|
1. |
Occupational Factors and Renal Disease |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 425-434
YaqoobMuhammad,
BellGordon M.,
Preview
|
PDF (613KB)
|
|
摘要:
The male-to-female ratio of patients requiring dialysis treatment commonly approaches 2:1. It is proposed that environmental factors, particularly occupational exposure to hydrocarbons, may account for the excess number of male patients. The term“hydrocarbon”refers to the aliphatic, alicyclic, aromatic, and halogenated hydrocarbons (carbon tetrachloride, chloroform); glycols (ethylene glycol, diethylene glycol, dioxane, glycerol); and organic solvents. Hydrocarbons commonly find use as solvents in industrial manufacturing practices because of their lipid solubility. Hydrocarbons have long been known to be neurotoxicants, affecting both peripheral and central nervous systems. Although benzene and its derivative have a known association with uroepithelial tumors, there is now a considerable body of evidence suggesting a possible role for hydrocarbon exposure in the development of non-neoplastic renal diseases. This article presents an epidemiological case for such an association and critically reviews the literature.
ISSN:0886-022X
DOI:10.3109/08860229409045074
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
2. |
Thyroid Hormone Induction of Ornithine Decarboxylase in Ischemic Acute Renal Failure |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 435-444
JohnsonJ. P.,
GrilloF. G.,
Preview
|
PDF (517KB)
|
|
摘要:
Thyroid hormone is an important interventional agent shown to be beneficial in a variety of models of acute renal failure (ARF). While its usefulness is clear, its mechanism of action remains unknown. Although there are a multitude of thyroid-inducible proteins and enzymes, the one singled out in these studies as of potential mechanistic significance in the protective effect of thyroid in ARF is ornithine decarboxylase (ODC). This enzyme catalyzes the entry step in the biosynthesis of polyamines, which possess several potential roles in fostering renal repair and recovery. Ischemic ARF was induced in rats by renal arterial clamp and functional assessment was made by inulin clearance 24 h after injury. Both T4(10µg/100 g) and T3(1 and 10µg/100 g) resulted in significant improvement in inulin clearance when compared to ischemia alone, while reverse T3was without effect. The activity of ODC was reduced 70% at 24 h in the kidney cortex but T3restored the level to near control. Pretreatment of rats with difluromethylornithine (DFMO), an irreversible inhibitor of ODC, resulted in nearly complete inhibition of this enzyme in the cortex and medulla, and blocked the increase in activity induced by T3. From the functional standpoint, DMFO did not worsen the severity of ischemic ARF but completely blocked the protective effect of T3. These data strongly suggest roles for ODC stimulation and, presumably, the consequent augmentation of polyamine biosynthesis, in the mechanism by which thyroid hormone enhances recovery from ARF.
ISSN:0886-022X
DOI:10.3109/08860229409045075
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
3. |
Oxygen Free Radicals Are Not the Main Factor in Experimental Gentarnicin Nephrotoxicity |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 445-455
StrattaPiero,
SegoloniGiuseppe Paolo,
CanaveseCaterina,
MuzioGiuliana,
DoglianiMargherita,
SerraAndrea,
AllemandiPaolo,
SalomoneMario,
CaramellinoCristina,
CanuteRosangela,
Preview
|
PDF (527KB)
|
|
摘要:
As a role for oxygen free radicals has been suggested in gentamicin (G) nephrotoxicity, we tested the hypothesis that exogenously administered glutathione (GSH), able to restore intracellular antioxidant potential, could be useful in reducing damage. Adult Sprague—Dawley rats were injected with saline (n = 30), subcutaneous (s.c.) G 100 (n = 23) and 150 mg/kg/day (n = 14), or s.c. G at the same dosages plus intraperitoneal (i.p.) GSH 1200 mg/kg/day (n = 24 and 14, respectively) for 7 days. In the G-100-day protocol, GSH-treated rats showed significantly lower renal G content (2.79±0.8 vs. 3.61±1.4µg/mg prot) coupled with lower plasma urea (153±79 vs. 188±61 mg/dL) and creatinine levels (1.63±1 vs. 2.45±1 mg/dL). As to renal oxidant/antioxidant balance, local GSH was increased (0.32±0.01 vs. 0.19±0.01µg/mg prot) while lipid peroxidation, determined-by production of thiobarbituric acid reactive substances (TBARS), was decreased (0.35±0.02 vs. 0.52±0.02 nmol/mg prot). In the G-150-mg protocol, GSH-treated rats showed no differences in renal gentamicin content or in blood urea and creatinine levels, in spite of a significantly lower renal TBARS production and a significantly higher GSH content. Urine enzyme excretion did not significantly change in GSH-treated vs. not-GSH-treated rats in both protocols. We conclude that: (a) GSH interferes with G nephrotoxicity mainly via a reduction in G uptake; (b) the oxidative renal stress is not crucial in inducing renal damage. In fact, when increased G dosages blunt the ability of GSH in reducing G uptake, no substantial protection is demonstrated.
ISSN:0886-022X
DOI:10.3109/08860229409045076
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
4. |
Acute, Subacute, and Chronic X-ray Effects on Glomerular Hemodynamics in Rats |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 457-470
de Paulo Castro TeixeiraVicente,
BoimMírian Aparecida,
SegretoHelena Regina Cômodo,
SchorNestor,
Preview
|
PDF (684KB)
|
|
摘要:
In order to evaluate the effects of x-rays on glomerular hemodynamics, surgically exposed left kidneys of Munich-Wistar rats were irradiated with 15 Gy in a single dose. The animals were studied 45 min (acute group, n = 8), 14 days (subacute group, n = 7), and 60 days (chronic group, n = 7) after irradiation and compared with their respective controls. A decrease in total glomerular filtration (55%) and renal plasma flow (40%) rates with marked elevation of total renal vascular resistance (180%), p<0.05, occurred within 45 min. Significant changes also occurred in the microcir-culation; i.e., single-nephron glomerular filtration (SNGFR), glomerular plasma flow (QA), and glomerular capillary hydraulic pressure (PGC) declined by 35%, 40%, and 12%, respectively, due to an increase in total ar-teriolar resistance (90%), p<0.05. Within 14 days, SNGFR was similar to control in spite of a moderate elevation of afferent arteriolar resistance (26%) and reduction in PGC(11%), p<0.05, and QA(20%). Kfwas significantly elevated (46%), p<0.05. The chronic group presented a response pattern similar to that of the acute group, although less severe. Histopathological changes were not relevant and were restricted to tubules. The present results suggest that: (a) Acutely, there was a marked reduction in filtration, flow, and PGCwith significant elevation of resistances, (b) Within 14 days, the maintenance of SNGFR was probably the result of an offsetting effect between QAand PGCdecreases and Kfelevation, (c) After 60 days, the homeostatic mechanism was not sufficient to maintain normal renal function, (d) A functional effect is probably the most important pathogenetic mechanism, at least during the initial phase, for the development of radiation nephropathy since no morphological alterations were observed.
ISSN:0886-022X
DOI:10.3109/08860229409045077
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
5. |
Iron Loading Enhances Susceptibility to Renal Ischemia in Rats |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 471-480
LongZhao,
PalterMark S.,
Preview
|
PDF (1155KB)
|
|
摘要:
Because chronic iron overload can cause organ injury in hemochromatosis and because iron participates in injury during renal ischemia-reperfusion, the effect of mild subacute renal iron loading on the susceptibility to ischemic acute renal failure was evaluated. Male Sprague-Dawley rats were injected with iron nitrilotriacetate (1 mg iron/kg BW i.p. daily) for 5 days. Controls were instead injected with nitrilotriacetate. Seventy-two hours later animals were subjected to 40-min renal artery ischemia. Iron loading produced a 28% increase in kidney iron content without any change in baseline renal function (plasma creatinine) or histology. Ischemic renal injury was far more severe in iron-loaded animals. Plasma creatinine 24 and 48 h after ischemia was significantly higher in iron-loaded rats (3.3 and 3.4 vs. 2.2 and 0.8 mg/dL) and GFR was significantly lower in iron-loaded rats (0.30 vs. 0.78 mL/min). In addition, iron-loaded rats showed a dramatically greater extent of damage by histologic evaluation using a semiquantitative scoring method. Therefore, a small increase in renal iron content greatly increased renal injury after an ischemic insult. These findings may be relevant to human renal disease because there is accumulating evidence of renal iron accumulation in a variety of proteinuric and chronic renal diseases.
ISSN:0886-022X
DOI:10.3109/08860229409045078
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
6. |
Endothelin-1 Potentiates ADP-Induced Platelet Aggregation in Chronic Renal Failure |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 481-489
HeintzBernhard,
SchmidtPeter,
MaurinNorbert,
KirstenRoland,
NelsonKaren,
WielandDagmar,
GüntherHeinz,
Preview
|
PDF (406KB)
|
|
摘要:
The effect of preincubation of heparinized whole blood with endothelin-1 (ET-1) on the ADP (adenosine diphosphate) and epinephrine-induced platelet aggregation was examined in 20 healthy donors compared with 20 patients with chronic renal failure (CRF). ET-1 significantly stimulated ADP-induced aggregation in CRF: EC (effective concentratiori)25= 2.3±0.20 with ET-1 vs. 2.7±0.22µmol/L without ET-1; EC50: 3.8±0.18 with ET-1 vs. 4.4±0.24µmol/L without ET-1; and EC75: 5.7±0.22 with ET-1 vs. 6.4±0.21µmol/L without ET-1). In healthy donors only the EC25was significantly increased: EC25= 2.5±0.13 with ET-1 vs. 2.8±0.20µmol/L without ET-1. No significant influence of ET-1 in epinephrine-induced aggregation was observed in CRF or in healthy donors. The basal values of determined ET-1 were significantly elevated in CRF: 6.99±0.29 pmol/mL vs. 5.65±0.33 pmol/mL in healthy donors. The high endogenous level of ET-1 in CRF patients together with an observed higher endogenous plasma level of camp (58±5.2 nmol/L compared to 29±2.0 nmol/L in healthy donors) may explain the enhanced pharmacological interaction of ET-1 and ADP in CRF patients. The data suggest that positive agonist interaction between ET-1 and ADP may result from effects on the concentrations of cAMP within the platelet rather than from direct interaction on the membrane receptors or the transmembrane coupling mechanisms. Our results demonstrate an in vitro effect of high-dose ET-1 on platelet function in whole blood, which is enhanced in patients with CRF.
ISSN:0886-022X
DOI:10.3109/08860229409045079
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
7. |
Fine Needle Aspirative Biopsy of the Liver in HBsAG-Positive Patients with End-Stage Renal Failure |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 491-499
FranceschiniNora,
GoncalvesLuis Felipe,
PromptCarlos Alberto,
BarrosSergio G. S.,
CerskiCarlos T. S.,
CostaCesar A. R.,
Preview
|
PDF (467KB)
|
|
摘要:
HBsAg-positive patients with end-stage renal failure have a high prevalence of asymptomatic chronic hepatitis. In order to determine the usefulness of hepatic cytology in the diagnosis of liver disease, the findings of hepatic needle core biopsy (NCB) and fine needle aspirative biopsy (FNAB) were compared in 75 HBsAg-positive uremic patients. The patients, aged 42±12 years, 14 males, were on hemodialysis for periods ranging from 13 to 105 months. The NCB was processed by standard histologic and immunohis-tochemical techniques and FNAB by the conventional technique, using the total corrected increment score (TCI). Plasma samples were collected for evaluation of hepatic function and for viral serologic tests. In 15 patients a diagnosis was made by NCB: normal, 7 cases; chronic persistent hepatitis, 4 cases', and chronic active hepatitis, 4 cases. When the patients were allocated into two groups according to the severity of the liver histologic findings [group I—minor changes (normal + chronic persistent hepatitis), 11 patients; group II—major changes (chronic active hepatitis), 4 patients], statistically higher values were found in the major changes group for alanine aminotransferase (49±33 vs. 24±11, p = 0.04),γ-glutamyl transpeptidase [148±53 vs. 38±28, p<(minor) 0.02] and TCI (3.7±1.2 vs. 2.5±0.8, p = 0.04). In conclusion, liver FNAB can be useful as a screening procedure for the identification of liver histologic changes (minor or major) in uremic HBsAG-positive patients.
ISSN:0886-022X
DOI:10.3109/08860229409045080
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
8. |
Lipid Parameters Including Lp(a) in Hemodialysis Patients |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 501-509
ElisafMoses,
BairaktariHelen,
TzatlasChristos,
GermanosNick,
KoulouridisEfstathios,
PappasMichael,
SiamopoulosKostas C.,
TsolasOrestis,
Preview
|
PDF (518KB)
|
|
摘要:
Chronic hemodialysis (CHD) patients have a high incidence and prevalence of atherosclerotic disease which may be related to numerous atherosclerotic risk factors. Among them dyslipidemia plays a significant role. Elevated Lp(a) levels, which are strongly associated with atherosclerosis, have been reported recently in uremic patients. The aim of our study was the determination of the levels of lipid parameters including Lp(a) in 151 CHD patients (76 male) aged 57 (12-81) years, who were on hemodialysis for a mean of 44.3 (range 1 to 189) months. Eighty-four normal individuals age and sex matched were used as controls. The median serum Lp(a) concentration in hemodialysis patients was 13 mg/dL compared with 6.5 mg/dL in healthy controls, p<0.001 by distribution-free Mann-Whitney test. The prevalence of subjects with Lp(a) levels above 25 mg/dL was significantly higher in CHD patients compared to normal subjects (30% vs. 8%, p<0.001). Even if CHD patients were matched for fasting lipid levels, they showed Lp(a) levels significantly higher than controls. No significant correlation was found between Lp(a) levels and either the age of the patients or the duration of hemodialysis. The etiology of primary renal disease did not influence the Lp(a) levels.
ISSN:0886-022X
DOI:10.3109/08860229409045081
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
9. |
Development of Renal Failure in IgA Nephropathy: The Importance of Interstitial Infiltration and Deposition of Fibrinogen |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 511-523
PolenakovićM.,
GrčevskaL.,
Preview
|
PDF (1414KB)
|
|
摘要:
We analyzed renal biopsy specimens of 60 patients with IgA nephropathy, 34 male and 26 female, aged 32, 8±9, 1. Patients were divided into 5 classes according to the morphological classification proposed on the basis of WHO criteria: 1, minimal lesions; 2, minor changes; 3, focal and segmental glomerulonephritis; 4, diffuse mesangial proliferation; and 5, sclerotic changes. Interstitial infiltration on optical microscopy and fibrinogen deposition on immunofluorescent microscopy were graded using a semiquantitative score. Clinical features (hypertension, proteinuria, erythruria/hematuria, renal function) were taken into consideration. The Mann—Whitney test was used for comparison of results between different classes. Classes 1 and 2 were younger (p<0.01) and had significantly better renal function than classes 3 and 4. Proteinuria was significantly higher in classes 2 and 3 (p<0.001) than the others. Macroscopic hematuria was more frequent in classes 1 and 2. Hypertension was absent in class 1 and correlated with the severity of histologic changes. Interstitial infiltration was absent in class 1 and also correlated with the degree of histological changes, but in contrast, fibrinogen deposits were more severe in earlier histological classes.
ISSN:0886-022X
DOI:10.3109/08860229409045082
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
10. |
Primary Disseminated Form of Ewing Sarcoma in Association with Hypercalcemia and Acute Renal Failure |
|
Renal Failure,
Volume 16,
Issue 4,
1994,
Page 525-534
LozanceLjubinka A.,
ZafirovskaKatica G.,
BogdanovskaStevka V,
ZafirovskiGjorgji J.,
Preview
|
PDF (1109KB)
|
|
摘要:
We present a case of an extremely rare form of Ewing sarcoma—primary disseminated, with fulminating course, severe hypercalcemia, extensive calcium deposition in parenchymatous organs, including kidneys, and acute renal failure as a clinical consequence. Correction of hypercalcemia was followed by prompt restoration of the glomerular filtration rate (GFR), suggesting that hypercalcemia had a direct effect on its regulation independent of the renal tubular damage. The effectiveness of the treatment with indomethacin indirectly supports the possibility of prostaglandin-mediated humoral hypercalcemia of malignancy.
ISSN:0886-022X
DOI:10.3109/08860229409045083
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
|
|