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Abstract

Y.F. Xia, S. Huang, X. Li, N. Yang, J. Huang, C. Xue, M. Zhang, J.C.K. Leung, M.F. Lam and J. Li

¹Department of Nephrology, First Affiliated Hospital, ²Department of Medical Genetics, ³Department of Medical Statistics, Zhongshan Medical College, Sun Yat-Sen University, Guangzhou, ⁴Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China
Aims: To investigate the association of megsin A23167G polymorphism with susceptibility and progression of IgA nephropathy in Chinese population. Methods: 435 IgA nephropathy patients and their family members were recruited for a family-based association study. Genotypes of megsin A23167G were determined by direct sequencing. The results were analyzed by transmission disequilibrium test (TDT) and haplotype relative risk (HRR). Clinical data and histological scores of renal lesions were compared between patients with different genotypes. According to disease stability, IgA nephropathy patients were divided into progressive group and stable group. The distribution of genotype frequencies were compared between the 2 groups. Results: TDT revealed that megsin 23167G alleles were transmitted more frequently from heterozygous parents to patients than expected (classical TDT: c2 = 5.435, p = 0.020, extended TDT: c2 = 5.017, p = 0.025). HRR analyses showed significant differences between transmitted and nontransmitted allele frequencies (c2 = 7.006, p = 0.008, HRR = 1.762). The scores of glomerular index and glomerular sclerosis index were higher in GG genotype patients than those in other genotypes (F = 4.570, p = 0.033, F = 4.324, p = 0.038, respectively). The distribution frequency of GG genotype in the progressive group was higher than that of the stable group (c2 = 4.370, p = 0.037). No statistical difference was found in tubulo-interstitial index, vascular index and clinical characteristics between the 2 groups. Conclusion: The polymorphism of megsin A23167G is associated with susceptibility and progression of IgA nephropathy in Chinese population. GG genotype is associated with severe histological lesions and progression of the disease.Correspondence to:
Prof. J. Li
Department of Nephrology
First Affiliated Hospital
Sun Yat-sen Universtiy
74 Zhongshan Road II
Guangzhou 510080, PR China
Email: bq0531@126.com

Abstract

Systemic Epstein-Barr virus infection associated with membranous nephropathy in children

Divisions of ¹Pediatric Nephrology, ²Gastroenterology, ³Immunology and Infectious Diseases, Department of Pediatrics, University of Florida College of Medicine, Gainesville, FL, USA
Epstein-Barr virus (EBV) infection can cause diverse renal manifestations ranging from microscopic hematuria to acute renal failure. Membranous nephropathy (MN) is an uncommon and usually secondary cause of nephrotic syndrome in children, and has been reported after chronic infections and antigenemia. We report two pediatric cases of secondary MN associated with acute and chronic systemic EBV infection. Patient 1 had a liver transplant for cirrhosis due to biliary atresia and developed chronic EB viremia. Membranous nephropathy occurred 3 years later and with aggressive therapy has partially subsided, in temporal association with a drop in blood EBV PCR levels. The other patient had a primary immunodeficiency and developed a lymphoproliferative disorder attributed to EBV. Nephrotic syndrome developed at initial presentation and was associated with MN on biopsy. The patient cleared the virus from blood, which was associated with eventual resolution of the MN. We postulate that EB viremia in patients lacking a fully competent immune system, but without a renal allograft, may create a susceptible environment for chronic systemic EB antigenemia that can then lead to immune-complex MN in the kidney. The association of EBV with renal histological changes consistent with MN has been suggested but not directly described before.Correspondence to:
V.R. Dharnidharka, MD Division of Pediatric Nephrology University of Florida Health Science Center 1600 SW Archer Road PO Box 100296 Gainesville, FL 32610-0296, USA
Email: vikasmd@peds.ufl.edu

Abstract

S. Nakamura, F. Yoshihara, K. Kamide, H. Nakahama, K. Nishigami, K. Fukuchi, H. Ogino and Y. Kawano

¹Division of Hypertension and Nephrology, ²Division of Cardiology, Department of Medicine, ³Department of Radiology and ⁴Department of Vascular Surgery, National Cardiovascular Center, Osaka, Japan
Aims: Renal dysfunction affects the prognosis of patients after aortic surgery. However, the factors associated with the postoperative deterioration of renal function has not been clarified precisely. Method: We prospectively examined renal function in 80 patients (age: 73 ± 7 years, 66 males) who required the elective repair of infrarenal abdominal aortic aneurysm (AAA). Serum creatinine (Scr) was measured. 24-h-creatinine clearance (Ccr) and urinary albumin excretion (UAE) were determined. Renal volume and mean renal length were calculated using the data obtained by ultrasonography. 48 patients showed normal UAE (< 30 mg/day), and 24 had microalbuminuria (30 – 300 mg/day) and 8 had overt proteinuria (> 300 mg/day). Scr were 0.9 ± 0.4, 1.0 ± 0.3 and 2.1 ± 1.3 mg/dl, respectively. Results: On Day 5 after surgery, 12 patients (15%) showed deterioration of renal function as defined either by an increase in Scr (³ 0.5 mg/dl) or by a decrease in Ccr (³ 20%). The acute deterioration of renal function was related to mean renal volume, mean renal length, duration of operation and the use of antibiotics. At Month 12 after surgery, Scr increased in the overt proteinuria group. The deterioration of renal function at Month 12 was found in 8 patients (10%) with microalbuminuria or overt proteinuria, and related to preoperative Ccr, UAE, mean renal volume, mean renal length, smoking status and blood pressure. Conclusion: We conclude that the deterioration of renal function occurred in considerable number of patients with AAA after elective operation on acute and chronic phase, although the development of end-stage renal failure is rare. Factors related to the acute and late deterioration appears to be different. UAE and renal size should be measured, even if Scr is in normal range at preoperative observation.Correspondence to:
S. Nakamura, MD, PhD
Division of Hypertension and Nephrology
Department of Medicine
National Cardiovascular Center
5-7-1 Fujishiro-dai, Suita
Osaka 565-8565, Japan
Email: snakamur@hsp.ncvc.go.jp

Abstract

M. Dickenmann¹, J. Steiger¹, B. Descœudres¹, M. Mihatsch² and V. Nickeleit³

¹Clinic for Transplantation Immunology and Nephrology, Department of Internal Medicine, ²Institute for Pathology, University Hospital, Basel, Switzerland, and ³Department of Pathology, Nephropathology Laboratory, The University of North Carolina, Chapel Hill, NC, USA
Background: C4d deposits in renal transplants are known to be an independent risk factor of graft failure. The current analysis evaluates the impact of C4d deposits on graft function and survival in renal transplants without morphological signs of rejection. Methods: We retrospectively analyzed diagnostic transplant biopsies performed due to allograft dysfunction from June 1994 to June 2001 at the University Hospital in Basel. Study group: Grafts/patients with focal or diffuse positivity of C4d along peritubular capillaries; absence of morphological signs of acute cellular and/or humoral rejection; up to 3 year follow-up analysis post index biopsy. Patients treated with anti-rejection therapy or an increase in maintenance immunosuppression post biopsy (intervention group = IG) were compared to patients with unaltered immunosuppression (standard group = SG). Results: Study group: 22 biopsies/patients out of 400 biopsies (5%) were included into the study, 17 in the SG and 5 in the IG. Patient survival (1-/3-years): SG: 100/94%, IG: 80/80%; graft survival censored for death (1-/3-years): SG: 82.5/68.8%, IG: 100/100%; serum creatinine (µmol/l) at index biopsy/1-year/3-years: SG: 221 ± 70/231 ± 103/245 ± 124, IG: 217 ± 100/143 ± 28/177 ± 55; acute rejection episodes within 1 year post index biopsy: SG: 4 (4 patients), IG: 1 (1 patient); all differences not significant. Lowest serum creatinine within 4 weeks post index biopsy (IG vs. SG): 108 ± 25 vs. 181 ± 61, p = 0.02. Conclusions: C4d positivity in kidney transplants lacking histological evidence of acute rejection is not associated with rapid functional graft deterioration, even in untreated cases. However, anti-rejection therapy results in the improvement of kidney function. Thus, even in grafts with normal histology, the detection of C4d in diagnostic biopsies can be interpreted as a sign of “smoldering” rejection that benefits from therapy.Correspondence to:
M. Dickenmann, MD
Clinic for Nephrology
University Hospital
4056 Basel, Switzerland
Email: mdickenmann@uhbs.ch

Abstract

K. Ulbricht¹, E. Bucha³, K.A. Pöschel¹, G. Stein¹, G. Wolf¹ and G. Nowak²

¹Department of Internal Medicine III, ²Research Unit “Pharmacological Hemostaseology”, Friedrich-Schiller-University Jena, and ³HaemoSys GmbH, Jena, Germany
Aim: The aim of our study was to investigate the use of polyethylene glycol (PEG)-Hirudin (PEG-H) as an anticoagulant in hemodialysis including drug monitoring with the Ecarin Clotting Time (ECT) in whole blood and to compare this regimen with standard anticoagulant unfractionated heparin (UFH) for influence on hemostatic parameters and clot frequency of the extracorporeal system. Patients and methods: The application of PEG-H as an anticoagulant in patients on chronic HD was studied in 20 patients (12 males, 8 females) from a single center in an exploratory, open-label, controlled, single-blind, dose-finding study. The patients were divided in 2 groups with 10 patients each (Group I and II); both received 3 dialyses with UFH, thereafter Group I received 5 dialyses with PEG-H and Group II 10 dialyses with PEG-H. Starting dose of PEG-H in the first dialysis was a bolus of 0.08 mg/kg bwt, the mean dose of the following HD was 0.041 mg/kg bwt (range 0.026 – 0.065 mg/kg bwt). PEG-H was applied as an intravenous bolus-dose followed by a 0.9% saline as a placebo-infusion. HD was performed regularly 3 times a week. All dialysis treatments were performed exclusively with a hollow fiber dialyzer type. Fibrinogen, antithrombin III, prothrombin fragments, thrombin-antithrombin and soluble fibrin were measured with commercial tests. ECT was determined in a mechanical coagulometer. A semiquantitative score was given for the presence of clots in the extracorporeal system after each dialysis. Results: PEG-H was effectively used as an anticoagulant in 150 chronic dialysis treatments using ECT as a simple monitoring method. The optimal whole blood concentration for PEG-H is 600 – 1000 ng/ml. Clotting in the whole extracorporeal system was decreased by 45% (p = 0.059) with PEG-H anticoagulated HD in comparison to UFH. Fibrinogen, prothrombin fragments (F1+2-fragments) and thrombin-antithrombin-complex showed no significant change in comparison with UFH, antithrombin III (AT III) increased to normal concentrations. Highly sensitive coagulation markers such as a soluble fibrin showed a significant decrease (p < 0.001) before and after HD with PEG-H compared with UFH. Conclusion: PEG-H can be used effectively as an alternative anticoagulant in patients on chronic HD using ECT as a simple drug monitoring method. The lower frequency of clots in the extracorporeal system, the stronger and more efficient inhibition of coagulation during HD as indicated by soluble fibrin, may have a positive influence on the disturbed blood coagulation of these patients.Correspondence to:
Dr. med. K. Ulbricht
Klinik für Innere Medizin III
Friedrich-Schiller-Universität Jena
Erlanger Allee 101
07747 Jena, Germany
Email: Kristina.Ulbricht@med.uni-jena.de

Abstract

W.F. Finn

Department of Medicine, University of North Carolina, Chapel Hill, NC, USA
Aims: No conventional phosphate binder is entirely satisfactory for the treatment of hyperphosphatemia in patients with end-stage renal disease (ESRD). Consequently, there is a need for new agents. One such agent is lanthanum carbonate (La). This large-scale study compares the safety of La with standard therapy (any approved phosphate binder) in patients who were treated for up to 2 years. Efficacy, having previously been demonstrated, was a secondary endpoint. Materials and methods: After washout, patients were randomized to receive La (n = 682) or their pre-study phosphate binder (n = 677). Over a 6-week period, La was titrated to a maximum daily dose of 3,000 mg elemental lanthanum (serum phosphorus target levels for titration were £ 5.9 mg/dl (1.90 mmol/l)). Safety assessments included adverse events (AEs), full laboratory parameters and blood profiles. Efficacy assessments included serum phosphorus, calcium, calcium × phosphorus product and parathyroid hormone (PTH) levels. Results: Average treatment exposure was greater in the standard therapy group (501.4 days) than in the La group (370.3 days) because standard therapy patients who switched or combined treatments were allowed to continue in the study. The most common AEs were gastrointestinal. The incidences of AEs in the La and treatment exposure-corrected standard therapy groups were nausea, 37 versus 29%; vomiting, 27 versus 22% and diarrhea (24% in each group). Hypercalcemia that was reported as an AE (La versus treatment exposure-corrected standard therapy) occurred in 4.3% and 8.4% of patients, respectively. There was no indication of liver toxicity, suppression of erythropoiesis or changes in the mini-mental state examination. Over 2 years, phosphorus control was similar in both groups; in the La group, however, serum calcium was lower and serum PTH levels were maintained in the range recommended by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI). Conclusions: The 2-year tolerability and efficacy of La are similar to those seen with standard therapy, although lower serum calcium levels and improved PTH levels were observed in the La group. These results support La as a viable new option for the management of hyperphosphatemia in ESRD.Correspondence to:
Prof. W.F. Finn
Department of Medicine
Division of Nephrology and Hypertension
University of North Carolina
CB 7155, 348 MacNider Building
Chapel Hill, NC 27599-7155, USA
Email: wffinn@med.unc.edu

Abstract

T.H. Westhoff, R. Waldherr, C. Loddenkemper, W. Ries, W. Zidek and M. van der Giet

¹Medical Clinic IV, Nephrology, Charité-Campus Benjamin Franklin, ²Institute of Pathology, Heidelberg, ³Institute of Pathology, Charité-Campus Benjamin Franklin, Berlin, ⁴Diakonissen Hospital, Flensburg, Germany
Background: Mesangial deposition of IgA (MCA) is a very rare finding in minimal change disease and has previously been considered a pure coincidence. In the US and Europe only anecdotal case reports exist. To date, there has been no consensus on nomenclature and categorization of this entity. We describe 2 cases of MCA with analogue histological findings but relevant differences in clinical presentation, and we discuss the clinical implications of mesangial IgA deposition in minimal change nephrotic syndrome. Patients: A 47-year-old female was admitted to hospital with nephrotic syndrome, microscopic hematuria, arterial hypertension and slight impairment of renal function 3 weeks after an unspecific upper airway infection. A 42-year-old male presented with nephrotic syndrome, microscopic hematuria, normotension and normal renal function. Both of the nephrotic syndromes were steroid-responsive and steroid-dependent. Findings: The clinical presentation of the male patient was consistent with the features of minimal change glomerulopathy, whereas the female patient combined signs of minimal change disease and IgA nephropathy. Light microscopy revealed mesangial IgA immune deposits and slight mesangial hypercellularity. Electron microscopic studies of MCA patients disclose diffuse effacement of glomerular foot processes. Conclusion: Our cases and a review of the literature indicate that the histological diagnosis of MCA may comprise different pathogenetic entities. From the clinical point of view, MCA has to be regarded as a minimal change nephrotic syndrome with symptomatic or asymptomatic mesangial IgA deposition. IgA deposition constitutes a risk factor for impairment of renal function and indicates a frequently relapsing course.Correspondence to:
Dr. med. T.H. Westhoff
Charité, Campus Benjamin Franklin
Medical Clinic IV, Nephrology
Hindenburgdamm 30
12200 Berlin, Germany
Email: timm.westhoff@charite.de

Abstract

N. Kanaan, Y. Horsmans and E. Goffin

Departments of ¹Nephrology and ²Gastroenterology, Université catholique de Louvain, Cliniques Universitaires St Luc, Brussels, Belgium
A 57-year-old man presented with nephrotic syndrome associated with active HBV infection. Liver biopsy showed severe portal and moderate lobular inflammation, patchy necrosis, moderate fibrosis and several “ground glass” cells. Immunofluorescence microscopical view of the renal biopsy showed diffuse granular IgG deposits along the glomerular basement membrane, compatible with MN. As symptomatic therapy with ACE inhibitors did not improve the nephrotic syndrome, lamivudine 100 mg o.d. was initiated. HBV-DNA became undetectable after 10 weeks and seroconversion of HBeAg and HBsAg to anti-HBe and anti-HBs occurred after 2 additional months; proteinuria normalized subsequently. This observation documents for the first time in an adult the beneficial effect of lamivudine in glomerulonephritis related to HBV infection with HBV seroconversion and complete remission of the nephrotic syndrome. Correspondence to:
Dr. N. Kanaan
Cliniques Universitaires St Luc
Université catholique de Louvain
Av Hippocrate 10
1200 Brussels, Belgium
Email: nada_kanaan@hotmail.com

Abstract

Y.K. Wen and M.L. Chen

¹Division of Nephrology, Department of Medicine, ²Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
We describe a 39-year-old man with hepatitis B virus- (HBV) related chronic hepatitis who presented with nephrotic syndrome and decompensated cirrhosis. A kidney biopsy revealed membranoproliferative glomerulonephritis (MPGN) which was thought to be related to the HBV infection. Because interferon-a therapy was generally not recommended in patients with advanced liver disease, we chose lamivudine as an alternate treatment for the HBV-associated glomerulonephritis (GN). After 3-month treatment with oral lamivudine, resolution of the renal disease dramatically occurred together with improvement in liver function. To our knowledge, this is the first case of HBV-associated MPGN successfully treated with oral lamivudine therapy. The possible role of lamivudine in the treatment of HBV-associated GN is discussed.Correspondence to:
Dr. Y.K. Wen Division of Nephrology Department of Medicine Changhua Christian Hospital 135 Nansiao St., Changhua, 500, Taiwan
Email: 9965@cch.org.tw

Abstract

W.M. Bernhardt, J.C. Schefold, W. Weichert, B. Rudolph, U. Frei, D.A. Groneberg and R. Schindler

¹Division of Nephrology and Hypertension, Friedrich Alexander University Erlangen-Nürnberg, Erlangen, ²Department of Nephrology and Intensive Care, ³Institute of Pathology, ⁴Otto Heubner Center, Pneumology and Immunology, Charité School of Medicine, Free University and Humboldt University, Berlin, Germany
Introduction: In small bowel disease such as M. Crohn, the intestinal absorption of oxalate is increased. Severe calcium oxalate deposition in multiple organs as consequence of enteric hyperoxaluria may lead to severe organ dysfunction and chronic renal failure. The management of hemodialyzed patients with short bowel syndrome may be associated with vascular access problems and oxalate infiltration of the bone marrow leading to pancytopenia. Although the risk of recurrence of the disease is very high after renal transplantation, it may be the ultimate therapeutic alternative in secondary hyperoxaluria. Case: Here, we report a patient with enteric oxalosis due to Crohn’s disease. He developed end-stage renal disease, erythropoietin-resistant anemia, oxalate infiltration of the bone marrow and severe vascular access problems. Following high-urgency kidney transplantation, daily hemodiafiltration of 3 hours was performed for 2 weeks to increase oxalate clearance. Despite tubular and interstitial deposition of oxalate in the renal transplant, the patient did not require further hemodialysis and the hematocrit levels normalized. Discussion: Early treatment of hyperoxaluria due to short bowel syndrome is essential to prevent renal impairment. Declining renal function leads to a further increase in oxalate accumulation and consecutive oxalate deposition in the bone marrow or in the vascular wall. If alternative treatments such as special diet or daily hemodialysis are insufficient, kidney transplantation may be a therapeutic alternative in severe cases of enteric oxalosis despite a possible recurrence of the disease.Correspondence to:
Dr. W.M. Bernhardt
Department of Nephrology and Hypertension
Friedrich Alexander University
Krankenhausstraße 12
91054 Erlangen, Germany
Email: wanja.bernhardt@med4.med.uni-erlangen.de

Abstract

T. Kusaba, T. Hatta, S. Tanda, H. Kameyama, K. Tamagaki, M. Okigaki, T. Inaba, C. Shimazaki and S. Sasaki

¹Division of Hypertension and Nephrology, ²Division of Hematology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan
A 48-year-old man was admitted to our hospital for investigation of mild renal dysfunction. A blood examination revealed mild elevation of creatinine level (1.77 mg/dl). Urinary examination revealed mild protein excretion (0.54 g/day) and microhematuria; renal biopsy revealed the focal proliferation of large mononuclear cells with mitosis in glomerular capillaries. According to immunohistochemical analysis, the intravascular lymphomatous cells stained positively with anti-leukocyte common antigen (LCA: CD45) and CD20, indicating a B lymphocyte lineage. In electron microscopy, the glomerular capillary was filled with lymphoma cells and epithelial foot process fusion was noted. Immunohistochemical analysis on adhesive molecules revealed a lack of CD11a expression on lymphoma cells, but positive CD54 expression on endothelial cells. Systemic 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) revealed no abnormal uptake of isotopes. On the basis of these findings, we diagnosed intravascular diffuse large B cell lymphoma localized in the kidney. Despite treatment with rituximab and CHOP (prednisolone, doxorubicin, vincristine, cyclophosphamide) for 3 cycles at 1-month intervals, the renal dysfunction did not change. In histopathological analysis of the second biopsy, lymphoma cells disappeared, but focal segmental glomerulosclerosis and moderate interstitial fibrosis were noted. Electron microscopic findings revealed severe subendothelial edema with mesangial interposition, indicating severe endothelial damage. Epithelial foot process fusion was improved. These pathological analyses let us conclude that a lack of CD11a could be a candidate factor for prevention of the extravasation of lymphoma cells from blood vessels in our patient. We also presumed that the intraglomerular endothelial damage occurred due to chemotherapy-associated cell injury.Correspondence to:
T. Kusaba, MD Division of Nephrology and Hypertension Department of Medicine Kyoto Prefectural University of Medicine 456 Kajii-cho Kamigyo-ku Kyoto-city, Japan, 602-8566
Email: fwnk5760@mb.infoweb.ne.jp

Abstract

Y. Yang, K. Ohta, M. Shimizu, A. Nakai, Y. Kasahara, A. Yachie and S. Koizumi

Abstract

K. Ohta

Abstract

A. Scholze, M. Borchert and M. Tepel

Abstract

A. Mountricha, E. Platsouka, C. Pappas, S. Vourli, E. Velonakis, V. Hadjiconstantinou, A. Vatopoulos and O. Paniara

Abstract

I. Tzanakis, E. Alifieris, N. Kareffylakis, A. Papadaki, S. Kagia, V. Spandidakis and N. Kallivretakis

Abstract

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Volume 65, No. 3/2006(March)