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Books: 236	Journals: 18	Articles: 21486

Abstract

S. Ahmed, A. Karim, M.M. Hoffman, T.A. Bhuiya and J. Mattana

Abstract

N. Bassilios, A. Restoux, F. Vincent, E. Rondeau and J.-D. Sraer

Abstract

U. Göbel, B. Mauersberger, R. Kettritz, J. Bohlender and F.C. Luft

Helios Klinikum Berlin, Franz Volhard Clinic, Medical Faculty of the Charité, Humboldt University of Berlin, Germany
Hydropericardium is a known cause of pericardial effusion related to severely expanded extracellular fluid volume. Nephrotic patients have expanded extracellular fluid volume but obviously may have other causes for pericardial effusion. We tested the hypothesis that pericardial effusion is related to inflammation and not to hydropericardium in patients with nephrotic syndrome. Twenty nephrotic patients with systemic lupus erythematosus (SLE) were compared to 20 patients with nephrotic syndrome of other causes. No patient in either group had symptoms or signs of pericardial disease. Pleural effusion and ascites were equally common in SLE-nephrotic patients compared to non-SLE-nephrotic patients. However, 8 SLE patients had pericardial effusion, while none of the non-SLE-nephrotic patients had pericardial effusion. We suggest that hydropericardium is rare in nephrotic patients and that an inflammatory or other secondary cause should be considered when pericardial effusion complicates nephrotic syndrome.

Abstract

A.A. Lopes, F.K. Port, S.A. James, M.A. Silveira, R. Martinelli, E. Brito and H. Rocha

¹Nephrology and Epidemiology, Federal University of Bahia, ²Medicine and Epidemiology, ³Center for Research on Ethnicity, Culture and Health, Department of Health Behavior and Health Education, The University of Michigan, Ann Arbor, USA, ⁴Edgar Santos Hospital, ⁵Nephrology and ⁶Pathology, Federal University of Bahia, Brazil
Background/aims: United States investigators have shown evidence of higher susceptibility to focal segmental glomerulosclerosis (FSGS) in blacks than in whites. This association between race and FSGS has not been assessed outside the US. The present study assesses the association between race and type of glomerulonephritis in a sample of Brazilian patients, taking into account the presence of the hepatosplenic form of Schistosomiasis mansoni (HSM). Methods: Eighty patients with focal segmental glomerulosclerosis (FSGS) were compared to 50 with membranoproliferative glomerulonephritis (MPGN). The association between race (i.e. black versus white) and type of glomerulonephritis was adjusted for age, gender and HSM by logistic regression. Results: Blacks were more likely than whites to have FSGS (as compared to MPGN), both among patients with HSM (odds ratio (OR) = 2.67; 95% confidence interval (CI) = 0.81 – 8.81) and without HSM (OR = 2.19; 95% CI = 0.79 – 6.05). After adjustment for age, gender and HSM, the odds of FSGS remained significantly greater for blacks (OR = 2.49; 95% CI = 1.05 – 5.95). Conclusion: The increased likelihood of FSGS in Brazilian blacks is consistent with findings from US patients. The association between race and type of glomerulonephritis was similar between patients with and without HSM. Future investigations should focus on the mediators factors that might explain these findings.

Abstract

J.G. Vlachojannis, S. Tsakas, C. Petropoulou, D.S. Goumenos and S. Alexandri

Department of Internal Medicine, Nephrology, University Hospital, Patras, Greece
Background: Endothelin-1 (ET-1) is a strong vasoconstrictive peptide that is involved in the pathogenesis of arterial hypertension. There is increasing evidence, based on studies in experimental animals, that endothelin-1 is produced by tubular epithelial cells in response to activation by filtered protein and is involved in the development of renal scarring. The aim of this study is to examine the distribution of ET-1 in the renal tissue of patients with heavy proteinuria and to estimate the changes in its urinary excretion after immunosuppressive therapy. Patients and methods: Twenty-four patients with severe proteinuria (7.5 ± 6.5 g/24 h) due to different types of glomerular disease and normal renal function (creatinine clearance 91 ± 14 ml/ min) were investigated. All patients underwent a renal biopsy and commenced on immunosuppressive therapy with corticosteroids and cyclosporin A. The localization of ET-1 in the renal tissue was examined by immunohistochemistry and compared to control renal tissue from 9 patients who underwent nephrectomies because of hypernephroma. In patients with proteinuria, endothelin-1 excretion in the urine at diagnosis was determined by radioimmunoassay and compared to that of 14 healthy subjects. A second measurement of urinary ET-1 excretion was performed after remission of proteinuria or 6 months after the initiation of treatment in patients with persistent nephrotic syndrome. Results: ET-1 in renal tissue of patients and controls was localized within the cytoplasm of endothelial cells. In nephrotic patients, it was also localized within the cytoplasm of tubular epithelial cells. Urinary ET-1 levels were higher in nephrotic patients compared to healthy subjects (746 ± 180 ng/24 h vs 410 ± 112 ng/ml, p < 0.001). In 17 of 24 patients who showed remission of proteinuria with immunosuppressive therapy, the urinary ET-1 levels decreased (from 803 ± 168 ng/24 h to 511 ± 80 ng/24 h, p < 0.001) whereas in 7 patients with persistent proteinuria, urinary ET-1 excretion remained elevated. Conclusions: The increased urinary excretion of ET-1 in patients with severe proteinuria followed by a significant decrease after remission of proteinuria with immunosuppressive treatment, along with its expression within tubular epithelial cells, suggests a possible relationship between proteinuria and renal ET-1 production.

Abstract

B. Kirschbaum

Department of Medicine, Virginia Commonwealth University, Richmond, VA, USA
Aims: Inflammation results in the production of free radicals which damage proteins, lipids, and nucleic acids. The products of these reactions are cleared, in part, by the kidney and appear in the urine. In this study, urine fluorescence was measured in individuals with various nephropathies to determine the value of these assays for detecting the excretion of endproducts of radical-mediated chemical reactions. Methods: Urine fluorescence was quantified at wavelengths which correspond to the presence of advanced glycosylation endproducts (AGE) and dityrosine (di-TYR). The samples were also tested for isoprostanes, nitrite/nitrate, hydrogen peroxide, and thiobarbituric acid reactive substances (TBARS). Results: Fluorescence values, expressed per ml urine or per mg creatinine (crt), were not normally distributed and covered a wide range. There were significant differences in fluorescence among groups of patients classified by diagnosis, but the differences did not allow sharp distinction of diagnostic categories. Fluorescence assays correlated significantly with TBARS but not with isoprostanes, nitrite/nitrate, or hydrogen peroxide. Fluorescence tended to increase with age. Gender and race did not affect the results. Conclusions: Because of the many factors which can affect free radical production and tissue injury, the value of urine fluorescence assays to screen for radical-mediated toxicity appears to be limited. Serial studies of patients will be needed to determine whether urine fluorescence will be useful to monitor responses to treatment or be predictive of progression vs. remission of renal disease.

Abstract

V. Tripodi¹, M. Nuñez², C. Carducci¹, A. Mamianetti³ and C. Agost Carreño⁴

¹Cátedra de Química Analítica, Facultad de Farmacia y Bioquímica, ²Cátedra de Matemática, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina, ³Departamento de Medicina Interna, Hospital Aeronáutico Central, and ⁴Hospital Aeronáutico Central, División Nefrología, Buenos Aires, Argentina
Background: A direct relationship between serum bile acids (SBA) and hepatic and hepatobiliary dysfunction has been demonstrated. However, there is little evidence that SBA are related to renal insufficiency. In a previous study, we showed that hemodialysis patients with advanced chronic renal failure (ACRF) have an increase of SBA in predialysis and a decrease in postdialysis. Consequently, it was assumed that the restoration of renal function in transplanted patients might decrease SBA levels. Aim of this study: Transplanted patients receiving cyclosporine A (CyA) were studied by monitoring CyA and SBA levels to determine if a probable relationship exists between renal function, CyA treatment and SBA levels. Subjects, materials and methods: SBA levels were determined in 15 recently transplanted patients receiving CyA for 18 months and longer. In addition, 22 renal patients transplanted not less than 6 years ago were also included in the study and were characterized as the stable group. Five patients from this group received mycophenolate or azathioprine instead of CyA as immunosuppressant. In addition to SBA and CyA, creatinine, cholesterol, g-GT, viral markers and triglycerides were also determined in all patients. Results: A significant and constant increase in SBA levels was observed in the recently transplanted group. However, after 18 months, SBA levels gradually decreased to those of patients considered stable under CyA treatment. In both recently transplanted and stable patients who received CyA, SBA values remained higher than normal, but stable patients under mycophenolate or azathioprine treatment showed no such increase. Conclusions: In recently transplanted patients, in patients studied for 18 months post transplant and in stable patients receiving CyA, the increase of SBA levels might be related to CyA treatment. This effect might be attributed to its cholestatic effect and also to a modification in uptake, metabolism, synthesis and excretion of SBA in the hepatocyte. These conclusions are supported by the results obtained in stable transplanted patients without CyA treatment showing normal SBA levels.

Abstract

G.H. Malik, A.S. Al-Harbi, S. Al-Mohaya, H. Al-Khawajah, M. Kechrid, A. Osman Al Hassan, K. Balbaid and M. Sabry Shetia

Division of Nephrology, Department of Internal Medicine, Security Forces Hospital Program, Riyadh, Saudi Arabia
Background: The aim of this retrospective study was to evaluate the incidence of tuberculosis (TB) in dialysis patients and to determine its clinical features and results of short-course (6 months) chemotherapy, mortality and risk factors of mortality. Methods: The study included 48 TB patients among 330 patients on dialysis of whom 37 were on hemodialysis and 11 were on peritoneal dialysis at Security Forces Hospital in the period from October 1989 to October 2000. The diagnosis of TB was established by a combination of clinical, radiological, biochemical, microbiological and histological examinations. Treatment with anti-TB drugs, the results of therapy and the outcome of patients were noted. Results: There were 32 males and 16 females with age ranges of 18 ? 89 (mean = 53.4) and 40 ? 70 (mean 57.9) years, respectively. Their duration on dialysis ranged from 1 month to 10 years (mean = 26 months). The presenting clinical features were fever (32), cough (16), weight loss (9), and anorexia (7). The organ systems involved were pulmonary (23), peritoneal (15), lymphadenopathy (11), pericardial (4), bone TB (3), bone marrow (2), epididimo-orchitis (1), right infraclavicular chest wall cold abscess (1), right infrascapular cold abscess (1) and right renal mass (1). Single organ system involvement was noted in 36 patients, 2 systems in 10 patients and 3 systems in 2 patients. Two patients were treated empirically with good response. Evidence of tuberculosis was obtained from chest X-rays (23), bone X-rays (3), spinal MRIs (1), AFB (stain and culture) of sputum and fluid (15), ascitic fluid examination with exudate and raised adenine deaminase (ADA) levels (12), lymph node biopsy (8), pleural fluid examination with exudate and raised ADA levels (5), bone marrow aspiration (2), exudative pericardial fluid with raised ADA levels (2), nephrectomy and histopathology (1), dorsal spine biopsy (1) and laparotomy and biopsy of peritoneum (1). Thirty-two patients received 4 anti-TB drugs: isoniazid (INH), rifampicin (Rif), pyrazinamide (Pyra) and ethambutol (Eth), 10 received 3 drugs (INH, Rif and Pyra or Eth), 2 received 2 drugs (INH + Rif) and a modified regimen was used in 3. The drug toxicities noted were hepatoxicity (5) and INH encephalopathy prior to the routine use of pyridoxine 100 mg daily (3), INH-induced SLE (1) and pyrazinamide-induced thrombocytopenia (1). The outcome of the patients was cured (35), expired (13), and 1 patient expired before starting therapy. Tuberculosis was not the direct cause of death in any of the patients. Conclusion: The incidence of TB in dialysis patients is 26 times more common than in the general Saudi population and a high index of suspicion is needed for early diagnosis and treatment. Extrapulmonary TB was noted in 52% of the patients. Short-course (6 months) chemotherapy is effective. INH-induced CNS toxicity is significant.

Abstract

W.-C. Chiang, T.-J. Tsai, Y.-M. Chen, S.-L. Lin and B.-S. Hsieh

¹Division of Nephrology, Department of Internal Medicine, En Chu Kong Hospital, Taipei County, Taiwan, Division of Nephrology, Department of Internal Medicine, National Taiwan University, Hospital, Taipei, Taiwan and ²Division of Nephrology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
Background: The diagnosis of iron deficiency using the current commonly used tests is usually difficult in hemodialysis patients. Soluble transferrin receptor (sTfR) has caught the attention of physicians recently as regards its use as a parameter for the evaluation of iron status. This study was conducted in order to evaluate the correlation of serum soluble transferrin receptor (sTfR) concentration with hematological parameters and iron profiles, in the role of identifying iron deficiency among dialysis patients. Methods: Seventy-three patients having received chronic hemodialysis and stable maintenance recombinant human erythropoietin (rHuEPO) therapy were included. Iron, total iron-binding capacity, ferritin and sTfR were measured in the first week. Following this, these patients began to receive intravenous iron dextran (2 mg/kg/week) for 4 weeks. The hematocrit (Hct), hemoglobin (Hb) levels and reticulocyte counts were evaluated weekly. At the beginning of fifth week, the sTfR level was measured again. Patients were classified as belonging to one of the following groups: serum ferritin < 100 mg/L – absolute iron-deficient group; initial ferritin level ³ 100 mg/L with an increase in hemoglobin of greater than 1 g/dL at the end of the study – occult iron deficiency group; others – non iron-deficient group. Results: Seventy-one patients completed the study. The concentration of sTfR was positively correlated with Hct, Hb and reticulocyte index at the beginning (r = 0.236, p = 0.047; r = 0.257, p = 0.04; r = 0.401, p < 0.01, respectively) and at the end of the study (r = 0.384, p < 0.01; r = 0.338, p < 0.01; r = 0.427, p < 0.001, respectively). After 4 weeks of iron and rHuEPO therapy, the sTfR concentration increased, rather than declined, from 21.85 ± 8.06 nM to 23.76 ± 7.42 nM (p = 0.04) and the change was positively correlated with the changes in Hct, Hb and reticulocyte index. The administered rHuEPO doses did not differ between the iron deficiency group (absolute deficiency, n = 3; occult deficiency, n = 10) and non-iron deficiency group (n = 58). The sTfR levels failed to identify the occult iron deficiency group because there was no difference between occult iron-deficient and non-iron-deficient patients (24.73 ± 9.09 nM versus 21.60 ± 7.89 nM, p = 0.34). Instead, transferrin saturation (TS) could be a differential marker between the 2 groups (19.0 ± 10.9% versus 30.1 ± 12.7%, p = 0.012). Conclusion: The serum sTfR concentration is indeed an appropriate marker for erythropoiesis. The erythropoitic effect of administered rHuEPO could mask the effect of iron status on the sTfR concentration. This might make the sTfR concentration no longer an appropriate index to identify the presence of occult iron deficiency. Thus, TS and ferritin currently remain better methods for the evaluation of iron status in rHuEPO-treated chronic hemodialysis patients.

Abstract

Y. Higashiuesato, T. Tana, M. Tozawa, C. Iseki, K. Iseki, K. Fukiyama and S. Takishita

¹Third Department of Internal Medicine, and ²Dialysis Unit, University of the Ryukyus, Okinawa, Japan
Background: There are conflicting reports regarding the relationship between the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism and the initiation and progression of cardiovascular disease. Moreover, there is no report regarding the relationship between the ACE I/D polymorphism and the prognosis of chronic dialysis patients. Methods: We examined the frequency of the ACE I/D polymorphism in 727 chronic hemodialysis patients in Okinawa, Japan, and observed the prognosis over 2 years in 407 men and 320 women with mean age (SD) of 55.5 (13.9) years with a mean duration of dialysis of 84.3 (66.6) months. Results: Genotype frequencies were 42.1% for II, 43.2% for ID, and 14.7% for DD. The relative risks of death were examined by Cox-proportional hazards analysis after adjusting for age, sex, age at the start of dialysis, presence of diabetes mellitus and hypertension and total cholesterol and serum albumin levels. The adjusted hazard ratio (95% confidence interval) was 1.03 (0.38 ? 2.85) for DD genotype and 1.50 (0.83 ? 2.70) for DD+ID genotype when compared to II genotype. Conclusion: ACE I/D polymorphism appears to have no relation to the short-term prognosis in chronic hemodialysis patients.

Abstract

C.W. McIntyre, R.J. Fluck, J.G. Freeman and S.H. Lambie

Department of Renal Medicine, Division of Gastroenterology, Derby City General Hospital, Derby, UK
Background: Acute liver cell failure (ALCF) commonly results in death and when complicated by acute renal failure (ARF), the mortality approaches 90%. Albumin dialysis allows partial replacement of some of the liver’s excretory functions. The molecular absorbents recirculating system (MARS®) has been recently introduced to provide this therapy. Thus allowing bridging to transplantation or hepatic regeneration. We have attempted to define the degree of “uremic” dialysis that this system can deliver as well as characterizing the dose of “hepatic” treatment, using a similar approach to solute remove as applied to assessing hemodialysis adequacy. As a secondary issue we also report on the clinical outcomes of this group of patients. Method: We treated 7 patients with ALCF and acute renal failure (6 of the patients having a formal diagnosis of hepatorenal syndrome), aiming to deliver a 5 treatment consecutive course consisting of 8 hours of albumin dialysis using the MARS® monitor, combined with hemodialysis. Clinical and biochemical outcomes were assessed, and dialysis adequacy measured using urea reduction ratios, calculated Kt/V and measured Kt/V (using ionic dialysance). Treatment dose, with respect to the highly protein bound and lipophilic toxins that accumulate in hepatic failure, was assessed by calculating the bilirubin reduction ratio and percentage reduction in plasma ammonia and total bile acids. Results: All of the patients had a degree of biochemical improvement with albumin dialysis. Urine output increased and the degree of encephalopathy improved. Mean bilirubin fell from 612 ± 105.5 mmol/l (range 165.6 – 1,024 mmol/l) to 370.4 ± 49.7 mmol/l (range 190.4 – 569.2 mmol/l), ALT reduced from 3,280 ± 2,266 IU/l (range 40 – 18,876) to 639 ± 230 IU/l (range 33 – 1677). Hepatic synthetic function improved with INR falling from 4.1 ± 0.5 (range 2.1 – 6.4) to 2.8 ± 0.6 (range 1.4 – 5.5). Plasma ammonia was reduced, falling from 162.4 ± 15.4 (range 131.1 – 191.9 mmol/l) to 73.1 ± 15 mmol/l (range 45.6 – 106.4 mmol/l). Bile acid levels fell from 132 ± 10.2 mmol/l (range 110.7 – 155.8 mmol/l) to 36.9 ± 6.1 mmol/l (range 24.6 – 49.6 mmol/l). The mean urea reduction ratio (URR) was 58.4 ± 3.2% (range 39 – 76%). Mean Kt/V as assessed by ionic dialysance was 1.7 ± 0.01 (range 0.8 – 2.4). Mean bilirubin reduction ratio (BRR) was 28.6 ± 1.4% (range 12.5 – 39%). BRR was proportional to both URR and Kt/V. BRR was also proportional to the percentage reduction of ammonia and bile acid levels. Three of the 7 patients survived to be discharged from hospital and 4 died. Conclusion: Albumin dialysis appears capable of improving the outcome in patients with ALCF and hepatorenal syndrome. Eight-hour intermittent treatments with the MARS® system in combination with hemodialysis deliver an adequate dose of dialysis with respect to urea. BRR may be an appropriate tool to allow further quantitative and comparative study of this technique.

Abstract

M. Karim, E. Vaux, D.R. Davies and P.D. Mason

¹Oxford Kidney Unit, Churchill Hospital, Oxford, UK, and ²Department of Cellular Pathology, John Radcliffe Hospital, Oxford, UK
Acute renal failure in association with microangiopathic hemolytic anemia and the pathological finding of thrombotic microangiopathy may occur in a number of conditions including hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and systemic sclerosis. Distinguishing between these conditions on clinical grounds may be difficult, and further investigations, including serological tests, are normally helpful. We present a patient who was treated with 5 doses of monthly carboplatin chemotherapy for stage IIb ovarian carcinoma and who subsequently developed acute renal failure and microangiopathic hemolysis together with some cutaneous features of systemic sclerosis. Initial serological tests, including anti-nuclear antibody titers measured using rat hepatocytes, were normal, and renal biopsy showed features of microangiopathic hemolysis, fibrinoid change, patchy tubular atrophy, and concentric intimal proliferation. A clinical diagnosis of diarrhea-negative hemolytic uremic syndrome was made and she was treated with plasma exchange and fresh frozen plasma infusion. However, she remained dialysis-dependent. Several weeks later she died following a cardiac arrest. Post-mortem examination revealed medial hypertrophy, concentric intimal proliferation, and thrombi within the small arteries of the kidneys and lungs. Subsequent results from tests taken at the time of her presentation with acute renal failure revealed a normal von Willebrand factor qualitative distribution, and a positive anti-nuclear antibody titer (using a human cell line) in association with positive autoantibodies to RNA polymerase types I, II, and III. Taken together, the clinical, laboratory, and post-mortem findings were suggestive of a diagnosis of systemic sclerosis. We discuss the differential diagnoses, and the associations between these and malignancy and chemotherapy. Finally, we consider the serological tests used for the diagnosis of systemic sclerosis that were, in this case, initially misleading.

Abstract

D.M. Graham, M.S. McMorris and J.T. Flynn

¹Departments of Internal Medicine and Pediatrics, Los Angeles County, University of Southern California Medical Center and Women’s and Children’s Hospital, Los Angeles, California, ²Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, and ³Department of Pediatrics, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA
Background: A relationship between allergy and the development of various renal diseases has been postulated, but never proven. Materials and methods: We present the case of a child with idiopathic episodic gross hematuria. The child also has significant environmental allergies, and his episodes of hematuria coincide with flares of his allergic symptoms. The available literature on hematuria and allergy was reviewed in order to further explore the potential role that allergy may play in the pathogenesis of genitourinary tract disease. Conclusions: This case, as well as others reported in the literature, suggest that allergy should be considered as a possible diagnosis in children with otherwise unexplained hematuria.

Abstract

K. Kaneko, K. Tuchiya, S. Fujinaga, R. Kawamura, Y. Ohtomo, T. Shimizu and Y. Yamashiro

Department of Pediatrics, Juntendo University School of Medicine, Tokyo, Japan
Aims: In view of the conflicting evidence of helper T cell type 1 (Th1) or type 2 (Th2) pattern of cytokine synthesis in childhood idiopathic nephrotic syndrome (INS) this study examined the balance of Th1 and Th2 which are characterized by intracellular cytokine production of interferon-g (IFNg) and interleukin-4 (IL-4), respectively. Subjects and methods: Sixteen children with steroid-sensitive INS (mean age 9.0 years) were included in this study, together with 15 healthy normal children (mean age 7.9 years) for the control group. Intracellular production of both IFNg and IL-4 in helper T cell (CD4+ cell) was investigated by a 3-color flow cytometry. Results: The cross-sectional data showed no significant differences of percentages of Th0 (IFNg+IL-4+ CD4+ cell), Th1 (IFNg+IL-4–CD4+ cell) and Th2 (IFNg–IL-4+ CD4+ cell) in CD4+ cells (p > 0.05). The Th1/Th2 ratio during nephrotic relapse did not differ from those during nephrotic remission and in normal healthy children (p > 0.05). Conclusion: We conclude that there is no significant skew of Th1/Th2 balance in childhood INS and that the cardinal immunological abnormality does not lie in helper T cells but in other cells, such as suppressor/cytotoxic T cells, natural killer cells or monocytes/ macrophage. To clarify the pathogenesis of INS, comprehensive studies for these cells would be worthwhile.

Abstract

V.M. Brandenburg, R.D. Frank and J. Riehl

Department of Nephrology, University Hospital, RWTH Aachen, Germany
Background: The exact incidence and clinical impact of arteriovenous fistulae (AVF) and pseudoaneurysms as complications emerging from renal allograft biopsy are not well established. We therefore conducted a prospective study using color-coded duplex sonography (CCDS) to determine the frequency, clinical presentation and spontaneous occlusion rate of biopsy-related AVF and pseudoaneurysms in kidney transplant recipients. Methods: We investigated 72 consecutive patients undergoing renal allograft biopsy using an automated biopsy technique. CCDS was performed before, immediately after and up to more than 6 months after biopsy. The diagnosis of AVF was based on the presence of perivascular vibration artifacts and detection of typical Doppler curves. Pseudoaneurysms were diagnosed based on the presence of “to-and-fro” signals. Results: In 5 patients (6.9%), an AVF was detectable before biopsy. Post-biopsy AVF were found in 12 additional patients (16.7%) with a spontaneous occlusion rate of 50% within 48 hours and 75% after 4 weeks. Three (25%) AVF persisted longer than 1 year. Four patients (5.6%) were found to have pseudoaneurysms. All pseudoaneurysms were located closely to AVF and closed spontaneously. None of the post-biopsy AVF and pseudoaneurysms required specific therapy. In 2 patients (2.8%), allograft biopsy lead to significant hemorrhage independent of AVF or pseudoaneurysms. Conclusion: These results indicate that post-biopsy AVF and pseudoaneurysms are a frequent finding after automated renal allograft biopsy. The natural history of these lesions shows a high rate of early occlusion. The present data fail to demonstrate significant clinical impact of AVF and pseudoaneurysms after renal allograft biopsy.

Abstract

A. Yildiz¹, M. Hursit¹, A.V. Çelik¹, S.M. Kayacan¹, H.Yazici¹, V. Akkaya¹, A.O. Gürol² and K. Karsidag²

¹Department of Internal Medicine, Division of Nephrology, Istanbul School of Medicine, and ²Department of Diabetology, Institute for Experimental Medical Research, Istanbul, Turkey
Doxazosin and insulin resistance
Insulin resistance (IR) in chronic renal failure (CRF) is well-known. In this randomized-controlled study, we aimed to compare the effect of doxazosin and amlodipine on IR in patients with CRF. Fifteen patients with CRF (male/female: 5/10, mean age: 46 ± 13 years) and 9 controls (male/female: 3/6, mean age: 35 ± 8 years) were included. Patients and controls had no family history of diabetes mellitus. Homeostasis model assessment (HOMA) was calculated as a marker of IR. Patients were grouped randomly to doxazosin (n = 8; 2 – 4 mg/day) and amlodipine (n = 7; 5 – 10 mg/day) arms. Baseline biochemical analysis (fasting serum glucose, BUN, creatinine, uric acid, cholesterol and cholesterol subgroups) and parameters related with insulin metabolism (insulin, C peptide, HOMA) were similar between amlodipine and doxazosin groups. There was no difference in age, gender and body mass index among study groups. The follow-up time was 12 weeks. Patients with CRF had higher HOMA (1.83 ± 0.55 vs 1.00 ± 0.36, p = 0.001), fasting insulin (8.06 ± 1.98 vs 4.46 ± 1.31 IU/l, p < 0.001) and serum triglyceride levels (197 ± 136 vs 112 ± 67 mg/dl, p = 0.04) as compared to controls. Serum HDL cholesterol levels were significantly lower in patients with CRF than controls (40 ± 10 vs 57 ± 14 mg/dl, p = 0.02). HOMA significantly decreased after doxazosin (1.91 ± 0.45 vs 1.41 ± 0.21, p = 0.02), however, no difference was found after amlodipine. Also, fasting insulin levels were decreased after a 12-week doxazosin therapy from 8.17 ± 1.22 vs 6.58 ± 0.84 IU/l, p = 0.02), but no change was seen after amlodipine. Lipid parameters did not significantly change during the study period in 2 groups. No adverse effect requiring drug discontinuation was observed during the 12-week period in the study groups. In conclusion, doxazosin decreases IR in patients with CRF, whereas amlodipine has no effect. This may be of advantage in the treatment of hypertension in this group of patients for preventing some long-term complication of IR.

Abstract

A. Ben-Haroush¹, R. Bardin¹, A. Erman², M. Hod¹, R.Chen¹, B. Kaplan¹ and J. Bar¹

¹Perinatal Division, Department of Obstetrics and Gynecology, and
²Nephrology and Hypertension Institute, Rabin Medical Center, Beilinson Campus, Petah Tiqva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Background and aim: b2-microglobulin (b2-m) is a polypeptide, which is freely filtered through the glomerular basement membrane and absorbed almost entirely by the proximal tubular cells. Preeclampsia, a common complication of pregnancy, is characterized by pathological renal changes, mainly glomerular lesions. The aim of the present study was to investigate whether serum b2-m measured in the early stages of pregnancy could be used as a marker to predict hypertensive complications in women at increased risk. Patients and methods: Serum b2-m concentrations were prospectively measured in 75 pregnant women with history of chronic hypertension, chronic renal disease, chronic vascular disease or preeclampsia and compared with those in 16 healthy pregnant women. Results: Of the 75 women in the study group, 10 (13%) developed preeclampsia and 20 (26%) had other complications, such as intrauterine growth restriction (n = 8), fetal or neonatal loss (n = 9) and delivery before 30 weeks of gestation (n = 8). Gestational age at delivery, birth weight and cesarean section rate were significantly worse in the patients with complications than in those without and in the healthy controls. No significant difference was detected in early serum b2-m concentrations between the women who later developed preeclampsia or other complications and those who did not. There was a significant positive correlation of b2-m concentrations with serum creatinine level (R2 = 0.394, p < 0.001), but not with gestational week at blood collection. Conclusion: Serum b2-m concentrations are not predictive of the development of preeclampsia or other complications in woman at risk.

Abstract

A. Bökenkamp¹, A. Grabensee¹, B. Stoffel-Wagner², C.Hasan¹, T. Henne³, G. Offner³ and M.J. Lentze¹

¹Medical Center of Bonn University, The Children’s Hospital,
²Institute for Clinical Chemistry, Medical Center of Bonn University, Bonn and ³Children’s Hospital, Hanover Medical School, Hanover, Germany
Background: As a consequence of more intensified immunosuppression, post-transplant lymphoproliferative disease (PTLD) is increasingly observed in patients after solid-organ transplantation. b2-microglobulin, a low-molecular weight protein (MW 11.8 kDa), is produced by all nucleated cells as part of the HLA complex. Its serum concentration is directly correlated with prognosis in patients with lymphatic neoplasms. Like other low-molecular weight proteins, b2-microglobulin is eliminated by glomerular filtration. This complicates its use as a tumor marker in renal insufficiency. Cystatin C, a low-molecular weight protein of 13.3 kDa, is a new marker of kidney function largely unaffected by extrarenal disease. We, therefore, sought to assess the potential of the b2-microglobulin/cystatin C ratio (b2M/Cys) as a marker of lymphoproliferation. Patients and methods: b2M/Cys was determined by particle-enhanced immunonephelometry in sera from 132 children with different degrees of renal insufficiency, 5 of whom had lymphoproliferative disease. Renal function was assessed using the Schwartz formula. Results: b2M/Cys was constant between 1.2 and 2.4 mg/mg for Schwartz GFR ³ 40 ml/min×1.73 m2. With lower GFR, b2M/Cys rose progressively, maximum values being found in the hemodialysis patients (4.85 – 11.73). Healthy renal transplant recipients had b2M/Cys comparable to controls. With acute lymphoproliferative disease, all but one patient had significantly elevated b2M/Cys between 2.68 and 3.68 mg/mg, which returned to normal in remission (1.67 – 2.35 mg/mg). The sensitivity of a b2M/Cys ratio > 2.4 mg/mg for the detection of PTLD was 80%, the specificity 100%, positive predictive value 100%, negative predictive value 90%. Conclusion: The b2-microglobulin/cystatin C ratio is a promising parameter of lymphoproliferation in patients with normal or mildly impaired renal function.

Abstract

R. Ranjan, H. Shah, J. Siu, E. Varghese, M. Bhaskaran, K. Reddy, A.A. Kapasi, J.D. Wagner and P.C. Singhal

Departments of Medicine, ¹Long Island Jewish Medical Center, and
²North Shore University Hospital, New York, USA
Background: The mononuclear phagocyte system plays an important role in host defense. Since dialysis patients have been reported to show enhanced leukocytes apoptosis, we evaluated the mechanism of increased apoptosis of monocytes in dialysis patients. Methods: Apoptotic studies were carried out on monocytes isolated from dialysis patients as well as healthy subjects. The effect of dialysis sera and membranes was evaluated on monocyte apoptosis as well as monocyte expression of proapoptotic proteins such as Fas and FasL. To confirm the role of FasL, we evaluated the effect of activated secretory products on T cell apoptosis. In addition, we studied FasL content of dialysis sera and supernatants of activated monocytes. Results: Monocytes isolated from dialysis patients (MDP) showed a greater magnitude of apoptosis when compared to monocytes isolated from healthy subjects (MHS) (MHS, 3.6 ± 1.1% vs. MDP, 24.3 ± 1.4%). Sera of hemodialysis patients (SHD) promoted (p < 0.001) apoptosis of MHS when compared to pooled control sera (HPS) (HPS, 0.8 ± 0.5% vs. SHD, 11.5 ± 0.5% apoptotic cells/field). Dialysis membranes, cellulose acetate membranes in particular, promoted monocyte apoptosis. Interestingly, anti-FasL antibodies partly inhibited dialysis sera-induced monocyte apoptosis. Dialysis membranes also modulated monocyte expression of both Fas and FasL. Secretory products of activated monocytes also promoted T cell apoptosis. Dialysis sera and activated monocyte secretory products showed increased FasL content. Conclusions: These results suggest that dialysis patients have an increased rate of monocyte apoptosis, which is mediated through a uremic milieu (serum factors). One of these serum factors seems to be FasL. In addition, dialysis membranes seem to promote apoptosis independent of the uremic milieu. The present study provides a mechanistical insight into the enhanced apoptosis of monocytes in dialysis patients.

Abstract

J. Chudek, M. Adamczak, F. Kokot, H. Karkoszka, W. Ignacy, D. Klimek and A. Wiecek

Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian University Medical School, Katowice, Poland
Background: Females are characterized by significantly higher plasma leptin concentration than males. It seems likely that sex hormones influence leptinemia independently from differences in body composition. The aim of the present study was to analyze the contribution of plasma concentrations of testosterone and estradiol on leptinemia in hemodialyzed patients. Methods: 110 hemodialyzed patients – HD (60 M, 50 F) and 70 healthy subjects (HS) (30 M, 40 F) were enrolled in this study. Plasma leptin, testosterone or estradiol and CRP concentrations and body composition by dual-energy X-ray absorptiometry (DEXA) were assessed. Results: Total body fat was significantly higher in females than in males (27.5 ± 1.5% vs. 17.2 ± 1.0% of body weight in HD and 36.0 ± 1.0% vs. 18.2 ± 1.4% in HS, respectively). Plasma leptin concentrations were markedly higher in females than in males both in HD (27.9 ± 5.4 ng/ml vs. 9.6 ± 1.9 ng/ml) and HS (16.5 ± 1.7 ng/ml vs. 3.1 ± 0.4 ng/ml). A highly significant, strong positive correlation was found between total fat mass (TFM) and leptinemia in all studied groups. No significant univaried correlation between plasma leptin and testosterone or estradiol concentrations respectively was found both in HD and HS. Multiple regression analyses showed that the main determinant of leptinemia is TFM (b = 0.623 and 0.798 in HS females and males respectively, and b = 1.058 and 0.797 in HD females and males respectively). Plasma concentration of testosterone (b = –0.139 and b = –0.075 in male HD and HS respectively) and estradiol (b = 0.199 and b = 0.046 in females HD and HS, respectively) contributed to leptinemia only in a minor degree. Conclusion: Both testosterone and estradiol are minor contributors to leptinemia both in HS and HD patients. The main determinant of leptinemia in these subjects is total body fat mass.

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