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1. |
Renal Tubular Cellular and Molecular Events in Acute Renal Failure |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 413-418
Adrian Iaina,
Down Schwartz,
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ISSN:1660-8151
DOI:10.1159/000188316
出版商:S. Karger AG
年代:1994
数据来源: Karger
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2. |
Treatment of Renal Anaemia with Recombinant Human Erythropoietin Results in Decreased Red Cell Uptake of45Ca |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 419-426
Torbjörn Linde,
Gunnar Ronquist,
Bo Sandhagen,
Björn Wikström,
Göran Frithz,
Leif Pettersson,
Bo G. Danielson,
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摘要:
The ability of erythrocytes to undergo deformation may be of importance to erythrocyte survival and to blood flow resistance. In a previous study a decreased deformability was demonstrated in the erythrocytes of uraemic patients treated with recombinant human erythropoietin (rhEPO). Erythrocyte deformability is, at least partly, determined by the intracellular concentration of free calcium ions. Six patients with renal anaemia (initial haemoglobin 95 ± 11 g/l) were treated with rhEPO. They were examined with regard to certain erythrocyte characteristics before treatment and after reaching a haemoglobin concentration exceeding 120 g/l. A decrease was noted upon treatment in erythrocyte deformability and uptake of 45Ca in vitro. The blood pressure tended to increase. The individual values of the decrease in 45Ca uptake and the increase in systolic blood pressure were positively correlated to each other (r=0.87; p < 0.05). No correlation was found between changes in erythrocyte deformability and 45Ca uptake. The decrease in 45Ca uptake may be interpreted in two different ways. It could reflect a reduced membrane permeability to calcium ions, or, which is more probable, it could be the end result of an increase in the intracellular metabolic pool of free calcium ions caused by the rhEPO treatment. We, therefore, conclude that rhEPO treatment has certain effects on calcium homeostasis in erythrocytes which may be related to blood pressure regulation
ISSN:1660-8151
DOI:10.1159/000188301
出版商:S. Karger AG
年代:1994
数据来源: Karger
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3. |
Delayed Decrease in Plasma Levels of Atrial Natriuretic Peptide during Cold Hemodialysis |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 427-432
Jörgen Hegbrant,
Hans Thysell,
Lena Mårtensson,
Anders Lassen Nielsen,
Fredrik Lindberg,
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摘要:
The high plasma levels of the vasodilating hormone atrial natriuretic peptide (α-ANP), observed in patients with chronic renal failure, decrease substantially during hemodialysis (HD), probably owing to volume reduction. Cardiovascular stability is better maintained by the use of cold dialysate although underlying mechanisms are unknown. In order to investigate the effects of different dialysate temperatures on hemodynamic stability and plasma levels of immunoreactive ANP (p-irANP), 10 stable HD patients were dialyzed with bicarbonate dialysis fluid for 240 min with each of 3 different dialysate temperatures: 36.5 °C (normal HD; NHD), 38.5°C (warm HD; WHD) and 34.5°C (cold HD; CHD). A Cuprophan plate dialyzer was used. The ultrafiltration volume and ultrafiltration rate were identical in each patient during the treatments. p-irANP was determined by radioimmunoassay, using 2 antisera which different cross-reactivity to ANP-related peptides. During NHD a nonsignificant decrease in mean arterial blood pressure from 111 ± 5 to 103 ± 8 mm Hg was observed. A significant (p < 0.05) decrease in mean arterial blood pressure from 109 ± 4 to 96 ± 6 mm Hg occurred during WHD, while during CHD it remained stable (111 ± 4 before, 112 ± 5mm Hg after). Irrespective of the dialysate temperature or the antiserum used, p-irANP decreased significantly (p < 0.05) during the treatment. The reduction in p-irANP was delayed during CHD, the decrease being significantly (p < 0.05) less pronounced after 120 min. At the end of the treatment no significant difference was observed between the regimes. In conclusion, together with the improvement of hemodynamic stability during CHD a delayed decrease in p-irANP was observed. Thus, α-ANP does not seem to be primarily involved in the stabilization of blood pressure duri
ISSN:1660-8151
DOI:10.1159/000188302
出版商:S. Karger AG
年代:1994
数据来源: Karger
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4. |
Increased Incidence of HLA-B40 Group Antigens in Children with Hemolytic-Uremic Syndrome |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 433-436
Kumudchandra J. Sheth,
Joan C. Gill,
Heinz E. Leichter,
Peter L. Havens,
Jay B. Hunter,
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摘要:
Hemolytic uremic syndrome (HUS) develops in 25-30% of children infected with Escherichia coli strains that produce Shiga-like toxins, also known as verocytotoxins. Mild HUS also occurs in 1 in 4 of the other family members, suggesting a familial predisposition to HUS. To understand the possible genetic predisposition, the frequency of HLA antigens was evaluated in 30 children (12 boys, 18 girls; mean age 3.8 years) with HUS following a prodrome of bloody diarrhea. When compared to a blood donor population from the same geographic area and ethnic background, no significant differences were noted in the frequency of HLA-A, HLA-C, HLA-DR, and HLA-DQ antigens. However, the frequency of HLA-B40 and its splits (B60,61 41 47) was significantly higher in the study population (corrected p < 0.005). The relative risk of developing HUS was 6.04 when HLA-B40 and HLA-B40 split products were present, and the risk increased to 8.5 when the analysis was extended to include the cross-reactive antigens B44 and B13. These HLA-B antigens share common amino acid sequences at positions 41-45 and 67-74 on the α-1 domain of the HLA class I molecule. Our data suggest that the inheritance of HLA-B40, its splits, and cross-reactive antigens increases the risk of developing HUS
ISSN:1660-8151
DOI:10.1159/000188303
出版商:S. Karger AG
年代:1994
数据来源: Karger
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5. |
Gene Expression and Release of lnterleukin-8 by Peritoneal Macrophages and Polymorphonuclear Leukocytes during Peritonitis in Uremic Patients on Continuous Ambulatory Peritoneal Dialysis |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 437-441
Ching-Yuang Lin,
Tung-Po Huang,
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摘要:
Interleukin-8 (IL-8) has been reported to be released by activated peritoneal macrophages (PMs) and a variety of other cell types, and it exhibits potent chemotactic activity for polymorphonuclear cells (PMNs). We have previously shown that IL-8 is detectable in the drain dialysate of uremic patients on continuous ambulatory peritoneal dialysis (CAPD) during peritonitis. The levels of IL-8 in infected drain dialysate caused by different microorganisms were variable. In this study, we evaluated the gene expression and release of IL-8 by PMs and PMNs during peritonitis caused by Staphylococcus aureus in uremic patients on CAPD. IL-8 levels were variable in the drain dialysate at the different episodes of peritonitis, even in the same patient. The IL-8 levels were highly correlated with PMN count in drain dialysate (r=0.9919, p < 0.001). PMs and PMNs obtained from drain dialysate at the onset of peritonitis increased mRNA expression for IL-8 and the amount of IL-8 mRNA from drainage cells was also highly correlated with PMN count. In contrast, cells isolated from drain dialysate without peritonitis failed to express mRNA for IL-8. These data suggest that increased expression of IL-8 may be a feature of peritonitis. The levels of IL-8 during peritonitis were not only related to the etiological microorganism but also to other unknown factor(s).
ISSN:1660-8151
DOI:10.1159/000188304
出版商:S. Karger AG
年代:1994
数据来源: Karger
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6. |
Analysis of Platelet Abnormalities in Uremia with and without Glanzmann’s Thrombasthenia |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 442-448
Shosaku Nomura,
Kenjiro Hamamoto,
Toshihiro Kawakatsu,
Hirofumi Kido,
Kazuyuki Yamaguchi,
Tsutomu Fukuroi,
Masahiko Suzuki,
Mutsumasa Yanabu,
Akira Shouzu,
Mitsushige Nishikawa,
Terutoshi Kokawa,
Shirou Fukuhara,
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摘要:
Uremia causes a bleeding tendency associated with platelet dysfunction, and previous studies have shown abnormalities of platelet glycoprotein (GP) lb or GPIIb/IIIa and a tendency for platelet activation in uremia. The present study compared the abnormalities of platelet function in uremia with (n=l) or without (n=18) associated Glanzmann’s thrombasthenia. There was a significant difference between ristocetin-induced agglutination of platelets from the uremic patients without Glanzmann’s thrombasthenia and platelets from healthy controls (n = 15). In addition, a reduction of GPIb expression by uremic platelets along with normal GPIIb/IIIa expression was confirmed using flow cytometry. Many coagulation markers were increased in the uremic patient with Glanzmann’s thrombasthenia, suggesting that the coagulation was enhanced and the platelets were prone to activation. However, the thrombasthenic platelets actually showed little increase in the binding of a monoclonal anti-CD63 antibody directed against lysosomal integral membrane protein (which is expressed after platelet activation), while uremic platelets showed a marked increase. In addition, the expression of GPIb by thrombasthenic platelets was normal, while that of GPIIb/IIIa was markedly decreased. Our results suggest that thrombasthenic platelets are resistant to activation and to the degradation of GPIb under uremic condition and that this difference from ‘ordinary’ uremic platelets be related to the difference in G
ISSN:1660-8151
DOI:10.1159/000188305
出版商:S. Karger AG
年代:1994
数据来源: Karger
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7. |
Glycosaminoglycans and Oxalocalcic Urolithiasis |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 449-453
F. Grases,
I. Llompart,
A. Conte,
R. Coll,
J.G. March,
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摘要:
A very simple analytical procedure with dimethylmethylene blue as photometric reagent was applied for the evaluation of glycosaminoglycan (GAG) urinary excretions and concentrations in both sexes, calcium oxalate stone formers, and a control group. The GAG concentrations varied significantly in stone formers (males and females) and in the control group; moreover, in some individual cases, a deficit of urinary GAGs was clearly detected. Apart from important inhibitory effects of GAGs on heterogenous calcium oxalate nucleation, the low urinary GAG content could be the cause of a pathological epithelium, favoring stone formation. The dimethylmethylene blue method is recommended as a quick screening procedure to determine a GAG deficit.
ISSN:1660-8151
DOI:10.1159/000188306
出版商:S. Karger AG
年代:1994
数据来源: Karger
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8. |
Toxic Acute Renal Failure in the Rat: Effects of Diltiazem and Urodilatin on Renal Function |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 454-461
L. Schramm,
E. Heidbreder,
J. Schaar,
K. Lopau,
J. Zimmermann,
R. Götz,
H. Ling,
A. Heidland,
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摘要:
Beneficial effects of natriuretic peptides have been reported in different models of acute renal failure (ARF). Calcium antagonists can also improve renal function, especially in ischemic models of ARF. The aim of our study was to investigate the effects of urodilatin and diltiazem alone and in combination in uranyl nitrate-induced toxic ARF in the rat. Three hours after induction of ARF glomerular filtration rate (GFR) was clearly diminished to about 50% compared to basal values. Intravenous infusion of diltiazem and urodilatin revealed a significant increase of GFR that even continued after cessation of drug delivery. Combined administration of urodilatin and diltiazem had no additional effect, probably due to a more pronounced fall in blood pressure in this group. Besides their vasorelaxing and blood pressure lowering effects both drugs also revealed diuretic activity. In conclusion both urodilatin and diltiazem are able to elevate GFR in the early phase of toxic ARF in the rat.
ISSN:1660-8151
DOI:10.1159/000188307
出版商:S. Karger AG
年代:1994
数据来源: Karger
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9. |
Progression of Chronic Renal Failure in a Rat Strain with Autosomal Dominant Polycystic Kidney Disease |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 462-467
N. Gretz,
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摘要:
Recently, the existence of a rat strain exhibiting autosomal dominant polycystic kidney disease (PKD) resembling human PKD has been described. An exact description of the course of chronic renal failure in this strain, however, is still missing. Thus the aim of this study was to analyze the long-term course of renal failure in these rats. In addition, unilateral nephrectomy (UNX) was performed in order to evaluate the impact of UNX on the occurrence of uremia. Our data clearly revealed that 70-80% of all animals of this rat strain developed uremia within 21 months. Additionally, proteinuria and hypercholesterolemia occurred, while the blood pressure was fairly unaffected. Also a slight degree of anemia was noted. In this long-term study death was due to uremia. The median survival time was significantly shorter in UNX PKD (median 11.6 months) than in non-UNX PKD animals (17.0 months; log-rank test: p = 0.001). In conclusion: with respect to renal function this rat model resembles human PKD disease. Furthermore, we could demonstrate that UNX is suitable to accelerate the rate of progression of renal failure in this model.
ISSN:1660-8151
DOI:10.1159/000188308
出版商:S. Karger AG
年代:1994
数据来源: Karger
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10. |
Allopurinol Fails to Protect against Gentamicin-lnduced Renal Damage in Normotensive and Spontaneously Hypertensive Rats |
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Nephron,
Volume 68,
Issue 4,
1994,
Page 468-472
B.J. Smyth,
W.G. Davis,
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摘要:
Recent research suggests the involvement of hydroxyl and superoxide free radicals in the development of gentamicin-induced acute renal tubular necrosis. Xanthine oxidase has been implicated as an important source of superoxide free radicals. Spontaneously hypertensive (Wistar-Kyoto) rats (SHR) have excessive oxidant stress which may render them more sensitive to the proported oxygen free radical producing effects of gentamicin. This study was undertaken to determine if the xanthine oxidase inhibitor allopurinol will ameliorate the effects of gentamicin. Normotensive Wistar-Kyoto (WKY) rats and SHR were administered allopurinol (40 mg/kg twice daily) orally 4 days before and throughout a 12-day gentamicin treatment period. The allopurinol only treatment group demonstrated no noticeable histological or functional changes considered to be indicative of nephrotoxicity. Gentamicin-injected WKY rats and SHR equally demonstrated extensive proximal tubular and glomerular damage characteristic of aminoglycoside-induced kidney damage. Allopurinol failed to protect either rat strain against the histological damage caused by gentamicin. Equivalent alterations in serum creatinine, serum gentamicin, urinary N-acetyl-β-D-glucos-aminidase excretion, body weight, urinary output, and blood pressure occurred in the gentamicin with allopurinol and gentamicin only treatment groups. Our results demonstrate allopurinol does not ameliorate the pathogenesis of gentamicin. SHR do not appear to be more sensitive to the effects of gentamicin induced kidney damage with or without allopurinol as compared with WKY rats
ISSN:1660-8151
DOI:10.1159/000188309
出版商:S. Karger AG
年代:1994
数据来源: Karger
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