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Abstract

B. Bicanski, M. Wenderdel, Peter R. Mertens, J. Senderek, U. Panzer, O. Steinmetz, R.A.K. Stahl, G. Cerullo, D. Diletta Torres, F.P. Schena, K. Zerres and J. Floege

¹Division of Nephrology and Clinical Immunology, ²Department of Genetics, RWTH University of Aachen, ³Department of Medicine, Division of Nephrology, Rheumatology and Osteology, University of Hamburg, Germany, ⁴Department of Nephrology, University of Bari, Italy
Background: Few genetic factors have been identified that determine susceptibility to and progression of IgA-nephropathy (IgAN). Given that IgAN is usually characterized by mesangioproliferative glomerulonephritis and that PDGF-B is of central pathophysiological relevance in this process, we analyzed four single-nucleotide polymorphisms (SNPs) of the PDGF-B gene to evaluate a possible association of these SNPs with disease onset and progression, histological grading and responses to ACE inhibitor (ACEi) therapy. Methods: The total study population consisted of 195 IgAN patients (127 from southern Italy and 68 from northern Germany) and 200 healthy controls (100 from each region). All four SNPs were in Hardy-Weinberg equilibrium and genotype distributions did not differ between patients and controls in either region. Results: SNP distribution in Italian patients reaching end-stage renal disease (n = 45) also was not significantly different from patients maintaining a serum creatinine below 1.2 mg/dl (n = 60) during 5.6 ± 5.5 years of follow-up. Furthermore, we failed to detect significant effects of any SNP on the slope of 1/serum creatinine, proteinuria level or the antiproteinuric response to ACEi. Additionally, particular PDGF-B genotypes did not correlate with histological grading using the Lee classification. Conclusion: We conclude that none of the four PDGF-B SNPs is related to the onset of IgAN in two different populations and that none of them has a major influence on the course of IgAN.Correspondence to:
B. Bicanski, MD Division of Nephrology and Clinical Immunology RWTH Aachen Pauwelstraße 30 52057 Aachen, Germany
Email: BojanBicanski@gmx.de

Abstract

C.S. Lim, S.M. Kim, Y.K. Oh, Y.S. Kim, D.-W. Chae, J.S. Han, S. Kim, J.S. Lee and H.J. Yoon

¹Department of Internal Medicine, Seoul National University Boramae Hospital, ²Department of Internal Medicine, Seoul National University College of Medicine, ³Seoul Clinical Genomics Inc., Seoul, Korea
Aims: Clara cell secretory protein (CC16) is a protein with anti-inflammatory and immunomodulatory properties. Moreover, both CC16 gene knockout and antisense-transgenic mouse models developed glomerulonephritis resembling IgA nephropathy (IgAN). In the present study, we evaluated the influence of the G38A polymorphism in the CC16 gene exon 1 on the development and progression of IgAN. Methods: Korean patients with biopsy-proven IgAN (n = 267) with a minimal follow-up of 4 years (mean ± SD 103.8 ± 52.6 months) were recruited. Healthy normal subjects (n = 315) were included as controls. The G38A polymorphism was determined using the polymerase chain reaction-restriction fragment length polymorphism method. Results: GG, GA and AA genotype frequencies were 36.3, 50.2 and 13.5% in IgAN patients, respectively, and 34.3, 50.2 and 15.5% in controls (chi2 = 0.596, p = 0.742). The G allele frequency was 0.614 in IgAN patients and 0.594 in controls (chi2 = 0.429, p = 0.512). Moreover, the GG genotype frequencies were 40.4% in patients showing stable disease course and 26.6% in those with progressive disease (chi2 = 4.029, p = 0.045). Patients with the GG genotype showed a better outcome by Kaplan-Meier analysis in terms of renal survival (p = 0.043). The CC16 polymorphism remained an independent risk factor for progression after multivariate analysis (Cox regression model, HR for CC16 AA genotype: 2.34, 95% CI 1.19 – 4.64, p = 0.014). Conclusion: Our results suggest that CC16 gene G38A polymorphism is not associated with the development of IgAN, but that it is an important marker of progression in IgAN.Correspondence to:
C.S. Lim, MD
Department of Internal Medicine
Seoul National University Boramae Hospital,
425 Sindaebang2-dong, Dongjak-gu, Seoul 156-707, Korea
Email: cslimjy@snu.ac.kr

Abstract

N. Thilly, S. Boini, C. Loos-Ayav, M. Kessler, S. Briançon and L. Frimat

¹Department of Clinical Epidemiology and Evaluation, CEC-CIE⁶ Inserm (EA ⁴⁰⁰³), ²Department of Nephrology, University Hospital of Nancy, Nancy, France
Background and aims: Despite guidelines concerning the management of renal anemia, the international literature reports that a large proportion of pre-dialysis patients have hemoglobin values lower than the recommended level. The present study analyzed the evolution of pre-dialysis Hb levels and erythropoietin use over a 4-year period and investigated factors associated with anemia. Methods: A total of 1,315 patients initiating dialysis in Lorraine, France, were enrolled since 2001 – 2004. For each year, anemia, defined by Hb < 11 g/dl, and erythropoietin use were investigated in three groups: all patients, patients whose dialysis was planned and patients whose dialysis was unplanned. Results: At initiation of dialysis, all groups showed increases over time in mean hemoglobin levels, proportion of patients without anemia and with erythropoietin therapy. Among patients whose first dialysis was planned in 2004, 43.8% had anemia and 67.9% had received erythropoietin, compared with 75.4% and 29.4%, respectively, when dialysis was unplanned. Patients receiving unplanned dialysis were more likely to have anemia (odds ratio (OR) = 2.6), as were those with a serum albumin level < 3.5 g/dl (OR = 2.1), body mass index < 30 kg/m2 (OR = 1.9) (all p < 0.001) or glomerular filtration rate < 10 ml/min/1.73 m2 (OR = 1.4, p = 0.04). The year of dialysis initiation was also associated with anemia (p = 0.024). Conclusion: The proportion of patients starting dialysis with anemia might be reduced by earlier nephrology referral leading to erythropoietin administration, planned first dialysis while residual renal function remains, and greater attention to nutritional status.Correspondence to:
Dr. N. Thilly, PhD Service d’Epidémiologie et Evaluation Cliniques (EA 4003) CHU Nancy, CO No. 34 54035 Nancy cedex, France
Email: n.thilly@chu-nancy.fr

Abstract

F.R. Hernandes, F.C. Barreto, L.A. Rocha, S.A. Draibe, M.E.F. Canziani and A.B. Carvalho

Nephrology Division, Federal University of São Paulo, São Paulo, Brazil
Background: Chronic kidney disease (CKD) patients are at a high risk of dying from a cardiovascular event, mainly due to coronary calcification. Among the various uremic and dialysis-specific risk factors for coronary calcification are mineral metabolism disorders. The role that secondary hyperparathyroidism (SHPT) consequent to the altered calcium and phosphate metabolism plays in the pathogenesis of coronary calcification remains unclear. The aim of this study was to evaluate the prevalence of coronary artery calcification in dialysis patients with severe SHPT submitted to multislice coronary tomography (MSCT) and to identify risk factors for coronary calcification. Methods: This study involved 23 adult dialysis patients (age > 18 years) with severe SHPT who were candidates for parathyroidectomy (PTX). All were submitted to MSCT and bone densitometry during the month preceding PTX. Fasting blood samples were collected immediately before surgery. Markers of mineral metabolism, including ionized calcium, phosphorus, alkaline phosphatase, intact-parathyroid hormone (iPTH), osteoprotegerin (OPG) and soluble receptor activator of nuclear factor-kappaB ligand, were analyzed. Dyslipidemia was assessed by determination of LDL, HDL and VLDL-cholesterol and triglyceride levels. Agatston units (AU) were used to calculate calcium scores. Results: No coronary calcification was found in 30% of the patients. Moderate (calcium score > 100 AU) and severe (calcium score > 400 AU) calcification was observed in 12 and 36% of the patients, respectively. In the univariate analysis, calcium volume correlated positively with VLDL-cholesterol (r = 0.44; p = 0.03) and, albeit less than significantly, with age (r = 0.35; p = 0.09), triglycerides (r = 0.39; p = 0.05) and Framingham risk index (r = 0.37; p = 0.07). We also found that OPG correlated negatively with bone mineral density at the L2-L4 lumbar vertebrae (r = –0.54; p = 0.007) and femoral neck (r = –0.43; p = 0.04). Conclusions: Although high levels of PTH should be considered a risk factor for cardiovascular death, the real role of severe SHPT on coronary calcification is to be clarified. Correspondence to:
F.R. Hernandes Rua Borges Lagoa, 960, 2nd floor, ZIP 04038-002, São Paulo, Brazil
Email: drafabi@hotmail.com

Abstract

J.G. Heaf

Department of Nephrology, Copenhagen University Hospital, Herlev, Denmark
Background: Acute initiation of dialysis is associated with increased morbidity due to access and uremia complications. It is frequent despite early referral and regular out-patient control. We studied factors associated with end-stage renal disease (ESRD) progression in order to optimize the timing of dialysis access (DA). Methods: In a retrospective longitudinal study (Study 1), the biochemical and clinical course of 255 dialysis and 64 predialysis patients was registered to determine factors associated with dialysis-free survival (DFS). On the basis of these results an algorithm was developed to predict timely DA, defined as > 6 weeks and < 26 weeks before dialysis initiation, with too late placement weighted twice as harmful as too early. The algorithm was validated in a prospective study (Study 2) of 150 dialysis and 28 predialysis patients. Results: Acute dialysis was associated with increased 90-day hospitalization (17.9 vs. 9.0 days) and mortality (14% vs. 6%). P-creatinine and p-urea were poor indicators of DFS. At any level of p-creatinine, DFS was shorter with lower creatinine clearance and vice versa. Patients with systemic renal disease had a significantly shorter DFS than primary renal disease, due to faster GFR loss and earlier dialysis initiation. Short DFS was seen with hypoalbuminemia and cachexia; these patients were recommended early DA. The following algorithm was used to time DA (units: µM and ml/min/1.73 m2): P-Creatinine – 50 × GFR + (100 if Systemic Renal Disease) > 200. Use of the algorithm was associated with earlier dialysis placement and a fall in acute dialysis requirements from 50% to 23%. The incidence of too early DA was unchanged (7% vs. 9%), and was due to algorithm non-application. The algorithm failed to predict imminent dialysis in 10% of cases, primarily due to acute exacerbation of stable uremia. Dialysis initiation was advanced by approximately one month. Conclusions: A predialysis program based on early dialysis planning and GFR-based DA timing may reduce the requirement for acute dialysis initiation and patient morbidity and mortality, at the cost of slightly earlier dialysis initiation.Correspondence to:
J. Heaf
Department B, KAS Herlev
2730 Herlev, Denmark
Email: heaf@dadlnet.dk

Abstract

L. Decelle, J.-P. Cosyns, B. Georges, M. Jadoul and C. Lefebvre

Departments of ¹Internal Medicine, ²Pathology, ³Nephrology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain, Brussels, Belgium
We report the case of a 42-year-old man who developed biopsy-confirmed acute interstitial nephritis (AIN) after cocaine sniffing. He required a few hemodialysis sessions but fully recovered within 3 weeks after cocaine withdrawal and a short course of corticosteroids. AIN should be recognized as a potential cause of acute renal failure in cocaine users, and a history of cocaine use should be carefully elicited in patients with unexplained AIN.Correspondence to:
Prof. M. Jadoul Department of Nephrology Cliniques Universitaires Saint-Luc Université catholique de Louvain 1200 Brussels, Belgium
Email: jadoul@nefr.ucl.ac.be

Abstract

C.K. Hsieh, Y.P. Hsieh, Y.K. Wen and M.L. Chen

¹Division of Nephrology, Department of Medicine, and
²Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
Focal segmental glomerulosclerosis (FSGS) may be idiopathic or secondary to a variety of causes. Clinical distinction between primary and secondary forms of FSGS has crucial therapeutic consequences. Whereas the former may respond to immunosuppressive therapy, treatment of secondary forms of FSGS must aim to resolve the underlying diseases. Although the combination of nephrotic syndrome and Cushing’s syndrome has been described anecdotally, the causal relationship between these two diseases remains controversial. We report herein a 37-year-old man who presented with lower extremity pitting edema. Heavy proteinuria and mild renal insufficiency prompted to perform a kidney biopsy and the specimen showed FSGS. On the other hand, admission physical examination was notable for a Cushingoid appearance. After endocrinological investigations, the patient was diagnosed as having Cushing’s disease caused by pituitary adrenocorticotropic hormone-producing microadenoma. Immunosuppressive therapy for the treatment of FSGS was not carried out and we treated his Cushing’s disease with transsphenoidal resection of the pituitary microadenoma. Surprisingly, resolution of heavy proteinuria occurred when the patient’s physical features characteristic of Cushing’s disease were gradually resolved 3 months later. This case suggests a possible association of Cushing’s disease with FSGS.Correspondence to:
Dr. Y.K. Wen
Division of Nephrology
Department of Medicine
Changhua Christian Hospital
135 Nansiao Street
Changhua, 500 Taiwan
Email: 45440@cch.org.tw

Abstract

C. Courtellemont, J. Guitard, M. Mehrenberger, S. Pontier, D. Ribes, N. Kamar, L. Esposito, A. Modesto and L. Rostaing

¹Department of Nephrology, Dialysis and Multiorgan Transplantation,
²Department of Histopathology, CHU Rangueil and
³Department of Pneumology, CHU Rangueil-Larrey, Toulouse, France
Background: Many etiologies lead to thrombotic microangiopathy (TMA), amongst which are antineoplastic chemotherapies. Gemcitabine, a nucleoside analogue, has been approved for the treatment of bladder and advanced non-small cell lung carcinomas (NSCLC). The reported incidence of gemcitabine-associated TMA in the literature is low, ranging from 0.015 – 0.31%. Methods: Herein, we describe the first reported case of gemcitabine-induced TMA in a renal transplant patient. This occurred in a 54-year-old male transplant recipient undergoing sirolimus-based immunosuppression. In February 2005, he was diagnosed to have NSCLC, for which he received dual chemotherapy, including carboplatin and gemcitabine. After the third cycle he developed TMA. Results: On admission, he presented with weakness, edema, normal blood pressure, leucopenia (2,440/mm3), thrombopenia (11,000/mm3), hemolytic anemia with hemoglobin at 8 g/dl, schistocytes between 18 – 33‰, increase in lactate dehydrogenase at 600 IU/l (N < 380), and decreased haptoglobin at 0.29 g/l. Renal function was stable: serum creatinine was 1.3 mg/dl, albuminemia 30 g/l, proteinuria was present at 3 g/l in association with microscopic hematuria, and sirolimus trough level was 6.4 ng/ml. Treatment included infusions of fresh frozen plasma, withdrawal of sirolimus, which was replaced by mycophenolate mofetil, and suspension of chemotherapy. He fully recovered from TMA within 4 weeks. The concomitant use of sirolimus, which inhibits vascular endothelial growth factor, plus gemcitabine may have resulted in TMA.Correspondence to:
Prof. L. Rostaing
Department of Nephrology, Dialysis and Transplantation,
CHU Rangueil,
1 avenue Jean Poulhes, TSA 50032,
31059 Toulouse Cedex 9, France
Email: rostaing.l@chu-toulouse.fr

Abstract

C. Shapiro and M. Coco

Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA
Calciphylaxis or calcific uremic arteriolopathy (CUA), not uncommon in the dialysis population, has also been reported in renal transplant recipients with varying stages of renal dysfunction. While cutaneous involvement in both populations is the most common feature, visceral involvement is rarely described. We report a patient with a long-standing functioning renal allograft who presented with visceral calciphylaxis in a Dieulafoy lesion requiring gastrectomy. Histopathology revealed typical features of CUA. The current literature describing CUA in post-transplant patients is reviewed.Correspondence to:
M. Coco, MD, MS Montefiore Medical Center 111 East 210th Street Bronx, New York 10467, USA
Email: mcoco@montefiore.org

Abstract

C. Johanssen, D. Mereles, S. Hardt, S.J. Buss and M. Zeier

¹Department of Cardiology, and ²Department of Nephrology, University of Heidelberg, Germany
Mitral annulus calcification is one of the most common cardiac calcifications. In patients with end-stage renal disease undergoing echocardiography, it can be detected in more than 40%. A specific form of mitral annulus calcification is liquefaction necrosis. It is often not adequately recognized by echocardiographers or clinicians and can be mistaken for cardiac tumor or infective vegetation. Here we report a case of liquefaction necrosis of mitral annulus calcification, mimicking an infective vegetation of the mitral valve apparatus in a patient with chronic renal failure.Correspondence to:
C. Johanssen, MD Division of Cardiology Department of Medicine Im Neuenheimer Feld 410 69120 Heidelberg, Germany
Email: Celine.Johanssen@med.uni-heidelberg.de

Abstract

Y. Uchiyama-Tanaka, Y. Mori and H. Matsubara

Department of Medicine, Division of Cardiology and Nephrology, Kyoto Prefectural University of Medicine, Kyoto, Japan
Correspondence to:
Y. Uchiyama-Tanaka, MD, PhD Department of Medicine Division of Cardiology and Nephrology Kyoto Prefectural University of Medicine Kamigyoku, Kyoto 606-8507, Japan
Email: mvkq97361@leto.eonet.ne.jp

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Volume 67, No. 2/2007(February)