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Abstract

V. Menon, X. Wang, T. Greene, G.J. Beck, J.W. Kusek, S.M. Marcovina, A.S. Levey and M.J. Sarnak

¹Department of Medicine, Division of Clinical Care Research, Tufts-New England Medical Center, Boston, MA,²Department of Biostatistics and Epidemiology/Wb⁴, Cleveland Clinic Foundation, Cleveland, OH,³National Institutes of Health, Bethesda, MD,⁴Departmen
Background and aims: Serum leptin levels are elevated in patients with kidney failure. Data on the associations of serum leptin and on the relationship of leptin with both kidney function and inflammation, are limited in patients with reduced glomerular filtration rate (GFR). We evaluated the independent associations of serum leptin in patients with reduced GFR. Material and methods: Serum leptin and C-reactive protein (CRP) were measured in samples from 798 participants of the Modification of Diet in Renal Disease Study. Multivariable analysis was used to evaluate the independent effects of kidney function and CRP on leptin levels. Results: Median (interquartile range) of serum leptin was 9.1 ng/ml (14.0). Female gender, higher percent body fat, higher insulin levels, older age, lower GFR and higher CRP were associated with higher serum leptin levels and explained 51% of the variability in the logarithm of serum leptin levels. After adjusting for the other variables, a 10 ml/min/1.73 m2 lower GFR was associated with 6% higher mean serum leptin levels. Percent body fat and gender, explained 45% of the variability in serum leptin levels. Conclusions: Level of kidney function and CRP are associated with serum leptin in patients with reduced GFR. However, there is a stronger association between serum leptin and indices of body fat and gender in patients in the earlier stages of chronic kidney disease. 50% of the variability remains unexplained in patients with reduced GFR.

Abstract

C. Garcia-Ruiz, A. Martinez-Vea, T. Sempere, A. Sauri, M. Olona, C. Peralta and A. Oliver

¹Departments of Nephrology, ²Institut d’ Estudis Avançats Universitat Rovira i Virgili, ³Radiology and ⁴Preventive, Hospital Universitari Joan XXIII, Tarragona, Spain
Background: Spiral computed tomography angiography (CTA) is a sensitive and specific technique for visualizing renal arteries and diagnosing renal artery stenosis (RAS). Whether spiral CTA is associated with increased risk of contrast nephropathy (CN) in patients with impaired renal function is unknown. Methods: We prospectively studied 50 patients with chronic renal insufficiency (serum creatinine concentration greater than 1.58 mg/dl) who underwent spiral CTA with iopromide, a nonionic, low-osmolar contrast agent. Fourteen patients had diabetes mellitus. Patients were encouraged to drink 1 l of water 12 hours before and 2 l over 24 hours after the procedure. The presence of CN was defined by an increase of 20% or more in the baseline serum creatinine level within or 72 hours after administration of the radiocontrast agent. Results: In the entire group, mean serum creatinine levels increased significantly from 2.92 ± 1.39 to 3.06 ± 1.55 mg/dl (p = 0.02) and mean creatinine clearance decreased from 29.8 ± 12.9 to 28.9 ± 12.8 ml/min (p = 0.009) 72 h after administration of the contrast medium. Two patients experienced an increase in serum creatinine level of 20%. Renal function returned to baseline within seven days in the 2 patients. Absolute changes in creatinine clearance after the administration of radiocontrast medium were similar in nondiabetic and diabetic patients and in the subgroup of patients, with a baseline serum creatinine of < 3 mg/dl and ³ 3 mg/dl. Conclusions: In patients with chronic renal insufficiency, spiral CTA performed with iopromide, a nonionic, low-osmolar contrast medium and a prophylactic oral hydratation, is a minimally invasive technique with low risk of contrast nephropathy.

Abstract

N. Cohen, O. Gorelik, D. Almoznino-Sarafian, I. Alon, Y. Tourovski, J. Weissgarten, S. Chachashvily, M. Shteinshnaider and D. Modai

¹Department of Internal Medicine “F”, and ²Nephrology Division, Assaf Harofeh Medical Center Affiliated to Sackler Faculty of Medicine, Tel-Aviv University,
Zerifin, Israel
Aims: Many congestive heart failure (CHF) patients suffer from various comorbidities, which may aggravate CHF or independently increase mortality risk. Renal failure (RF) is one of them. We defined bed-side clinical, laboratory and electrocardiographic parameters characterizing CHF patients with and without concomitant RF, and analyzed their impact on mortality. Methods: We studied symptomatic unselected consecutive furosemide-treated CHF patients hospitalized for various acute conditions. On admission, history taking, physical examination, chest x-ray, ECG and routine laboratory tests were performed. Subsequently, patients were divided into 2 subgroups, those with serum creatinine ³ 1.5 mg/dl (RF) and those with lower values. Following discharge, information concerning mortality and circumstance of death was obtained from hospital records and outpatient death certificates. Results: Included were 398 patients, 163 (40.9%) with RF and 235 free of RF. Prevailing in the RF subgroup were older age (mean age 75.5 vs 70.8, p < 0.001), male gender (p < 0.001), admission pulmonary edema (p = 0.007), cardiac arrhythmias (p = 0.05), cardiac conduction disturbances (p = 0.002), severe CHF (p = 0.005), lower ejection fraction (p = 0.03), anemia (p = 0.009), higher furosemide maintenance dosages (p < 0.001), insulin treatment (p = 0.03) and receiving less ACE inhibitors (p = 0.006). On median follow-up of 43 months, mortality was 54.9% in the RF vs 31.9% in the non-RF subgroup (p < 0.001), RF being the parameter most significantly associated with low survival (OR 1.97, p < 0.001). In the RF subgroup older age (p < 0.02), female gender (p < 0.003) and not using ACE inhibitors (p = 0.04) or drugs with antiarrhythmic effects (p < 0.005), emerged significantly associated with low survival, while diabetes mellitus (DM) and admission pulmonary edema tended to be so associated (p < 0.2). Using multivariate analysis in the RF subgroup, older age, female gender and DM proved most significantly associated with poorer survival (p = 0.004, OR 1.5, p = 0.03, OR 1.72, p = 0.04, OR 1.28, respectively). In the non-RF subgroup, only older age (p = 0.005) and DM (p = 0.05) were significantly associated with low survival. Sudden death occurred in 21 patients, 14 (8.6%) in the RF and 7 (3%) in the non-RF subgroup (p < 0.001). Conclusions: RF is a marker of severity in CHF. Its full-blown deleterious prognostic effect is already manifested at serum creatinine 1.5 mg/dl. Older age, DM and female gender most significantly heralded a shorter survival. Such patients require special care.

Abstract

N. Maki, A. Komatsuda, H. Wakui, Y. Oyama, T. Kodama, H. Ohtani, A. Kigawa, H. Imai, M. Motegi, A. Yamaguchi and K. Sawada

¹Third Department of Internal Medicine, Akita University School of Medicine, ²Department of Internal Medicine, Akita City Hospital, and
³Department of Internal Medicine, Senboku General Hospital, Akita, Japan
Background: Fabry disease is an X-linked recessive disorder resulting from a deficiency of lysosomal a-galactosidase A (a-Gal A). Chronic renal failure is an important cause of death in patients with Fabry disease. We report on patients with Fabry disease (a hemizygous male and his mother) due to a nonsense mutation (R220X) in the a-Gal A gene. Methods: The proband, a 41-year-old man, and his 71-year-old mother presented with renal and cardiac manifestations of Fabry disease. Histological examination and molecular analysis of the a-Gal A gene were performed. Results: Typical histological findings of Fabry disease were observed in a renal biopsy specimen from the proband and in renal and myocardial necropsy specimens from the mother. Sequencing of a full-length a-Gal A cDNA from the proband indicated a C – T transition at codon 220, resulting in substitution of the predictable termination for arginine (R220X). Examination of genomic a-Gal A DNA revealed that the proband was a hemizygote and the mother was a heterozygous carrier for the mutation. Conclusion: This is the first detailed report of family members with Fabry disease due to a nonsense mutation (R220X) in the a-Gal A gene. Our study indicates that this mutation causes the typical disease in both genders.

Abstract

A. Klemm¹, C. Franke¹, M. Busch¹, A. Müller¹, S. Franke¹, D. Lang², J. Passlick-Deetjen² und G. Stein¹

¹Department of Internal Medicine III, Friedrich Schiller University, Jena, and ²Fresenius Medical Care, Bad Homburg, Germany
Backround: Advanced glycation end products (AGEs), total homocysteine (tHcy) and the homocysteine metabolites cystathionine (Cysta) and dimethylglycine (DMG) are increased in serum of patients with end-stage renal disease. The aim of this prospective randomized study was to compare the efficacy of polysulfone high-flux vs. polysulfone low-flux hemodialysis (HD) treatment regarding removal of AGEs, tHcy, Cysta and DMG. Patients and methods: Twenty-nine patients on chronic HD treatment were randomly assigned to 2 groups in a 3-period 2-treatment design with low flux (A) – high flux (B) – low flux (A) for group I and B-A-B for group II, 6 weeks each period. The following parameters were measured in pre- and postdialytic serum samples at baseline and the end of each period: total serum fluorescence, Ne-carboxymethyllysine (CML), free and protein-bound pentosidine, tHcy, Cysta and DMG. Results: There was increased removal of free pentosidine during high-flux HD treatment compared to low-flux HD treatment, attaining significance between the second and third treatment periods (group I: 86.0 ± 4.7% vs. 79.2 ± 8.8%, p = 0.007; group II: 84.0 ± 6.3% vs. 79.8 ± 9.8%, p = 0.049 for high vs. low flux). The intradialytic reduction rates for total serum fluorescence, tHcy, Cysta, DMG did not differ between high- and low-flux HD treatment. Protein-bound pentosidine and CML did not decrease during the dialysis sessions, neither with high-flux nor with low-flux HD membrane. Despite a strong decrease during single HD session, the predialytic levels of free pentosidine, tHcy, Cysta and DMG remained unchanged during the study period both for high- and low-flux HD treatment. Conclusion: The more pronounced effect of high-flux dialysis on the removal rate of free pentosidine, found in this randomized crossover study, could not translate into a significant difference in predialysis levels after a 6-week treatment period. We could not find any differences between polysulfone high- and low-flux membranes for lowering predialytic serum concentrations of the measured AGEs, which are mainly bound on albumin.

Abstract

R.J. Walker, W.H.F. Sutherland and S.A. De Jong

¹Department of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, and ²Department of Nephrology, Dunedin Hospital, Dunedin, New Zealand
Background: In vitro, synthetic dialysis membranes induce less activation of blood components to produce pro-inflammatory cytokines and reactive oxygen species compared with cellulose acetate membranes. However, the long-term effect of switching from a cellulose-based dialysis membrane to a synthetic membrane on protein oxidation and systemic inflammation in hemodialysis patients is not well defined. Methods: Nineteen patients receiving hemodialysis were followed prospectively after changing from a low-flux cellulose acetate membrane to a low-flux polysulphone membrane for 11 – 17 months (n = 15) and then returning to the cellulose acetate membrane for 1 month (n = 13). Plasma markers of protein oxidation, cell activation and systemic inflammation and concentrations of soluble cell adhesion molecules were measured at baseline and at the end of each intervention period. Results: Plasma levels of protein thiols (18%), IL-6 (34%), VCAM-1 (33%), ICAM-1 (21%) and b2-microglobulin (21%) increased significantly and dityrosine fluorescence (– 36%), protein lipofuscin-like fluorophores (–18%) and TNF-a (–20%) decreased significantly in the patients after they switched to the polysulphone membrane. After reverting to the cellulose acetate membrane for 1 month, plasma levels of protein thiols and IL-6 returned to baseline while levels of other variables were not significantly different from values at the end of the polysulphone dialysis period. There was substantial intra-individual variation between 2 baseline measurements of plasma cytokines. Conclusions: Switching from a cellulose acetate membrane to a low-flux polysulphone dialysis membrane for a year or more may decrease the level of protein oxidation suggesting a decrease in oxidant stress and greater biocompatibility of the polysulphone membrane. The effect of this change in dialysis membrane on systemic inflammation is uncertain due to increases in some but not other inflammation-sensitive molecules.

Abstract

R. Bergner, M. Hoffmann, H. Brass und M. Uppenkamp

Medizinische Klinik A, Klinikum der Stadt Ludwigshafen, Ludwigshafen
Mycophenolate mofetil is an immunosuppressive agent in transplantation which inhibits the purin neogenesis. Proliferating lymphocytes are suppressed and antibody production is decreased. Many cases of successful therapy in different kidney diseases are reported, such as diffuse proliferative lupus nephritis, pauci-immune necrotizing glomerulonephritis, focal segmental glomerular sclerosis and IgA nephropathy. We report 3 patients with IgA nephropathy who were treated with mycophenolate mofetil for more than 1 year. In all patients, proteinuria decreased significantly and the renal function remained stable. In 2 patients, kidney biopsy was repeated after 12 months and 18 months, respectively. There were no histological signs of progression of the disease. Two patients developed infections during treatment. One patient had a pneumonia, and a second patient an infection with varizella zoster. Based on our data, mycophenolate mofetil can be a potential treatment of IgA nephropathy. Further controlled studys are warranted to investigate the role of mycophenolate mofetil in IgA nephropathy.

Abstract

T.-C. Chen, F.-R. Chung, C.-H. Lee, S.-C. Huang, J.-B. Chen and K.-T. Hsu

¹Division of Nephrology, Department of Internal Medicine and ²Department of Pathology, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan
Henoch-Schoenlein purpura (HSP) crescentic glomerulonephritis with acute renal failure in adults is extremely rare. The condition carries a grave renal outcome if it is not appropriately managed. Oral corticosteroids, intravenous methylprednisolone pulse therapy and plasmapheresis with concomitant plasma replacement have been used alone or in various combinations to treat patients with HSP nephritis, yet the effects are uncertain. We describe a 33-year-old man with oliguric acute renal failure in the setting of HSP crescentic glomerulonephritis that is refractory to intravenous methylprednisolone pulse therapy (1,000 mg/day for 3 days) with maintained oral prednisolone (1 mg/kg/day) and oral cyclophosphamide (2 mg/kg/day) for 3 weeks, resulting in successful recovery of renal function after 9 sessions of simple double-filtration plasmapheresis treatment without concomitant plasma replacement. There was no recurrence of vasculitic events within 18 months. In this case, we emphasize that simple double-filtration plasmapheresis without concomitant plasma replacement is an effective and safe modality therapy for adult patients with HSP crescentic glomerulonephritis and acute renal failure, especially when conventional therapy has failed.

Abstract

P. Eller, A.R. Rosenkranz, W. Mark, I. Theurl, J. Laufer and K. Lhotta

¹Department of Internal Medicine, Clinical Nephrology Division, ²Department of Transplant Surgery, ³Institute of Pathology, Innsbruck University Hospital, Innsbruck, Austria, and ⁴Institute of Pathology, SLK-Klinikum, Heilbronn, Germany
We report a patient with complete adenine phosphoribosyltransferase deficiency and urolithiasis, in whom 4 consecutive cadaveric renal transplantations were performed; 2,8-dihydroxyadenine crystal nephropathy recurred within weeks in the first and second graft when the patient was not treated with allopurinol immediately after transplantation. In the third graft, recurrence of disease could be prevented by immediate allopurinol treatment. This graft was lost due to chronic allograft nephropathy without significant crystal deposition. After a fourth transplantation, again without initial allopurinol, the disease recurred following an initial vascular rejection. Addition of allopurinol significantly improved renal function of the 2nd and 4th graft. This case indicates that outcome of renal transplantation in patients with adenine phosphoribosyltransferase deficiency critically depends on immediate postoperative pharmacotherapy with allopurinol, which is able to prevent 2,8-dihydroxyadenine nephropathy in the graft. Furthermore, rapid recurrence of disease without allopurinol seems to be triggered by delayed graft function and acute rejection.

Abstract

M.J. Hausmann, M. Vorobiov, M. Zlotnik, B. Rogachev and A. Tomer

¹Department of Nephrology and ²Blood Bank and Transfusion Medicine Service, Soroka Medical Center and Faculty of Health Sciences, Ben-Gurion University, Beer-Sheva, Israel
A patient with end-stage kidney disease is described, who lost his renal allograft in the early post-transplant period due to allograft renal vein thrombosis. Prior to transplantation, he had been treated by hemodialysis and lost several vascular accesses because of thrombosis. A search for potential thrombophilic factors disclosed a unique combination of increased clotting factor levels, i.e. FVIII, FIX, FXI and homocysteine. More common hereditary and acquired hypercoagulability factors have been excluded in this patient. While clotting factor deficiencies are well known causes of hemophilia, their levels should also be measured in the workup of transplant candidates with a history of multiple vascular access thrombosis.

Abstract

S.I. Park, S. Lee, W. Kim, W.H. Yoo and S.K. Park

Abstract

M. Viljoen and A.M. Koorts

Abstract

A. Rodríguez-Cuartero, F. Pérez-Blanco, M. Riera, J. Canora and J. Roldán

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Volume 61, No. 3/2004(March)