M. Fleet, F. Osman, R. Komaragiri, A. Fritz and D.S.C. Raj Department of Medicine/Nephrology, University of New Mexico, Health Sciences Center, Albuquerque, NM, USA Background: Protein energy wasting is a maladaptive metabolic state often associated with inflammation, which is common in patients with chronic kidney disease (CKD). Methods: A literature search was performed using MEDLINE and the reference lists of relevant review articles. The following key words were used in the MEDLINE search: “cytokines”, “inflammation”, “protein metabolism”, “acute-phase protein”, “cachexia”, “chronic kidney disease”, “end-stage renal disease” and “hemodialysis”. The search was limited to English-language articles. Results: While experimental models have shown that uremic animals are more prone for proteolysis, the results from the human studies are controversial. Intradialytic loss of amino acids and activation of proinflammatory cytokines lead to potein catabolism during hemodialysis (HD). At the whole-body level, intradialytic parenteral nutrition (IDPN) increases protein synthesis and decreases proteolysis. Amino acid infusion during HD increases muscle protein synthesis, but does not decrease protein catabolism. Activation of interleukin-6 during HD induces protein catabolism, impairs amino acid utilization for protein synthesis and increases acute-phase protein synthesis. Conclusion: The changes in albumin, fibrinogen and muscle protein kinetics during HD could be due to competing and complementary effects of availability of amino acids and activation of proinflammatory cytokines.Correspondence to:
D.S.C. Raj, MD, DM,
Professor of Medicine,
Division of Nephrology and Epidemiology,
5th Floor-ACC, 2211 Lomas Blvd. NE,
Albuquerque, NM 87131-5271, USA
Email: draj@salud.unm.edu

C.S. Lim¹,², S.M. Kim², Y.K. Oh¹,², K.W. Joo², Y.S. Kim², J.S. Han² and S. Kim^{2 1}Department of Internal Medicine, Seoul National University Boramae Hospital and ²Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea Aims: Megsin is a mesangial cell-predominant gene which belongs to the serpin superfamily. The expression of megsin was upregulated and coincided with mesangial proliferation and extracellular matrix expansion in IgA nephropathy (IgAN). In the present study, we evaluated the influence of the C2093T and C2180T polymorphism within the 3’ untranslated region (3’UTR) of megsin gene and its haplotypes on the development and progression of Korean IgAN patients. Methods: Korean IgAN patients (n = 260) with a minimal follow-up of 4 years were recruited. Healthy subjects with normal renal function, normal urinalysis and normotension (n = 315) were included as controls. The polymorphisms were determined by the 5’ nuclease allelic discrimination assay, and the haplotypes were constructed using the Phase program. Results: The C2093T and C2180T genotype and allele frequencies were not different significantly between IgAN patients and controls. In C2093T polymorphism, patients with CC genotype showed a better renal survival than those with CT or TT genotypes by Kaplan-Meier analysis (p = 0.027). The megsin C2093T polymorphism remained an independent risk factor for progression (Cox regression model, HR for TT genotype: 3.52, 95% CI 1.69 – 7.34; HR for CT genotype: 2.15, 95% CI 1.30 – 3.57). In C2180T polymorphism, patients with TT genotype showed a better outcome than those with CC or CT genotypes (p = 0.025). The C2180T polymorphism was also an independent risk factor for progression (HR for CC genotype: 4.05, 95% CI 1.93 – 8.51; HR for CT genotype: 2.35, 95% CI 1.40 – 3.94). The two alleles showed linkage disequilibrium in phased haplotype. The patients with 2093T-2180C haplotype showed a poor renal survival compared to those with 2093C-2180T haplotype (p = 0.028). The haplotype remained an independent risk factor for progression (HR for 2093T-2180C haplotype: 2.01, 95% CI 1.44 – 2.81). Conclusions: Our results suggest that the 2093T-2180C haplotype at the 3’UTR of megsin gene is associated with rapid disease progression in Korean IgAN patients. This is the reverse of the results from the Chinese IgAN patients. Further studies are strongly needed to elucidate the reasons of disparity.Correspondence to:
C.S. Lim, MD
Department of Internal Medicine, Seoul National University Boramae Hospital, 425 Sindaebang 2-dong, Dongjak-gu, Seoul 156-707, Korea
Email: cslimjy@snu.ac.kr

B. Seiberlich¹, N. Hunzelmann², T. Krieg², M. Weber¹ and E. Schulze-Lohoff^{1 1}Department of Medicine I, Merheim Medical Center, Cologne General Hospital, Cologne and ²Department of Dermatology, University of Cologne, Germany Background: Renal involvement and systemic vascular damage have been shown to significantly affect prognosis in systemic sclerosis (SSc). However, it is often difficult to assess damage to the renal and systemic vasculature in SSc patients. Methods: Using detailed urinary protein analysis we sought to detect scleroderma renal disease at an early stage and to assess systemic vasculopathy due to SSc. We examined 80 patients with SSc as well as 18 healthy control subjects using urinary protein analysis including determination of urinary albumin excretion rate and urinary total protein excretion as well as urinary polyacrylamide gel electrophoresis. Results: Albuminuria was found in 25% (20/80) of the SSc patients (2.5% macroalbuminuria, 22.5% microalbuminuria), increased total protein excretion in 17.5% (14/80), and intermediate molecular weight proteinuria (IMWP) as determined by urine electrophoresis in 31.3% (25/80). None of these abnormalities was found in the control group (0/18). Presence of IMWP correlated with the diffuse type of SSc (p < 0.01), gastrointestinal involvement (p < 0.05) and increased systolic blood pressure (p < 0.01). Increased total protein excretion was found to correlate with pulmonary involvement (p < 0.05). Albuminuria was associated with prolonged duration of the disease (> 4 years) (p < 0.05) and increased systolic blood pressure (p < 0.01). Conclusions: Leakage of proteins into the urine in patients with SSc appears to indicate not only renal involvement but also systemic vasculopathy which is associated with increased morbidity. Patients with SSc should be regularly examined using sensitive urinary protein tests such as albumin assays or urine electrophoresis, to detect kidney involvement at an early stage.Correspondence to:
Prof. Dr. E. Schulze-Lohoff
Katholisches Klinikum Duisburg, Medizinische Klinik – Marienhospital, Wanheimer Straße 167a, 47053 Duisburg, Germany

Email: E.Schulze-Lohoff@uni-koeln.de

N. Kamar¹, A. Jaafar², L. Esposito¹, D. Ribes¹, D. Durand¹, F. Di-Giambattista³, I. Tack² and L. Rostaing^{1 1}Nephrology, Dialysis and Multi-Organ Transplantation, ²Renal Functional Explorations Unit, CHU Rangueil, Toulouse Cedex ⁴ and
³Novartis Pharma SAS, Rueil-Malmaison, Cedex, France Aim: To provide data on conversion of kidney transplant patients from sirolimus to everolimus. Materials and methods: In this 6-month prospective, open-label pilot study, maintenance renal transplant patients receiving sirolimus, mycophenolic acid and corticosteroids without concomitant calcineurin inhibitor (CNI) therapy were converted to everolimus 8 mg/day (8 – 15 ng/ml), and followed for 6 months. Mycophenolic acid and corticosteroid therapy were continued unchanged. Patients with acute rejection within the previous 3 months were excluded. Results: 11 patients were recruited and completed the study (mean 5.1 ± 1.8 years post transplant). Mean everolimus trough level remained within target throughout the study. Mean GFR remained stable (Day 0, 48.4 ± 8.4 ml/min/1.73 m², Month 6, 49.5 ± 17.3 ml/ min/1.73 m² (p = 0.966), as did mean renal phosphate threshold (TmPO₄/GFR) (Day 0, 0.41 ± 0.15 mmol/l, Month 6, 0.40 ± 0.17 mmol/l (p = 0.966)). Serum phosphates increased significantly from 0.71 to 0.77 mmol/l (p = 0.01), but tubular reabsorption of phosphates and 24-h phosphaturia remained unchanged and mean PTH concentration tended to decrease. No patient died, lost their graft or experienced biopsy-proven acute rejection after conversion. There were no cases of CMV infection. Tolerability remained similar post conversion. Hematological and lipid parameters remained stable. Liver enzymes and sex hormones remained within normal ranges. Conclusion: This pilot study suggests that converting kidney transplant patients receiving CNI-free maintenance immunosuppression from sirolimus to everolimus, at relatively high exposure levels, is safe and easily manageable. There was no consistent evidence for a change in GFR or proximal tubular function.Correspondence to:
N. Kamar, MD, PhD
Department of Nephrology and Multi-Organ Transplantation, CHU Rangueil, 1 avenue Jean Poulhès, 31059 Toulouse, France
Email: kamar.n@chu-toulouse.fr

R.M. Schaefer¹, J. Bover², F. Dellanna³, D. Sanz⁴, C. Asensio⁵, M.C. Sánchez González⁶, P. Gross⁷, V. Zani⁸, D. Carter⁸ and P.M. Jehle^{9 1}Department of Medicine D, University of Münster, Germany, ²Fundació Puigvert, Barcelona, Spain, ³Dialysepraxis, Düsseldorf, Germany, ⁴Hospital Puerta del Hierro, Madrid, Spain, ⁵Hospital Virgen de las Nieves, Granada, Spain, ⁶Hospital La Paz, Madrid, Spain, ⁷Medizinische Fakultät Carl-Gustav-Carus, Dresden, Germany, ⁸Amgen, Switzerland and United Kingdom and ⁹Klinik für Innere Medizin and KfH, Nierenzentrum, Lutherstadt Wittenberg, Germany Background: Cinacalcet, a novel calcimimetic, simultaneously lowers parathyroid hormone (PTH), phosphorus (P), calcium (Ca) and Ca × P in patients who are on dialysis with secondary hyperparathyroidism (sHPT) associated with CKD. Previous studies have required cinacalcet to be administered during the dialysis session and at the same time on non-dialysis days. The aim of the SENSOR study was to demonstrate that cinacalcet given in a more clinically practical manner with the first major meal after dialysis is noninferior to cinacalcet given with food during the dialysis session. Methods: In this open-label study dialysis patients with poorly controlled sHPT (intact PTH (iPTH) ³ 300 pg/ml) were randomized to receive cinacalcet either daily with their post-dialysis meal (n = 337) or with food during the dialysis session (n = 336). The primary endpoint was the proportions of patients with mean iPTH £ 300 pg/ml (£ 31.8 pmol/l) at Weeks 11 and 13 of a 21-week treatment period. Secondary endpoints included the proportion of patients with Ca × P < 55 mg²/dl² (< 4.44 mmol²/l²) at Weeks 11 and 13 and patients who discontinued the study due to nausea or vomiting. Results: Comparable proportions of patients in the cinacalcet “during dialysis” and “post-dialysis meal” groups had a mean iPTH £ 300 pg/ml (54 vs. 57%, respectively, 95% confidence interval (CI) difference –4, +10%) and Ca × P < 55 mg2/dl2 (78 vs. 73%, respectively, 95% CI difference –11, +2%) at Weeks 11 and 13. The groups were also comparable at Week 21. Cinacalcet was well tolerated, with < 3% of patients in both groups discontinuing due to nausea or vomiting. A combined post-hoc analysis of both groups showed the incidence of nausea and vomiting was lower if cinacalcet was administered during the evening. Conclusions: Administering cinacalcet with the first main meal after dialysis was as effective as administration with food during the dialysis session. Cinacalcet was well tolerated. The incidence of gastrointestinal adverse events appeared to be lower when cinacalcet was administered in the evening.Correspondence to:
R.M. Schaefer, MD
Department of Medicine D, University of Münster, Albert-Schweitzer-Straße 33, 48149 Münster, Germany
Email: schaefe@uni-muenster.de

R. Nissel¹,², S. Faraj¹, K. Sommer¹,², L. Henning³, M. van der Giet³ and U. Querfeld¹,^{2 1}Department of Pediatric Nephrology, ²Center for Cardiovascular Research and ³Department of Nephrology/Endocrinology, Charité University Hospital Berlin, Germany Aims: Studies in young hemodialysis patients without significant comorbidities might increase the understanding of incipient vascular pathology in uremia. We investigated whether a specific pattern of oxidative stress markers with potential prognostic significance could be identified in this population. Material and methods: We performed a cross-sectional matched case control study of 25 young hemodialysis patients (age 18 – 40 years) without known comorbidity factors. Patients were matched pairwise to healthy controls, and markers of oxidative stress were analyzed for associations with surrogate parameters of vascular structure and function. Results: Oxidized low-density lipoproteins (OxLDL) were similar in patients and controls whereas conjugated dienes were increased in the very low-density lipoproteins (VLDL) fraction (20 ± 6 vs. 12 ± 5 mmol/l, p < 0.0001), but not in the low-density lipoproteins (LDL) fraction (16 ± 6 vs. 18 ± 6 mmol/l). Superoxide dismutase (SOD) activity was diminished in patients (1,117 ± 151 vs. 1,299 ± 88 U/g Hb, p < 0.0001), but there was no difference in glutathione peroxidase (GPx) activity. Oxidative stress expressed as the ratio of oxidized and reduced glutathione (GSSG/GSH) was increased in patients (0.25 ± 0.18 vs. 0.13 ± 0.04, p = 0.0048). Intima-media thickness (IMT) of the common carotid artery (0.70 ± 0.12 vs. 0.62 ± 0.08 mm, p = 0.0007) was significantly increased, and postischemic peak flow (PIPF) by venous occlusion plethysmography was severely diminished in patients (632 ± 319 vs. 1,057 ± 543% of basal flow, p < 0.0001). None of the markers of oxidative stress was independently associated with IMT or PIPF or a significant discriminator between patients and controls by multivariate regression. Conclusions: In this pilot study of exclusively young patients on hemodialysis, oxidative stress markers were of limited clinical value in identifying young patients at risk for vascular complications.Correspondence to:
U. Querfeld, MD
Department of Pediatric Nephrology, Charité
University Hospital, Augustenburger Platz 1, 13353 Berlin, Germany
Email: uwe.querfeld@charite.de

M. Thaha¹, Pranawa¹, M. Yogiantoro¹, Sutjipto², Sunarjo², M. Tanimoto³, T. Gohda³ and Y. Tomino^{3 1}Department of Internal Medicine, Division of Nephrology-Hypertension, Airlangga University School of Medicine, ²Airlangga University School of Medicine, Surabaya, Indonesia and ³Department of Internal Medicine, Division of Nephrology, Juntendo University School of Medicine, Tokyo, Japan Background: Impairment of nitric oxide generation caused by gene polymorphism is considered as a major factor in the deterioration of progressive renal disease, including diabetic nephropathy and hypertension. The aim of the present study was to examine the Glu298Asp polymorphism of endothelial nitric oxide synthase (eNOS) in patients with end-stage renal disease (ESRD). Methods: The Glu298Asp polymorphism in exon 7 was determined in 100 ESRD patients who were maintained on hemodialysis at Dr. Soetomo Hospital, Surabaya, Indonesia, and in a control group of 100 unrelated healthy individuals. In the patient group, 39 patients had Type 2 diabetes mellitus (DM), 44 hypertension (HT) and 17 miscellaneous conditions. The mean length of time from onset of ESRD to the start of this study was 24.37 ± 32.37 months (Mean ± SD). Results: The positivity of Glu298Asp in the ESRD group was significantly higher than that in the control group (p < 0.0001). The odds ratio for this group was 4.57 (95% confidence interval 2.52 – 8.31). The positivity of 298Asp in Type 2 DM ESRD with subgroup was significantly higher than that in healthy controls (p < 0.0001). The positivity of 298Asp in the subgroup of patients with HT-derived ESRD was also significantly higher (males p < 0.036, females p < 0.005) than that in healthy control group. Homozygotes with glutamate to aspartate substitution at nucleotide position 7702 showed a single band at 457 bp. Conclusion: It appears that Glu298Asp may be a predisposing factor in DM-derived and HT-derived ESRD.Correspondence to:
Y. Tomino, MD
Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-Ku, Tokyo 113-8421, Japan
Email: yasu@med.juntendo.ac.jp

B.J. Lim¹, K.S. Suh¹, K.R. Na², K.W. Lee² and Y.T. Shin^{2 1}Department of Pathology, Lancer Research Institute and ²Department of Internal Medicine, Chungnam National University College of Medicine, Moonhwa-dong, Jung-gu, Daejeon, Korea Superimposition of poststreptococcal glomerulonephritis (PSGN) on the course of IgA nephropathy (IgAN) is uncommon. A case of PSGN during IgA nephropathy is presented. A 30-year-old man who had alternating gross and microscopic hematuria for 7 months underwent a renal biopsy. The first renal biopsy revealed IgAN with mesangial deposits of IgA and C3. Two months later, the patient suffered generalized edema, proteinuria, hematuria, an increased ASO titer and a decreased C3 level. A second renal biopsy revealed diffuse endocapillary proliferative glomerulonephritis with epimembranous hump-like electron-dense deposits of C3, but the original mesangial IgA deposits had disappeared. A diagnosis of acute PSGN was indicated. Two months after the onset of acute nephritic syndrome, the patient remained asymptomatic, except for microscopic hematuria and proteinuria. Some cases with persistent proteinuria or hematuria after PSGN are probably related to preexisting IgAN.Correspondence to:
K.S. Suh, MD
Chungnam National, University College of
Medicine, 6, Moonhwa-dong, Jung-gu, Daejeon, Korea
Email: Kssuh@cnu.ac.kr

S.M.S. Ting¹, T. Toth² and F. Caskey^{3 1}Renal Specialist Registrar, Renal Department, Birmingham Heartlands Hospital, Birmingham, ²Consultant Histopathologist, Richard Bright Renal Unit, Southmead Hospital, Westbury-on-Trym, Bristol, West Midlands and ³Consultant Renal Physician, Richard Bright Renal Unit, Southmead Hospital, Westbury-on-Trym, Bristol, West Midlands, United Kingdom The role of severe a1-antitrypsin (A1AT) deficiency in the predisposition of early-onset pulmonary emphysema and juvenile hepatic cirrhosis is well-established. Associated glomerulonephritis is unusual although it is well-recognized in children and young adults with the severe phenotype. We report the first adult case of A1AT deficiency presenting with nephrotic syndrome secondary to IgA nephropathy and explore the direct role of A1AT deposits in the pathogenesis of the renal involvement.Correspondence to:
Dr. S.M.S. Ting
The Renal Directorate, Birmingham Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS, West Midlands, United Kingdom
Email: stephen_ting@yahoo.com

G. Mazzucco¹, C. Costa², M. Bergallo², G.P. Segoloni³ and G. Monga^{4 1}Department of Biomedical Sciences and Human Oncology, ²Department of Public Health and Microbiology, ³Department of Internal Medicine, Faculty of Medicine and Surgery, University of Turin, and ⁴Department of Medical Sciences, University of Piemonte Orientale, Novara, Italy Herein reported is a severe case of BK virus nephropathy, probably caused by an intense/overimmunosuppression and identified 17 months after transplantation. The diagnostic biopsy showed extracapillary proliferation and typical cytopathic lesions, both in tubular epithelial cells and in those of the glomerular crescents. Severe inflammatory infiltrates, tubulitis, tubular atrophy and fibrosis were also observed. Immunohistochemistry and molecular biology disclosed the presence of an AS variant of the BK virus with a high viral load, both in renal tissue and urine. Immunosuppression was reduced and Leflunomide therapy administered for a month. Although this led to an improvement in the renal function, the therapy had to be suspended due to the onset of a skin rash. A second biopsy was performed 7 months later. The cellular crescents were no longer present and there was no evidence of either histologic or immunohistochemical findings consistent with an active BK virus infection. Tubular atrophy and interstitial fibrosis were still present. In addition, fibrotic crescents, which may be interpreted as late scarring changes of previous epithelial proliferation, were found. Although molecular investigation still showed the presence of the BK virus, the viral load in renal tissue, urine and serum was greatly reduced. Indeed, serum and urine viral load was still low at the last control, five months after the second biopsy. The morphologic and clinical evolution are reported and the possible role of the therapy is discussed.Correspondence to:
G. Monga, MD
Dipartimento di Scienze Mediche. Via Solaroli 17, 28100 Novara, Italy
Email: guido.monga@med.unipmn.it

J. Warncke¹, S. David¹, P. Kümpers¹, J.P. Opherk², H. Haller¹ and D. Fliser^{1 1}Department of Internal Medicine/Nephrology and ²Department of Diagnostic Radiology, Medical School Hannover, Germany Ischemic preconditioning has been first described by Murry and coworkers as the protection conferred to ischemic myocardium by preceding brief periods of sublethal ischemia separated by periods of reperfusion. Another phenomenon closely associated to IPC is hibernation and stunning. The hibernating myocardium refers to resting left ventricular dysfunction due to reduced coronary blood flow that can be partially or completely reversed by myocardial revascularization and/or by reducing myocardial oxygen demand. Similarly as for the myocardium, these effects are reproducible for other solid organs. Here we report a case of a renal transplant recipient with decompensated proximal transplant artery stenosis due to ACE inhibition resulting in acute renal failure. The transplant perfusion was strictly dependend on systemic arterial blood pressure leading to intermittent episodes of renal ischemia and reperfusion. Renal function was severely decreased (glomerular filtration rate ~ 8 ml/min) with the need of hemodialysis treatment over a period of 4 weeks after transplantation. After dilatation of the stenosis, the patient’s renal function improved rapidly and achieved values better than ever before. Referring to the definition of hibernating myocardium, here we postulate a case of a hibernating kidney in context of ischemic preconditioning.Correspondence to:
S. David, MD
Department of Internal Medicine/Nephrology, Medical School Hannover, Carl-Neuberg-Straße 1, 30625 Hannover, Germany
Email: david.sascha@mh-hannover.de

S. Costanzi¹, A. Zoli², P.M. Ferraro¹, F.M. Danza³ and G.F. Ferraccioli^{2 1}Renal Unit, ²Rheumatology and ³Radiology, Catholic University of the Sacred Heart, Rome, Italy Retroperitoneal fibrosis (RPF) is a rare disease characterized by an inflammatory proliferative fibrosing process occurring in the retroperitoneum, often causing urinary tract obstruction. Medical therapy is not well-defined, but glucocorticoids have been the mainstay of therapy. Recently, positive response to tamoxifen, an antiestrogen drug, has been reported among patients with RPF. We report the case of a 65-year-old male with a renal cell carcinoma in the upper pole of the right kidney showing acute renal failure due to a biopsy-confirmed RPF determining bilateral hydronephrosis. After polar resection of the right kidney, a high-dose oral steroid therapy did not modify the hydronephrosis. At 6 months, therapy with tamoxifen determined the retroperitoneal fibrotic mass regression and resolved the ureteral obstruction, that persists at the 13th month of follow-up. Tamoxifen can be considered as an effective alternative to corticosteroids and immunosuppressors in treating RPF.Correspondence to:
Dr. S. Costanzi
Complesso Integrato Columbus, Via G. Moscati 31, 00168 Roma, Italy
Email: stefano.costanzi@fastwebnet.it

N. Demoulin¹, M. Jadoul¹, J.P. Cosyns² and L. Labriola^{1 1}Department of Nephrologyand ²Department of Pathology, Cliniques Universitaires St. Luc, Université Catholique de Louvain Medical School, Brussels, Belgium We report moderate renal failure in a 50-year-old man with a history of recent colonoscopy after oral sodium phosphate purgative use. We initially missed the correct diagnosis, but renal biopsy revealed signs of acute phosphate nephropathy. The patient had residual renal impairment at 8-month follow-up. Greater awareness of this complication is needed amongst health care professionals. The preventive strategies are discussed.Correspondence to:
Prof. M. Jadoul, MD
Cliniques Universitaires St. Luc, Université Catholique de Louvain Medical School, Avenue Hippocrate 10, 1200 Brussels, Belgium
Email: jadoul@nefr.ucl.ac.be

B. Simsek, A. Noyan, A.K. Bayazit, M. Soran and A. Anarat Department of Pediatric Nephrology, Cukurova University, School of Medicine, Balcali, Adana, Turkey Pleural effusions are seen relatively common in end-stage renal disease (ESRD) patients, on the other hand, hydrothorax secondary to pleuroperitoneal leak in continuous ambulatory peritoneal dialysis (CAPD) patients is rare. Since treatment modalities differ widely from that of other causes of pleural effusion seen in CAPD patients such as uremia, volume overload, congestive heart failure, infection and malignancy, pleuroperitoneal leak should always be kept in mind in the differential diagnosis and should be excluded urgently. To draw attention to this point, in this paper, 2 children on CAPD who developed a hydrothorax secondary to a pleuroperitoneal communication are presented with an overview of diagnostic tools and treatment modalities.Correspondence to:
Dr. B. Simsek
Department of Pediatric Nephrology, Cukurova University, School of Medicine, Balcali, Adana, 01330 Turkey
Email: drmago@hotmail.com

S. Shaldon Monte Carlo, Monaco

S.-O. Moon, K.P. Kang, S.K. Park, A.S. Lee, H.J. Kim and W. Kim

I. Mimura, Y. Hori, T. Matsukawa, H. Uozaki, A. Tojo and T. Fujita

H. Inagaki, T. Satoh, K. Kamiya, T. Mori, T. Nomura, T. Hamazaki and K. Hamazaki