disease, with 1 due to haemorrhagic shock in the renal biopsy area. There were no deaths in the transplant immune activation group. In the vasculitis group, there were 3 deaths (2 secondary to septic shock). Of the 10 patients who died, 9 did so within the first three months after diagnosis. Of the 26 renal biopsies performed, the most frequent indications were: vasculitis (23%), humoral rejection (42%), humoral rejection with calcineurin-inhibitor toxicity (12%) and HUS (8%), among others. Haemodialysis (HD) was required by 24 patients at the start of clinical symptoms: 9 of the 11 patients with vasculitis, 4 of the 5 patients with HUS and 5 of the 15 patients with transplant immune activation. At the end of evolution, 14 of them remained on the HD programme: 5 of the 11 patients with vasculitis, 2 of the 15 transplant patients and 3 of the 5 HUS patients. Significantly, patients who developed end kiney disease (EKD) in the vasculitis group were older and had higher creatinine at the onset of the disease. The transplant patients were monitored for anti-HLA class I or II before and after PP; there was a mean decrease of antibody titres in all but one patient; with an average decrease of 51% to 31%. In general, the PP technique was virtually free of complications. There were only 5 (3%) mild-moderate reactions to fresh plasma (perioral tingling and urticarial reactions) requiring pre-medication with steroids, but which did not lead to discontinuation of the treatment., Conclusion: Taking into account the wide variety of diseases that can benefit from PP and the nature of some of them, publishing our experience with this therapeutic method is of great importance. By increasing the description of case series by centre, we can add survival and renal function evidence in many uncommon diseases. Our study provides useful information for clinical practice and has also led us to reflect on future strategies to optimise outcomes in our patients.

Introduction: Important differences in patient survival exist between peritoneal dialysis (PD) and haemodialysis (HD). Several different studies have shown that PD yields a better survival rate than HD in the first and second years of treatment, especially in younger patients and non-diabetic patients with low comorbidity, whereas HD produces better results in diabetic patients, elderly patients, and in patients with greater comorbidity. In recent years, interesting changes have occurred in PD units in the Canary Islands, such as the introduction of peritoneal dialysis solutions with bicarbonate dialysate and low content of glucose degradation products, extended use of automated dialysis, and continuity of physicians and nurses in PD units, in addition to enhancing visits for advanced chronic kidney disease (ACKD)., Objective: This situation led us to perform our study with the primary objective of comparing medium-term survival among incident dialysis patients on HD versus PD in recent years in the Canary Islands, and as a secondary objective, to compare survival between these two types of dialysis by subgroups as defined by age, sex and diabetes., Material and Methods: This was a retrospective cohort study comparing survival between HD and PD patients starting dialysis in the Canary Islands between 01/01/2006 and 31/12/2009, with adjustment based on the propensity score analysis. We analysed data from the RERCAN database, which collects data on demographic variables, changes in type of dialysis, province and hospital of the patient, and mortality and its causes. We calculated Kaplan-Meier estimates of survival based on the overall population and stratified by age, sex and diabetes. We applied a Cox proportional hazards model for survival to estimate the relative mortality risk of PD compared with HD, using as independent variables: age, sex, quartiles of propensity score, the province of the patient, and diabetes. Finally, we applied a Cox model with time-dependent effects, using as a fixed risk factor the initial type of dialysis in order to assess the effect of PD versus HD on short and medium-term survival., Results: The cohort included 1469 patients (173 PD and 1296 HD), with a mean age of 62.5 years, 65% male. Mean follow-up was 16.2±12.4 months. Factors associated with greater probability of choosing PD were younger age and living in the province of Las Palmas. The cumulative mortality in the intention to treat (ITT) analysis was 27.1% in the HD group and 8.7% in the PD group, P<.0001. The cumulative probability of survival by ITT using PD vs HD was 96.6% versus 89% at 6 months (P<.001), 96% versus 80% at 12 months (P<.001), 90% versus 65% at 24 months (P<.001), 82% versus 58% at 36 months (P<.001) and 73% versus 45% at 46 months (P<.001). In the subgroup analysis, survival was also higher in PD patients compared to HD patients both over and under 65 years old, in both diabetic and non-diabetic patients, and in both genders. The same analysis from the 90th day onward produced similar results. In the ITT analysis, the Cox-adjusted mortality risk for PD was 61% lower than for HD (RR: 0.398, 95% CI 0.237-0.669, P=.001), adjusted for age, diabetes, sex, patient's province and propensity score. Broken down by years of survival on the technique used, the relative risk of death for PD compared with HD in the first year was also significantly lower (RR 0.509, 95% CI: 0.259-0.999, P=.049). From year 2 onwards, only age was a risk factor for mortality (RR: 2.785, 95% CI: 1.525-5.086, P=.001) and no differences were shown between the two dialysis techniques., Conclusion: In the Canary Islands, PD has demonstrated survival advantages over HD in the short and medium term. It is remarkable that this benefit was found in young and old patients, men and women, and diabetic and non-diabetic patients, and that this advantage was maintained even after years of being on dialysis.

Background: Hemodialysis (HD) cost analysis provides information about the economic impact of the disease on the community. Its knowledge is crucial to adequate and optimize health resources. Our aim was to study sanitary and non-sanitary direct costs of HD, based on patients individual data. Furthermore, the effect of sociocultural factors and comorbidity on costs was evaluated., Material and Methods: Retrospective and observational study of prevalence costs produced during one year of HD therapy. All patients from North Health District of Tenerife province (Canary Islands, Spain) included for at least 3 months on HD were considered for the study. Sociodemographic parameters and comorbidity data were collected from a generic individual survey and reviewing database records. Direct sanitary and non-sanitary costs were organized in 6 categories: HD sessions, medication costs, hospitalization costs (evaluated by Diagnosis-Related Groups classification system), outpatient care (including consultation and complementary studies); healthcare material and patient transportation., Results: Finally, 161 patients were included (63 +/- 16 years, 63% males, 38% diabetics). Of note, the proportions of sociocultural deprivation was high among this population (75-85% did not complete first school and had non-qualified jobs). Mean cost of global therapy was 43,070 +/- 13,932 euro. Proportional allocation of costs was as follow: HD sesion 51%, pharmacy 27%, hospitalization 17%, transportation 3% and ambulatory care 2%. There was no association between sociocultural profile, comorbidity and therapy cost., Conclusions: This is the first study of HD costs, itemized by components of expenses, based in individual data and introducing GRD model for hospitalization cost. The highest expenses corresponded to HD sessions and medication (79%), both very homogeneous to this patient population. The saving in economic terms should be, fundamentally, the prevention of CKD.

Introduction: Cardiovascular disease and other complications of atherosclerosis are the most common cause of death in patients with chronic renal failure in maintenance hemodialysis (MHD). Carotid ultrasonography is a simple non-invasive tool to investigate the vascular system, by means of intima media thickness (IMT) measurement and carotid wall calcifications., Objective: To determine IMT and the presence of plaques, and their possible clinical relationships; finally we tried to investigate whether they would predict cardiovascular morbidity and mortality in patients in MHD., Methods: We studied 60 MHD patients (age 68 +/- 13 years, 48% male, 50% diabetics, time on MHD 32 +/- 11 months) and a control group of 274 people matched for age and sex. Follow-up period was 66 +/- 13 months., Measurements: Demographic and clinical data, serum levels of homocysteine (tHcy), folic acid (FA) and B6 and B12 vitamins. IMT was measured by high-resolution B-mode ultrasonography., Results: IMT was higher in MHD patients than in those in the control group (0.947 +/- 0.308 vs 0.619 +/- 0.176 mm; P < 0.001). IMT was related with age (r = 0.268; P = 0.038), diabetic (r = 0.650; P < 0.001) and hypertensive condition (r = 0.333; P = 0.012), but not wih lipids, tHcy or FA. Patients who suffered from coronary artery disease, peripheral artery disease or stroke had higher IMT than those without those events (1.156 +/- 0.371 vs 0.875 +/- 0.285 mm; P < 0.001; 1.205 +/- 0.374 vs 0.911 +/- 0.231 mm; P = 0.007; 1.195 +/- 0.264 vs 0.844 +/- 0.251; P < 0.001 respectively). Something similar occurred with the presence of plaques. During the follow-up period 36 patients died (60%), 67% of them due to cardiovascular causes. IMT was higher in patients who died than those who survived (1.020 +/- 0.264 vs 0.858 +/- 0.334 mm; P = 0.044). The survival rate during the observation period was significantly lower in the final IMT fourth (20%) than in the first (72%) (P = 0.014). The presence of carotid plaques was an independent predictor of cardiovascular mortality., Conclusions: These findings suggests that measurement of carotid IMT and the presence of wall plaques are useful tools to predict cardiovascular events and mortality in patients in MHD.

Prescription of protein intake in CKD is complicated by potential conflicts between goals to delay progression of CKD and preserve nutritional status. Providing a protein intake of about 0.75 g/kg/day appears reasonable in patients with GRF > 30 mL (CKD stages 1-3). In CKD stage 4 and 5, it is recommended to provide a protein intake of about 0.6 g/kg/day to slow progression and minimize accumulation of uremic toxins. - Maintaining adequate energy intake is essential in all stages of CKD. - Assessment of nutritional status in CKD requires multiple markers to assess protein status, fat stores, body composition, and protein and energy intake. - PEM can be considered as an indication for the initiation of kidney replacement therapy. If PEM develops or persists despite attempts to optimize intake, and there is no apparent cause for malnutrition other than intake or anorexia, initiation of dialysis or kidney transplant is indicated in patients with GFR > 15 mL/min. - Nutritional treatment for patients with CKD should include nutritional assessment and education and nutritional planning and follow-up.

Unlabelled: With progression of chronic kidney disease (CKD), disorders of mineral metabolism appear. The classic sequence of events begins with a deficit of calcitriol synthesis and retention of phosphorus. As a result of this, serum calcium decreases and parathyroid hormone (PTH) is stimulated, producing in the bone the high turnover (HT) bone disease known as osteitis fibrosa while on the other extreme we find the forms of low turnover (LT) bone disease. Described later and initially associated with aluminum intoxication, these diseases are now seen primarily in older and/or diabetic patients, who in a uremic setting have relatively low levels of PTH to maintain normal bone turnover. Osteomalacia is also included in this group, which after the disappearance of aluminum intoxication is rarely observed. LT forms of hyperparathyroidism facilitate the exit of calcium (Ca) and phosphorus (P) from bone, whereas the adynamic bone limits the incorporation of Ca and P into bone tissue. Therefore, both forms facilitate the availability of Ca and P, which ends up being deposited in soft tissues such as arteries. The link between bone disease and vascular calcifications in CKD is now a well-established phenomenon. 2. Diagnostic strategies Calcium, Phosphorus They have little capacity to predict underlying bone disease, but their regular measurement is decisive for therapeutic management of the patient, especially in the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics. Ideally, Ca++ should be used, but total Ca is routinely used. It is recommended to adjust albumin levels in the event of hypoalbuminemia (for each g/dL of decrease in albumin, total serum Ca decreases 0.9 mg/dL). The following formula facilitates rapid calculation of corrected total calcium: Corrected total Ca (mg/dL) = total Ca (mg/dL) + 0.8 [4-albumina (g/dL)]. Parathyroid hormone "Intact" PTH is the biochemical parameter that best correlates with bone histology (levels measured with the Allegro assay from Nichols Institute Diagnostics, no longer available). Various assays are currently available that use antibodies against different fragments of the molecule, but they have significant intermethod variability and have not been validated. A whole PT assay (1-84) is currently unavailable. A consensus to establish uniform criteria for PTH measurement remains to be established. During the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics, more frequent measurement may be required based on clinical judgment. Calcifediol (25(OH)D3) It is important to maintain adequate levels of 25(OH)D3 (> 30 ng/mL), since they will be the substrate for production of 1- 25(OH)2 D3, and their deficiency aggravates hyperthyroidism. Determining 25(OH)D3 levels every 6-12 months is a recommended guideline. Other markers of bone turnover (osteocalcin, total and bone alkaline phosphate, free pyridolines in serum, and C-terminal telopeptide of collagen) do not improve the predictive power of PTH and therefore their systematic use is not justified. Radiologic studies Radiologic studies are of little diagnostic utility, because biochemical changes precede radiologic changes. Systematic radiologic evaluation of the skeleton in asymptomatic patients is not justified at present. They are useful as the first step in the study to detect vascular calcifications and amyloidosis due to b2-microglobulin and in symptomatic and at risk patients to detect vertebral fractures. Bone densitometry: Dual energy x-ray absorptiometry (DEXA) is the standard method to determine bone mineral density (usually in the femoral neck and vertebrae). It provides information on changes in bone mineral content, but not on the type of underlying bone disease. It is useful for follow-up of bone mass or for the study of bone mass changes in the same patient. Its value as a predictor of the risk of fracture has not been demonstrated in patients on kidney replacement therapy or with advanced chronic kidney disease. It is indicated in patients with fractures or risk factors for osteoporosis. Bone biopsy: The "gold standard" for diagnosis of bone disease. With improved knowledge of the value of noninvasive parameters, its use is infrequent., Indications: Pathological fractures in the presence or absence of minor trauma. Symptomatic patients in the presence of incongruent clinical parameters. A typical case is the presence of unexplained hypercalcemia from systemic disease, with inconclusive serum PTH values (between 120-450 pg/mL as an estimated range). Evaluation and follow-up of cardiovascular calcifications There are no consensuated clinical practice guidelines for the evaluation and follow-up of extraosseal calcifications in CKD. The clinical tools for evaluation and follow-up of cardiovascular disease are used based on clinical judgment. The periodicity of follow-up has not been established . 3. Recommended biochemical values The biochemical values recommended in clinical practice guidelines for the evaluation of bone mineral metabolism are summarized in Figure 3. The recommended PTH values do not fully coincide with the K/DOQI guidelines. The wide variability in PTH values depending on the assays used has led us to expand the recommended PTH range in stage 3 and 4 CKD. 4. Treatment 4.1. Diet. The recommended diet for the patient with CKD is traditionally based on protein restriction and phosphorus restriction for control of mineral metabolism. A favorable circumstance is that there is a close relationship between protein and phosphorus intake. In CKD stages 3, 4 and 5, it is recommended to restrict phosphorus intake to between 0.8-1 g/day when serum levels of phosphorus and PTH are above the recommended range. This is approximately equivalent to a diet of 50-60 g of protein. This reasonable antiproteinuric strategy that also restricts phosphorus intake is nutritionally safe. What should we tell them to eat? In a practical and oversimplified way, we recommend the following daily intake: Animal proteins: 1 serving (100-120 g), dairy products: 1 serving (equivalent to 200-240 mL of milk or 2 yoghourts), bread, cereals, pastas (1 cup of pasta, rice or legumes + some bread or cookies), vegetables and fruits relatively freely, but with moderation. 4.2. Medication Vitamin D supplements should be provided if serum levels are less than 30 ng/mL. In Spain, vitamin D3 (cholecalciferol) is marketed as Vitamin D3 Berenguer 2,000 IU/mL of solution. Combinations of calcium with cholecalciferol are also available. Most of the dosage forms contain approximately 500 mg of Ca+ and 400 IU of cholecalciferol. Alternatively, calcifediol (25(OH)D3), as Hidroferol 100 mcg/mL, has been used, although the dose range is very variable and has not been established. 4.3. Phosphorus binders. Use if hyperphosphatemia occurs. Start with calcium-containing phosphorus binders (calcium carbonate or calcium acetate), which also provide calcium if dietary intake is inadequate. Do not exceed 1.5 g of Ca++ per day. The most used are calcium carbonate and calcium acetate. Calcium acetate shows a similar binding potency to calcium carbonate but with a lesser calcium overload, and thus would have certain advantages as well as its greater effect at different pH ranges. However, gastric intolerance is more frequent with this dosage form. Aluminum hydroxide may sometimes be required to control phosphoremia or the occurrence of hypercalcemia. Serum aluminum values should be maintained below 30 mcg/L. Avoid use for longer than 6 months and daily doses greater than 1.5 g. Sevelamer is associated with an increased risk of acidosis and has not been approved for use in predialysis stages. Lanthanum carbonate has been recently marketed in Spain, although its indication for use in the predialysis stage of CKD is still not approved. 4.4. Vitamin D derivatives. Indicated when PTH levels are elevated. A prerequisite for their use is that Ca and P serum levels are adequately controlled. Vitamin D derivates available in Spain are 1,25(OH)2D3 (Calcitriol)and 1a(OH)D3 (a-Calcidiol). Doses should be titrated until PTH levels are normalized. Phosphate binder doses often need to be increased because these vitamin D derivatives increase intestinal absorption of calcium and phosphorus. Low doses do not cause hypercalcemia or hyperphosphatemia and do not worsen the course of renal function. Recommended doses: Calcitriol 0.25 mcg every 48 hours and alpha-Calcidiol 0.50 mcg every 48 hours. Soon to be available on the Spanish market is the oral dosage form of paricalcitol (recommended initial dose of 1 mcg/24 h), with a lesser hypercalcemic and hyperphosphoremic effect. Clinical use of calcimimetics in the predialysis state is not yet recommended and is currently under investigation.

Mineral metabolism abnormalities in chronic kidney disease (CRK) have adverse effects, particularly on the skeleton and cardiovascular system. Among the classic biochemical abnormalities, hyperphosphoremia plays a significant role. It stimulates parathyroid hormone production by the parathyroid gland both directly (it increases PTH synthesis and secretion and induces cell proliferation) and indirectly (it suppresses calcitriol synthesis by the kidneys and reduces vitamin D receptor and calcium sensor expression). It induces phenotypical activation of vascular smooth muscle cells, causing them to acquire an osteoblastic profile and produce procalcifying factors. As a result of both effects, numerous studies (retrospective) have shown an increase in mortality associated with hyperphosphoremia (usually P > 5.5 mg/dL). Finally, recent observations suggest a direct association between phosphoremia and CKD.Undoubtedly, all these are powerful arguments in favor of increasingly strict control of P in CKD.

Unlabelled: A pathological Oral Glucose Tolerance test (OGTT) is early marker of peripheral insulin resistance. Nevertheless, its utility in nondiabetic patients with CRF stage IV-V is undetermined., Aim: We wanted to detect, in a population of non diabetic patients with CRF, the presence of carbohydrates metabolism anomalies, by means of the OGTT and to relate it with metabolic, anthropometric, cardiovascular parameters and renal function. We studied 45 non diabetic patients with advanced CRF (stage IV-V), 26 men, mean age 66.5 years, with average Cockroft-Gault of 23.6 ml/min. We measured weight, height, waist and BMI. BIOCHEMICAL: glucose, insulin, OGTT, C peptide, lipid profile, HbA1C and Hto. Cardiovascular comorbidity, mean proteinuria and systolic and diastolic blood pressure (6 months pre and post analytical measure) were measured. Pulse pressure was also calculated., Results: 47% of the patients presented normal fasting glucose, whereas 53% had isolated impaired fasting glucose (IFG). After the OGTT, 36% of the patients presented impaired glucose tolerance (IGT) and 14% diabetes (>200 mg/dl). Of the patients with normal fasting glucose, 38% had IGT after OGTT and 5% diabetes. Patients with abnormal OGTT were older (71+/-13.6 versus 60+/- 18.8 years, p=0.03), had greater HbA1C (5.6+/-0.5 versus 5.2+/-0.3%, p=0.02), total cholesterol (193+/-37.7 versus 169.8+/-44.9 mg/dl, p=0.03), pulse pressure (63.4+/- 14.5 versus 52.3+/-9.7 mmHg, p=0.0001) and greater prevalence of ischemic heart disease (28% versus 5%, p=0.05). Creatinine Clerance negatively correlated with the OGTT (r=-0.39, p=0.01) and plasma creatinine positively with fasting insulin (r=0.33, p=0.02) and C-peptide (r=0.42, p=0.006). Urinary Proteins were correlated with fasting glucose (r=0.30, p=0.04), C-peptide (r=0.52, p=0.001), triglycerides (r=0.36, p=0.01) and with the HOMA-IR index (r=0.30, p=0.05)., Conclusion: Fasting Glucose did not predict OGTT results in patients with CRF. For this reason, we think that the OGTT can be very usefull tool to identify states of "prediabetes" and diabetes in patients with CRF, specially in those whose present an elevated Pulse Pressure, age greater than 65 years, hyperlipidaemia and HbA1C above 5.2%. The early detection of these metabolic anomalies, may lead to intensify dietetic and pharmacological measures directed to delay or to attenuate the appearance of diabetes and its serious complications in a population in which the cardiovascular risks factors are very elevated.

Unlabelled: High levels of homocysteine (tHcy) are frecuent in MHD patients, and recognized as a risk factor for cardiovascular events. Vitamin supplements have been shown to lower serum Hcys, although optimal dose and efficacy is not well defined. Moreover, methylenetetrahydrofolate reductase (MTHFR) gene polymorphism can modulate its prevalence and response to treatment., Objective: To evaluate efficacy and safety of two vitamin supplement regimens on Hcys serum levels over a 12 month period., Methods: We conducted a prospective, randomised, double-blind trial in 60 stable MHD patients (68 +/- 13 years, 48% male, 50% diabetics). Patients were randomly assigned to one of two treatment regimens: 1) daily renal multivitamin containing folate (FA), vitamin B6 and B12 (5 mg, 10 mg and 0.4 mg respectively) (N = 27); and 2) supraphysiological daily doses (15 mg, 100 mg and 1 mg) (N = 33). These regimens were continued throughout the study period. Hcys levels were compared with a control group from the general population (N = 276) matched for age and gender., Measurements: demographic and clinical data, serum levels of Hcys, FA, B6, B12 at baseline and after 1, 3, 6 and 12 months of treatment; MTHFR gene polymorphism (PCRRT)., Results: At baseline, global prevalence of hyperhomocysteinemia (tHcy > or = 15 micromol/L) was 100% in patients and 22% en controls. Hcys levels were significantly higher in patients versus controls (32.4 +/- 8.9 vs 12.9 +/- 6.8; P < 0.0001). Both regimens were equally effective in reducing Hcys levels. As a whole, Hcys levels were reduced by 23.6% (P < 0.001) after one month of treatment. The highest reduction was observed at the sixth month (28.3%, 32.4 +/- 8.9 vs 22.7 +/- 6.4, P < 0.001) and remained stable thereafter. However, only 12% of patients normalised their plasma levels after 12 months of therapy. The effect of treatment was not influenced by age, gender, diabetes, body weight or time on MHD. Reduction rate of tHcy levels was related to baseline tHcy level (r = 0.500, P < 0.001) and baseline FA levels (r = -0.332, P = 0.009). The MTHFR polimorfism did not significantly modified the effect of the treatment. No side effects were associated with either regimen., Conclusions: Hyperhomocysteinemia is common in patients with conventional HD schedules and this is not related to vitamin deficiencies. Vitamin supplements significantly reduce Hcys levels in a sustained but suboptimal way. Supraphysiological doses did not improve the results. Further studies are requiered to demonstrate that this effect is associated with an improval in morbidity and mortality.

Early after renal transplantation (RT) a rapid decrease in bone mineral density at the lumbar spine, femoral neck, and femoral shaft has been documented. In addition, an appreciable proportion of patients still remain losing bone late after RT. As a consequence, RT patients are at a high risk of bone fractures as compared to general population. Most fractures involve appendicular skeleton, particularly the feet and ankles, and the diabetic patient is at increased risk of fractures. Thus, early institution of preventive measures and treatment of established osteoporosis are central. The major cause of post-transplantation bone loss is corticosteroid treatment, and this should be used at the lower dose compatible with graft survival. Preexisting hyperparathyroidism also affects the early cancellous bone loss at the spine, and post-transplantation bone loss reflects variable individual susceptibility, resembling the polygenic determination of bone mineral density in general. Clinical trials have demonstrated that bisphosphonates or vitamin D plus calcium supplementation, prevent post-transplantation bone loss during the first 6-12 months. However, their role in preventing bone fractures has not been proven. Finally, recommendations for management, prevention and treatment, are summarized.