CKD LAB METHODS, PROGRESSION & RISK FACTORS 2

Nephrology Dialysis Transplantation, May 2014

Introduction and Aims: Despite decades of research, our complete understanding of the determinants and natural history of CKD-ESRD progression is immature. CKD to ESRD progression is unanimously and classically depicted as a predictable, linear, progressive and time-dependent decline in renal function, ultimately leading to ESRD and the need for RRT. The National Kidney Foundation KDOQI 2002 staging of CKD stages I, II, III, IV and V is most fortuitously based on this untested unproven premise. There is however accruing evidence that quite often, CKD to ESRD happenstance is unpredictable, precipitate and unexpected in otherwise a priori stable CKD patients. Moreover, in 2010, we first described the new unrecognized syndrome of rapid onset end stage renal disease (SORO-ESRD). This is acute yet irreversible ESRD after AKI; its contribution to the incident general adult US ESRD population is uncertain and unstudied. Methods: A retrospective computer-based analysis of real-time individual patient-level serum creatinine trajectories from CKD to ESRD of the last 100 adult consecutive ESRD patients on maintenance outpatient in-center hemodialysis for >90 days. Definition: SORO-ESRD defines a patient with an apriori stable GFR ≥30 mL/min/1.73 m2, on or before the 90th day preceding first RRT, who developed irreversible ESRD thereafter. Results: Excluding 9 patients (deficient laboratory data), 31 of 91 (34%) ESRD patients, 18M:13F, age 72 (50-92) years, had SORO-ESRD. The remaining 60 patients had "classic" progressive time-dependent ESRD (Figure 1). Two of 31 (6%) SORO-ESRD patients were renal transplant recipients (Figure 2). AKI in 31 SORO-ESRD patients followed Pneumonia (8), Acute decompensated heart failure (7), Pyelonephritis (4), Post-operative states (5), General sepsis (3), Contrast-induced nephropathy (2), and others (2). The SORO-ESRD patients were older than the 60 “classic ESRD” patients - 71 ± 12 (49-91) years vs 69 ± 13 (38-93), p NS. Moreover, concurrent angiotensin inhibition was commoner in the 31 SORO-ESRD patients, 7 of 31 (23%) versus 3 of 60 “classic ESRD” patients (5%), t (89)=2.587, p=0.0113. Conclusions: The syndrome of rapid onset end stage renal disease (SORO-ESRD) is not uncommon in the general incident US adult ESRD population. Older age, associated renal senescence, and exposure to nephrotoxics including angiotensin inhibition, may predispose to SORO-ESRD. Larger studies are mandated to assess its impact on CKD care in general, RRT planning, AV-Fistula First programs, and renal allograft loss. Finally, SORO-ESRD once again reemphasizes the need for more preventive nephrology or ‘renoprevention’ to reduce AKI in our CKD patients. View larger version: In this window In a new window Download as PowerPoint Slide

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CKD LAB METHODS, PROGRESSION & RISK FACTORS 2

0 Schneider's Children Medical Center of Israel , Petah Tiqva , Israel 1 Rabin Medical Center , Petah Tiqva , Israel 2 Amaryllis H Van Craenenbroeck 3 Antwerp University Hospital , Antwerp , Belgium 4 University of Antwerp , Edegem , Belgium 5 Department of Nephrology, School of Medicine, Faculty of Medicine, Toho University , Tokyo , Japan 6 The Division of Diabetes and Metabolism, the Institute for Adult Diseases, Asahi Life Foundation , Tokyo , Japan 7 Kakuta Clinic , Saitama City , Japan 8 Jichi Medical University Saitama Medical Center , Saitama-City , Japan 9 Saitama Medical Center Jichi Medical University , Saitama City , Japan 10 Kathrin Untersteller 11 Saitama Social Insurance Hospital , Saitama City , Japan 12 Mashiko Hospital , Kawaguchi City , Japan 13 Saitama Red Cross Hospital , Saitama City , Japan 14 Saitama Tsukinomori Clinic , Saitama City , Japan 15 Department of Renal, Urological and Infectious Diseases, Faculty of Medicine, University of Porto , Porto , Portugal 16 University of Pittsburgh Medical Center In Italy , Palermo , Italy 17 University of Messina , Messina , Italy 18 Department of Renal, Urological and Infectious Diseases, Faculty of Medicine , Porto , Portugal 19 Nephrology and Infectious Diseases Research and Development Group , INEB-(I3S), Porto , Portugal 20 Saarland University Medical Center , Homburg , Germany 21 Federal University of Ceara , Fortaleza , Brazil 22 University of Fortaleza , Fortaleza , Brazil 23 Geraldo Silva Junior 24 Humanitas Clinical and Research Center , Rozzano , Italy THE PATHWAY FROM CKD TO ESRD: THE SYNDROME OF RAPID ONSET END STAGE RENAL DISEASE IN THE LAST CONSECUTIVE 100 ADULT ESRD PATIENTS IN A MAYO CLINIC DIALYSIS SERVICES MAINTENANCE OUTPATIENT IN-CENTER HEMODIALYSIS UNIT © The Author 2014. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. - Introduction and Aims: Despite decades of research, our complete understanding of the determinants and natural history of CKD-ESRD progression is immature. CKD to ESRD progression is unanimously and classically depicted as a predictable, linear, progressive and time-dependent decline in renal function, ultimately leading to ESRD and the need for RRT. The National Kidney Foundation KDOQI 2002 staging of CKD stages I, II, III, IV and V is most fortuitously based on this untested unproven premise. There is however accruing evidence that quite often, CKD to ESRD happenstance is unpredictable, precipitate and unexpected in otherwise a priori stable CKD patients. Moreover, in 2010, we first described the new unrecognized syndrome of rapid onset end stage renal disease (SORO-ESRD). This is acute yet irreversible ESRD after AKI; its contribution to the incident general adult US ESRD population is uncertain and unstudied. Methods: A retrospective computer-based analysis of real-time individual patient-level serum creatinine trajectories from CKD to ESRD of the last 100 adult consecutive ESRD patients on maintenance outpatient in-center hemodialysis for >90 days. Definition: SORO-ESRD defines a patient with an apriori stable GFR ≥30 mL/min/ 1.73 m2, on or before the 90th day preceding first RRT, who developed irreversible ESRD thereafter. Results: Excluding 9 patients (deficient laboratory data), 31 of 91 (34%) ESRD patients, 18M:13F, age 72 (50-92) years, had SORO-ESRD. The remaining 60 patients had "classic" progressive time-dependent ESRD (Figure 1). Two of 31 (6%) SORO-ESRD patients were renal transplant recipients (Figure 2). AKI in 31 SORO-ESRD patients followed Pneumonia (8), Acute decompensated heart failure (7), Pyelonephritis (4), Post-operative states (5), General sepsis (3), Contrast-induced nephropathy (2), and others (2). The SORO-ESRD patients were older than the 60 “classic ESRD” patients 71 ± 12 (49-91) years vs 69 ± 13 (38-93), p NS. Moreover, concurrent angiotensin inhibition was commoner in the 31 SORO-ESRD patients, 7 of 31 (23%) versus 3 of 60 “classic ESRD” patients (5%), t (89)=2.587, p=0.0113. Conclusions: The syndrome of rapid onset end stage renal disease (SORO-ESRD) is not uncommon in the general incident US adult ESRD population. Older age, associated renal senescence, and exposure to nephrotoxics including angiotensin inhibition, may predispose to SORO-ESRD. Larger studies are mandated to assess its impact on CKD care in general, RRT planning, AV-Fistula First programs, and renal allograft loss. Finally, SORO-ESRD once again reemphasizes the need for more preventive nephrology or ‘renoprevention’ to reduce AKI in our CKD patients. BLOOD UREA NITROGEN/SERUM CREATININE RATIO PREDICTS MORTALITY AFTER HEMODIALYSIS INITIATION IN PREDIALYSIS CHRONIC KIDNEY DISEASE PATIENTS Introduction and Aims: Blood urea nitrogen/serum creatinine (BUN/Cr) ratio has been widely used clinically to identify the pre-renal azotemia and dehydration. The study aimed to evaluate whether elevated BUN/Cr ratio could predict mortality in patients with advanced chronic kidney disease (CKD) after hemodialysis initiation. Methods: The prospective cohort study enrolled 906 patients who entered regular hemodialysis between 2003 and 2010. The primary endpoint is the mortality rate within first 3 months after the initiation of regular hemodialysis. Results: The mean age was 59.2 ± 16.1 years, 43.9% patients have BUN/Cr ≥12, and 33.1% patients had treatment of keto acids. Overall mortality rate was 19.8%. Compared to BUN/Cr < 12, patients with BUN/Cr ≥12 at 6 months before dialysis have significantly higher mortality rate, 34.9% vs 9.8%. Elderly patients (aged ≥75) had higher percentage of BUN/Cr ≥12 (61.7%) and elderly patients with BUN/Cr ≥12 had the highest mortality rate (43.4%). The use of keto acids associated with less patients with BUN/Cr ≥12 (16.4%) and lower mortality rate (12.2%). Moreover, elevated BUN/ Cr associated with rapid decline of renal function. The use of keto acids associated with slower decline of renal function and longer duration between serum creatinine over 6 mg/dL and the initiation time of regular hemodialysis. Conclusions: In summary, elevated ratio of BUN/Cr is not uncommon and could be a strong predictor of mortality after hemodialysis initiation in advanced CKD patients, especially elderly population. The use of keto acids is associated with lower BUN/Cr ratio and slower decline of renal function. C REACTIVE PROTEIN AND LONG-TERM RISK FOR CHRONIC KIDNEY DISEASE Introduction and Aims: C-reactive protein (CRP) is an acute phase protein that is produced predominantly by hepatocytes under the influence of cytokines such as interleukin-6 and tumor necrosis factor-alpha. C reactive protein may also be locally expressed within renal cortical tubular epithelial cells. Among apparently healthy individuals, elevated CRP levels have been associated with increased risk of future cardiovascular events. The aim of the present study was to assess the association of CRP and the risk for long-term chronic kidney disease (CKD). Methods: We conducted a retrospective analysis on a prospectively collected data from a large screening center in Israel. All participants who had a follow up interval of more than 5 years in the screening center, and presented with an estimated glomerular filtration rate (eGFR) above 60 ml/min/1.73 m2 at baseline were included. High sensitive mean CRP levels of all visits were calculated for each subject. Risk for CKD (defined as eGFR<60 ml\min) at the end of follow up was assessed in relation to mean CRP levels. The confounding effects of other predictors of CKD (age, sex, diabetes mellitus (DM), hypertension (HTN), total cholesterol, HDL cholesterol, current smoking status and body mass index) were examined in a multivariate analysis using multiple logistic regressions. Results: Out of 4,345 patients (see Table 1 for patients' characteristics), 42 (1%) developed CKD in a mean follow up of 7.6 ±2 years. Elevated levels of CRP were associated with greater risk for CKD (crude OR 4.2, 95% CI 1.5-12). The OR for the association of CRP with CKD when controlling for age and gender simultaneously was 5.28 (95% CI 1.7-16.2). In a multivariate analysis using multiple logistic regressions for confounding variables, elevated CRP levels remained significantly associated with greater risk for CKD (OR 5.5, 95% CI 1.8-17.0), see Table 2. In addition, when applying logistic regression models treating CRP as a continuous variable, it appears that for patients with DM, HTN or presenting with eGFR<90ml\min\1.73 m2, the predictive role of CRP for CKD was highly significant (Figures 1-3). Conclusions: Elevated levels of CRP in are independently associated with long-term risk for future CKD development. The predictive role of high CRP level is especially enhanced in patients with DM, HTN and in patients presenting with eGFR<90ml\min \1.73 m2. MP129 Figure 2: CKD predicted probability according to CRP and hypertension. MP129 Figure 1: CKD predicted probability according to CRP and diabetes. MP129 Figure 3: CKD predicted probability according to CRP and hypertension. iii | Abstracts DEVELOPMENT OF FUNCTIONAL HUMAN PROXIMAL TUBULE CELL MONOLAYERS ON POLYMERIC MEMBRANES Introduction and Aims: Chronic kidney disease (CKD) patients suffer from heterogeneous clinical complications and are at high morbidity risk. A major cause relates to the accumulation of protein-bound uremic toxins. The Biological Kidney (BioKid) aims at developing living membranes for intra-dialytic human renal epithelial cells aided removal of these toxins. In this study, human conditionally immortalized proximal tubule epithelial cell (ciPTEC) monolayer integrity when cultured on polyethersulfone (PES)-based membranes coated with L-3,4-dihydroxyphenylalanine (L-DOPA) and collagen IV was evaluated. Methods: PES flat sheet and hollow fiber (HF) membranes were coated with both L-DOPA2 and collagen IV at different concentrations. First, the cell-free permeability properties of flat membranes were studied using pure water at selected pressures. Subsequently, ciPTEC were cultured on selected flat and HF membranes, and after 7 days, the expression of the tight junction protein zonula occludens-1 (ZO-1) was detected using laser scanning confocal microscopy. Finally, functional properties were studied in real-time using matured ciPTEC cultured on HF membranes by uptake of ASP+, a known substrate of Organic Cation Transporters (OCTs), under flow conditions. Results: The application of L-DOPA (2 mg/ml) in combination with collagen IV (25 μg/ml) coatings onto the PES membranes resulted in acceptable cell-free membrane permeability. Using this optimized coating strategy, matured ciPTEC showed a clear ‘cobble stone’ and tight epithelial morphology on both flat- and HF-coated membranes, and ZO-1 was abundantly expressed along the tight junctions of the cells. Moreover, matured ciPTEC cultured on coated HF exposed to 5 μM ASP+ during 20 min, under a constant flow of 3 ml.h-1, demonstrated a clear fluorescent intracellular signal indicating an active basal uptake of ASP+. The signal appeared after 2 min of ASP+ exposure and was saturated after 14 min. Preliminary results showed a reduced ASP+ uptake of 57.0 % ± 0.4 in the presence of 100 μM metformin, a known OCT inhibitor, indicating the specificity of the uptake via OCTs. Conclusions: A coating combination of L-DOPA and collagen IV has proven to be favourable for the formation of a functional ciPTEC monolayer. Hence, we expect that the application of this coating in the BioKid device will positively contribute to the excretion of uremic toxins by ciPTEC. References 1. Wilmer M.J. et al, Cell and Tissue Research 339, 2010, p.449 - 457 2. Ni M. et al, Biomaterials 32 (6), 2011,p.1465-1476 EFFECT OF A SINGLE MAXIMAL EXERCISE BOUT ON MONOCYTE SUBSETS IN CHRONIC KIDNEY DISEASE Introduction and Aims: Monocytes play a substantial role in chronic low-grade inflammation that is associated with atherosclerosis in chronic kidney disease (CKD). Recently, three functionally distinct subgroups have been described. The response to acute exhaustive exercise is complex and involves immune cells and inflammatory cytokines. In healthy subjects, an acute exercise bout induces leuko- and monocytosis and results in mobilisation of Mon2 and Mon3 from the microvasculature. In overt atherosclerotic disease, this response is blunted. We are the first to evaluate the effect of a maximal exercise bout on monocyte subsets, interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in CKD. Methods: Twenty patients with CKD and 15 age-matched healthy subjects (HS) were included {Table 1}. Venous blood was sampled before a maximal cardiopulmonary exercise test and within 5 minutes after recovery. Next to standard leukocyte counts and differentiation, flow cytometry was applied to quantify monocyte subsets; CD14+ +CD16-CCR2+ cells (Mon1; inflammatory), CC14++CD16+CCR2+ cells (Mon2; pro-atherogenic and anti-inflammatory) and CD14+CD16++CCR2- cells (Mon3-tissue healing). Levels of IL-6 and MCP-1 were determined by ELISA. Results: Baseline data are in Table 1. Mean eGFR in CKD patients was 44.42 ± 19.7 ml/ min/1.73m2, and aerobic capacity was severely reduced. Baseline levels of MCP-1 were higher in CKD compared to HS ( p=0.013). Total monocyte count was lower in CKD, but the monocyte subset distribution did not differ between groups. Mon1 comprised the largest subset followed by Mon3 and Mon2. After an acute exercise challenge, total monocyte count increased in both groups (HS 450 ± 128 to 728 ± 205 cells/μl, p<0.001; CKD 352 ± 103 to 597 ± 161 cells/μl, p<0.001). Within the total monocyte group, Mon1 decreased whereas Mon2 and Mon3 increased ( p<0.05){Figure 1}. The response of the monocyte subsets was comparable between HS and CKD; for Mon3 there was a trend towards a blunted response in CKD compared to HS ( p=0.055). Post-exercise, levels of MCP-1 and IL-6 increased in HS (MCP-1 330.76 ± 163.53 to 392.02 ± 191.44 pg/mL, p<0.05; IL-6 1.07 ± 1.76 to 1.57 ± 2.17 pg/mL, p<0.05), but no change was observed in CKD. VO2peak correlated with exercise-induced decrease in %Mon1 (r= 0.503, p= 0.03) and increase in %Mon3 (r= 0.509, p= 0.002). VO2peak correlated with change in MCP-1 (r= 0.612, p<0.001), but the latter did not relate to the shifts in monocyte subsets. Conclusions: Despite a lower exercise capacity and presence of low-grade inflammation at baseline, CKD patients showed a comparable acute exercise-induced change in monocyte subsets as healthy subjects. These observations can add insight into the long-term anti-inflammatory effects of exercise training. MP131 Baseline comparisons RELATIONSHIP BETWEEN PROTEINURIA AND PULSE WAVE VELOCITY IN PATIENTS WITH STAGE 1-4 CHRONIC KIDNEY DISEASE Introduction and Aims: Cardiovasculary disease is the leading cause of mortality and morbidity in chronic kidney disease (CKD) patients. In this study, we aimed to evaluate the relationship between proteinuria and arterial stiffness in stage 1-4 CKD patients. Methods: Sixty patients with stage 1-4 CKD from our outpatient clinic were enrolled into the study. All patients were evaluated for their standard clinical (age, gender, CKD duration, body mass index) and biochemical parameters. Anthropometric and body composition analyses were performed for all patients. Pulse wave velocity (PWv) was determined from pressure tracing over carotid and femoral arteries using the SphygmoCor system. 24 hours urine sample was collected to calculate proteinuria and creatinine clearance. Results: Mean duration of CKD for all patients were 47,00 (40,5) months. Mean PWv value for all patients were higher from normal range as 8,54±2,49 ms. Patients were divided into 3 groups according to their GFR values; Group 1: GFR≥60 ml/dk/1,7 m2 (n:21, 35%), Group 2: GFR 30-60 ml/dk/1,7 m2 (n:27, 45%) ve Group 3: GFR < 30ml/ dk/1,7 m2 (n:12, 20%). Serum hemoglobin and albumin values were significantly decreased and serum PTH levels were significantly increased between groups while GFR levels were decreasing. When patients were divided into two groups according to PWv levels; patients with higher PWv values (PWv > 8 m/s, n:29) had significantly higher proteinuria/24 hours (1421,4 vs 488,5 mg/24 hours) and microalbuminuria (656,1 vs 191,7 mg/24 hours) levels compared with patients with lower PWv levels (PWv ≤8 m/s, n:31). PWv levels were negatively correlated with GFR (r:-0,259, p:0,046) levels; and positively correlated with HT duration (r:0,298, p:0,021), serum creatinine (r:0,285, p:0,027) and PTH (r:0,017, p:0,009) levels. Conclusions: In this study we demonstrated higher PWv levels in patients with stage 1-4 CKD and significant correlation between PWv levels and GFR values, HT duration, hyperparathyroidism and proteinuria. These factors should be evaluated and treated seriously for prevention of cardiovasculary disease and renal disease progression in predialysis patients. POLPMORPHISMS IN MYH9 ARE ASSOCIATED WITH THE CHRONIC KIDNEY DISEASE IN CHINESE Liping Liu1 and Caili Wang1 1Division of Nephrology, The First Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, China Introduction and Aims: In recent genome-wide association study(GWAS)indicated that the MYH9 gene was significantly associated with Chronic Kidney Disease in African-Americans and Europeans. In the present study,we aims to explore the association between polymorphisms in MYH9 and Chronic kidney disease in Chinese. Methods: Five hundred and ninety-five persons, including 301 patients with chronic kidney disease and 294 healthy controls, were enrolled in the present study. Two single nucleotide polymorphisms (SNPs) (rs3752462,rs4821480) were genotyped by TaqMan assay or a restriction fragment length polymorphism assay for a further case-control study. The discrepancies of the patients’ quantitive traits (including age, sex, urinary protein in 24 hour, Serum creatinine, glomerular filtration rate, systolic and diastolic blood pressure, frequency of different primary diseases and frequency of using different kinds of antihypertensive drugs) among different genotypes of the two MYH9 SNPs were analyzed. The association between polymorphisms in MYH9 and hypertension susceptibility in CKD patients were analyzed in the rs3752462 site. Meanwhile analysis of the relationship between different genotypes associated with disease progression of chronic kidney disease Rs3752462 sites. Results: 1. Single factor analysis showed that systolic blood pressure of CT genotype patients is significantly higher(147.94±27.40)than that of CC genotype patients(136.43 ±19.09)(P<0.05). 2. The frequency of using all kinds of antihypertensive drugs for CC genotype patients (7.4%) is below that of TT (43.9%) and CT (48.7%) genotype patients (P<0.05). 3. After correcting the age factor, Logistic regression indicated that CC genotype is a protective factor of systolic blood pressure increasing. The probability of high blood MP133 Baseline clinical characteristics of CKD in subgroups divided by rs3752462 TT(n=153) 55.19±15.60 146.50±26.12 87.79±19.26 21.99±24.18 51.21±15.97 136.43±19.09 85.00±12.91 32.00±29.98 54.49±17.04 147.94±27.40 87.51±17.85 21.62±23.67 Age(year) Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) eGFR (ml/min per 1.73m2) iii | Abstracts MP133 rs3752462 site binary logistic pressure for CT genotype patients with CKD is 0.175 times that of CC genotype (95% CI:0.071~0.431). 4. Glomerular filtration rate of CC genotype of patients significantly higher than the genotype CT patients (P=0.045), and TT patients (P=0.048) Conclusions: Based on a Chinese cohort, we found an association between MYH9 gene polymorphism and chronic kidney disease, adding to the mounting evidence of MYH9 as an important gene in CKD. The CKD patients who carry the rs3752462 site CC genotype of MYH9 gene are not prone to high blood pressure. Polymorphism of MYH9 gene rs3752462 site is associated with systolic blood pressure in CKD patients. It may indicate that allele C mutation for T can lead to the increase in systolic blood pressure. It can be a useful bio-mark for predicting the hypertension susceptibility in chronic kidney disease patients. CC genotype is the independent protective factors of CKD progression to ESRD, gene mutations in C allele to T allele may cause ESRD. PREDICTORS OF THE EFFECT ON PRESERVATION OF RENAL FUNCTION BY SODIUM BICARBONATE SUPPLEMENTATION FOR ACIDEMIA IN CHRONIC KIDNEY DISEASE Introduction and Aims: Sodium Bicarbonate (S.B) supplementation is usually administrated to patients with chronic kidney disease (CKD) and metabolic acidemia, and slows the rate of progression of renal failure to ESRD. However, CKD includes various pathological states and which pathology is adequate to obtain optimal response to S.B supplementation remained unclear. Therefore we investigated to predictive factors for the effect of S.B supplementation in patients with CKD and diabetic (DM) or non-DM. Methods: 351 CKD patients with acidemia (eGFR<50ml/min, serum bicarbonate level<24mmol/l) was enrolled at The Institute for Adult Diseases, Asahi Life Foundation and Kidney Center in Toho University Omori Medical Center Tokyo, Japan from July 2002 to January 2013. 200 patients (DM 100, non-DM 100, mean age 65.6y/o, eGFR 11.2±5.7ml/min, urinary protein excretion 3.0±3.3g/g Cr, serum bicarbonate concentration 17.4±2.5mmol/l) treated with conventional therapies were given additional oral S.B supplementation and the effect on retardation of renal function decline was evaluated. The responder group (improved eGFR trajectory) was defined that eGFR slope during pretreatment for 3 month was more declined than eGFR slope during treatment for 3 month with oral S.B, non-responder group (aggravated eGFR trajectory) was defined vice versa. Baseline clinical and laboratory findings were compared in the two groups. The predictive factors for response to treatment were analyzed. The statistical analysis was used t-test, chi square test, logistic regression model and receiver- operator characteristics (ROC) curve. Results: The slope of eGFR was -0.6±1.5ml/min/month before S.B treatment and was significantly slowed down ( p=0.01) after treatment to -0.2±1.2ml/min/month. The eGFR slope in DM before S.B treatment (-0.7±1.3ml/min/month) was steeper than in non-DM (-0.4±1.6) and ameliorated by S.B treatment (slope during treatment DM -0.2 ±1.2ml/min/month, non-DM 0.30±1.31)110 CKD patients among 200 patients had improved eGFR trajectory after S.B and were assigned to responder group, the rest were to non-responder group. Responder group showed lower serum bicarbonate concentration (17.0±2.6 mmol/l in responder, vs. 17.8±2.3 in non-responder, p=0.02), and more rapid progress of eGFR slope pretreatment (-1.2±1.2ml/min/month vs. 0.2 ±1.3, p<0.0001) than non-responder group. In logistic regression model, responder was predicted by steep eGFR downslope during pretreatment. eGFR downslope steeper than -0.4ml/min/month (AUC0.9, p<0.0001) was cut-off point by ROC analysis. Low serum bicarbonate level (OR 0.8, 95%C.I. 0.7-0.9, p=0.02), use of antiplatelet agents (OR 1.8, 95%C.I. 1.0-3.2, p=0.04) or diuretics (OR 2.4, 95%C.I. 1.3-4.3, p=0.002) was associated with responder. DM tended to more strongly respond (OR 1.6, 95%C.I. 0.9-2.8, p=0.08) than non-DM, however, it is almost based on steep eGFR slope during pretreatment. In non-DM, antiplatelet agents was significantly (OR 2.4, 95%C.I. 1.0-5.8, p=0.03) associated with response and in DM, diuretics (OR 2.5, 95%C.I. 1.1-6.0, p=0.02) was associated. Conclusions: S.B treatment added on conventional management achieved retardation of renal function decline in CKD. DM patients have steeper eGFR slope at S.B supplementation, but tended to be more responsive than non-DM patients. Use of antiplatelet agents in non-DM patients and diuretics in DM is possibly useful for combination with S.B supplementation. NT-PROBNP VERSUS ECHOCARDIOGRAPHIC MARKERS AS PREDICTORS OF CARDIOVASCULAR EVENTS IN CKD G2 - G4 PATIENTS Introduction and Aims: Chronic kidney disease (CKD) patients experience an enormous cardiovascular event (CVE) rate. Both circulating biomarkers (i. e. natriuretic peptides) and echocardiographic parameters (left atrial volume index [LAVI], left volume mass index [LVMI]) have been suggested for prediction of CVE in CKD patients. We aimed to analyze whether natriuretic peptides and echocardiographic markers yield complementary prognostic information. Methods: In a prospective cohort study, we recruited 402 stable CKD patients with an estimated glomerular filtration rate (eGFR) of 15 - 89 ml/min/1.73 m2. No patient received renal replacement therapy at study initiation. In all participants, plasma NT-proBNP was measured, and LAVI and LVMI were assessed. During a mean follow-up of 2.5 ± 1.3 years, the occurrence of CVE (acute myocardial infarction, stroke, amputation above the ankle, surgical or interventional coronary / cerebrovascular and / or peripheral arterial revascularization and / or death of any cause) was recorded. In univariate Kaplan-Meier analyses and multivariate Cox regression analyses, we assessed NT-proBNP, LAVI and LVMI as outcome predictors. Results: NT-proBNP, LAVI and LVMI all predicted CVE in univariate analyses. However, in Cox regression analysis which included NT-proBNP, LAVI (or LVMI, respectively), eGFR and traditional cardiovascular risk factors, NT-proBNP (HR forth vs first quartile: 3.495; 95% CI 1,684 - 4,413; p = 0.011) remained an independent predictor for cardiovascular events, whereas LVMI (HR forth vs first quartile: 1.946; 95% CI 0.997 - 1,011; p = 0.128) or LAVI (HR forth vs. first quartile: 0.645; 95% CI 0,976 - 1,024; p = 0.311) lost their predictive power. Conclusions: NT-proBNP, LAVI and LVMI all predicted CVE in univariate analyses. However, in Cox regression analysis which included NT-proBNP, LAVI (or LVMI, respectively), eGFR and traditional cardiovascular risk factors, NT-proBNP (HR forth vs first quartile: 3.495; 95% CI 1,684 - 4,413; p = 0.011) remained an independent predictor for cardiovascular events, whereas LVMI (HR forth vs first quartile: 1.946; 95% CI 0.997 - 1,011; p = 0.128) or LAVI (HR forth vs. first quartile: 0.645; 95% CI 0,976 - 1,024; p = 0.311) lost their predictive power. RENOPROTECTIVE EFFECT OF PITAVASTATIN IN PATIENTS WITH CHRONIC KIDNEY DISEASE Introduction and Aims: Statins improve lipid metabolism disorder and then reduce cardiovascular complications in patients with chronic kidney disease (CKD). Recently, several studies have reported that stains slow renal progression in patients with early CKD. However, it is unclear whether statins have a renoprotective effect in all CKD patients, including those with advanced stage disease. This study aimed to evaluate the effect of pitavastatin on annual decline in estimated glomerular filtration rate (eGFR) in patients with CKD, including those with advanced stage disease. Methods: We conducted a multi-centre clinical trial to examine the renoprotective effect of pitavastatin on annual decline in eGFR in CKD patients, and 40 patients were recruited. We included CKD patients who met the following criteria: (1) continuation of statin (except pitavastatin) therapy for more than 1 year and follow-up data for 1 year after switching to pitavastatin and (2) eGFR <60 mL/min/1.73 m2 at initiation of pitavastatin therapy. The exclusion criteria were (1) initiation of haemodialysis during the observation period and (2) incorrect laboratory data on renal function and lipid metabolism. Annual decline in eGFR was calculated using linear regression based on the eGFR values during 1 year before and after initiation of pitavastatin therapy. Results: The concentration of low-density lipoprotein cholesterol did not change significantly between initiation of pitavastatin therapy and at 1 year after initiation of therapy (100.0 ± 27.2 and 101.5 ± 32.5, respectively; NS). The value of eGFR was 27.3 ± 16.0 mL/min/1.73 m2 at initiation of pitavastatin therapy and 26.8 ± 17.7 mL/min/1.73 m2 after 1 year of therapy. Annual decline in eGFR at 1 year before and after initiation of pitavastatin therapy was -1.9 ± 4.6 and -0.2 ± 5.2 mL/min/1.73 m2, respectively. Comparison of these values showed that annual decline in eGFR after pitavastatin initiation was significantly lesser than that before initiation ( p < 0.05). Furthermore, annual decline in eGFR, as derived using cystatin C level, at 1 year after Pitavastatin initiation was 0.3 ± 5.9 mL/min/1.73 m2, and there was no difference between annual decline in eGFR derived using serum creatinine level and the value derived using cystatin C level ( p=0.35; NS). During this study, there were no significant changes in body weight, blood pressure, or proteinuria. Conclusions: The renoprotective effect of pitavastatin is stronger than that of other statins, even in patients with advanced stage of CKD. CHRONIC KIDNEY DISEASE EVOLUTION IN HIV INFECTED PATIENTS, TWO YEARS OF FOLLOW UP Pedro Campos1, Clara Dias2, Joana Baptista1, Ana Luisa Papoila3, Alberto Ortiz4, Luis Inchaustegui1 and Karina Soto1,2 1Hospital Prof. Doutor Fernando Fonseca, Amadora, Portugal, 2Faculdade Ciencias Médicas - Universidade Nova de Lisboa, Lisboa, Portugal, 3Universidade Nova de Lisboa, Lisboa, Portugal, 4Fundacion Jimenez Dias, Madrid, Spain Introduction and Aims: In the last decades the life expectance in the HIV+ population has improved significantly and the prolongation of survival has been accompanied by long term exposure to traditional risk factors for chronic kidney disease (CKD). We aimed to determine the evolution of kidney function in HIV infected patients under stable antiretroviral therapy (ART), searching for the prevalence of CKD and its risk factors. Additionally, we studied the influence of Cystatin C as a marker of GFR on CKD diagnosis. Methods: As a part of a prospective study, a cross-sectional and retrospective analysis was performed in a cohort of 969 HIV+ patients. Enrollment was consecutive for outpatients that signed the informed consent. All clinical data were registered at admission and urinary and blood samples collected after 4 to 6 months of follow-up. Previous biochemistry data were collected from Outpatient of Infectious diseases Department Register. The primary endpoint was CKD (eGFR <60 ml/min). GFR was estimated using the CKD-EPI and MDRD equations based on creatinine (Cr) and CKD-EPI based on Cystatin C (CysC). McNemar test, Chi-squared test and a logistic regression model were used. Significance was set at α=0.05. Results: Among 969 patients (mean age 46 ±0.4); 55% were male; 44% African ancestry 92.2% HIV type1; 23.3% Hypertension; 7.1% Diabetic. Mean CD4 count 494 ±8.7cels/μL; Mean viral load 19534 ± 4958copies/mL At baseline, 71.8; 23.1; 4; 0.8 and 0.2% were in stage I, II, III, IV and V CKD respectively (KDOQI CKD classification, CKD-EPI equation). Thus, 5% had eGFR < 60 ml/min. At the end of the study, median CKD-EPI-Cr eGFR was 102 (IQ 87.7 - 113.2) and percent of CKD (GFR<60) were 3.9%, 4.4%; and 6.1% by CKD-EPI-Cr, MDRD and CKD-EPI-CysC respectively. Among patients with CKD-EPI-CysC <60 ml/min, 60.7% and 57.1% were classified as GFR>60 by MDRD and CKD-EPI-Cr respectively. CKD-EPI based on Cr and CysC showed 33.3% of CKD misdiagnosis ( p=0.052). An increase in eGFR (CKD-EPI-Cr) was observed in 428 (51.4%) patients and a decrease in 366 (44 %) ( p < 0.01). After 2 years 8.6% of patients worsened the CKD stage. Of them new 14 (1.4%) patients developed CKD (GFR<60) and 60 (7.2%) worsened from I to II CKD stage. Factors associated with progression of CKD include Hypertension OR = 2.42 (95%CI 1.28-4.60); African ancestry OR = 2.04 (95% CI 1.08-3.85), age [OR 1.04 (95% CI 1.02-1.07 and ART including lamivudine OR 2.83 (95% CI 1.47-5.46)]. [ao1]correct? Conclusions: The prevalence of CKD was low in this cohort, but still higher than in the general population of the same age. Overall renal function remained stable, but a subset of patients progressed. Modifiable factors associated with progression were hypertension and ART with lamivudine. CKD-EPI-CysC is a more sensitive CKD marker in this population. SPOT URINE ALBUMIN−TO−CREATININE RATIO EQUIVALENT TO PROTEIN−TO−CREATININE RATIO Kyoung Hyoub Moon1, Soohyun Yang1, Dong-Young Lee1, Hye Won Kim1 and Beom Kim1 1Veterans Health Service Medical Center, Seoul, Republic of Korea Introduction and Aims: Proteinuria is a cardinal sign of chronic kidney disease. The quantitative analysis by timed urine collection is the gold standard for detecting proteinuria. However, due to its cumbersome process, the spot urine protein corrected by urine creatinine is more frequently used. Recently, it is reported that albumin-to-creatinine ratio (ACR), rather than urine total protein-to-creatinine ratio (PCR), is more closely related with kidney disease prognosis, and KDIGO 2013 guideline recommended ACR rather than PCR. Therefore, we estimated ACR equivalent to PCR in outpatients. Methods: ACR and PCR were simultaneously measured in outpatients who visited our center. The predicted value of ACR for PCR was calculated using linear regression analysis. Results: Total of 3,873 tests (M: 94.1%) were performed in 3,685 patients. The mean age was 67.7 ± 6.2 years. Forty-one percent was diabetic, 79% was hypertensive patients. The estimated GFR was 74.0 ± 18.8 mL/min/1.73m2. Linear regression analysis revealed that ACR increased by 70.8 mg/g (95% CI: 70.2-71.3) as PCR increased by 100 mg/g (R2 = 0.95) (Figure). ACR equivalent to 500 mg/g was 323(95% CI: 317-330) mg/g. Conclusions: The ACR (mg/g) equivalent to PCR (mg/g) was estimated as -30 + 0.71 x PCR (mg/g). MEDICATION ADHERENCE TO PHOSPHATE BINDERS : THE CHEOBS STUDY Corinne Isnard Bagnis1, Abdallah Guerraoui2, Franck Zenasni3, Laetitia Idier4 and Philippe Chauveau5 1Groupe Hospitalier Pitie Salpetriere et Chaire de Recherche En Education Therapeutique, Paris, France, 2Calydial, Vienne, France, 3Institut de Psychologie, Boulogne- Billancourt, France, 4AURAD Aquitaine, Bordeaux, France, 5AURAD Aquitaine, Gradignan, France Introduction and Aims: Noncompliance (NC) is not always intentional. The medical team, in the absence of objective evidence, rarely takes into account the non-intentional NC linked to the difficulty of taking drugs regularly and feelings of the patient, unless objective evidence is present. Better understanding of the triggers and determinants of NC would allow elaboration of educational tools designed to help out chronic patients with their treatment. Methods: 340 hemodialysis patients in 9 centers in three areas in France were included on a voluntary basis in this descriptive study. Among them, 10 patients responded to a qualitative interview focused on individual beliefs, attitudes and motivations towards phosphate binders’ therapy. 26% of patients attended an educational program. Statistical methods consist of frequencies analysis and Exploratory Factor Analysis to determine combination of factors which significantly influence the compliance to phosphate binders. The semi-structured interviews were analyzed according to qualitative content analysis. Results: 329 self-administered questionnaires (50 items) were analyzed, 297 were complete for analysis (mean age 61 years, 62% male, dialysis duration 4.5 years, number of medication 9 per day). The majority of patients considers treatment as important (80%). However, they mostly relativizes the treatment as vital (45%). Factor analysis helped to identify two kind of independent behaviors: those which indicate concerns for the treatment and those relative to the use of the treatment as a necessity. Age, level of education and gender influence these two factors. Older patients are more compliant. The higher the level of education the more frequently patients adapt the treatment. The swallowable tablets are preferred (75%). The shape and color has little influence on decision. 60% of the patients consider they received enough pre therapeutic information. The involvement into educational formation has a not high enough influence on adherence. Conclusions: In conclusion, this large study provides clues to better understanding of non compliance to phosphate binders determinants. Based on these assumptions, educational program should be more efficient and fruitful to chronic dialyzed patients. This work was funded by an unconditional grant from Sanofi. ENDOTHELIAL FUNCTION ASSESSED BY PERIPHERAL ARTERIAL TONOMETRY IS NOT RELATED WITH FGF-23 SERUM LEVELS IN PREDIALYSIS CKD PATIENTS Ana Cerqueira1,2,3, Janete Quelhas-Santos4,5 and Manuel Pestana1,2,3 Introduction and Aims: Cardiovascular (CV) diseases are the leading causes of morbidity and mortality in patients with chronic kidney disease (CKD) that encompass the mildest degrees of renal impairment. Endothelial dysfunction (ED) represents the earliest abnormality in the development of vascular disease linked to CV diseases. Fibroblast growth factor 23 (FGF-23), a recently described regulator of phosphate metabolism increase early in CKD patients was associated with increased CV events in this population. In this study we aimed to examine the relationship between FGF-23 serum levels and endothelial function in a pre-dialysis CKD patient population. Methods: We examined 43 CKD patients followed-up in our outpatient clinic. The patients were distributed according to the GFR calculated by CKD-EPI formula (CKD stages 1-2 [n=16, M37%, age 48.6±3.2], CKD stage 3 [n=14, M33%, age 58.0±4.1], CKD stages 4-5 [n=13, M33%, age 59.8±4.0]. Renal function, blood pressure, proteinuria, phosphate serum levels and a validated comorbidity index (Charlson Index) were evaluated in the studied patients. Intact FGF-23 levels were assessed by ELISA (Immutopics, Inc.). Endothelial function was assessed by peripheral arterial tonometry (Endo-Pat 2000) where lower reactive hyperaemia index (RHI) values correspond to greater ED. Results: RHI was significantly lower in CKD patients included in stages 4-5 in comparison with CKD patients included in stages 1-2 (1.60±0.18 vs 2.22±0.16, p<0.05), and this was accompanied by a positive relationship in the studied population between CKD-EPI and RHI (r=0.35; p<0.04). On the other hand, a negative relationship was observed between CKD-EPI and FGF-23 serum levels (r=-0.42; p<0.05). RHI negatively correlated with age (=-0.59; p<0.0001), proteinuria (=-0.50; p<0.03), phosphate serum levels (=-0.34; p<0.04) and Charlson index (=-0.56; p<0.0003). By contrast, no significant relationship was observed between RHI and FGF-23 serum levels (r=-0.11, n.s.). Conclusions: In summary, our results provide evidence favoring the view that peripheral arterial tonometry, a non-invasived method for evaluation of endothelial function, can provide clinically important information to identify vulnerable patients, and stratify cardiovascular risk in CKD population. Our results also agree with the view that serum phosphate and FGF-23 levels promote vascular disease through distinct mechanisms. EXPRESSION OF CALPONIN IN THE GLOMERULAR PARIETAL EPITHELIAL CELLS OF CHRONIC NEPHROPATHY IS RELATED TO THE DEVELOPMENT OF GLOMERULOSCLEROSIS: 3-DIMENSIONAL STUDY Jae-Youn Choi1, Dong-Chan Jin2, Yeong-Jin Choi1, Wan-Young Kim1, Sun-Ah Nam1 and Jung-Ho Cha1 1College of Medicine, the Catholic University of Korea, Seoul, Republic of Korea, 2College of Medicine, the Catholic University of Korea, Seoul, Republic of Korea Introduction and Aims: Progressive glomerulosclerosis lead to a common histological and functional end point referred to as end-stage renal disease. We previously have reported that periglomerular calponin expression in two chronic nephropathy rat models, puromycin aminonucleoside nephropathy and subtotal nephrectomy. In present study, to investigate the role of calponin in the glomerulosclerosis, we carried out 3-dimensional analysis of expression pattern of calponin and structural changes of calponin-positive periglomerular cells in chronic nephropathy rat model using serial semithin sections. Methods: Male Sprague-Dawley rats were used, and nephropathy models were established at 8 and 12 weeks after single intraperitoneal injection of adriamycin (5mg/ kg bw; N=5). Preembedding-immunohistochemistry was performed to 50-um vibratome renal sections using monoclonal calponin antibody. After flat epon-embedding, serial semithin sections were prepared for another immunohistochemistry and 3-dimensional analysis. Results: In nephropathy models, 16.3% (8 weeks) ~ 22.7% (12 weeks) glomeruli were shown calponin-positive at periglomerular area. All the glomeruli with periglomerular calponin-immunoreactivity were under sclerotic changes. At periglomerular area, only both the glomerular parietal epithelial cells (GPEC) and myofibroblasts were demonstrated as calponin-positive. However, in the glomeruli with weak periglomerular calponin-positive, immunoreactivity was mostly detected only in GPEC not in myofibroblasts, suggesting that calponin may be expressed in GPEC earlier than in myofibroblasts in the glomerulosclerotic change. 3-dimensional analysis demonstrated that some calponin-positive GPEC invaded glomerular tuft with loop-shaped projection. In the glomerular tuft around this projection, nestin expression which is strong in normal state was much reduced. Conclusions: These results suggested that calponin-positive GPEC and periglomerular myofibroblasts may play a key role in the development of glomerulosclerosis, and direct contact with GPEC and glomerular tuft may be more important to degenerative changes of glomeruli. SEMAPHORIN 3A IS A NEW BIOMARKER OF CHRONIC KIDNEY DISEASE Introduction and Aims: Semaphorin 3A is a secreted protein involved in vascular morphogenesis, axon guidance, immune responses and tumour progression. Its expression has been demonstrated in the developing nephron and mature podocytes and collecting tubules in mice as well as in renal biopsies from lupus iii | Abstracts glomerulonephritis patients. As recently observed, semaphorin 3A may represent an early, predictive biomarker of acute kidney injury both in paediatric and in adult intensive care patients. The aim of the present study has been to evaluate the serum levels of semaphorin 3A in CKD (chronic kidney disease) and haemodialysis patients and the potential correlation with renal function. Methods: We recruited 16 CKD patients not on haemodialysis (5 men, 11 women; mean age 58 ± 15 years) and 18 patients (14 men, 4 women; mean age 63 ± 12 years) receiving haemodialytic treatment three times a week in 4-hour sessions with AFB (Acetate-Free Biofiltration) technique using the Integra® machine (Gambro). Moreover, we enrolled 8 healthy subjects as controls. Peripheral venous blood was taken from haemodialysis patients at different time intervals: start of dialysis, middle and end of dialysis. We also collected samples of dialysate by the monitoring system known as Quantiscan, in order to determine whether Semaphorin 3A was removed during the haemodialysis session. To minimize circadian variation in CKD patients and in the control group, all blood samples were taken at the same time of the day corresponding to pre-dialysis time in haemodialysis patients. Biochemical parameters were measured according to the standard methods of the routine clinical laboratory. Semaphorin 3A was assessed using an enzyme-linked immunosorbent assay kit (Catalogue no. MBS732622; My Biosource®, CA, USA) according to the manufacturer's instructions. Results: The difference in serum levels of Semaphorin 3A between healthy subjects and CKD patients was statistically significant (92 ng/ml [95% CI: 21-163] versus 30 ng/ml [95% CI: 3-64], p = 0.05) while no significant differences have been observed between CKD and haemodialysis patients ( p = 0.62). Semaphorin 3A is removed throughout a haemodialysis session (40 ng/ml [95% CI: 15-65] versus 9 ng/ml [95% CI 0-20], p = 0.0185), especially during the first half of the treatment (P = 0.05). In support of this statement, semaphorin 3A has been also found in the dialysate. In CKD patients, semaphorin 3A serum levels were correlated with creatinine (r = 0.61, p = 0.01), blood urea nitrogen (r = 0.72, p = 0.005) and presence of diabetes mellitus (r = -0.65, p = 0.02). Conclusions: Our data suggest that semaphorin 3A is a new biomarker of renal impairment, not only for acute kidney injury but also for CKD. Moreover, it is significantly removed during a haemodialysis session with AFB technique, but whether this may have clinical consequences is still unknown. S-ADENOSYLHOMOCYSTEINE IN CKD ASSOCIATED CARDIOVASCULAR DIESASE Introduction and Aims: Although homocysteine has been discussed as a cardiovascular risk factor in patients with chronic kidney disease (CKD), interventional studies in which homocysteine was lowered via B vitamin supplementation failed to demonstrate a survival benefit. Recently, it has been suggested that the homocysteine metabolite S-Adenosylhomocysteine (SAH), which is a potent inhibitor methylation reactions and thus a central epigenetic regulator, may be the real culprit in cardiovascular disease and thus explain the hitherto paradoxical findings. Against this background we now aimed to analyze (1) to which degree SAH accumulates in CKD and (2) whether SAH, compared to homocysteine, is associated more strongly with prevalent cardiovascular disease. Methods: : Plasma homocysteine and SAH concentrations were assessed among 297 CARE FOR HOMe participants suffering from CKD (K/DOQI stages G1 - G5). SAH was analysed using a Waters 2795 alliance HT, coupled to a Quattro micro API tandem mass spectrometer. Homocysteine was assessed by using a fluorescence polarization immunoassay on the Abbott AxSym system. Kidney function was determined as estimated glomerular filtration rate (eGFR), using the MDRD equation. Results: Among the 297 CKD patients, mean eGFR was 44 ± 19 ml/min/1.73 m², and mean plasma SAH and homocysteine were 50.1 ± 30.1 μmol/l and 18.4 ± 7.2 nmol/l, respectively. 32 % patients had prevalent cardiovascular disease at baseline. eGFR correlated more strongly with plasma SAH (r = 0.497) than with plasma homocysteine (r = 0.424). Patients with prevalent cardiovascular disease had higher plasma SAH than patients without prevalent cardiovascular disease ( p = 0.007). Nevertheless, plasma SAH did not independently predict prevalent cardiovascular disease in logistic regression analysis. Conclusions: In CKD, plasma SAH accumulates to a higher degree than plasma homocysteine. Follow-up of study participants will reveal whether SAH independently predicts future cardiovascular events. Moreover, further studies are needed to examine if an increase of plasma SAH represents a novel non-traditional cardiovascular risk factor and to identify strategies to lower SAH, after B vitamins failed to reduce SAH levels. URINARY MONOCYTE CHEMOTACTIC PROTEIN-1 IS ASSOCIATED WITH URINARY OXIDATIVE STRESS, MICROALBUMINURIA AND THE BACTERIOLOGICAL INDEX IN LEPROSY Gdayllon C. Meneses1, Geraldo Silva Junior2,1, Marcus Felipe B. Costa1, Heitor S. Gonçalves3, Elizabeth F. Daher1, Alexandre B. Libório1 and Alice M.C. Martins1 1Federal University of Ceara, Fortaleza, Brazil, 2University of Fortaleza, Fortaleza, Brazil, 3Centro de Dermatologia Dona Libania, Fortaleza, Brazil Introduction and Aims: Renal lesions in leprosy have been extensively described in medical literature. Leprosy patients can present with kidney disease from glomerular (glomerulonephritis, amyloidosis) or tubule-intertitial etiology. The aim of this study is to evaluate renal abnormalities in leprosy patients through traditional biomarkers of renal disease and Monocyte Chemotactic Protein-1 (MCP-1). Methods: This is a cross-sectional study with 44 patients with clinical and laboratory diagnosis of leprosy and with no previous anti-mycobacterium treatment and reaction episode. Patients were recruited in public health centers in Fortaleza, Ceara, Brazil, between August 2012 and August 2013. A group of 15 healthy subjects were included as a control group. Glomerular filtration rate (GFR), protein excretion, microalbuminuria and urinary oxidative stress (malondialdehyde-MDA) were estimated. Urinary MCP-1 was determined by sandwich enzyme-linked immunosorbent assay. All urine measurements were normalized by urinary creatinine concentration. Results: Patients’ average age was 36±10 years, and 61% were male. Age and gender were similar between leprosy patients and control group. Time from symptoms to leprosy diagnosis varied from one month to 8 years, with a median time of 17 months. Twenty-six patients had skin smear-positive test (59.1%) and 18 were negative (40,1%). Clinically, there were 14 (31.8%) tuberculoid polar form (TT/BT), 19 (43.2%) borderline (BB) and 11 (25%) lepromatous polar form (LL/BL). Regarding renal function, no patient had chronic kidney disease. Leprosy patients had a higher urine protein excretion (97.6±69.2 vs. 6.5±4.3mg/g-Cr, p<0.001), urinary MDA (1.77±1.31 vs. 1.27±0.66mmol/ g-Cr, p=0.0372) and urinary MCP-1 (101±79.8 vs. 34.5±14.9mg/g-Cr, p=0.006) than healthy controls. Urinary MCP-1 was higher in multibacillary than in paucibacillary patients (122.1±91.9 vs. 72±46.1mg/g-Cr, p=0.023) and there was a positive correlation between urinary MCP-1 and bacteriological index in skin smear (r=0.104, p=0.035), urinary MCP-1 and albumin excretion rate (r=0.171, p=0.006) and urinary MCP-1 and urinary MDA (r=0.205, p=0.002). Conclusions: We demonstrated that leprosy patients with no clinical kidney disease have increased urinary MCP-1 and its levels are even higher as patients approximates to lepromatous polar form. Moreover, urinary MCP-1 was associated with urinary oxidative stress and urine albumin excretion, suggesting that these patients are at increased risk of developing clinical kidney disease in the future. ALBUMINURIA DURING AND AFTER PARICALCITOL TREATMENT IN CHRONIC KIDNEY DISEASE PATIENTS Robert Ekart1, Nina Hojs1, Sebastjan Bevc1 and Radovan Hojs1 1University Clinical Centre Maribor, Maribor, Slovenia Introduction and Aims: Albuminuria is associated with chronic kidney disease (CKD) progression, cardiovascular disease and death. Reduction of albuminuria is one of the goals in the management of CKD patients. Therefore the aim of our study was to evaluate the effect of paricalcitol treatment on albuminuria in non-dialysis CKD patients. Methods: Non-dialysis CKD patients with secondary hyperparathyroidism and albuminuria were included in our study. All patients were examined at the beginning of our study, after 6 months of paricalcitol treatment (1 μg/day), 3 and 6 months after drug withdrawal. Three patients stopped treatment after 3 months because of low parathyroid hormone. We measured urine albumin/creatinine ratio (UACR), 24-hour albuminuria (24hA) and cystatin C. 24-hour ambulatory blood pressure monitoring was done at the beginning, after 6 months of treatment and 6 months after drug withdrawal. 24-hour mean ambulatory blood pressure (MAP) was used for statistical analysis. Fixed doses of angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers and/or statins were kept for 3 months before and during the study. None of the patients received a vitamin D analogue at least 1 month before the beginning of the study. Results: Forty-two non-dialysis CKD patients (29 men, 13 women), aged 62.3±11.9 years (range 31-84 years), all of white race, were included in our study. To get an approximately normal distribution, laboratory data for albuminuria were log transformed. Paricalcitol treatment significantly reduced UACR ( p=0.001) and 24hA ( p=0.001). Three months after drug withdrawal only UACR ( p=0.023) significantly increased, while 6 months after drug withdrawal UACR ( p=0.014) and 24hA ( p=0.032) significantly increased compared to albuminuria at the end of paricalcitol treatment. Paricalcitol treatment ( p=0.443) and withdrawal ( p=0.239) did not affect MAP. Cystatin C significantly increased during treatment ( p=0.001), but 3 ( p=0.312) and 6 ( p=0.311) months after drug withdrawal it stayed stable. Conclusions: Paricalcitol treatment (1 μg/day) in non-dialysis CKD patients significantly reduced albuminuria (UACR, 24hA). Six months after drug withdrawal UACR and 24hA increased. Paricalcitol treatment did not affect MAP. Cystatin C significantly increased during treatment, after drug withdrawal it stayed stable. EFFECTS OF LOW SODIUM INTAKE ON THE ANTIPROTEINURIC EFFICACY OF OLMESARTAN IN HYPERTENSIVE PATIENTS WITH ALBUMINURIA (ESPECIAL): A RANDOMIZED CLINICAL TRIAL Chun Soo Lim1, Jin Ho Hwang1, Ho Jun Chin2, Sejoong Kim2, Dong Ki Kim3, Suhnggwon Kim3, Jung Hwan Park4, Sung Joon Shin5, Sang Ho Lee6 and Bum Soon Choi7 1Seoul National University Boramae Medical Center, Seoul, Republic of Korea, 2Seoul National University Bundang Hospital, Seong-Nam, Republic of Korea, 3Seoul National University Hospital, Seoul, Republic of Korea, 4Konkuk University School of Medicine, Seoul, Republic of Korea, 5Dongguk University Ilsan Hospital, Goyang, Republic of Korea, 6Kyung Hee University Medical Center, Seoul, Republic of Korea, 7Seoul St Mary’s Hospital, Seoul, Republic of Korea Introduction and Aims: Several studies revealed an additive effect of dietary salt restriction with renin-angiotensin-aldosterone system blockade on blood pressure and proteinuria. Most of these studies include a small number of patients or the methods for implementing low-salt or high-salt diets used are not suitable for application in clinical practice. We tried to determine the proteinuria-lowering effects of intensive low-salt diet education on urine protein excretion and blood pressure in nondiabetic hypertensive patients with albuminuria who are already taking renin-angiotensin-aldosterone system blocker. Methods: This study is a multicenter, open-label, randomized, controlled trial conducted between March 2012 and March 2013 in 7 Korean hospitals. Outpatients with age of 19-75 years, the use of antihypertensive medication or a diagnosis of hypertension, Modification of Diet in Renal Disease estimated glomerular filtration rate≥30mL/min/1.73 m2, and random urine albumin/creatinine ratio≥30mg/gCr more than twice with ≥1-week interval in the last 6 months. After a run-in period of 8 weeks, all patients received the angiotensin-II receptor blocker olmesartan for 8 weeks, 40mg daily. Patients were then divided into two groups. One group was treated for another 8 weeks with olmesartan plus conventional low-salt diet education, and the other group was treated for 8 weeks with olmesartan plus a weekly 30-minute phone call with intensive education. A total of 269 adult participants were enrolled, and we performed the final analyses with 235 participants who completed the study. Results: Patients who completed intensive education exhibited greater decreases in urinary albumin excretion than the control group (Δalbuminuria, 154.4mg/day vs. 2.6mg/day; P=.02, from week 8 to week 16). The amount of albuminuria was significantly decreased with 8 weeks of olmesartan treatment (930.0±969.2mg/day vs. 515.7±685.5mg/day; P<.001, from week 0 to week 8). Twenty-four-hour urinary sodium excretion from week 8 to week 16 was decreased by 34.8mEq/day in the intensive education group and 9mEq/day in the conventional education group. Urinary albumin excretion tended to decrease as the 24-hour urinary sodium excretion amount decreased. Conclusions: The reduction in salt intake induced by intensive low-salt diet education effectively reduced urine albumin excretion in olmesartan-treated non-diabetic patients with hypertension. Weekly intensive education for low-salt diet would be a suitable method for clinical practice. CYSTATINE C BASED EQUATION DOES NOT OUTPERFORM CREATININE BASE FORMULAS IN OBESE CKD PATIENTS Sandrine Lemoine1, Marine Panaye2, Laurent Juillard2, Laurence Dubourg2, Aoumeur Hadj-Aïssa2 and Fitsum Guebre-Egziabher2 1Hôpital Edouard Herriot, Hospices Civils de Lyon, Lyon, France, 2Hospices Civils de Lyon - Hôpital Edouard Herriot, Lyon, France Introduction and Aims: Recent findings suggest that cystatin C is independently associated with obesity, body mass index and waist circumference. Hence, cystatin C based equation could overestimate the chronic kidney disease (CKD) prevalence for overweight and obese patients. The objective of this study was to evaluate the accuracy of cystatin C based equation for glomerular filtration rate (GFR) estimation. Methods: This prospective study included 108 patients with BMI > 25 kg/m2 referred to the department of renal function study in Lyon between January 2013 and October 2013 for measurement of gold standard clearance by inulin or iohexol (mGFR) without BSA indexation for suspected or established renal dysfunction. All patients underwent cystatin C measurement. GFR was also estimated by equations derived from creatinine (eGFRCKD-EPI) or cystatin (eGFRcyst) or both (eGFRcyst-creat). The mean Bias (mGFR - eGFR) and accuracy within 30% were calculated for the three equations. Results: Mean age was 56 ± 1.5 years and BMI was 32 kg/m2. Among this cohort, 56% of patients had a GFR < 60 mL/min/1.73m2. The mGFR was 64 ± 3 mL/min, eGFRCKD-EPI was 60 ± 3.1, eGFRcyst 62 ± 3.6 and eGFRcyst-creat 63 ± 3.6 mL/min/ 1.73m2. The bias between mGFR and eGFRCKD-EPI, eGFRcyst or eGFRcyst-creat are not different (2.8 ± 1.6, 1.43±2 and 3.12 ± 1.6 mL/min/1.73m2, p= 0.5 and p=0.8 vs eGFRCKD-EPI respectively); The accuracy 30% was 87%, 75% and 90 % for eGFRCKD-EPI, eGFRcyst and eGFRcyst-creat respectively. In the subgroup of patients with a GFR < 60 mL/min/1.73m2, we found no difference with the bias between mGFR, eGFRCKD-EPI, eGFRcyst and eGFRcyst-creat. Conclusions: eGFRcyst and eGFRcyst-creat could be used as an accurate estimation of GFR in obese and overweight subjects, but do not outperform eGFRCKD-EPI. PROTEINURIA IN ADULTS WITH SICKLE CELL DISEASE: THE ROLE OF HYDROXYUREA AS A PROTECTIVE AGENT Introduction and Aims: Renal abnormalities are one of the main complications of sickle cell disease (SCD). The aim of this study is to investigate the role of hydroxyurea as a protective factor in sickle cell nephropathy. Methods: This is a prospective study with 26 SCD patients. Renal function evaluation was performed and a comparison between patients and control group was done. iii | Abstracts Patients using hydroxyurea were compared to those not taking this drug. Results: Patients mean age was 32.1±9.9 years, and 16 (61%) were males. Glomerular hyperfiltration was found in 9 patients with SCD (34.6%). GFR300mg/day) in 1 patient (3.8%). All patients presented urinary concentrating deficit, and inability to acidify urine was found in 10 cases (38.4%). The comparison of patients according to the use of hydroxyurea showed lower levels of serum creatinine in those using the drug (0.6 ±0.1 vs. 0.8±0.3mg/dL, p=0.03), as well as lower levels of 24h-proteinuria (226±16 vs. 414±76mg/dL, p=0.0001), but not microalbuminuria (79±15 vs. 55±86mg/dL, p=0.35). Conclusions: SCD is associated with important renal abnormalities. Hydroxyurea seems to protect kidney function in SCD by decreasing proteinuria. Further studies are required to better establish the mechanisms through which hydroxyurea protects kidney function in SCD. ASSOCIATION BETWEEN ANNUAL ESTIMATED GFR DECLINE AND NEPHROLOGIST REFERRAL IN ADVANCED CKD AND DM PATIENTS Kiyonori Ito1, Susumu Ookawara1, Haruhisa Miyazawa1, Yuichiro Ueda1, Yoshio Kaku1, Keiji Hirai1, Taro Hoshino1, Honami Mori1, Izumi Yoshida1 and Kaoru Tabei1 1Saitama Medical Center, Jichi Medical University, Saitama, Japan Introduction and Aims: Patients with chronic kidney disease (CKD) and diabetes mellitus (DM) have the potential of proceeding CKD and reaching dialysis. Furthermore, there are not many reports about a change of estimated glomerular filtration rate (eGFR) decline before and after nephrologist referral. In this study, we aimed to clarify the effect on renal function in patients referred to nephrologist. Methods: We intended consecutive incident dialysis patients at our single center in Japan from January 2005 to December 2012. A total of 729 dialysis patients (426 males and 283 females, mean age at the initiation of dialysis 66.0± 12.7 years) was recruited, and we analyzed an annual eGFR declines before and after nephrologist referral in each patient, and nephrologist referral timing retrospectively in the extracted group of all patients. Referral timing was classified as: late (<3 months), early (3-12 months) or very early (≥12 months). Results: 24% of all dialysis patients were late referred, 22% early and 56% very early. 43% had DM, and 89% of DM patients were eGFR <30 ml/min/1.73m2 in referral. Early and very early referrals suppressed the annual eGFR decline after nephrologist than before. Furthermore, annual eGFR declines of DM patients were suppressed by nephrologist referral (before vs after (ml/min/year), stage G4; -17.9 vs -8.4, p<0.001, stage G5; -15.1 vs -6.6, p<0.001). Conclusions: Early and very early referral to nephrologist is the potential to suppress annual eGFR decline even in advanced CKD stage and DM patients. IS RENAL RESISTIVE INDEX RELATED TO GENDER IN CKD PATIENTS? Gabriel Stefan1, Cristina Capusa1,2, Simona Stancu1,2, Diana Margarit1, Ligia Petrescu1,2, Elena D Nedelcu3 and Gabriel Mircescu1,2 1“Dr Carol Davila” Teaching Hospital of Nephrology, Bucharest, Romania, 2“Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania, 3Ponderas Hospital, Bucharest, Romania Introduction and Aims: Since high renal resistive index (RRI) correlates with atherosclerotic organ damage and the prevalence of cardiovascular (CV) disease varies according to age and gender (higher in men prior to the fifth decade of age, balanced in the sixth decade, and greater in women thereafter), we aimed to analyze the RRI gender differences in chronic kidney disease (CKD) patients. Methods: Seventy-eight stable, non-dialysis CKD patients over 50 years old, with known history of systemic atherosclerosis (50% male, median age 70 [65-73] years, and eGFR 33.9 [30.4-37.3] ml/min) were prospectively enrolled over a 8 months period in this cross-sectional, single-center study. Subjects with obstructive nephropathy and valvular heart disease were excluded. Doppler sonography was performed for the RRI measurements. Medical history for traditional CV risk factors (age, smoking, arterial hypertension, diabetes mellitus, obesity) and primary kidney disease was obtained. Markers of atherosclerosis (carotid intima-media thickness - IMT by ultrasound, abdominal aortic calcification score - ACS according to Kaupilla on X-ray and ankle-brachial index - ABI by the waveform device VaSera), arterial stiffness (cardio-ankle vascular index - CAVI, VaSera), and biochemical parameters (lipid profile, serum calcium, phosphate, albumin and C-reactive protein - CRP) were also assessed. The patients were gouped and compared according to their gender. Multiple regression analysis was used to investigate the relationship between RRI and CV risk factors. Results: Primary kidney disease was not associated with either female or male group ( p=0.2). No differences in regard of age and eGFR were observed between women and men (70 [66-75] vs. 67 [62-73] years, p=0.1 and 34.5 [29.2-39.9] vs. 33.2 [28.7-37.7], p=0.7, respectively) The female group had higher total serum cholesterol (189 [167-214] vs. 171 [153-183], p=0.02) and HDL-cholesterol (59.1 [49.9-64.3] vs. 49.1 [45.9-54.4], p=0.02), but lower CRP (3 [2-6] vs. 7 [3-19], p=0.008). All the other investigated traditional CV risk factors and biochemical parameters were similar between the studied groups. Among the atherosclerosis and arterial stiffness markers, only the ACS was increased in women (7 [2-10] vs. 3 [0-7], p=0.03). In this group, higher RRI values were also found (0.69 [0.66-0.73] vs. 0.63 [0.56-0.67], p=0.003). The relationship between RRI and CV risk factors was further investigated by multiple regression analysis. Only gender seemed to influence significantly and independently the RRI (F=5.22, p=0.02). No relationships with age, smoking, body mass index, atherosclerotic indices (IMT, CAVI, ACS), lipid profile, CRP were found. Conclusions: With the reserve of small cohort, single center, and cross-sectional design - our study shows that women have higher RRI and ACS than men, despite a lower inflammatory status and an elevated HDL-cholesterol. EVALUATION OF CHOSEN RISK FACTORS OF THE CARDIOVASCULAR SYSTEM IN DIFFERENT STAGES OF CHRONIC KIDNEY DISEASE Anna Szarejko-Paradowska1 and Jacek Rysz1 1Medical University of Lodz, Lodz, Poland Introduction and Aims: Chronic kidney disease becomes more and more important epidemiological, social and health problem worldwide. Disturbed renal function was observed in 16% of patients in the epidemiological PolNef 2004 survey conducted in Poland in 2004 which gives about 4.5 million of persons. It is estimated that the number of persons with chronic kidney disease will grow significantly every year. Extending life expectancy, growing CKD morbidity due to diabetes and arterial hypertension and too late recognition of early stages of chronic kidney disease and its risk factors are the most important reasons of such situation. Cardiovascular disorders is the main cause of deaths amongst patients with chronic kidney disease. Mortality in this group of patients is about 10-20 times higher than that in general population. The greatest risk of death from diseases of the cardiovascular system occurs in young people and it decreases with age. In 30-year-olds diagnosed with chronic kidney disease the risk is comparable to that seen in 70-year-olds without CKD and it is 100 times higher than in their peers without kidney disease. So far, no glomerular filtration rate (GFR) at which linear relationship with cardiovascular risk occurs has been clearly established. Increased risk of atherosclerosis in these patients results from the overlapping of so-called traditional (characteristic of the general population) and non-traditional (characteristic of this disease) risk factors for cardiovascular disease. The aim of this study was to evaluate the prevalence of selected cardiovascular risk factors, such as age, sex, lipid disorders, hypertension, obesity, smoking, disorders of calcium and phosphate metabolism, anemia, inflammation in various stages of chronic kidney disease. Methods: The study included 60 patients with chronic kidney disease in the predialysis stages hospitalized in the Department of Nephrology, Hypertension and Family Medicine, WAM University Hospital in Lodz. Chronic kidney disease stadium was determined on the basis of estimated (eGFR) calculated on the basis of abbreviated MDRD formula. The study analyzed data obtained in an patients, interview concerning the previous occurrence and treatment of hypertension, smoking and the duration of chronic kidney disease. Blood pressure measurement and anthropometric analyses evaluating height and weight were performed for each patient. Laboratory tests determining the concentration of hemoglobin, creatinine, total cholesterol, HDL cholesterol, LDL cholesterol, triglyceride, CRP, serum total calcium, inorganic phosphorus, parathyroid hormone were also made. In addition, all patients underwent ultrasound assessment of carotid intima - media thickness (IMT) and cardiac CT scan to evaluate indicator of coronary artery calcification score (CACS). Results: 1 Age, co-occurrence of hypertension and the decline of glomerular filtration rate affect the growth of the intima - media thickness (IMT) in patients with chronic kidney disease. 2 Age, exposure to tobacco smoke is associate with the increase in calcification score (CACS) in patients with chronic kidney disease. 3 Thickening of the intima - media thickness (IMT) influence the increase in calcification score in the patients with chronic kidney disease. Conclusions: The measurement of the intima - media thickness (IMT) can be a valuable non-invasive method for the assessment of early atherosclerotic lesions, which allows to point a group of subjects particularly susceptible to cardiovascular system complications. GLYCOSURIA AND RENAL OUTCOME IN NON-DIABETIC CHRONIC KIDNEY DISEASE STAGE 3-5 PATIENTS WITH PROTEINURIA Chi-Chih Hung1 and Hung-Chun Chen1 1Kaohsiung Medical University Hospital, Kaohsiung, Taiwan Introduction and Aims: Detection of glucose in urine (glycosuria) in non-diabetic patients is a sign of impaired renal tubular reabsorption. Glycosuria may be more frequent in chronic kidney disease (CKD). Whether glycosuria is associated with worse renal outcome is not known. In contrast, impaired renal tubular reabsorption could prevent renal tubules from the protein overload of the glomerular filtrates. It is possible that glycosuria is associated with less renal damage by proteinuria. We would thus study glycosuria and its association with renal outcome in non-diabetic CKD patients with proteinuria. Methods: We recruited 988 non-diabetic CKD stage 3 to 5 patients with proteinuria between 2002 and 2009. Glycosuria was defined as more than one measurements of urine glucose +~++++ by dipstick during the follow-up period and at least once in the first three tests. Serum glucose, glycated hemoglobin and chart review were applied to exclude diabetes. Results: The mean age was 60.9 years, estimated glomerular filtration rate (eGFR) was 19.1 mL/min per 1.73 m2 and urine protein-to-creatinine ratio was 1962 mg/g. Percentage of glycosuria was 2.4%, 12.8% and 46.9% in non-diabetic CKD stage 3, 4 and 5, respectively. It was also higher in those with heavy proteinuria. In multivariate logistic regression, glycosuria was associated with eGFR, proteinuria, hemoglobin, albumin, and phosphorus. In survival analysis, glycosuria was associated with a decreased risk for end-stage renal disease (ESRD) (hazard ratio= 0.79; CI=0.63-0.98; p=0.034) and for rapid renal function progression (odds ratio= 0.64; CI=0.43-0.95; p=0.027); but glycosuria was not associated mortality or cardiovascular event. Conclusions: Glycosuria was associated better renal outcome in non-diabetic CKD stage 3-5 patients with proteinuria. This may indicate that impaired renal tubular reabsorption of filtered protein is associated with less renal function progression. NEPHROLITHIASIS AND URINARY TRACT INFECTIONS INCREASE THE PROGRESION OF THE RENAL FAILURE IN AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE Vesna Ristovska1 and Ladislava Grcevska2 1University Clinic of Nephrology, University Sts Cyril and Methodius, Skopje, Republic of Macedonia, 2Univeristy Clinic of Nephrology, University STS Cyril and Methodius, Skopje, Republic of Macedonia Introduction and Aims: The prevalence of nephrolithiasis is considerably greater in patients with autosomal dominant polycystic kidney disease, than in general population. The anatomic factors because of increased intrarenal obstruction, such as cyst growth, renal tubular stasis and methabolic disorders, are important and may predisposed to stone formation. Methods: In order to evaluate the nephrolithiasis in polycystic kidneys, 60 patients with autosomal dominant polycystic kidney disease, mean age 42.6+/- 12.8 years, underwent echosonography and computed tomography scan. Routine blood analysis and urine samples, including 24 h urine collections were done. Patients were also evaluated from the aspect of urinary tract infection. Criteria for presence of urinary tract infection were: more than 10 leucocytes in the urine sediment and positive urine culture. The follow-up included urine analysis every 6 months, during the period of 3 years. Results: Renal stones were detected in 22 out of 60 patients (36,6%). The morphologic data presented that patients with autosomal dominant polycystic kideny disease and nephrolithiasis had more renal cysts and larger predominant cyst size than patients without nephrolithiasis ( p<0,05). Renal function expressed by creatinin clearance was also different between the 2 groups of patients (72,6+/-9,4 in patients with nephrolithiasis, and 93,7+/-8,6 in patients without nephrolithiasis). Twenty-four hours urine analysis showed that patients with nephrolithiasis had significantly lower urine volumes and levels of uric acid. Presence of urinary tract infections in patients with adult polycystic kidney disease, can influence the progression of the disease. Kaplan-Meier's statistical analysis demonstrated that the progression of the renal disease, depends on the presence of the infections in these patients. Comparising the 2 groups of patients (with and without infections), we found that patients with infections had worse renal survival ( p<0.05). Conclusions: The authors consider that nephrolithiasis is important factor for the progression of the renal demage in patients with autosomal dominant polycystic kidney disease, because of complications that may accelerate the progression of the renal disease and the chronic renal failure. Together with the urinary tract infections increases the possibility of renal failiure IMPROVEMENT OF ERDHEIM−CHESTER DISEASE −RELATED RENAL FAILURE FOLLOWING TREATMENT WITH ANAKINRA Introduction and Aims: Erdheim Chester disease (ECD) is a rare non-Langherans cell histiocytosis characterized by massive infiltrates of lipid-laden CD68+/CD1ahistiocytes, affecting heart, lungs, central nervous system and bones. About 30% of patients with ECD have renal failure, often caused by vascular, ureteral or kidney infiltrates. Due to the large pleomorphism of ECD, the diagnosis is challenging, and the treatment is generally based on administration of Interferon-alpha (IFNα). Preliminary results have also showed the therapeutic efficacy of Anakinra, an antagonist of the receptor of interleukin 1 (IL-1Ra). Results: A 76-year old man was admitted to our unit for hypertension and renal function deterioration. His medical history was remarkable for chronic kidney disease with a baseline creatinine of 1.6 mg/dL. Physical examination was unremarkable. Laboratory investigations showed: creatinine 2.6 mg/dL, phosphate 5.2 mg/dL, Hb2Ac 7.2%. All the other tests were normal. Urinary tract ultrasonography (US) showed bilateral hydronephrosis. A contrast-enhanced computed tomography (CT) revealed also the presence of an extra-pelvic fibrous tissue extended up to the ureteral origin, determining a significant bilateral constriction of the renal pelvis, with retro-dilatation of the calyces. At subsequent magnetic resonance imaging (MRI) the extra-pelvic tissue signal resulted compatible with a slowly evolutionary fibrous tissue [Fig. 1].A biopsy showed a fibro-muscular tissue diffusely infiltrated by foamy histiocytes, along with areas of steatonecrosis. On direct immunofluorescence the histiocytes were CD68+ and CD1a-. A diagnosis of ECD was made and treatment with standard dosage IFNα was started. The treatment was poorly tolerated because of weakness, dependent edema and hypotension. Of more concern, serum creatinine progressively increased up to 3.9 mg/ dL. IFNα was withdrawn, and subcutaneous Anakinra (100 mg/day) was started. After one year of therapy, the patient symptoms improved, along with renal function, and a follow-up ultrasound showed the absence of hydronephrosis. After one further year of follow-up serum creatinine was still stable around 2 mg/dL. Conclusions: Anakinra is a recombinant, form of IL-1 Receptor antagonist, which binds to IL-1 membrane receptor and down-regulates the biologic activities of IL-1, including inflammation. Aouba et al first reported a significant reduction of IL-1α (expressed at the monocytes membrane surface after cell stimulation) following treatment with Anakinra, a finding that, along with clinical improvement, supported the hypothesis of IL-1 as a primary actor in ECD systemic Th1-oriented immune perturbation. Anakinra also showed important results in some ECD patients with skeletal and cardiac involvement. In all cases a reduction of inflammatory markers, fever and ECD symptoms was observed. We used Anankira as a rescue therapy: general conditions of the patient improved and plasma creatinine reduced from 4 to 2 mg/dl. Neither renal artery nor ureteral stenting were necessary to obtain this result. iii | Abstracts Moreover, in contrast to IFNα therapy, which caused severe side-effects, Anakinra was well tolerated, even in the long-term. ETHNIC COEFFICIENT FOR GLOMERULAR FILTRATION RATE ESTIMATION BY THE MODIFICATION OF DIET IN RENAL DISEASE STUDY EQUATION IN THE IRANIAN POPULATION Nader Nouri-Majalan1, Sarasadat Moghadasimousavi1 and Zahra Eshaghyeh1 1Shahid Sadoughi University of Medical Sciences, Yazd, Iran, Islamic Republic of Introduction and Aims: Estimation of the glomerular filtration rate (GFR) is used clinically for the detection of chronic kidney disease. GFR is estimated from serum creatinine using the Modification of Diet in Renal Disease (MDRD) study equation that is significantly affected by race and ethnically. The aim of the study was to find the Iranian coefficient for the MDRD study equation. Methods: Patients who were older than 18 years with renal clearance of 99mTc-DTPA more than 30 ml/min were included. An estimated GFR (eGFR) derived from the abbreviated MDRD study equation was tested in 152 Iranian people and compared with the dual plasma sampling 99mTc-DTPA plasma clearance method as a reference for GFR (rGFR) measurement. The Iranian coefficient was determined by minimizing the sum of squared errors between rGFR and eGFR. Results: According to rGFR, frequency of GFR between 30-59, 60-89 and more than 90 ml/min per 1.73m2 were 37, 50 and 13%, respectively. The Iranian coefficient for abbreviated MDRD study equation was 0.925. The mean differences was significantly smaller with the 0.925 × MDRD equation than that with 1.0 × MDRD study equation (-0.5 vs -5.5 ml/min per 1.73m2; p<0.05). Conclusions: The abbreviated MDRD study equations with ethnic coefficient improve the estimation of GFR for overall renal function. EXERCISE TRAINING IMPROVES KIDNEY FUNCTION, CARDIOVASCULAR HEALTH, CARDIO-RESPIRATORY FITNESS AND QUALITY OF LIFE IN PATIENTS WITH PROGRESSIVE STAGES 3-4 CHRONIC KIDNEY DISEASE: A RANDOMISED CONTROLLED STUDY Sharlene Greenwood1, Pelagia Koufaki2, Helen Maclaughlin1, Robert Rush3, Bruce M Hendry4, Iain C Macdougall1, Thomas Mercer2 and Hugh Cairns1 1King's College Hospital, London, United Kingdom, 2Queen Margaret University, Edinburgh, United Kingdom, 3Queen Margaret University, Queen Margaret University, United Kingdom, 4King's College London, London, United Kingdom Introduction and Aims: This pilot and feasibility study examined the effect of 12 months of moderate-intensity exercise training and motivational interviewing on kidney function, indices of cardiovascular risk, and quality of life in patients with progressive stages 3-4 chronic kidney disease (CKD). Methods: 20 patients (age, 18-80 yrs) were randomly assigned to either exercise (Ex, n = 10) or usual care (UC, n = 10) for 12 months. The Ex group received resistance and aerobic training (3 days per week) whereas individuals in the UC group received standard of care and were instructed not to start a structured exercise programme during the study. Estimated glomerular filtration rate by MDRD (eGFR), Pulse Wave Velocity (PWV), VO2peak, waist circumference, resting heart rate, blood pressure, plasma lipids, high sensitivity C-reactive protein, and quality of life as assessed by the SF-36 and the Duke’s Activity Status Index (DASI) were assessed at baseline, 6 and 12 months. A paired t-test was used to compare glomerular filtration rate slopes between groups, whereas all other data were analyzed with univariate analysis using the baseline value as the covariate. Pearson correlations were performed between change in main outcome measures and other secondary outcome measures. Results: There were no statistically significant differences in any of the baseline parameters between the groups. 2 patients were lost to follow-up in the Ex group. The 12-month exercise intervention led to a significant improvement in kidney function (eGFR +5.02±5.51 ml/min/1.73m2/year p<0.02) in the Ex group compared with a continued decline in kidney function in the UC group (-2.34±6.4ml/min/year, p<0.02) when comparing the slope. This was accompanied by a significant mean difference in change of pulse wave velocity of 2.30±0.33 m/sec ( p<0.001) between the Ex and UC groups at 12 months (Ex=-1.58±0.87 m/s UC=+0.98±0.69 m/s). There was a significant correlation ( p<0.001) between the improvement in eGFR and PWV in the Ex group at 12 months. There was a significant mean difference in VO2peak of 5.7ml/kg/min ( p<0.01) when comparing the Ex group and the UC group at 12 months (Ex=20.1±5.8 ml/kg/min to 23±5.3 ml/kg/min, UC= 18.3±4.6 to 16.2±5 ml/kg/min ( p<0.01). There was a significant difference of -7.08±2.18cm ( p<0.01) in mean waist circumference between the Ex and UC groups at 12 months (Ex=-5.43±1.61cm, UC=+2.37±1.45cm). This improvement in waist girth was correlated with a significant improvement in VO2peak ( p=0.05). There was an observed improvement in the Short form 36 (SF36) of 4.46 points (45.99±8.45 to 50.45±7.47) in the Ex group compared with a mean decrease of 4 points (50.77±3.14 to 46.75±6.92) in the UC group. Conclusions: A 12-month aerobic and resistance training programme has the potential to improve kidney function, VO2peak, PWV, waist circumference and quality of life in patients with progressing stages 3-4 CKD.


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Macaulay Onuigbo, Nneoma Agbasi, Ming Ju Wu, Kuo Hisung Shu, Eytan Kugler, Eytan Cohen, Irit Krause, Elad Goldberg, Moshe Garty, Ilan Krause, Jitske Jansen, Ilaria E De Napoli, Carolien MS Schophuizen, Martijn J Wilmer, Henricus A Mutsaers, Lambertus P Heuvel, Dirk W Grijpma, Dimitrios Stamatialis, Joost G Hoenderop, Rosalinde Masereeuw, Amaryllis H Van Craenenbroeck, Emeline M Van Craenenbroeck, Katrijn Van Ackeren, Christiaan J Vrints, Vicky Y Hoymans, Marie M Couttenye, Mehtap Erkmen Uyar, Emre Tutal, Zeynep Bal, Orhan Guliyev, Siren Sezer, Liping Liu, Caili Wang, Kentaro Tanaka, Akifumi Kushiyama, Ken Sakai, Shigeko Hara, Yoshifumi Ubara, Yasushi Ohashi, Yujin Kunugi, Shoji Kawazu, Kathrin Untersteller, Sarah Seiler, Kyrill S Rogacev, Insa E Emrich, Claudia S Lennartz, Danilo Fliser, Gunnar H Heine, Taro Hoshino, Susumu Ookawara, Haruhisa Miyazawa, Yuichiro Ueda, Kiyonori Ito, Yoshio Kaku, Keiji Hirai, Honami Mori, Izumi Yoshida, Sachiko Kakuta, Naoaki Hayama, Morimasa Amemiya, Hidekazu Okamoto, Shuji Inoue, Kaoru Tabei, Pedro Campos, Clara Dias, Joana Baptista, Ana Luisa Papoila, Alberto Ortiz, Luis Inchaustegui, Karina Soto, Kyoung Hyoub Moon, Soohyun Yang, Dong-Young Lee, Hye Won Kim, Beom Kim, Corinne Isnard Bagnis, Abdallah Guerraoui, Franck Zenasni, Laetitia Idier, Philippe Chauveau, Ana Cerqueira, Janete Quelhas-Santos, Manuel Pestana, Jae-Youn Choi, Dong-Chan Jin, Yeong-Jin Choi, Wan-Young Kim, Sun-Ah Nam, Jung-Ho Cha, Valeria Cernaro, Saverio Loddo, Antonio Lacquaniti, Adolfo Romeo, Giuseppe Costantino, Gaetano Montalto, Domenico Santoro, Domenico Trimboli, Carlo Alberto Ricciardi, Viviana Lacava, Michele Buemi, Insa E. Emrich, Adam M. Zawada, Kyrill S. Rogacev, Sarah Seiler, Rima Obeid, Jürgen Geisel, Danilo Fliser, Gunnar H. Heine, Gdayllon C. Meneses, Geraldo Silva Junior, Marcus Felipe B. Costa, Heitor S. Gonçalves, Elizabeth F. Daher, Alexandre B. Libório, Alice M.C. Martins, Robert Ekart, Nina Hojs, Sebastjan Bevc, Radovan Hojs, Chun Soo Lim, Jin Ho Hwang, Ho Jun Chin, Sejoong Kim, Dong Ki Kim, Suhnggwon Kim, Jung Hwan Park, Sung Joon Shin, Sang Ho Lee, Bum Soon Choi, Sandrine Lemoine, Marine Panaye, Laurent Juillard, Laurence Dubourg, Aoumeur Hadj-Aïssa, Fitsum Guebre-Egziabher, Geraldo Silva Junior, Ana Patricia F. Vieira, Amanda X. Couto Bem, Marília P. Alves, Gdayllon C. Meneses, Alice M.C. Martins, Alexandre B. Libório, Elizabeth F. Daher, Kiyonori Ito, Susumu Ookawara, Haruhisa Miyazawa, Yuichiro Ueda, Yoshio Kaku, Keiji Hirai, Taro Hoshino, Honami Mori, Izumi Yoshida, Kaoru Tabei, Gabriel Stefan, Cristina Capusa, Simona Stancu, Diana Margarit, Ligia Petrescu, Elena D Nedelcu, Gabriel Mircescu, Anna Szarejko-Paradowska, Jacek Rysz, Chi-Chih Hung, Hung-Chun Chen, Vesna Ristovska, Ladislava Grcevska, Manuel A Podestà, Francesco Reggiani, David Cucchiari, Salvatore Badalamenti, Michele Buemi, Claudio Ponticelli, Giorgio Graziani, Nader Nouri-Majalan, Sarasadat Moghadasimousavi, Zahra Eshaghyeh, Sharlene Greenwood, Pelagia Koufaki, Helen Maclaughlin, Robert Rush, Bruce M Hendry, Iain C Macdougall, Thomas Mercer, Hugh Cairns. CKD LAB METHODS, PROGRESSION & RISK FACTORS 2, Nephrology Dialysis Transplantation, 2014, iii369-iii379, DOI: 10.1093/ndt/gfu165