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Abstract

K.M. Koch, H.H. Malluche, Jörg Feistle and Frank Feistle

Medizinische Hochschule Hannover, Zentrum für Innere Medizin, Hannover, Germany
On July 16th 2007, Professor Dr. Reinhold Kluthe, the first editor and together with Dr. Karl Feistle the founder of Clinical Nephrology (CN), died a week after his 79th birthday. We extend our condolences to his family.

Reinhold Kluthe was the first Editor-in-Chief of CN from 1973 until 1991. At that time, when we succeeded him, CN was already known as one of the leading nephrological journals with a clinical focus. People called it the “Green Journal”, and it enjoyed an excellent reputation.

Reinhold Kluthe’s successful editorship was based on an equally impressive academic career. After studying medicine in Homburg/Saar and Freiburg/Breisgau and receiving his doctor’s degree in 1956, he worked as research fellow at the Freiburg University Institute of Hygiene and thereafter as a resident in Internal Medicine at the Medizinische Universitätspoliklinik under Prof. H. Sarre, one of the leading German Clinical Nephrologists at that time. After research stays in Biochemistry in Berlin and at the Basel Canton Hospital, R. Kluthe was designated in 1964 to be a University lecturer, after having already written his postdoctoral thesis on the pathogenesis and protein metabolism of nephrotic syndrome at Freiburg University. He became senior physician of the Freiburg University Medizinische Poliklinik in 1965 and Associate Professor of Medicine in 1970.

From 1975 to 1976 he served as a temporary director of the Medizinische Poliklinik Freiburg and in 1977 was appointed to be the director of the newly established section of Nutritional Medicine and Dietetics.

Reinhold Kluthe’s scientific work found expression in more than 350 publications on renal, hypertensive, metabolic and nutritional diseases and their treatment. He played a major role in enabling dietetics to regain its former importance as an essential treatment of metabolic diseases in this age of pharmacotherapy. One of his outstanding achievements was the development of a low protein potato-egg diet for patients with chronic terminal renal failure. This strict dietary regime enabled many patients to stay alive until treatment with the artificial kidney became available for them.

Reinhold Kluthe can be considered as one of the pioneers in the development of our understanding of the relationships between metabolic disturbances such as diabetes and obesity and renal disease/arteriosclerosis.

After retirement in 1991 he dedicated himself more intensively to his activities as head of the German Academy for Nutritional Medicine, which he founded in 1983. Among his many achievements after leaving academic medicine are the development of the nutritional medical curriculum for the German Federal Medical Chamber and planning and supervising a large National Pilot Project on Clinical Nutritional Medicine. For his achievements he was awarded the medal of the International Society of Nutrition and became the first recipient of the Konrad Lang Medal of the German Society of Nutritional Medicine in 2003.
Reinhold Kluthe’s great achievements and his landmark contributions to the understanding and treatment of renal disease as well as his merits as co-founder and first editor of Clinical Nephrology will not be forgotten.
Correspondence to:
Prof. Dr. med. K.M. Koch, Medizinische Hochschule Hannover, Zentrum für Innere Medizin, Building K25, I. Stock, Carl-Neuberg-Straße 1, 30625 Hannover, Germany
Email: clin.nephrol@t-online.de

Abstract

P. Dennen and C.R. Parikh

¹Section of Nephrology and Critical Care, Denver Health Medical Center, University of Colorado Health Sciences Center, Denver, CO, and ²Section of Nephrology and Clinical Epidemiology Research Center, Yale University School of Medicine, New Haven, CT, USA
Acute kidney injury (AKI) is frequent in hospitalized critically ill patients and mortality associated with AKI is largely unchanged over many decades. The new nomenclature, AKI, reflects the entire spectrum of acute renal failure, recognizing that an acute decline in kidney function can be secondary to an injury that causes functional or structural changes in the kidneys [Mehta et al. 2007]. An abrupt change in serum creatinine level has been the primary method for diagnosing AKI for nearly 60 years despite its well recognized limitations [Addis et al. 1947, Barrett and Addis 1947, Fisher and Wilhelmi 1937, Star 1998]. These limitations are mainly related to the delayed diagnosis of AKI associated with delayed rise in serum creatinine and the lack of specificity and sensitivity associated with small changes in serum creatinine. It is believed that these limitations associated with diagnosis of AKI have prevented progress by interfering with the design of clinical trials for newer therapies. It is now widely believed that the availability of accurate and objective early biomarkers of AKI will stimulate progress in the development of early interventions in AKI. Recognition of this concept has led to a surge in preclinical, translational and clinical research for discovery and validation of biomarkers in AKI. In this review we will discuss the role of biomarkers in AKI and the promising biomarkers on the horizon.Correspondence to:
C. Parikh, MD, PhD, Section of Nephrology, Yale University and VAMC, 950 Campbell Ave, Mail Code 151B, Bldg 35 A, Room 219, West Haven, CT 06516, USA
Email: chirag.parikh@yale.edu

Abstract

A. Boscheri, C. Weinbrenner, B. Botzek, K. Reynen, E. Kuhlisch and R.H. Strasser

¹Department of Internal Medicine and Cardiology, ²Department of Medical Informatics and Biometry, University of Technology, Dresden, Germany
Aims: Contrast-media induced nephropathy (CIN) remains a common complication after contrast dye exposure especially in patients with chronic renal impairment (CRI). We sought to evaluate the efficacy of the antioxidant ascorbic acid as an adjunct to hydration in limiting the incidence of contrast induced nephrotoxicity after coronary procedures. Materials and methods: In a randomized, double-blind, prospective, single center-study, 143 consecutive patients with CRI (creatinine level > 120 µmol/l) referred to coronary angiography/intervention were randomly assigned to receive 1 g ascorbic acid or placebo in adjunct to saline hydration prior to and after angiography. Creatinine and urea nitrogen levels were measured prior to and up to 6 days after exposure to contrast agent. Results: The development of CIN occurred totally in 8/143 (5.6%) patients. Between the two groups no significant difference was detected (Vitamin C 5/74 (6.8%) patients; placebo 3/69 (4.3%) patients). After adjusting for the amount of contrast dye, drug treatment, cardiovascular risk factors, ejection fraction, or sex, again no differences were detected. No patient required dialysis. More patients with diabetes had development of CIN (7/85; 8.2%) compared with nondiabetic patients (1/58; 1.7%), although not significant (p = 0.14). The incidence of CIN was elevated in patients with high amounts (> 140 ml) of contrast volume used (6/8). Conclusions: Our study does not support the prophylactic use of ascorbic acid in patients with renal dysfunction exposed to contrast dye.Correspondence to:
A. Boscheri, MD, Department of Internal Medicine and Cardiology, University of Technology, Fetscherstraße 76, 01309 Dresden, Germany
Email: Aboscheri@aol.com

Abstract

M. Abe, F. Kikuchi, K. Kaizu and K. Matsumoto

¹Division of Nephrology and Endocrinology, Department of Medicine, Nihon University School of Medicine, ²Department of Nephrology and Blood Purification, Yamato Hospital, Tokyo, ³Department of Nephrology and Blood Purification, Yokohama Social Insurance Central Hospital, Yokohama, Japan
Aims: Unfortunately, clinicians are diagnosing a growing number of patients on hemodialysis (HD) with insulin-resistant, Type 2 diabetes in Japan. While α-glucosidase inhibitors (α-GI) such as oral antidiabetic agents are indicated for Japanese diabetics on HD, pioglitazone and other PPARgamma agonists are now contraindicated. No prospective study has evaluated the use of thiazolidinediones in diabetics with end-stage renal disease (ESRD) in combination with α-GI. In this study we evaluated the efficacy and safety of pioglitazone in Japanese diabetics on HD. Methods: An open-label randomized study was performed on 31 Type 2 diabetics on HD with unstable glycemic control receiving constant doses of voglibose. The patients were randomly assigned to two groups: a combination therapy group (pioglitazone group) administered pioglitazone (fixed dose 30 mg) plus voglibose, and a monotherapy group (control group) administered voglibose alone. The efficacy of the treatments was determined by monitoring glycemic control (plasma glucose and HbA1c) and insulin resistance. Insulin resistance was assessed using the homeostasis model assessment for insulin resistance (HOMA-R). Safety and tolerance were determined by monitoring clinical and laboratory parameters. Results: The pioglitazone was effective in reducing plasma glucose and HbA1c from the baseline levels from Week 4 onward. It was also effective in reducing triglycerides. HOMA-R decreased significantly at 4 weeks in the pioglitazone group, and the decrease continued up to the last measurement at Week 12. Systolic and diastolic blood pressures at 4 weeks were statistically lower in the pioglitazone group than in the control group. No serious adverse effects such as hypoglycemia, liver impairment or rhabdomyolysis were observed in any of the patients. Conclusions: Pioglitazone was safe and effective as a treatment for diabetics on dialysis therapy. The 30 mg daily dose of pioglitazone was sufficient for Japanese HD patients, obese and nonobese alike. The combination therapy of pioglitazone with voglibose will add to the list of first-line drug treatments for glycemic control in uremic Type 2 diabetes.Correspondence to:
M. Abe, MD, Division of Nephrology and Endocrinology,
Department of Medicine, Nihon University School of Medicine, 30-1, Oyaguchi-Kamimachi, Itabashi-ku, Tokyo, 173-8610, Japan
Email: mabe@med.nihon-u.ac.jp

Abstract

Q. Yao, E. Rodr�guez Ayala, J.Q. Qian, P. Stenvinkel,

¹Department of Clinical Science, Intervention and Technology, Divisions of Baxter Novum and Renal Medicine, Karolinska Institute, Stockholm, Sweden, ²Renal Division, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China, ³Unida
Background: Human peritoneal mesothelial cells (HPMCs) have been shown to regulate the inflammatory response and the subsequent peritoneal extracellular matrix accumulation (ECM) induced by bioincompatible peritoneal dialysis solutions. Recently, attention has been given to the possible antiinflammatory effect exhibited by angiotensin receptor blockers (ARB) or PPAR- γ agonists in several tissues including glomerular. As no data on the potential role of these commonly used drugs in reducing peritoneal fibrosis exist, we examined the in vitro effects of an ARB (losartan) and a PPAR-γ agonist (rosiglitazone) on inflammatory and profibrotic pathways in cultured HPMCs subjected to high glucose. Methods: HPMCs were incubated for 48 hours with 3 different concentrations of glucose: 5 mM (G5), 50 mM (G50) and 100 mM (G100), as well as G50 with either losartan (5 or 10 �M) and/or rosiglitazone (1 or 10 �M). IL-6, IL-8, VEGF and TGF-β₁ in the supernatants were measured by cytokine multiplex assays or ELISA. Smad7, the inhibitor of the TGF/Smad signaling pathway, was measured using immunocytochemistry. Results: All the measured cytokines increased in proportion to increased concentration of glucose. Unexpectedly, this effect was not inhibited, but rather further enhanced, by rosiglitazone and losartan separately. However, only the combination of the two drugs had an inhibitory effect on TGF-β₁ and IL-6, while the expression of inhibitory Smad7 was increased. Conclusion: We conclude that high glucose exposure stimulates an inflammatory response in HPMCs in a dose-dependent manner. Rosiglitazone and losartan appear to have synergetic effects which could decrease fibrosis by inhibiting inflammation and regulating the TGF/Smad signaling pathway, but further studies are needed to elucidate the complex pathways modulated by these drugs.Correspondence to:
B. Lindholm, MD, PhD, Divisions of Baxter Novum and Renal Medicine, Department of Clinical Science, Karolinska Institute, K-56 Karolinska University Hospital Huddinge, 141 86 Huddinge, Sweden
Email: bengt.lindholm@ki.se

Abstract

M. Schneider, K. Thomas, L. Liefeldt, D. Kindgen-Milles, H. Peters, H.-H. Neumayer and S. Morgera

¹Department of Nephrology, ²Department of Infectious Disease, Campus Charité Mitte, Charité-Universitätsmedizin Berlin and ³Anesthesiology Clinic, University of Düsseldorf, Germany
Background: The use of trisodium-citrate for regional anticoagulation of the extracorporal circuit during renal replacement therapy (RRT) has received increased interest, particularly in critically ill patients with increased risk of bleeding. Continuous renal replacement therapies are the most extensively investigated and used procedures in this regard. However, when patients recover from critical illness, RRT is often switched to intermittent procedures. In this prospective study, we investigated the efficacy and safety of citrate anticoagulation during intermittent hemodialysis (IHD) performed with a standard roller blood pump device. Methods: We treated 11 critically ill patients with acute renal failure. These patients received a total of 31 intermittent IHD treatments. The targeted IHD treatment time was 6 h (4.5 l/h treatment dose). For anticoagulation, a 4% trisodium-citrate solution was continuously infused into the arterial line of the extracorporeal circuit. A calcium-free, lactate-based dialysis solution was used in all treatment procedures. Calcium was continuously substituted via a separate central line. Electrolyte and acid-base changes as well as the cardiovascular hemodynamics were analyzed. Results: All patients achieved the targeted filter life time. Filter clotting did not occur. Electrolytes and acid base values were well-maintained throughout the study period. Particularly metabolic derangements were not observed. All treatments were hemodynamically well-tolerated. Conclusions: Intermittent hemodialysis with citrate anticoagulation can be safely applied in critically ill patients at high risk of bleeding.Correspondence to:
PD Dr. med. S. Morgera, Medizinische Klinik mit Schwerpunkt Nephrologie, CCM, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
Email: stanislao.morgera@charite.de

Abstract

K. Katano, Y. Hayatsu, T. Matsuda, R. Miyazaki, K. Yamada, M. Kawano, N. Takahashi, H. Kimura and H. Yoshida

¹Department of Internal Medicine, Fujita Memorial Hospital, Fukui, ²Department of Internal Medicine, Division of Rheumatology, Kanazawa University Graduate School of Medicine, Kanazawa and ³Division of Nephrology, Faculty of Medicine, Fukui University, Fukui, Japan
Renal lesions of IgG4-related disease have been reported recently. Most of them are tubulointerstitial nephritis, and a definite glomerulonephritis complicating IgG4-related disease is very rare. We report here a case of definite glomerulonephritis and concurrent tubulointerstitial nephritis complicating retroperitoneal fibrosis with a high serum level of IgG4. A 68-year-old Japanese woman was referred to our hospital for investigation of anasarca. We diagnosed her disease as a nephrotic syndrome and left hydroureteronephrosis due to retroperitoneal fibrosis. Her laboratory data revealed a high serum level of IgG4, renal injury, hypoproteinemia, hypocomplementemia, a positive finding of circulating immunocomplex (CIC), and negative findings of autologous antibodies suggesting systemic lupus erythematosus (SLE) or Sjögren’s syndrome (SS). A diagnosis of SLE or SS could not be made clinically. Right renal biopsy revealed endocapillary proliferative glomerulonephritis with crescent formation and concurrent tubulointerstitial nephritis. Infiltration of plasma cells in interstitium was more conspicuous than seen with ordinary tubulointerstitial nephritis, and in most of them IgG4 was positive. We placed a percutaneous nephrostomy catheter in her left kidney, and prescribed prednisolone and cyclosporine. The responses to prednisolone and cyclosporine therapies were very good. Further studies are needed to clarify the relationship between glomerulonephritis and IgG4-related disease. However, when considering renal lesions of IgG4-related disease, we think that hypocomplementemia, a positive finding of CIC, negative findings of autologous antibodies suggesting SLE or SS, conspicuous interstitial infiltration of IgG4-positive plasma cells, and a good response to steroid or immunosuppressant therapy are key points.Correspondence to:
K. Katano, MD, Department of Internal Medicine, Fujita Memorial Hospital, 4-15-7, Houei, Fukui, 910-0004, Japan
Email: yukaken@p2332.nsk.ne.jp

Abstract

K. Ohta, M. Shimizu, T. Yokoyama, K. Ohta, A. Nakai, A. Seno, Y. Kasahara, A. Yachie, M. Fujieda and S. Koizumi

¹Department of Pediatrics, ²Department of Laboratory Sciences, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, ³Department of Pediatrics, School of Medicine, Faculty of Medicine, Kochi University, Kochi and ⁴Department of Pediatrics, Kanazawa Medical Center, National Hospital Organization, Kanazawa, Ishikawa, Japan
Background: We report a 16 year-old girl with propylthiouracil (PTU)-induced antineutrophil cytoplasmic antibody (ANCA)-positive glomerulonephritis combined with Henoch-Schönlein purpura nephritis (HSPN) and antiphospholipid syndrome (APS). Case and methods: The patient had Graves’ disease and had been treated with PTU for about 6 years. She complained of arthralgia, epigastralgia, purpura of the lower extremities, anemia, and abnormal urinalysis. Lupus anticoagulant was positive. Additionally, a high level of anti-myeloperoxidase (MPO) antibodies (IgG) and a low level of coagulation factor XIII were recognized. She had several complications including lung bleeding, lacuna infarctions of the right frontal and parietal brain lobes, and deep vein thrombosis of the left lower extremity. We studied tissue histology and carried out MPO-ANCA subtype analysis by immunofluorescence and flow cytometry and MPO-ANCA epitope analysis. Results: Histologically, purpura showed leukocytoclastic vasculitis with perivascular depositions of IgA and complement C3. Renal biopsy showed necrotizing glomerulonephritis with crescents and mesangial IgA deposits. Notably, IgG, IgM, and IgA ANCA were detected in the patient’s serum by flow cytometry and immunofluorescence. We diagnosed an overlap syndrome of ANCA-positive vasculitis, HSPN, and APS. A change in the reactivity of MPO-ANCA from recognition of only the Hg epitope in the C-terminal region to recognition of multiple MPO epitopes was accompanied by a remission of symptoms. Conclusions: This report may provide a very rare description of an overlap syndrome of PTU-induced ANCA vasculitis, HSPN, and APS in which not only IgG ANCA but also IgA and IgM ANCA were found. Epitope analysis may be a useful marker for disease-monitoring of PTU-induced ANCA-positive vasculitis. This case may provide insight into the pathological mechanism underlying each of these diseases.Correspondence to:
K. Ohta, MD, PhD, Department of Pediatrics, Graduate School of Medical Science, Kanazawa University, 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan
Email: kohta@ped.m.kanazawa-u.ac.jp

Abstract

T. Hermle, A.-K. Goestemeyer, P. Sweny and A. Burns

Centre for Nephrology, Royal Free and University College Medical School,
UCL and Royal Free Campus, London, United Kingdom
Wegener’s granulomatosis is a significant cause of end-stage renal disease requiring renal replacement therapy. Treatment of relapses is often difficult as immunosuppressive therapy can be limited by various factors including graft survival in renal transplantation. Rituximab is a novel therapeutic approach in those conditions. We present the case of a 42 year-old Caucasian woman who had been diagnosed with Wegener’s granulomatosis 15 years ago. Predominantly affected organs were kidneys and pituitary gland. Five years later she reached end-stage renal failure and received a renal transplant soon after. She suffered from continuous relapses involving pulmonary hemorrhage and treatment became increasingly difficult. Symptoms resolved soon after single administration of low dose rituximab.Correspondence to:
T. Hermle, MD, Uhlandstrasse 38, 78628 Rottweil, Germany
Email: tobias.hermle@gmail.com

Abstract

L. Esposito, N. Kamar, C. Guilbeau-Frugier, M. Mehrenberger, A. Modesto and L. Rostaing

¹Department of Nephrology, Dialysis and Multiorgan Transplantation,
²Department of Histopathology, CHU Rangueil, Toulouse, France
Linezolid is a recent oral antibiotic used in drug-resistant Gram-positive cocci infections. Herein, we report on the first case of linezolid-related acute renal failure in a kidney-transplant patient. A 60-year-old male having autosomic polycystic kidney disease with liver involvement, on cyclosporin A, mycophenolate mofetil and very low dose prednisolone, presented with an Enterococcus faecium abscess of a huge liver cyst, which was treated by percutaneous drainage and linezolid therapy. Eight days after starting linezolid, he presented with acute renal failure, i.e. serum creatinine increased from 136 – 221 µmol/l, associated with mild hypereosinophilia, anemia and thrombocytopenia. There was no skin rash, arthralgia, eosinophiluria or proteinuria. The transplant kidney biopsy, performed 15 days after the beginning of linezolid therapy, showed interstitial nephritis and focal tubular atrophy. After linezolid withdrawal and increasing prednisolone daily dose to 20 mg/d, within a few days, serum creatinine had decreased; after 2 and 4 weeks post linezolid withdrawal, his serum creatinine was 166 and 159 µmol/l, respectively. Because of the potential side effects of linezolid, i.e. myelosuppression and possibly nephrotoxicity, we recommend close monitoring of these parameters when linezolid therapy is attempted in kidney transplant patients.Correspondence to:
L. Rostaing, CHU, Multiorgan Transplant Unit, University Hospital, 1 avenue Jean Poulhès, TSA 50032, 31059 Toulouse Cedex 9, France
Email: rostaing.l@chu-toulouse.fr

Abstract

M. Sedlak, G. Biesenbach and R. Margreiter

¹Second Department of Medicine, General Hospital Linz, ²Department of General and Transplant Surgery, Medical University of Innsbruck, Austria
Preemptive simultaneous kidney-pancreas transplantation (SKPT) was performed in two patients with Type 1 diabetes and nephrotic syndrome due to diabetic nephropathy, although the native kidneys exhibited near-normal function. Before and 3 months as well as 12 months after SKPT S-creatinine, creatinine clearance (Cr-Cl) and urinary protein excretion were measured. Additionally, 99mTC scintigraphic examinations of the kidneys were performed 3 and 12 months after SKPT. Thereby, the injected 99mTC activities were assessed in the kidney graft as well as in the patient’s native kidneys. Aim of the study was to find out the impact of successful SKPT on proteinuria and further functioning of the patient’s own kidneys after transplantation. Indication for pancreas transplantation was severe diabetic autonomic neuropathy and Brittle diabetes, respectively. In Patient 1, we registered 3 months after SKPT a near-normal protein excretion of mean 0.20 g/24-h urine at a Cr-Cl of 82 ml/ min. The scintigraphic examinations showed 60% of the radioactivity in the kidney graft and 40% in the patient’s own kidneys (22% right and 18% left). Data 1 year after SKPT were: mean protein excretion 0.28 g/24-h urine, Cr-Cl 78 ml/min and in the scan, furthermore, 30% of the activity in the patient’s native kidneys (16% right and 14% left). In Patient 2 after 3 months we obtained a mean protein excretion of 0.18 g/24-h urine at a Cr-Cl of 80 ml/min. Scintigram of the kidneys: 58% of the injected activity were measured in the kidney graft and 42% in the patient’s own kidneys (22% right and 20% left). After 12 months of SKPT we measured a mean protein of 0.26 g/24-h urine and Cr-Cl 78 ml/min. Scintigram of the kidneys: 36% of the activity was in the patient’s native kidneys (18% right and left). We conclude that in diabetic patients with nephrotic syndrome and near-normal function of the native kidneys SKPT leads to rapid and nearly complete diminution of proteinuria although the residual function of the patient’s native kidneys was about 40% at 3 months after transplantation and slightly lower at 12 months after SKPT.Correspondence to:
Dr. G. Biesenbach, 2nd Department of Medicine, General Hospital Linz, Krankenhausstraße 9, 4020 Linz, Austria
Email: georg.biesenbach@akh.linz.at

Abstract

K. Karstila, M. Korpela, S. Sihvonen, H. Helin and J. Mustonen

¹Department of Internal Medicine, Tampere University Hospital, Tampere, ²Division of Pathology, HUSLAB, Helsinki University Hospital and ³Medical School, University of Tampere, Finland
Correspondence to:
Dr. K. Karstila, Department of Internal Medicine, Tampere University Hospital, P.O. Box 2000, 33521, Tampere, Finland
Email: krista.karstila@fimnet.fi

Abstract

H. Matsukura, K. Miya, M. Arai, T. Miyawaki and S. Inaba

¹Department of Pediatrics, Saiseikai Toyama Hospital, Toyama, ²Department of Pediatrics, Faculty of Medicine, University of Toyama, Toyama, and ³Inaba Pediatric Clinic, Uozu city, Toyama, Japan
Correspondence to:
H. Matsukura, Department of Pediatrics, Saiseikai Toyama Hospital, 33-1 Kusunoki, Toyama, 931-8533, Japan
Email: matsukura-npr@umin.net

Abstract

H. Matsukura, K. Kida, K. Miya, H. Kanegane, M. Arai and T. Miyawaki

¹Department of Pediatrics, Saiseikai Toyama Hospital, Toyama, ²Kida Pediatric Clinic, Imizu city, ³Department of Pediatrics, Faculty of Medicine, University of Toyama, Toyama, Japan
Correspondence to:
H. Matsukura, Department of Pediatrics, Saiseikai Toyama Hospital, 33-1 Kusunoki, Toyama, 931-8533, Japan
Email: matsukura-npr@umin.net

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Volume 68, No. 5/2007(November)