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Books: 232	Journals: 18	Articles: 21403

Abstract

T. Onoe, T. Konoshita, K. Miyagi, K. Yamada, H. Mutoh, I. Koni and H. Nomura

¹Second Department of Internal Medicine, Kanazawa University School of Medicine, and ²Department of General Medicine, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan
Background: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited renal disorders in the world. Mutations in PKD1 are responsible for 80 – 95% of all autosomal dominant polycystic kidney disease (ADPKD). Although the need for linkage analysis of ADPKD is decreasing after the success of mutation detection at whole exons of PKD1, linkage analysis still has some advantages in detecting non-PKD1 families, thereby avoiding hopeless mutation analysis. Methods: We evaluated ten microsatellite markers beside or inside PKD1 on chromosome 16p. Allele frequency and heterozygosity of each marker were calculated based on the 100 genotypes obtained from 50 normal Japanese. Automated microsatellite genotyping using ABI Prism 377 and GeneScan software was applied. Markers were mapped using radiation hybrid mapping. Finally, this strategy was applied in the linkage analysis of 6 independent Japanese ADPKD families. Results: D16S3024, D16S3082, D16S3027 and D16S423 showed high heterozygosity (> 0.80) in a normal Japanese population and sufficient proximity to the PKD1 gene for linkage analysis. We could successfully analyze 144 genotypes within 7 hours. This strategy produced theoretically near-maximum LOD scores in 4 independent Japanese families inheriting ADPKD. Conclusions: Automated genotyping using microsatellite markers, D16S3024, D16S3082, D16S3027 and D16S423 are very useful in the linkage analysis of ADPKD.

Abstract

H. Burkhardt, T. Hahn and R. Gladisch

Specialty Geriatrics, IV. Medical Department, University of Heidelberg, Klinikum Mannheim, Mannheim, Germany
Background: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited renal disorders in the world. Mutations in PKD1 are responsible for 80 – 95% of all autosomal dominant polycystic kidney disease (ADPKD). Although the need for linkage analysis of ADPKD is decreasing after the success of mutation detection at whole exons of PKD1, linkage analysis still has some advantages in detecting non-PKD1 families, thereby avoiding hopeless mutation analysis. Methods: We evaluated ten microsatellite markers beside or inside PKD1 on chromosome 16p. Allele frequency and heterozygosity of each marker were calculated based on the 100 genotypes obtained from 50 normal Japanese. Automated microsatellite genotyping using ABI Prism 377 and GeneScan software was applied. Markers were mapped using radiation hybrid mapping. Finally, this strategy was applied in the linkage analysis of 6 independent Japanese ADPKD families. Results: D16S3024, D16S3082, D16S3027 and D16S423 showed high heterozygosity (> 0.80) in a normal Japanese population and sufficient proximity to the PKD1 gene for linkage analysis. We could successfully analyze 144 genotypes within 7 hours. This strategy produced theoretically near-maximum LOD scores in 4 independent Japanese families inheriting ADPKD. Conclusions: Automated genotyping using microsatellite markers, D16S3024, D16S3082, D16S3027 and D16S423 are very useful in the linkage analysis of ADPKD.

Abstract

D. Meier-Allmendinger

Abstract

N. Kishimoto, Y. Mori, T. Nishiue, Y. Shibasaki, O. Iba, A. Nose, Y. Uchiyama-Tanaka, H. Masaki, H. Matsubara and T. Iwasaka

¹Renal Division and ²Cardiovascular Center, Department of Medicine II, Kansai Medical University, Osaka, Japan
Background: An accessible non-invasive method for evaluating renal regional blood flow in real time is highly desirable in the clinical setting. Recent progress in ultrasonography with microbubble contrast has allowed quantification of regional blood flow in animal models. Aims: Goal of this study was to establish a convenient contrast-enhanced harmonic ultrasonography (CEHU) method for evaluating renal cortical blood flow in humans. Methods: We carried out intermittent second harmonic imaging in 9 healthy volunteers. Pulse interval was progressively decreased from 4 s ? 0.2 s during continuous venous infusion of the microbubble contrast agent. Results: Pulse interval versus CEHU-derived acoustic intensity plots provided microbubble velocity (MV) and fractional vascular volume (FVV) during renal cortical perfusion in humans. Low-dose dopamine infusion (2 mg/min/kg) resulted in a significant increase in MV which correlated well with the increase in total renal blood flow (RBF) determined by a conventional study of p-aminohippurate clearance (CPAH) (r = 0.956, p < 0.0001). Although FVV was not significantly increased, alterations in CEHU-derived renal cortical blood flow calculated by the products of MV and FVV were also correlated with alterations in total RBF (r = 0.969, p < 0.0001). Thus, low-dose dopamine infusion increases renal cortical blood flow observed in CEHU, mainly by increasing MV. Conclusions: The present study shows that renal cortical blood flow in humans can be measured non-invasively by CEHU and that CEHU can be used for quantitatively evaluating changes induced by a therapeutic agent such as dopamine in flow velocity and in FVV.

Abstract

S. Seeliger¹, M. Hausberg², I. Eue², T. Usdin³, K.H. Rahn² and M. Kosch²

¹Department of Paediatrics, ²Department of Internal Medicine D (Nephrology), University Hospital Münster, Germany, and ³Unit of Cell Biology, Laboratory of Genetics, National Institute of Health, Bethesda, Maryland, USA
Background: Parathyroid hormone (PTH) has specific effects on function, migration and proliferation of human leukocytes. These effects may contribute to accelerated atherosclerosis and impaired immune response observed in patients with renal insufficiency. Recently, a new G protein-coupled receptor with substantial implications for vascular function – the PTH2 receptor (PTH2-R) – has been identified, however, expression and distribution in humans and a possible regulation has not yet been studied. We therefore investigated the expression of the PTH2 receptor on human leukocytes in healthy subjects and in patients with hyperparathyroidism. Methods: PTH2 receptor expression was quantified by flow cytometry (FACS) analysis on monocytes, lymphocytes and granulocytes that were isolated from peripheral blood (hypotonic density gradient centrifugation) and by immunohistochemistry using a specific a-PTH2-R antibody produced in rabbit. Results of 22 patients with hyperparathyroidism (12 renal allograft recipients, 10 hemodialysis patients, mean age 43 ± 8 years) were compared to 22 age and sex-matched healthy controls. Results: Mean relative antigen density of the PTH2 receptor and percentage of positive cells in healthy subjects was 19 ± 5 and 90 ± 6% on granulocytes, 5 ± 2 and 55 ± 19% on monocytes, and 24 ± 7 and 21 ± 7% on lymphocytes. In patients with hyperparathyroidism, mean antigen density was significantly lower on granulocytes and monocytes (17 ± 4% and 3 ± 1%, p < 0.01, respectively). The percentage of positive cells and mean expression on lymphocytes was not significantly different. A significant and inverse correlation was found between plasma PTH concentrations and the mean PTH2 receptor expression on granulocytes (r = –0.41, p < 0.05). Conclusions: The PTH2 receptor is expressed on human granulocytes and – to a lesser degree – on monocytes and lymphocytes. In patients with hyperparathyroidism the PTH2 receptor is down-regulated as function of plasma PTH levels.

Abstract

R.D. Poduval and M.S. Hammes

Division of Nephrology, University of Chicago Hospitals, Pritzker School of Medicine, Chicago, IL, USA
Aim: Patients with end-stage renal disease are at increased risk for tuberculosis (TB). The Centers for Disease Control and Prevention (CDC) has recommended annual skin testing for TB, with tuberculin-purified protein derivative (PPD), in patients with chronic renal failure. The aim of this study was to identify the incidence and prevalence of tuberculin positivity and assess the utility of the tuberculin test in an inner city dialysis population. Methods: All patients on chronic hemodialysis at a center affiliated to the University of Chicago, who were tuberculin-tested between 1997 and 2000 or had previously documented PPD positivity precluding retesting, were included. Demographics, comorbidity, and tuberculin and anergy reactivity were recorded. A positive PPD was an induration of > 10 mm in response to 5 tuberculin units of PPD, and anergy an induration of < 2 mm in response to the anergy antigens (Candida and Mumps), at 48 h. PPD-positive patients were compared with PPD-negative patients; Fisher’s exact test and t-test were used, p < 0.05 was considered significant. Results: Of 131 patients at the dialysis center, 118 were studied. The remaining 13 refused consent to PPD testing. 41 (35%) were PPD-positive, 77 (65%) were negative. Of the 77 PPD-negative patients, 62 (81%) were anergic. None of the PPD-positive patients had clinical or radiographic signs of active TB. Only 20 patients received INH prophylaxis, the others refused or had contraindications to therapy. The conversion rate ranged from 3 – 8% per year. Demographics, nutritional parameters, comorbidity and adequacy of dialysis did not help predict PPD positivity. Conclusion: There is a high prevalence of PPD positivity and anergy among dialysis patients. As the diagnostic utility of the time-tested PPD test is unclear in an anergic dialysis population, the need for a high index of suspicion for active tuberculosis and timely diagnostic work up should be reinforced and not replaced by total dependence on the tuberculin test.

Abstract

H. Trimarchi, M.R. Mongitore, P. Baglioni, M. Forrester, E.A.R. Freixas, M. Schropp,H. Pereyra and M. Alonso

Division of Nephrology and Biochemistry Laboratory, Hospital Británico de Buenos Aires, Argentina
Background: Oxidative stress has been implicated in the development of endothelial damage in hemodialysis (HD). We have assessed the effects of N-acetylcysteine (NAC), a compound with antioxidant effects, on malondialdehyde (MDA), a marker of oxidative stress on lipid peroxidation. Methods: A clinical trial was conducted in which 24 chronic HD patients were divided into 2 groups according to gender, age, time on HD and cause of renal failure. The NAC group (n = 12) received 600 mg of NAC twice a day for 30 days. The remaining patients constituted the control group (n = 12). MDA levels were measured pre- and post-dialysis at the beginning of the study (baseline) and on day 30 (30 days). Results: Baseline pre- and post-dialysis MDA levels were not different between both groups and were above normal values. A significant decrease was found in the NAC group when either pre- or post-dialysis MDA levels were compared to the corresponding control group levels on day 30 (pre-dialysis NAC vs control group 3.01 ± 0.6 vs 4.5 ± 0.73 mmol/l, p < 0.0001, post-dialysis NAC vs control group 2.76 ± 0.5 vs 4.39 ± 0.7 mmol/l, p < 0.0001). Only in the NAC group were pre-dialysis MDA 30-day levels different from pre-dialysis baseline levels (3.01 ± 0.6 vs 5.07 ± 1.6 mmol/l, p < 0.002). Post-dialysis MDA 30-day concentrations were significantly lower than post-dialysis MDA baseline levels (2.76 ± 0.5 vs 4.32 ± 0.7 mmol/l, p < 0.002) and pre-dialysis MDA 30-day measurements (2.76 ± 0.5 vs 3.01 ± 0.6 mmol/l, p < 0.011). Conclusions: MDA levels are elevated in chronic HD patients and are not significantly reduced by HD. NAC significantly reduces malondialdehyde levels in chronic HD patients.

Abstract

R. Schindler, F. Christ-Kohlrausch, U. Frei and S. Shaldon

¹Department of Nephrology and Internal Intensive Care Medicine,
Charité Campus Virchow-Klinikum, Humboldt University, Berlin, Germany and ²Monaco
Aims: The increasing use of high-flux membranes for hemodialysis has raised concerns that patients dialyzed with these membranes may be at higher risk of being exposed to cytokine-inducing bacterial substances in the dialysate than patients dialyzed with low-flux membranes. We investigated the permeability of various high-flux membranes for both purified E. coli lipopolysaccharide (LPS) as well as for LPS derived from Stenotrophomonas (Sten.) maltophilia. Materials and methods: An in vitro dialysis circuit with saline in the blood compartment of 3 dialyzers containing different membranes (polysulfone, helixone and Diapes) was employed. The dialysate was challenged with increasing doses of sterile filtrates derived from Sten. maltophilia cultures or with purified LPS from E. coli. Samples from the blood compartment were tested for cytokine induction (IL-1b, IL-6 and TNF) in mononuclear cells as well as for LPS by limulus amebocyte lysate test (LAL). Results: IL-6 induction above sterile controls (< 0.02 ng/ml IL-6) was observed by samples from the blood side of DIAPES dialyzers (1.2 ± 0.7 ng/ml IL-6) after challenging the dialysate with 4.1 ± 3.6 U/ml E. coli LPS (9.9 ± 4.5 ng/ml IL-6). In contrast, at the same challenge dose no significant IL-6 induction above sterile controls was observed by blood side samples of polysulfone (0.15 ± 0.07 ng/ml) and helixone (0.09 ± 0.05 ng/ml) dialyzers. Increasing the amount of E. coli LPS in the dialysate further augmented IL-6 induction by blood side samples of Diapes but not of polysulfone and helixone dialyzers. Similar results were obtained for IL-1b and TNF. After challenging the dialysate with E. coli LPS as well as with cultures of Sten. maltophilia, significantly more LAL reactivity was observed in the blood compartment of Diapes compared to polysulfone and helixone. Conclusions: There are considerable differences between high-flux membranes regarding their permeability for cytokine-inducing substances from E. coli as well as for LPS derived from E. coli and Sten. maltophilia. Dialyzers that leak CIS under aqueous conditions in vivo should not be used unless the dialysate has passed through an ultrafilter.

Abstract

L. Labriola, M. Jadoul, M. Daudon, Y. Pirson and M. Lambert

Divisions of ¹General Internal Medicine and ²Nephrology, Cliniques Universitaires St. Luc, Université Catholique de Louvain, Brussels, Belgium, and ³Laboratoire de Biochimie, G.H. Necker – Enfants Malades, Paris, France
The authors report the case of a 45-year-old woman admitted for pneumonia who presented anuric acute renal failure after 12 days of intravenous amoxycillin-clavulanate treatment. Acute renal failure resolved rapidly and completely after antibiotic withdrawal. Analysis of the first post-anuric urine specimen showed many crystals. Infrared spectrophotometry revealed that the crystals were composed of trihydrated amoxycillin. The possibility of intrarenal obstruction due to massive drug crystalluria should not be overlooked in the face of abrupt anuria.

Abstract

H. Takahashi, S. Muto, E. Nakazawa, S. Yanagiba, Y. Masunaga, Y. Miyata, K. Tamba, E. Kusano, M. Matsuo, T. Matsuo and Y. Asano

¹Department of Nephrology, Jichi Medical School, Tochigi, and ²Department of Central Laboratory and Internal Medicine, Hyogo Prefectural Awaji Hospital, Hyogo, Japan
We report on the management of a 36-year-old hemodialysis patient with heparin-induced thrombocytopenia (HIT, type II) and clot formation in extracorporeal circulation. Platelet aggregation test and measurement of anti-platelet factor 4/heparin complex antibody by enzyme-linked immunosorbent assay revealed to us that our patient had developed HIT. Instead of heparin, we used nafamostat mesilate (NM) as an anticoagulant during hemodialysis, but could not completely prevent HIT-induced thrombocytopenia or clot formation in the extracorporeal circuit. Combined use of NM and aspirin completely inhibited platelet aggregation, decrease in platelet count and clot formation in the extracorporeal circuit.

Abstract

B.R. Don and A.I. Chin

Division of Nephrology, University of California Davis Medical Center, Sacramento, CA, USA
Calcific uremic arteriolopathy (calciphylaxis) is one of the more devastating complications that can develop in patients with chronic renal failure. This disorder is associated with calcium-phosphorus deposition in the subcutaneous arterial vessels and presents as a progressive ischemic necrosis of the skin resulting in large subcutaneous ulcerations with eschar formation. Mortality rates are substantially greater in chronic renal failure patients with calciphylaxis, and the major cause of death is infection and sepsis. We have developed a treatment strategy that employs a combination of therapies, which is based on reducing the known risk factors for the development of calciphylaxis as well as utilization of a number of treatment modalities that have been proven successful in the treatment of this disorder.

Abstract

M.S. Parisi, B. Oliveri, J. Somoza and C. Mautalen

Sección Osteopatías Médicas, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina
The efficacy and safety of the vitamin D analog, doxercalciferol (1a-hydroxyvitamin D2, 1aD2) in the treatment of secondary hyperparathyroidism in hemodialysis patients has been previously reported. We report thse effect of 16-week 1aD2 treatment on mineral metabolism and bone mineral density (BMD) in a hemodialysis patient with persistent secondary hyperparathyroidism post parathyroidectomy, resistant to previous calcitriol treatment. Levels of iPTH, bone-specific alkaline phosphatase and serum type I collagen C telopeptide were above normal at baseline and were substantially decreased with 1aD2 treatment (–92%, –63% and –53%, respectively). BMD increased in all areas: total skeleton (+6.5%), lumbar spine (+6.9%) and total femur (+4.3%). The patient showed no hypercalcemia, and phosphorus levels remained between 3.3 and 6.2 mg/dl.

Abstract

M. Guglin, C. Dey, G.M. Meny, W. Sultan and L.S. Weisberg

¹Divisions of Cardiology and ²Nephrology, UMDNJ/Robert Wood Johnson Medical School, The Cooper Health System, Camden, New Jersey, and ³The American Red Cross, Penn Jersey Region, Philadelphia, Pennsylvania, USA
Aims: To describe a patient with end-stage renal disease who developed non-cardiogenic pulmonary edema after transfusion of packed red blood cells. Design: Case report and literature review. Results: The patient under consideration is a 60-year-old woman who developed acute pulmonary edema after transfusion of packed red blood cells without concomitant dialysis. The initial diagnosis of fluid overload was managed by isolated ultrafiltration. Minimal fluid removal led to significant hypotension that was resistant to vasopressors. Subsequent pulmonary artery catheter readings were consistent with non-cardiogenic pulmonary edema. The patient improved spontaneously over the next few days with supportive care only. Plasma from the donors was checked for granulocyte antibodies and antibodies to HLA class I antigens. No granulocyte antibodies were detected in donor plasma but of one the HLA antibodies detected in donor plasma had specificity for a recipient HLA-A antigen. These characteristics supported a final diagnosis of transfusion-related acute lung injury (TRALI). Conclusions: Acute pulmonary edema following blood transfusion in a dialysis-dependent patient does not always signify fluid overload and nephrologists should be aware of the alternative diagnosis of TRALI. Proper awareness of TRALI will lead to prompt diagnosis and appropriate management.

Abstract

M. Sato, T. Kogure, N. Yanagisawa, H. Haizuka and Y. Nakashima

Abstract

K.T. Woo and Y.K. Lau

Abstract

I. Tzanakis, A. Papadaki, S. Kagia, N. Karefyllakis, V. Spandidakis, N. Girousis and N.Kallivretakis

Abstract

H. Kamimura, K. Tsuchiya, K. Honda, H. Kobayashi, T. Ogawa, H. Nihei and T. Mochizuki

Abstract

G. Gillerot and O. Devuyst

Division of Nephrology, Université Catholique de Louvain Medical School, Brussels, Belgium
Over time, a significant proportion of patients an peritoneal dialysis (PD) develop an increased permeability for small solutes, which induces a faster absorption of glucose, and ultrafiltration failure by early dissipation of the osmotic gradient. Vascular proliferation and vasodilatation of preexisting vessels might represent the structural basis for increased effective peritoneal surface area encountered in these PD patients. Animal models have shown that local release of growth factors and nitric oxide in the peritoneal membrane (PM) may lead to the development of areas of neovascularization and/or submesothelial fibrosis. Long-term exposure to conventional, glucose-based dialysis fluids plays a central role in the pathogenesis of these structural modifications. Glucose degradation products and reactive carbonyl species, which are present both in glucose-based dialysates and uremic plasma, accelerate the formation of the advanced glycation end products in the PM, which may in turn initiate a range of cellular responses including stimulation of monocytes, secretion of inflammatory cytokines, proliferation of vascular smooth muscle cells, stimulation of growth factors, and secretion of matrix proteins. The changes in the PM may also be potentiated by uremia and hyperglycemia per se. These new insights into the molecular mechanisms operating in the PM have provided rationale for novel therapeutic strategies including the development of glucose-free PD solutions and two-chamber bags.

Abstract

D.C. Cattran, R. Wald, P.E.C. Brenchley and B. Coupes for the North American Nephrotic Syndrome Group and the Genes, Gender and Glomerulonephritis Group

¹Department of Medicine, Toronto General Hospital/University Health Network and University of Toronto, Canada and ²Renal Research, Manchester Institute of Nephrology and Transplantation, Manchester Royal Infirmary, Oxford Head, Manchester, UK
Aims: The membrane attack complex (MAC) plays a key role in the pathogenesis of experimental membranous nephropathy. However, the clinical significance of urinary MAC (UMAC) excretion in human idiopathic membranous nephropathy (IMGN) and other proteinuric glomerulopathies is not fully elucidated. Patients and methods: We studied 16 patients with IMGN and 4 with focal segmental glomerulosclerosis (FSGS) who participated in clinical trials. Serial measures of UMAC, proteinuria and serum indices of renal function were conducted over the 26 weeks of treatment. Patients with UMAC excretion at treatment outset were identified as UMAC (+). We compared UMAC (+) and UMAC (?) patients with respect to several parameters at treatment initiation and study completion including age, disease duration, serum creatinine, creatinine clearance and proteinuria. In the UMAC(+) group we compared changes in UMAC values over time with patient outcome. Results: There were no demographic or clinical characteristics at presentation and study completion that distinguished the 8 UMAC (+) patients from the 12 UMAC (?) patients. As well, UMAC positivity did not predict response to therapy. Among the 8 UMAC (+) patients, 4 (3 IMGN and 1 FSGS) responded to therapy and in all cases, UMAC became undetectable. Non-responders to therapy (2 IMGN and 2 FSGS) continued to excrete UMAC at the conclusion of treatment. Initial UMAC levels of responders and non-responders were similar. Conclusions: UMAC levels parallel proteinuria not only in IMGN but also in FSGS patients. Immunomodulation may reduce glomerular formation of MAC in IMGN. In both histologic subtypes, the reduction in filtered protein may diminish the activation of MAC at the tubulointerstitial interface. However, the clinical utility of measuring UMAC is limited by its low prevalence, the absence of histopathologic specificity and its equivocal role in predicting outcome.

Abstract

J. Panos, M.F. Michelis, M.V. DeVita, R.H. Lavie and B.M. Wilkes

Nephrology Section, Department of Medicine, Lenox Hill Hospital and

The New York University School of Medicine, New York, NY, USA
Patients with various renal diseases receiving an angiotensin-converting enzyme inhibitor (CEI) were enrolled in a protocol to determine whether adding an angiotensin type 1 receptor blocker (ARB) reduces urinary protein excretion (UPE). All patients had significant proteinuria (range 517 – 8,562 mg/24 h) despite administration of CEI for at least 4 weeks. Following baseline measurements, losartan (50 mg/d) was started and testing was repeated at 1 month. Compared with CEI alone, combined CEI plus ARB reduced UPE by 45 ± 8% (p < 0.005). Compared with CEI alone, CEI + ARB lowered UPE in each patient independent of baseline protein excretion or renal diagnosis. Reduction in proteinuria occurred independent of changes in mean arterial blood pressure (MAP), suggesting that the mechanism involved local changes in glomerular dynamics. If renal angiotensin II (ANG II) formation occurred despite CEI, the ANG II formed would suppress plasma renin activity (PRA), and adding an ARB would cause PRA to rise. In 7 of 10 subjects, addition of ARB to CEI increased PRA (p < 0.03) suggesting that intrarenal ANG II formation occurred in CEI-treated subjects. As a second marker of ANG II tissue activity, we measured the effects adding ARB on plasma aldosterone (ALDO). In 9 of 10 subjects, ALDO was acutely lowered (p < 0.009) suggesting that ANG II levels were incompletely blocked by CEI. We conclude that: combined CEI and ARB reduces UPE greater than CEI alone; reduction in proteinuria is independent of changes in MAP or renal diagnosis; and the additive effects of CEI and ARB are due at least in part to greater inhibition of ANG II action at the tissue level in the kidneys and adrenal glomerulosa.

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