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Dustri-Verlag
Volume 58, No. 5/2002(November)
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Originals
Pericardial effusion in the nephrotic syndrome
329
20$
Abstract
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.
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.
Originals
Race and glomerulonephritis in patients with and without hepatosplenic Schistosomiasis mansoni
333
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Abstract
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.
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.
Originals
Endothelin-1 in the kidney and urine of patients with glomerular disease and proteinuria
337
32$
Abstract
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.
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.
Originals
Correlative studies of urine fluorescence and free radical indicators
344
28$
Abstract
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.
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.
Originals
Total serum bile acids in renal transplanted patients receiving cyclosporine A
350
28$
Abstract
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.
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.
Originals
Eleven years of experience with dialysis associated tuberculosis
356
32$
Abstract
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.
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.
Originals
Serum soluble transferrin receptor reflects erythropoiesis but not iron availability in erythropoietin-treated chronic hemodialysis patients
363
32$
Abstract
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.
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.
Originals
Angiotensin-converting enzyme (ACE) insertion/deletion polymorphism and survival in a cohort of chronic hemodialysis patients
370
28$
Abstract
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.
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.
Originals
Characterization of treatment dose delivered by albumin dialysis in the treatment of acute renal failure associated with severe hepatic dysfunction
376
36$
Abstract
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.
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.
Case reports
Renal failure due to scleroderma with thrombotic microangiopathy developing in a woman treated with carboplatin for ovarian cancer
384
24$
Abstract
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.
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.
Case reports
Episodic gross hematuria in association with allergy symptoms in a child
389
20$
Abstract
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.
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.
