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Abstract

A. Chang, J. Kowalewska, K.D. Smith, R.F. Nicosia and C.E. Alpers

Department of Pathology, University of Washington Medical Center, Seattle, WA, USA
Background: IgA nephropathy is the most common glomerulonephritis in the world. Thrombotic microangiopathy occurs in a number of clinical settings, including but not limited to thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, malignant hypertension, anti-phospholipid antibody syndrome and radiation nephropathy. Renovascular complications, such as thrombotic microangiopathy, in the setting of IgA nephropathy may be overlooked and their significance as a concomitant histologic finding is unclear. Methods: We conducted a clinicopathologic study to understand the possible relationship between IgA nephropathy and a concurrent thrombotic microangiopathy injury process. We identified 10 patients with an established diagnosis of IgA nephropathy and concurrent findings of thrombotic microangiopathy based on their renal biopsies. Results: Six patients presented with malignant hypertension, while three others had severe hypertension (³ 100 mmHg, diastolic). Five patients had nephrotic-range proteinuria. Seven patients had occasional arteriolar thrombi identified by light microscopy and prominent glomerular subendothelial space widening by electron microscopy, while three patients demonstrated only ultrastructural features of thrombotic microangiopathy. Other possible etiologic causes of thrombotic microangiopathy were not identified with the available clinical information. Conclusion: Our study suggests that a thrombotic microangiopathy injury, when present, is usually found in advanced stages of IgA nephropathy and can be associated with severe proteinuria. Although other possible causes of thrombotic microangiopathy, such as anti-phospholipid antibody syndrome, were excluded in only two patients, the thrombotic microangiopathy injury process may be a cause or a consequence of the severe hypertension encountered in most of the patients which, in turn, may be a consequence of the disease progression of IgA nephropathy.Correspondence to:
A. Chang, MD
University of Chicago Hospitals
Department of Pathology
5841 S. Maryland Ave.
Room S-628 (MC6101)
Chicago, IL 60637, USA

Email: anthony.chang@uchospitals.edu

Abstract

H. Matsumura, A. Ashida, K. Hirano, H. Nakakura and H. Tamai

Department of Pediatrics, Osaka Medical College, Osaka, Japan
Aim: Recent studies have indicated that reactive oxygen species (ROS) play a role in the pathogenesis of glomerular injury leading to proteinuria in nephrotic syndrome. In the present investigation, we examined the effects of the radical scavenger edaravone administered at various time points to rats with puromycin nephrosis. Materials and methods: 35 Wistar rats were divided into five groups: treatment with puromycin aminonucleoside (PAN) alone, treatment with PAN followed by edaravone in the early period, treatment with PAN followed by edaravone administration in the late period, treatment with PAN and administration of edaravone for the whole experimental period, and untreated controls. On Days 3, 6 and 9, urinary protein excretion was measured. The levels of glomerular thiobarbituric acid-reactive substance (TBArs) were determined in all animals on Day 10. Results: On Day 9, rats that had been administered edaravone showed reduced urinary protein excretion and reduced glomerular TBArs. In particular, edaravone administration in the late period, during which proteinuria was most acute, had the effect of reducing the severity of proteinuria. Glomerular TBArs were suppressed to the control level. Our results indicate that edaravone exerts a protective effect in the acute phase of PAN nephrosis when administered as antioxidant therapy at the onset of proteinuria. Conclusions: Edaravone can ameliorate urinary protein excretion after the onset of proteinuria in nephrotic syndrome.Correspondence to:
A. Ashida, MD; Department of Pediatrics, Osaka Medical Colleg, 2-7 Daigakumachi Takatsuki Osaka, 569-8686, Japan
Email: ped006@poh.osaka-med.ac.jp

Abstract

S. Muray, M.P. Marco, L. Craver, M. Rue, J.M. Valdivielso and E. Fernandez

¹Hospital Universitari Arnau de Vilanova, Lleida, ²University of Lleida, Spain
Background: The role of mineral metabolism in cardiovascular pathologies has been studied almost exclusively in chronic kidney disease patients. There are no studies that relate mineral metabolism to pulse pressure in healthy populations. Methods: 692 subjects were initially selected. After applying clinical exclusion criteria, 659 subjects were recruited. Creatinine clearance was then calculated to detect subjects with occult chronic kidney disease. Statistical analysis was applied to the remaining population after excluding subjects with occult chronic kidney disease (n = 466). Pulse pressure, creatinine clearance, calcium, phosphorus, intact parathormone, 25-hydroxivitamin D₃ and Bsm I genotype of the vitamin D receptor were determined. Means and frequencies were compared by ANOVA and Chi-square, respectively. Multivariate analysis was applied to the whole population and then to Caucasians, Sub-Saharans, Caucasian men and Caucasian women separately. Pulse pressure (PP) was the dependent variable, and adjustments were made for clinical and laboratory data. Results: The prevalence of occult chronic kidney disease was 32%. In subjects without kidney disease, phosphorus and vitamin D were independent predictors of elevated PP in Caucasian males whereas Bsm I genotype of the vitamin D was an independent predictor of elevated PP in the Caucasian population in both genders. No covariable showed relationship with PP in Sub-Saharan subjects. Conclusion: Mineral metabolism influences pulse pressure in Caucasian men.Correspondence to:
Dr. M.P. Marco Nephrology Service Hospital Arnau de Vilanova of Lleida Rovira Roure 80 25198 Lleida, Spain
Email: mmarco@arnau.scs.es

Abstract

M.E. Suliman¹, P. Stenvinkel¹, T. Jogestrand², Y. Maruyama¹, A.R. Qureshi¹, P. Bárány¹, O. Heimbürger and B. Lindholm¹

¹Department of Clinical Science and ²Department of Clinical Physiology, Divisions of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska University Hospital Huddinge, Karolinska Institutet, Stockholm, Sweden
Background: Homocysteine and advanced glycation end-products (AGEs), which accumulate in chronic kidney disease (CKD), are recently proposed cardiovascular risk factors. In this study, we evaluated the association between changes in calculated intima media (cIM) area of the common carotid artery during the first year of dialysis therapy and plasma total homocysteine (tHcy) level as well as circulating AGEs such as plasma pentosidine level. Methods: We studied 63 CKD patients (38 males) aged 52 ± 12 years at a time-point close to start of dialysis treatment and after 12 months of dialysis treatment (41 on peritoneal and 22 on hemodialysis). The tHcy and plasma pentosidine levels were measured by HPLC. Change in cIM area was evaluated by non-invasive B mode ultrasonography. Malnutrition was assessed by subjective global assessment (SGA). Results: At basal, 70% of the patients had carotid plaques, 32% had symptomatic CVD, 38% had malnutrition, 30% had inflammation (CRP ³ 1 mg/dl) and 23% had diabetes mellitus, respectively. At baseline, the mean plasma pentosidine levels were similar in the patients with and without carotid plaques (36 ± 21 vs 36 ± 19 pmol/mg albumin, respectively), whereas the median plasma tHcy was significantly lower in the patients with carotid plaques than in the patients without carotid plaques (32 ± 21 vs 52 ± 42 mmol/l, p < 0.01, respectively). The prevalence of hyperhomocysteinemia (tHcy level > 13.7 mmol/l) was 95%. In univariate analysis, the change in cIM area during the first year of dialysis was significantly correlated with basal plasma pentosidine level (r = 0.31, p = 0.01), but not with basal tHcy (r = –0.11). However, neither pentosidine nor tHcy levels were correlated with cIM area at basal or at 12 months. In a stepwise multiple regression model, age and plasma pentosidine content, but not the tHcy level, associated with changes in the cIM area. Conclusion: Progression of atherosclerosis, as indicated by changes in carotid intima-media area during the course of dialysis treatment, was associated with pentosidine, but not with tHcy, levels at baseline in these CKD patients. This suggests that the accumulation of AGEs in CKD patients may have a role in the pathogenesis of CVD in these patients. Since almost all CKD patients have hyperhomocysteinemia, this finding, however, does not exclude a role of homocysteine as a risk factor for CVD in CKD patients.Correspondence to:
B. Lindholm, MD, PhD

Divisions of Baxter Novum and Renal Medicine

Department of Clinical Science

Intervention and Technology

Karolinska University Hospital Huddinge

K-56, 141 86 Stockholm, Sweden

Email: bengt.lindholm@klinvet.ki.se

Abstract

M. Sato, H. Morita, H. Ema, S. Yamaguchi and I. Amano

¹Department of Kidney and Dialysis, Social Insurance Chukyo Hospital, Nagoya, ²Department of Kidney Disease, Shizuoka City Hospital, Shizuoka, ³Department of Kidney and Dialysis, Tenri Yorodu Soudanjo Hospital, Tenri, Japan

Aim: Biocompatibility profiles of synthetic membranes may vary. In this prospective crossover study, we examined the effect of various membranes on cutaneous microcirculation during HD. Subjects and methods: 11 HD patients without cardiovascular complications were enrolled in this study. They were dialyzed using three types of membrane in a randomized order: ethylene-vinyl alcohol copolymer (EVAL), vitamin E-bonded cellulose (VE-C) and polysulfone (PS). The transcutaneous oxygen tension (TcPO2) was examined on the dorsum of foot to assess the cutaneous microcirculation. Serum biochemical parameters were also measured. Results: The TcPO2 as a percentage of the predialysis level decreased from the beginning of HD, and significant differences were observed after 15 min of HD between EVAL and the other 2 membranes (98 ± 6% (mean ± SD) for EVAL versus 89 ± 7% for VE-C (p < 0.01) and 88 ± 10% for PS (p < 0.01)). Furthermore, there were significant differences at 30 and 60 min between EVAL and PS (30 min: 93 ± 9% for EVAL versus 85 ± 7% for PS (p < 0.05); 60 min: 92 ± 10% for EVAL versus 79 ± 10% for PS (p < 0.01)). The serum level of thiobarbituric acid reactants (TBARs), a marker of lipid peroxidation, increased significantly at the end of HD relative to that at the beginning of HD when using a PS membrane (from 1.9 ± 0.5 to 2.1 ± 0.5 nmol/ml, p < 0.05). Conclusion: Our results indicate that an EVAL membrane is superior to PS and VE-C membranes in terms of its smaller influence on cutaneous microcirculation. The repeated occurrence of microcirculatory disturbance during HD sessions may cause chronic endothelial dysfunction and even cardiovascular complications in HD patients.Correspondence to:
M. Sato, MD
Department of Kidney and Dialysis
Social Insurance Chukyo Hospital
1-1-10 Sanjou, Minami-ku, Nagoya 457-8510, Japan
Email: motoyoshi_sato@chukyo-hosp.jp

Abstract

T. Weinreich¹, T. De los Ríos², A. Gauly² and J. Passlick-Deetjen²,³

¹Nephrologisches Zentrum Villingen-Schwenningen, ²Fresenius Medical Care, Bad Homburg and ³Heinrich-Heine-Universität, Düsseldorf, Germany
Cardiovascular mortality is still high and many risk factors are inadequately controlled in patients on conventional chronic hemodialysis. Recent studies on intensified treatment schedules by either increasing length or frequency of dialysis sessions have shown promising results with better control of blood pressure, reduction of left ventricular hypertrophy and easier control of calcium/phosphate metabolism. Aim: The present observational study compared the effect of different forms of “intensified dialysis treatment” i.e. either long nightly intermittent (LNHD, 3 × 7.5 – 8 h) or short daily dialysis sessions (DHD, 6 × 2.5 – 3 h) on cardiovascular parameters, phosphate and anemia control in comparison to standard treatment schedules (SHD, 3 × 4 – 5 h). Methods: All patients stable on hemodialysis between 18 and 80 years of age and with either uncontrolled hypertension and/or left ventricular hypertrophy and/or frequent intradialytic hypotension, were asked to participate in intensified dialysis therapy by either LNHD or DHD. Patients not willing to change their dialysis regime were asked to participate as control group (SHD). Primary end point was 24-h ambulatory blood pressure, secondary end points were predialysis blood pressure, left ventricular mass index (LVMI) and fractional shortening (FS), control of calcium, phosphate and anemia. Patients were followed up for 1 year. Results: 17 patients opted for LNHD, 8 for DHD, 19 patients served as control group. After 1 year of treatment 24-h blood pressure was unchanged in all groups. Predialysis systolic blood pressure decreased in LNHD and DHD, but increased in SHD. Mean LVMI decreased in all treatment groups (DHD –20.1 ± 24.0%, SHD –13.6 ± 33.4%, LNHD –6.1 ± 32.2%). The mean number of antihypertensive tablets/day was reduced in DHD by 3.3 tablet units, in LNHD by 1.2 tablet units, but increased in SHD patients. FS improved in patients on LNHD and DHD, but decreased in patients on SHD. Regression of LVMI was independent of dry weight which was unchanged in LNHD and SHD but increased in DHD. In contrast to SHD, phosphate control and Ca × P product improved in DHD and LNHD with less phosphate binding tablets. Intact PTH did not change in SHD, but decreased in DHD and LNHD. Hemoglobin increased in groups on intensified treatments, but fell in SHD. EPO resistance index fell in LNHD, but increased in DHD and SHD. Conclusion: While reduction in 24-h blood pressure was not achieved by intensified dialysis, both schedules showed favourable effects on LVMI and FS with less antihypertensive medication. This was independent of reduction in dry weight. These effects were more pronounced in DHD patients. In contrast, in SHD patients, stable 24-h blood pressure and reduction in LVMI were achieved on the expense of an increasing amount of antihypertensive medication and with worsening of FS.Correspondence to:
T. Weinreich, MD

Nephrologisches Zentrum

Schrambergerstraße 28

78054 Villingen-Schwenningen,Germany
Email: weinreich@dialyse-schwenningen.de

Abstract

A. Kawauchi, Y. Inoue, T. Hashimoto, N. Tachibana, S. Shirakawa, Y. Mizutani, T. Ono and T. Miki

¹Department of Urology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, ²Japan Somnology Center, Neuropsychiatric Research Institute, Tokyo, ³Department of Urology, Tojinkai Hospital, Kyoto, ⁴Osaka Medical Center for Health Science and Promotion, Osaka, ⁵Department of Psychogeriatrics, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Japan
Aims: To compare clinical data, sleep quality and health-related quality of life (HRQOL) with and without RLS in HD patients. Materials and methods: The international RLS study group diagnosis questionnaire was completed by 228 HD patients. The Pittsburg Sleep Quality Index (PSQI) for the evaluation of sleep quality and the Kidney Disease Quality of Life (KDQOL-SF) for the analysis of HRQOL were also used. Results: 53 (23%) patients were diagnosed as RLS. Age and age at the initiation of HD were significantly younger in the RLS group. Serum calcium concentration (Ca) was significantly higher in the RLS group. Sleep quality evaluated by PSQI was significantly lower in the RLS group. In SF-36 domains of KDQOL-SF, bodily pain, general health perceptions, vitality, role functioning emotional, mental health and mental component score were significantly lower in the RLS group. In kidney targeted scales of KDQOL-SF, symptoms/problems, burden of kidney disease, cognitive function, quality of social interaction, sleep and patient satisfaction were significantly lower in the RLS group. Conclusion: High Ca was possibly connected to the pathophysiology of RLS which impaired sleep quality as well as HRQOL including mental health and many kidney disease related scales.Correspondence to:
A. Kawauchi, MD, PhD
Department of Urology, Graduate School of Medical Science
Kyoto Prefectural University of Medicine
Kawaramachi-Hirokoji, Kyoto 602-8566, Japan

Email: kawauchi@koto.kpu-m.ac.jp

Abstract

N. Kishimoto, Y. Mori, H. Yamahara, Y. Kijima, A. Nose, Y. Uchiyama-Tanaka, T. Tokoro, T. Nagata, Y. Umeda, N. Takahashi, H. Yoshida and H. Matsubara

¹Division of Cardiology and Nephrology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, ²Department of Medicine II, Kansai Medical University, Osaka, and ³Division of Nephrology, University of Fukui Hospital, Fukui, Japan
Renal deterioration often occurs in cases of infectious endocarditis (IE), but, IE- associated nephritis with rapidly progressive glomerulonephritis (RPGN) is rare. Patients with severe infection (e.g., IE) sometimes show positivity for cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA). Therefore, diagnosis and treatment are very difficult in cases of RPGN with IE and positivity for C-ANCA. Such cases are rare, only 12 have been reported in the English literature. Herein, we describe the case of a 50-year-old man who presented with RPGN with IE and tested positively for C-ANCA. He was referred to our hospital because of leg edema, purpura and renal dysfunction. Laboratory tests revealed serum creatinine elevation and positivity for C-ANCA and proteinase 3-specific (PR3)-ANCA. RPGN and acute renal failure were diagnosed. Hemodialysis and steroid therapy were started. Streptococcus oralis was isolated by blood culture. Transthoracic echocardiography revealed grade III mitral valve insufficiency with two vegetations. Therefore, IE was diagnosed. The steroid therapy was stopped, and antibiotic therapy was begun. Because there was no improvement, surgical therapy was performed. The operation was successful, but the patient died of brain hemorrhage. Our experience in this case indicates C/PR3-ANCA positive RPGN must be ruled out in patients with infectious disease, particularly IE, together with renal symptoms, and renal biopsy should be performed. Correspondence to:
Y. Mori, MD Division of Cardiology and Nephrology Department of Medicine Kyoto Prefectural University of Medicine 465 Kajii-cho Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan
Email: moriy@koto.kpu-m.ac.jp

Abstract

S. Belmouaz, E. Desport, R. Abou Ayache, A. Thierry, A. Mignot, M. Bauwens, J.-M. Goujon, F. Bridoux and G. Touchard

¹Department of Nephrology, ²Department of Pathology, Hôpital Jean Bernard, Poitiers, France

Fluindione is a vitamin K antagonist that is commonly prescribed for the treatment of cardiovascular disease and venous thromboembolism in France. Bleeding is the most common side effect of fluindione, whereas hypersensitivity reactions are rare. We describe here a patient with acute immuno-allergic interstitial nephritis caused by fluindione. Initial symptoms included fever, eosinophilia, low albuminuria, microscopic hematuria, eosinophiluria and acute renal failure. Kidney biopsy showed severe interstitial nephritis with interstitial edema, inflammatory infiltrates and tubulorrhexis. Fluindione withdrawal and corticosteroid treatment resulted in rapid recovery of renal function. A review of the literature revealed a very low incidence of fluindione-induced interstitial nephritis, with variable renal and extrarenal signs. Early recognition of this rare complication may prevent the development of severe chronic renal injury.
Correspondence to:
Dr. S. Belmouaz
Department of Nephrology
Hôpital Jean Bernard
Centre Hospitalier Universitaire
Rue de la Miletrie, BP 577, 86021 Poitiers Cedex, France
Email: s.belmouaz@chu-poitiers.fr

Abstract

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
Although parasitic infections have been known to be associated with immune complex-mediated glomerular lesions, strongyloidiasis-related glomerulopathy has not been well documented. We report a patient with delayed-recognized disseminated strongyloidiasis who developed nephrotic syndrome 3 months after the beginning of the manifestations related to strongyloidiasis. A kidney biopsy showed minimal change disease. We treated strongyloidiasis and hesitated to give steroid therapy for the treatment of minimal change nephrotic syndrome (MCNS) because of the risk of aggravation of Strongyloides stercoralis infection. Surprisingly, resolution of heavy proteinuria occurred after anthelmintic therapy with ivermectin. This case suggests a possible causal relationship between S. stercoralis infection and MCNS. In addition, a review of another 4 cases previously reported in the literature demonstrates the importance of detecting underlying S. stercoralis infection in patients with nephrotic syndrome since steroid therapy can cause hyperinfection or disseminated strongyloidiasis, and which may lead to fatal outcome.Correspondence to:
Dr. Y.K. Wen Division of Nephrology Department of Medicine Changhua Christian Hospital 135 Nansiao St. Changhua, 500, Taiwan
Email: 45440@cch.org.tw

Abstract

M.J. Izquierdo¹, C. Gomez-Alamillo¹, F. Ortiz², E.R. Calabia¹, J.C. Ruiz¹, A.L.M. de Francisco¹ and M. Arias¹

¹Nephrology and ²Neumology Departments, “Marques de Valdecilla” Hospital, University of Cantabria, Santander, Cantabria, Spain
Aminoglycoside nephrotoxicity is a well-known clinical entity that complicates the course of infectious diseases treated under this antibiotic regime. Recently, a new administration form of tobramycin, inhaled tobramycin (TOBI), has been approved to improve the antibacterial activity and reduce nephrotoxicity. We describe the clinical case of a 73-year-old woman with chronic-obstructive pulmonary disease (COPD) who developed acute renal failure (ARF) after using TOBI. Clinical presentation and biochemical parameters were compatible with aminoglycoside-induced renal failure. Based on the clinical findings presented here, a surveillance program should be established to monitor the presence of factors predisposing to renal failure, and to measure serum levels of tobramycin. Correspondence to:
Dr. M. Arias Rodriguez
Department of Nephrology
Hospital Universitario Marqués de Valdecilla
Avda Marques de Valdecilla s/n
39008 Santander, Cantabria, Spain
Email: nefarm@humv.es

Abstract

G. Guron, J. Holmdahl and L. Dotevall

¹Department of Nephrology, Department of Metabolism and Cardiovascular Research, Institute of Medicine, ²Department of Infectious Diseases, Institute of Biomedicine, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden
A 20-year-old, previously healthy woman, presented with high fever, headache and myalgia 3 days after her return from a holiday in Southeast Asia. Laboratory data on admission demonstrated a pronounced increase in plasma creatinine, marked thrombocytopenia and moderately elevated liver aminotransferases. After having ruled out malaria, dengue fever was primarily suspected and supportive intravenous fluid therapy was initiated. Still, 1 day after admission, platelet counts dropped even further and she became anuric although she did not appear hypovolemic. On day 2 after admission, urine production commenced spontaneously and the patient slowly recovered. All laboratory test results had returned to normal approximately 2 months later. Serological analysis for dengue fever was negative. It turned out that the patient had been trekking in the jungle while in Thailand and we, therefore, analyzed serology for Leptospira spirochetes which was clearly positive. The patient was diagnosed with leptospirosis which is a serious condition associated with a high mortality when complicated by acute renal failure. Differential diagnoses in patients with acute renal failure and tropical infections are reviewed. The importance of early recognition of leptospirosis, and prompt treatment with antibiotics in suspected cases, is emphasized.Correspondence to:
G. Guron, MD, PhD Department of Nephrology at the Department of Metabolism and Cardiovascular Research Institute of Medicine The Sahlgrenska Academy at Gothenburg University Bla Straket 7, 413 45 Gothenburg, Sweden
Email: gregor.guron@kidney.med.gu.se

Abstract

T.H. Westhoff¹, C. Loddenkemper², M.P. Hörl¹, S. Schmidt¹, I. Anagnostopoulos², M. Hummel², W. Zidek¹ and M. van der Giet¹

¹Medizinische Klinik IV, Nephrology, ²Institute of Pathology, Charité, Campus Benjamin Franklin, Berlin, Germany
Background: In end-stage renal disease patients, the incidence of both infections and malignancies is increased leading to a higher incidence of peripheral lymphadenopathy. In the present work we describe a rare but probably underdiagnosed cause for enlarged lymph nodes in uremic patients. Patient: A 43-year-old male patient was admitted to our hospital with inguinal lymphadenopathy and pruritus. He turned out to be uremic due to focal segmental glomerulosclerosis (creatinine 4.5 mg/dl, MDRD creatinine clearance 12 ml/min). Findings: Sonography revealed enlarged lymph nodes (up to 4 cm) with intact corticohilar border differentiation. After extirpation of an inguinal lymph node, histological examination established the diagnosis of dermatopathic lymphadenopathy. T cell lymphoma was excluded by PCR for T cell receptor-g rearrangements and subsequent GeneScan analysis. Intravenous fluid supplementation with subsequent decline of creatinine, UVB treatment, clemastine, and topical use of emollients led to a relief of the uremic pruritus and the lymph nodes’ size normalized within 8 weeks. Conclusion: Dermatopathic lymphadenopathy refers to the reactive condition seen in lymph nodes that drain areas with disruption of the skin integrity, e.g. due to scratch marks. The present case report describes dermatopathic lymphadenopathy as a harmless cause of enlarged lymph nodes in uremic pruritus for the first time. This entity should be considered in the differential diagnosis of peripheral lymphadenopathy of unknown origin in patients with renal failure. Correspondence to:
Dr. T.H. Westhoff
Charité, Campus Benjamin Franklin
Medizinische Klinik IV, Nephrology
Hindenburgamm 30
12200 Berlin, Germany
Email: timm.westhoff@charite.de

Abstract

T. Sanai, M. Hirakawa, M. Yokoyama, M. Soejima, M. Nakayama, N. Uesugi, N. Takeshita, A. Iguchi and F. Nanishi

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Volume 66, No. 6/2006(December)