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Abstract

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Abstract

V. Guru and S.E. Fremes

Divisions of Cardiovascular Surgery, Sunnybrook and Women’s College Health Sciences Center, University of Toronto, Toronto, Canada
Introduction: There have been many small randomized controlled trials evaluating the effectiveness of N-acetylcysteine (NAC) in preventing radiographic contrast-induced nephropathy. Most studies have suggested a beneficial NAC effect. This meta-analysis describes the effect of NAC in the prevention of radiographic contrast-induced nephropathy in the aggregated trial data. Methods: A search using MEDLINE from 1966 to December 2003 identified all randomized control trials that evaluated NAC in those patients at risk of acute renal failure (ARF) following either angiographic or CT scan contrast exposure. All studies included in the review employed the use of either low-osmolar (n = 9 trials) or iso-osmolar (n = 2 trials) contrast agents. The outcome of interest was ARF as defined by a rise in serum creatinine (Cr ³ 0.5 mg/dl rise or > 25% increase from baseline) after exposure to contrast. The data were aggregated by the methods of Mantel and Haenszel. Results: The overall summary odds ratio estimate of 0.46 (95% confidence interval 0.32 – 0.66) suggests a strong protective effect of NAC in preventing radiographic-induced nephropathy. Conclusion: In summary, there is good aggregate trial evidence to suggest that patients who have an elevated serum creatinine level at baseline benefit from receiving periprocedure NAC in the prevention of contrast-induced ARF.Correspondence to:
V. Guru, BSc, MD
Sunnybrook and Women’s College Health Sciences Center
2075 Bayview Avenue, H-410
Toronto, Ontario M4N 3M5, Canada
Email: veena.guru@utoronto.ca

Abstract

R. Ficek, F. Kokot, J. Chudek, M. Adamczak, J. Ficek and A. Wiecek

Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of Silesia, Katowice, Poland
Background: Acute renal failure (ARF) is characterized by impaired excretory, endocrine, homeostatic and metabolic function of the kidneys. It is well-known that leptin is an adipose-derived polypeptide hormone which is predominantly biodegraded by the kidneys. Therefore, plasma leptin concentration is increased in chronic renal failure (CRF). However, its’ concentrations in patients with ARF were not investigated until now. The aim of the present study was to evaluate plasma leptin concentration in patients with ARF. Patients and methods: 27 patients with ARF (age 44 ± 4 years, BMI 26.0 ± 0.9 kg/m2, means ± SEM, 17 patients 15 M, 2 F recovered kidney function and 10 patients 7 M, 3 F died during the anuric phase), 27 hemodialysis patients (22 M, 5 F; age 45 ± 2 years; BMI 26.2 ± 0.8 kg/m2) with chronic renal failure (CRF) and 27 healthy subjects (HS) (22 M, 5 F; age 42 ± 3 years; BMI 25.9 ± 0.6 kg/m2) were examined. In patients with ARF, blood samples for plasma leptin and routinely assessed biochemical parameters were withdrawn before the first HD session (I), and in patients who survived a second time 5 days later during the anuric/oliguric phase (II), and a third one during the polyuric phase before discharge of the patient from hospital (III). In patients with CRF all examined parameters were estimated only once before a subsequent HD session. Results: Patients with ARF (before the first HD session) and CRF did not differ significantly with respect to BMI, serum creatinine and blood hydrogen ion concentrations. Plasma leptin level in patients with ARF before the first HD session was similar to values obtained in HS, but significantly lower (p < 0.01) than in patients with CRF (2.5 (1.9 – 8.2) vs. 3.4 (2.5 – 8.3) vs. 8.4 (2.9 – 16.9) ng/ml in ARF, HS and CRF, respectively). There was no significant difference in leptinemia between patients with ARF who survived and who died. In patients with ARF who survived, improvement of renal function was accompanied by a slightly (not significant) declining tendency in plasma leptin concentration (5.6 ± 2.2 vs. 4.8 ± 1.7 vs. 4.5 ± 1.3 ng/ml; I, II, III phases of ARF, respectively). Conclusions: In contrast to hemodialysis patients with chronic renal failure, patients with acute renal failure are characterized by normal plasma leptin concentration. Thus, difference in leptinemia between patients with chronic and acute renal failure seems to be due to preservation of large amounts of active renal parenchyma in ARF patients. Correspondence to:
Prof. Dr. A. Wiecek
Department of Nephrology
Endocrinology and Metabolic Diseases
Medical University of Silesia
Katowice, ul. Francuska 20/24
40-027 Katowice, Poland
Email: awiecek@spskm.katowice.pl

Abstract

O. Schück, V. Teplan, M. Stollová and J. Skibová

Institute for Clinical and Experimental Medicine, Prague, Czech Republic
Background: Serum cystatin C (Scyst) has an obvious advantage in recognizing the initial stages of renal impairment. However, several recent studies suggest that Scyst may also be affected by some nonglomerular factors such as thyroid dysfunction, glucocorticoid administration or metabolic status of the diabetic patient. The aim of this study was to evaluate whether obesity could affect Scyst. Patients and methods: The study was performed in 33 patients (mean age 49.1 ± 6.3 years) with chronic renal disease (Scr = 227 ± 118 mmol/l) and BMI = 35.6 ± 1.8 kg/m2, and in 78 patients (mean age 43.4 ± 5.1 years) with chronic renal disease (Scr = 245 ± 111 mmol/l) and BMI = 24.0 ± 1.8 kg/m2. Glomerular filtration rate (GFR) was determined using renal inulin clearance (Cin) under conditions of stabilized plasma concentrations and water loading. Scyst was measured using immunonephelometry. For statistical evaluation, linear regression analysis and receiver-operating characteristic (ROC) curve analysis were used. Results: A significant correlation (r = 0.956, p < 0.001) between 1/Scyst and Cin was demonstrated in patients with BMI ³ 30 kg/m2 (Group A). Similarly, a significant correlation (r = 0.900, p < 0.001) between 1/Scyst and Cin was found in patients with BMI < 30 kg/m2 (Group B). There was no significant difference between the regression straight lines characterizing these relationships. ROC curve analysis (using a cut-off value for Cin = 30 ml/min/1.73 m2) did not show significant differences in AUC, sensitivity and specificity for Scyst between obese and nonobese patients. Conclusion: The results suggest that evaluation of GFR based on Scyst in obese patients need not differ from that in nonobese ones. Correspondence to:
Dr. O. Schück
Institute for Clinical and Experimental Medicine
Vídeòská 1958/9
140 21 Prague 4, Czech Republic
Email: otto.schuck@medicon.cz

Abstract

A. Saracino, L.F. Morrone, V. Suriano, A. Niccoli-Asabella, A. Ramunni, M. Fanelli, G. Rubini and P. Coratelli

Nephrology and ²Nuclear Medicine Units, Department of Internal and
Public Medicine, University of Bari, Italy
Aim: The Cockcroft and Gault formula is a quick and reliable method for calculating creatinine clearance without a 24-hour urine collection (CG-cl). In obese subjects an excess of fat mass provokes a reduction in daily creatinine urine excretion per body kilo weight and is responsible for overestimated renal function when calculated by CG-cl. The aim of this study was to devise a simple correction method which could also make use of CG-cl in obese subjects. Patients and methods: In 52 subjects with a body mass index (BMI) > 25, renal function was assessed by simultaneously determining creatinine clearance using 24-hour urine collection (Cr-cl) and the CG-cl. The percentage difference between the 2 clearances (_VP_EQN_0.GIF %) was correlated with BMI for each patient using simple linear regression analysis. The estimated regression model (_VP_EQN_1.GIF % = 1.217 BMI – 24.81) provided the following CG-cl correction formula for obese subjects: Corrected CG-cl = CG-cl (1.25 – 0.012 BMI). Its validity was evaluated in another group of 20 subjects with BMI > 25 by comparing the results obtained with Corrected CG-cl to those obtained by CG-cl and MDRD formula (MDRD-cl) using the clearance of 51Cr-EDTA (51Cr-EDTA-cl) as the GFR measurement gold standard. Results and Conclusion: Linear regression analysis of CG-cl, MDRD-cl and Corrected CG-cl compared to 51Cr-EDTA-cl (considered as the independent variable) resulted in the following determination coefficients (R2): 0.687; 0.818; 0.947, respectively. In conclusion, this formula can be considered a quick and reliable method for CG-cl correction in obese subjects.
Correspondence to:
Dr. A. Saracino
Chair of Nephrology
Policlinico, Piazza Giulio Cesare 11
I-70124 Bari, Italy
Email: asaracino@inwind.it

Abstract

J. Braun, H.-G. Asmus, H. Holzer, R. Brunkhorst, R. Krause, W. Schulz, H.-H. Neumayer, P. Raggi and J. Bommer

¹KfH Dialysezentrum Nürnberg, Germany, ²KfH Dialysezentrum Sonnenallee, Berlin, Germany, ³Universitätskinikum Graz, Austria, ⁴KfH Dialysezentrum, Hannover, Germany, ⁵KfH Dialysezentrum Moabit, Berlin, Germany, ⁶Klinikum Bamberg, Germany, ⁷Universitätsklinikum Charité, Berlin, Germany, ⁸Tulane University, New Orleans, LA, USA, and ⁹Department of Nephrology, Universitätsklinikum Heidelberg, Germany
Background: Calcium carbonate used as a phosphate binder may contribute to cardiovascular calcification. Long-term comparisons of sevelamer, a non-calcium polymeric phosphate binder, and calcium carbonate (CC) are lacking. Methods: 114 adult hemodialysis patients were randomly assigned to open label sevelamer or CC for 52 weeks. Study efficacy endpoints included changes in serum phosphorus, calcium, calcium-phosphorus product, and lipids. In addition, initial and sequential electron beam computerized tomography scans were performed to assess cardiovascular calcification status and change during follow-up. Safety endpoints were serum biochemistry, blood cell counts and adverse events. Results: Patients receiving sevelamer had a similar reduction in serum phosphorus as patients receiving CC (sevelamer –0.58 ± 0.68 mmol/l, CC –0.52 ± 0.50 mmol/l; p = 0.62). Reductions in calcium-phosphorus product were not significantly different (sevelamer –1.4 ± 1.7 mmol2/l2, CC –0.9 ± 1.2 mmol2/l2; p = 0.12). CC produced significantly more hypercalcemia (> 2.8 mmol/l in 0% sevelamer and 19% CC patients, p < 0.01) and suppressed intact parathyroid hormone below 150 pg/ml in the majority of patients. Sevelamer patients experienced significant (p < 0.01) reductions in total (–1.2 ± 0.9 mmol/l, –24%) and LDL cholesterol (–1.2 ± 0.9 mmol/l, –30%). CC patients had significant increases in coronary artery (median +34%, p < 0.01) and aortic calcification (median +32%, p < 0.01) that were not observed in sevelamer-treated patients. Patients on sevelamer required more grams of binder (sevelamer 5.9 g vs. CC 3.9 g) and experienced more dyspepsia than patients on calcium carbonate. Conclusions: Sevelamer is an effective phosphate binder that unlike calcium carbonate is not associated with progressive cardiovascular calcification in hemodialysis patients. Correspondence to:
Prof. Dr. med. J. Bommer
Klinikum der Universität Heidelberg
Sektion Nephrologie
Bergheimerstraße 56a
D-69115 Heidelberg, Germany
Email: juergen_bommer@ t-online.de

Abstract

M.H. Schwenk and D.A. Blaustein

¹Division of Nephrology and Hypertension, The New York Hospital Medical Center of Queens, Flushing, and
²Division of Nephrology, The Long Island College Hospital, Brooklyn, NY, USA
Aims: Two patients with chronic kidney disease presented with severe anemia and iron deficiency. Because of their religious beliefs, red blood cell transfusions were not possible, and an aggressive therapeutic regimen of iron replenishment was instituted. Material and methods: The regimen included epoetin, folic acid and high-dose intravenous iron sucrose infusions over multiple successive days (total dosages of 2 and 3.5 g). Results: The patients’ iron stores were replenished and an erythropoietic response ensued subsequent to this aggressive and unique therapeutic regimen. There were no side effects observed which could be attributed to iron sucrose, and both patients stabilized and were discharged after 3 – 4 weeks. Conclusion: In patients with chronic kidney disease who are severely anemic and iron-deficient and where transfusions are not possible, an aggressive regimen of multiple high-dose iron sucrose infusions may be both safe and effective. Correspondence to:
M.H. Schwenk
The New York Hospital Medical Center of Queens
Division of Nephrology and Hypertension
56-45 Main Street, Flushing
NY 11355, USA
Email: mhschwen@nyp.org

Abstract

S. Sund¹, A.V. Reisæter², H. Scott¹, T.E. Mollnes³ and T. Hovig¹

¹Department/Institute of Pathology, ²Department of Internal Medicine, and ³Institute of Immunology, Rikshospitalet University Hospital, Oslo, Norway
Background: The specific role of monocytes/macrophages (MO) in kidney graft rejection is not yet fully elucidated. In a recent protocol biopsy study of living-donor recipients, we demonstrated massive capillary influx of MO, associated with severe complement activation and acute rejection (AR) 1 week after transplantation [Sund et al.]. To gain further insight into the possible relationship between MO and complement activation, we analyzed glomerular and interstitial MO in these biopsies. Methods: Twenty-seven protocol biopsies were stained with antibodies to calprotectin (L1) and CD68 as markers for MO. Cells were counted as an average number per glomerulus and as an average number per defined visual field in the interstitium. Polymorphonuclear leukocytes (PMN) were counted in glomeruli and interstitium by light microscopy. Baseline specimens from 10 of the patients served as controls. The results were compared with data on deposition of complement from the foregoing study, and with histopathologic and clinical data on AR. Results: Cases with diffuse C4d deposition in peritubular capillaries consistent with acute antibody-mediated rejection (AbAR) (n = 4) had significantly higher numbers of intraglomerular MO than the other protocol biopsies (L1: median 20.7 vs 3.6, p = 0.0002; CD68: median 10.1 vs. 2.0, p = 0.0008). With a cut-off of 10 L1-positive and 6 CD68-positive MO, the specificity for the diagnosis of AbAR was 96% and 91%, respectively. The number of interstitial MO was significantly higher in patients with AR than in those without, but in contrast to glomerular MO, interstitial MO could not discriminate between complement positive and negative AR. The number of glomerular and interstitial PMNs was significantly higher in the AbAR group than in the other protocol biopsies. Conclusions: The strong correlation between complement activation and early glomerular influx of MO in the kidney allograft suggests a causal relationship between these 2 events. At 1 week after transplantation, a number of 10 L1-positive and 6 CD68-positive MO per glomerulus indicates AbAR.

Correspondence to:
Dr. S. Sund
Department of Pathology
Førde Central Hospital
6807 Førde, Norway
Email: Stale.sund@ helse-forde.no

Abstract

F. Antolini, F. Valente, D. Ricciardi and R.M. Fagugli

¹Department of Internal Medicine and Metabolic and Endocrinologic Sciences, Laboratory of Clinical Biochemistry, University of Perugia, and
²Nephrology – Dialysis Unit, Silvestrini Hospital, Perugia, Italy
Background: It is well-known that hemodialysis patients experience increased oxidative stress, which is believed to cause numerous uremia-related complications. Retention of water-soluble toxins as well as protein-bound toxins is due to renal failure. Kidney transplantation restores, at least partially, the fundamental processes of glomerular filtration which eliminates toxic solutes. The aim of this study was to determine the levels of several different glycoxydative stress-related parameters after kidney transplantation. Patients and methods: A cross-sectional study was carried out on 30 subjects: 10 kidney-transplanted patients with chronic renal failure (Tx-CRF), 10 kidney-transplanted patients with normal renal function (Tx-N) and 10 controls (Ctr). The groups were comparable with respect to age and gender. The following glycoxydative stress markers were determined by HPLC analysis: albumin-bound and free pentosidine, low-molecular weight-advanced glycation end products (LMW-AGEs), advanced oxidation protein products (AOPP) and low-molecular weight carbonyls (LMW-C). The total antioxidant serum capacity was monitored by measuring both the ferric reducing/antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC). Results: With respect to the controls, the Tx-CRF patients had higher levels of pentosidine (2.66 ± 0.98 vs 1.45 ± 1.1 pmol/mg), LMW-AGE (47.55 ± 39.74 vs 15.45 ± 6.39 a.u./ml), and AOPP (6.71 ± 0.78 vs 4.81 ± 0.32 a.u./mg) while Tx patients with normal kidney function had levels of these compounds that were comparable to the controls, except for the LMW-AGEs which were higher. Levels of LMW-AGEs, pentosidine, LMW-C and AOPP were inversely correlated to creatinine clearance. The total antioxidation serum capacity was paradoxically higher in Tx patients than in the controls, regardless of kidney function. FRAP as well as ORAC, were correlated to uric acid (r = 0.62, p < 0.001; r = 0.54, p < 0.01). Conclusions: The reported data indicate that kidney transplantation seems to restore a nearly normal level of glycoxidative stress markers, but a complete remission is only possible when the renal function is normal. An increase of total antioxidant power of serum in transplanted patients was reported, as probable effect of uric acid high levels. Correspondence to:
Dr. F. Antolini
ENEA Materials Science and Technology Unit
S.S.7 Km 714
I-72100 Brindisi, Italy
Email: francesco.antolini@brindisi.enea.it

Abstract

S.R. Cheema, F. Arif, D. Charney, I.S. Meisels and S.S. Cheema

¹Division of Nephrology, and ²Department of Pathology, St. Luke’s-Roosevelt Hospital Center, College of P&S of Columbia University, New York, NY, USA
Unlike hepatitis B and C, renal involvement has been extremely uncommon in patients with hepatitis A virus (HAV) infection. Nephrotic syndrome has been documented as a rare complication in association with HAV infection. In this report, we describe a patient with serologically documented HAV infection, who presented with nephrotic syndrome. The renal biopsy showed an immunoglobulin A- (IgA) dominant glomerulonephritis (GN) with subendothelial immune deposits. This is the second biopsy-proven case report of a patient with acute HAV associated with IgA-dominant immune complex glomerulonephritis and nephrotic syndrome. This is perhaps the first case in which a patient experienced both IgA-dominant glomerulonephritis and cutaneous cryoglobulinemic vasculitis.Correspondence to:
Dr. S. Cheema
Division of Nephrology
St. Luke’s-Roosevelt Hospital Center
College of P&S of Columbia University
1111 Amsterdam Ave
New York, NY 10025, USA
Email: shafiqcheema@yahoo.com

Abstract

A. Bauer¹, W.J. Jabs¹, S. Süfke¹, M. Maass² and B. Kreft¹

¹Department of Medicine I and ²Institute of Medical Microbiology and Hygiene, University of Lübeck School of Medicine, Lübeck, Germany
Subacute bacterial endocarditis is frequently associated with extracardiac manifestations and renal failure. Clinical variety of endocarditis manifestation is wide and has the potential to mimic vasculitis. Whereas Streptococcus bovis is often isolated and associated with colonic tumors, Neisseriaceae are rarely found. An association of subacute bacterial endocarditis and antineutrophil cytoplasmic antibodies has been described. We report on a 62-year-old man who was admitted to our hospital with acute oliguric renal failure and a nonpruritic purpural rush without fever. Antineutrophil cytoplasmic antibody diagnostic revealed perinuclear staining with a titre of 1 : 512 and antiproteinase-3 specificity. Immune complex-mediated glomerulonephritis without extracapillary proliferation was diagnosed in renal biopsy. Finally, blood cultures became positive for Streptococcus bovis and Neisseria flava. Echocardiography showed mobile vegetations on tricuspid valve. Under treatment with penicillin G and gentamicin, skin efflorescences and renal function recovered, but vegetations increased. A colonic tumor could be excluded, a disastrous dental status may have been a predisposal factor. When classical findings of subacute bacterial endocarditis are less clear, the presence of renal failure and antineutrophil cytoplasmic antibodies in absence of fever may lead to misdiagnosis and deleterious immunosuppressive therapy. Neisseria subflava, an upper respiratory tract commensal, may cause subacute bacterial endocarditis without typical symptoms. Correspondence to:
Dr. A. Bauer
Department of Medicine I
University of Lübeck School of Medicine
Ratzeburger Allee 160
D-23538 Lübeck, Germany
Email: bauer-alex@gmx.de

Abstract

D. Dinour, S. Mini, S. Polak-Charcon, D. Lotan and E.J. Holtzman

¹Department of Nephrology and Hypertension, ²Department of Pathology, and ³Division of Pediatric Nephrology, The Chaim Sheba Medical Center, Tel-Hashomer, and the Faculty of Medicine, Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel
Mitochondrial DNA plays a crucial role in oxidative production of energy. Thus, defects in mitochondrial DNA can affect virtually all organ systems. The point mutation A à G at position 3243 in the mitochondrial tRNAleu(UUR) gene is the cause of several distinct types of mitochondrial cytopathy and several clinical phenotypes, including encephalomyopathy with lactic acidosis and stroke-like episodes and maternally inherited diabetes and deafness. This mutation has been recently described also in association with kidney disease, mainly focal and segmental glomerulosclerosis. At present, little is known about the prevalence of this mitochondrial nephropathy, its clinical course and the pathogenesis of glomerular damage. We describe 2 unrelated patients, who presented with proteinuria and progressed to end-stage renal failure. Other clinical features were short stature, severe headache, hearing loss, diabetes mellitus and hypertrophic cardiomyopathy. The main histological finding was an increased number of abnormal mitochondria in tubular cells and podocytes. Analysis of mitochondrial DNA from leukocytes and urine sediment revealed heteroplasmy for the A3243G mutation in tRNAleu(UUR) gene in both patients. Recognition of the characteristic clinical and histological features of the mitochondrial A3243G mutation-associated glomerulopathy will enable correct diagnosis and better management of a disease which is likely to be underdiagnosed. Correspondence to:
D. Dinou MD
Department of Nephrology and Hypertension
The Chaim Sheba Medical Center
Tel-Hashomer, Israel 52621
Email: dinourad@yahoo.com

Abstract

M. Tintillier, J.-M. Pochet, J.-P. Cosyns, E. Delgrange and J. Donckier

Departments of ¹Nephrology, ³Internal Medicine and Endocrinology,
Cliniques Universitaires de Mont-Godinne, Yvoir, and
²Pathology, Cliniques Universitaires Saint-Luc, Brussels, Belgium
Primary hyperoxaluria type 1 (PH1) is a rare autosomal metabolic recessive disease, caused by the deficiency of the liver peroxysomal alanine:glyoxylate aminotransferase (AGT), characterized by accumulation of calcium oxalate crystals in kidneys and others organs. We present the case of an elderly woman with PH1, presenting as acute renal failure. Precipitation of calcium oxalate crystals was probably due to amiodarone-induced severe hypothyroidism. Residual AGT activity is associated with the G170R (G630A) mutation. A new mutation of AGT, called R36C, was also discovered; the role of this new mutation is actually not known.
Correspondence to:
Dr. M. Tintillier
Department of Nephrology
Cliniques Universitaires de Mont-Godinne
B-5530 Yvoir
Email: Belgiumm.tintillier@ibelgique.com

Abstract

S. Kandutsch¹, A. Feix², M. Haas², M. Häfner³, G. Sunder-Plassmann² and A. Soleiman¹

¹Clinical Institute of Pathology, ²Division of Nephrology, Department of Medicine III, and ³Division of Gastroenterology and Hepatology, Department of Medicine IV, Vienna General Hospital, University of Vienna, Austria
A renal transplant recipient with stable allograft function presented with massive hemorrhagic diarrhea and severe anemia. No microbial infection could be found in stool cultures. Early colonoscopy showed severe colitis with ulceration. Histological samples confirmed granulomatous inflammation with acid-resistant Ziehl-Neelson-positive microorganisms of mycobacterial type. Polymerase chain reaction (PCR) analysis of native mucosal biopsies specified the infectious organism as Mycobacterium tuberculosis complex. The patient responded well to antimycobacterial therapy and was still asymptomatic after 6 months with a stable graft function. Our case shows that tuberculosis can be a severe clinical problem in transplant recipients. Most of the patients with intestinal tuberculosis, reported to literature, were diagnosed post mortem or after explorative laparotomy and bowel resection. Thus, intestinal tuberculosis should be considered when a transplant recipient shows abdominal symptoms with no clear evidence of another infection. Proper diagnosis and treatment resulted in a beneficial outcome in our patient. Correspondence to:
Dr. A. Soleiman
'Clinical Institute of Pathology
University of Vienna
Vienna General Hospital, Währinger Gürtel 18-20
A-1090 Vienna, Austria
Email: Afschin.Soleiman@akh-wien.ac.at

Abstract

H.-S. Hsieh, H.-T. Liao, C.-J. Wei and D.-C. Tarng

¹Division of Nephrology, Department of Medicine, ²Department of Radiology, Taipei Veterans General Hospital, and ³Faculty of Medicine, National Yang-Ming University School of Medicine, Taiwan
Non-cuffed, double-lumen hemodialysis (HD) catheters can be inserted at the bedside in the femoral, internal jugular or subclavian position. The femoral route is less risky, and the incidence of life-threatening complications is lower for femoral cannulation than for internal jugular and subclavian cannulations. However, here we describe a life-threatening complication of an extensive deep vein thrombosis and subsequent pulmonary thromboembolism following femoral cannulation of a double-lumen HD catheter. The possible mechanisms and treatment for this potentially fatal thromboembolic event are discussed in this report.

Correspondence to:
D.-C. Tarng MD PhD Division of Nephrology Department of Medicine Taipei Veterans General Hospital No. 201, Section 2 Shih-Pai Road Taipei 112, Taiwan
Email: dctarng@vghtpe.gov.tw

Abstract

H. Tanaka, T. Nakahata, K. Tsugawa, K. Tsuruga, W. Yumura and E. Ito

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Volume 62, No. 2/2004(August)