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1. |
Adam Linton—The Man |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 1-2
ClarkW. F.,
LindsayR. M.,
NaylorC. D.,
TurnbullD. I.,
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ISSN:0886-022X
DOI:10.3109/08860229409044842
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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2. |
Diuretics in Acute Renal Failure |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 3-17
ShillidayIlona,
AllisonMarjorie E. M.,
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摘要:
Studies on the ability of loop diuretics, mannitol, dopamine, and atrial natriuretic peptide to ameliorate or reverse human acute renal failure are reviewed. A precise role for diuretic therapy in this clinical setting has not been established. Most reports are retrospective, poorly controlled, or simply anecdotal. There is a need for prospective, randomly allocated studies on adequate numbers of patients. While the use of diuretic agents may improve fluid balance management in patients at risk of developing acute renal failure, maintenance of adequate effective circulating volume and oxygen delivery probably provides the best-proven protection.
ISSN:0886-022X
DOI:10.3109/08860229409044843
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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3. |
Accelerated Recovery from Toxic Acute Renal Failure with Thyroxin: Stimulation of Renal Phospholipid Biosynthesis |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 19-26
NegriArmando Luis,
AlvarezClarisa,
del Carmen FernandezMaria,
KaneLaura,
SterinNorma,
ArrizurietaElvira,
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摘要:
Thyroxine (T4) seems to accelerate recovery from various forms of acute renal failure. The mechanisms of this effect are still debated. We decided to evaluate if thyroxine enhances the recovery of HgCl2renal failure through an increment in the mitotic activity or through an increase in membrane phospholipid biosynthesis of the regenerating tubular cells. Male Wistar rats were allocated to four groups: one group received 0.4 mg/100g BW HgCl2SC and saline IP (HgCl2group); the second received the toxin and 24 and 48 h after it, T4 15µg/100g BW IP (HgCl2+T4 Diuretics in Acute Renal Failure group); a third group received saline SC and T4 IP (T4 group), and the last group received saline SC and IP (control group). On the third day GFR was evaluated by 24-h creatinine clearance and afterward rats were sacrificed and the kidneys removed. Some of them were studied histologically, evaluating the severity of the tubular lesion using a semiquantitative score (0–4) and the mitotic index (N mitotic figures per 10 high-power fields). In the other kidneys we studied phospholipid synthesis through the incorporation of 32 P into the different renal phospholipids of the several kidney regions. The T4-treated group had a better recovery of GFR after the toxin (HgCl2+ T4: 0.44±. 09 vs. HgCl2: 0.23±. 06, p<. 05). Both HgCl2-treated groups had similar lesional scores and mitotic indexes. Phospholipid synthesis, evaluated as the % change of 32 P incorporation to phosphatidylcholine compared to control rats, showed a 21% decrease in incorporation in the HgCl2group and a 95% increase in the HgCl2+ T4 group in the outer medulla. We conclude that T4 accelerates the recover of HgCl2through an increase in membrane phospholipid biosynthesis, and not through an increase in the replication of tubular cells.
ISSN:0886-022X
DOI:10.3109/08860229409044844
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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4. |
End-Stage Reflux Nephropathy |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 27-35
BaileyRoss R.,
LynnKelvin L.,
RobsonRichard A.,
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摘要:
Forty-two of 371 patients (11.3%) entering a dialysis—transplant program had end-stage reflux nephropathy. Thirteen of these 371 patients were under 16 years of age, with 6 of them having reflux nephropathy. Most patients presented with severely impaired renal function, hypertension, and proteinuria. Documented urinary tract infections occurred in only 4 of the 18 male and 14 of the 24 female patients. Thirty-five patients had hypertension, which in 22 had not been detected before presentation. Five presented with accelerated hypertension. Eight of the 24 women presented during a pregnancy. Twentynine patients are still alive, 20 with a functioning renal transplant. Reflux nephropathy is an important cause of end-stage renal failure, particularly in younger people. All patients presenting with renal insufficiency and proteinuria, with or without urinary tract infections or hypertension, should have reflux nephropathy excluded.
ISSN:0886-022X
DOI:10.3109/08860229409044845
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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5. |
Acute Renal Cortical Necrosis—A Study of 113 Patients |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 37-47
ChughK. S.,
JhaV.,
SakhujaV.,
JoshiK.,
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摘要:
Over a 28-year period, 113 out of 2986 (3.8%) patients dialysed for acute renal failure at a referral center in North India were diagnosed to have acute renal cortical necrosis (ACN). Obstetric causes were responsible for ACN in 56.6% patients and nonobstetric causes in 43.4%. Within the obstetric group, ACN developed in association with complications of late pregnancy in 37.1% and following septic abortion in 19.5%. The various nonobstetric causes included viperine snake bite in 14.2%, hemolytic uremic syndrome in 11.5%, renal allograft rejection in 5.3%, acute gastroenteritis in 4.4%, acute pancreatitis in 3.5%, septicemia in 2.7%, and trauma and drug-induced N hemolysis in 0.9% patients. Total anuria was the commonest presenting feature and was noted in 78.8% of patients. Renal histology showed diffuse cortical necrosis in 62.8% and patchy lesions in 37.2% patients. Computerized tomography (CTscan) of the kidneys revealed characteristic diagnostic findings in all the 5 patients in whom it was done. Dialytic support could be withdrawn as a result of improvement in renal function in 19 patients with patchy cortical necrosis. Dialysis-free survival of as long as 12 years has been recorded. The present study shows that, in contrast to the Western world, ACN continues to be a common cause of acute renal failure in developing countries. CT scan of the kidneys is helpful in establishing an early diagnosis.
ISSN:0886-022X
DOI:10.3109/08860229409044846
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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6. |
Epidermal Growth Factor in Acute Renal Failure |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 49-60
NouwenEtienne J.,
VerstrepenWalter A.,
De BroeMarc E.,
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摘要:
Epidermal growth factor (EGF) is produced in large amounts in the kidney in the form of a membrane-bound high molecular weight precursor. This precursor is inserted in the apical plasma membrane of the EGF-producing cells, which are localized in the thick ascending limb and distal convoluted tubule in mouse and rat kidney, and probably also in human kidney. High levels of EGF are excreted in urine, although renal tissue contains little mature EGF. It modulates renal cell proliferation and differentiation in vitro, but the role of the distal tubular EGF and/or its precursor in vivo is unknown. The expression of EGF in the kidney and its liberation into the urine are quickly abolished during several types of drug- or ischemia-induced acute renal failure and also in ureteral obstruction. Moreover, its expression is restored only after morphological and functional recovery of the kidney. This absence of EGF in conditions in which its mitogenic properties would be most appropriate suggests that the EGF of renal origin is not acting as a mitogen during kidney regeneration. Nevertheless, since the number of EGF receptors, which are localized at the basolateral cell surface in most nephron segments, is increased in regenerating renal epithelia, EGF of systemic origin or other members of the EGF family of growth factors, released from infiltrated inflammatory cells at the sites of injury, could enhance cellular proliferation by interacting with the EGF receptor. Administration of EGF indeed has a mildly beneficial effect on recovery from acute renal injury.
ISSN:0886-022X
DOI:10.3109/08860229409044847
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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7. |
Zinc-Induced Metallothionein Synthesis Could Protect from Gentamicin Nephrotoxicity in Suspended Proximal Tubules of Rats |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 61-69
LingChao,
HaiXue,
HuaJin,
ChenWen,
XinYong,
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摘要:
We have reported that preinjection of zinc could ameliorate gentamicin-induced nephrotoxicity in vivo via the induction of metallothionein. The present project was designed to study whether preinjection of zinc could protect from the harmful effects of gentamicin on DNA synthesis, Na+-K+-ATPase activity, and free radical production in rat renal proximal tubules (PT) in vitro. PT were prepared and cultured from normal, saline-preinjected, and Zn-preinjected (Zn 10 mg/k/day s.c. 5 days) Wistar male rats weighing 80–120 g. The results showed that DNA synthesis and Na+-K+-ATPase activity were significantly suppressed in the normal and saline-preinjected rats' PT by addition of gentamicin to the media in the concentration of 12.4 mg/mL; however, these reactions were not suppressed by gentamicin in Zn-preinjected rats' PT, and malondialdehyde and hydroxyl radical production in Zn-preinjected rats' PT were significantly lower than those in the normal and saline-preinjected rats' PT (p<. 01). On the other hand, the metallothionein in Zn-preinjected rats' PT was very significantly higher than that in the normal and saline-preinjected rats' PT (p<. 001). Our data indicate that gentamicin-induced suppression of DNA synthesis and Na+-K+-ATPase activity in rat PT, which lead to renal injury, may be relevant to free radicals generated by gentamicin; and that preinjection of zinc could ameliorate gentamicin-induced nephrotoxicity via the induction of the metallothionein synthesis in rat PT to scavenge free radicals generated by gentamicin.
ISSN:0886-022X
DOI:10.3109/08860229409044848
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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8. |
Effects of Gentamicin on Glomerular Renin Release |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 71-89
FernándezEmma,
FantauzziRebecca,
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摘要:
Gentamicin nephrotoxicity is associated with impaired glomerular function. To examine whether the effects of gentamicin on glomerular function are mediated through alterations in the renal-angiotensin system, basal and stimulated glomerular renin release was assessed in isolated glomeruli from control and gentamicin-treated rats. Male Sprague-Dawley rats (220±20 g) were studied immediately after treatment with gentamicin sulfate (4 mg/kg BW/day, n = 6) for 1 or 2 consecutive weeks and after 1 week of recovery from 2 weeks of treatment. Control rats received an equivalent volume of saline (n = 9). After the respective treatment, renal renin content was measured. In addition, glomeruli from control and gentamicin-treated rats were isolated and glomerular renin release was measured under basal conditions and after stimulation with the calmodulin inhibitor trifluoperazine (1×10−4M). Renin concentration was determined in aliquots of the supernatant by measuring the generation of angiotensin I using radioimmunoassay techniques at 15-min intervals. Renal renin content was significantly increased after 2 weeks of gentamicin treatment (+47%) and remained elevated (+ 62%) 1 week after discontinuing a 2-week gentamicin treatment. Both basal and stimulated glomerular renin release were lower in glomeruli isolated from gentamicin-treated rats. The effect of gentamicin added in vitro to glomeruli isolated from untreated rats was also evaluated. Exposure of normal glomeruli to in vitro gentamicin (1 mM) resulted in a Significant inhibition of both basal (-47%, p<. 05) and stimulated (-84%, p<. 05) glomerular renin release. To determine whether the inhibitory action of gentamicin on glomerular renin release was dependent on extracellular calcium concentration, the effects of gentamicin on glomerular renin release were also assessed in the absence of extracellular calcium. Our data revealed that in the absence of extracellular calcium, the inhibitory effect of gentamicin on both basal and stimulated glomerular renin release was abolished. Taken together, these findings strongly suggest an inhibitory effect of gentamicin on glomerular renin release. Furthermore, the inhibition of glomerular renin release induced by gentamicin appears to be dependent on extracellular calcium.
ISSN:0886-022X
DOI:10.3109/08860229409044849
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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9. |
A Study of 500 Cases of Acute Renal Failure (1978-1991) |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 91-99
FirmatJ.,
ZucchiniA.,
MartinR.,
AguirreCristina,
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摘要:
A retrospective study of 500 consecutive cases of acute renal failure (ARF) in a period covering 1978 through 1991 is presented. A total of 316 females and 182 males with an average age of 46.4 years (14 to 84) had a global survival rate of 68%. Oligoanuric ARF was present in 77% of the patients and, except in 13 cases, all were dialyzed with varied techniques. The treatment plan consisted of early and repetitive dialysis, rational use of antibiotics, and parenteral and/or oral nutritional support. The patients have been divided into three main categories according to etiology: gyneco-obstetric, medical, and postsurgical cases, the latter having the poorest survival rate, With regard to ARF post-septic abortion, we strongly believe that a hysterectomy should not be carried out except in the presence of gangrene or proven uterine perforation, as surgery increases the morbomortality rate in these septic patients.
ISSN:0886-022X
DOI:10.3109/08860229409044850
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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10. |
Glycine Prevents Toxic Tubular Cell Injury |
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Renal Failure,
Volume 16,
Issue 1,
1994,
Page 101-108
GabbaiFrancis B.,
PetersonOrjan W.,
BlantzRoland C.,
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摘要:
Glycine prevents tubular injury as suggested by in vitro cell culture studies, studies in the isolated perfused kidney, and in vivo studies, We have previously demonstrated that intratubular administration of uranyl nitrate (UN) produces proximal tubular cell injury and decreases proximal tubular reabsorption (APR). The decrease in APR activates tubuloglomerular feedback and lowers nephron filtration rate (SNGFR). This study was designed to evaluate if glycine administration could prevent the decrease in SNGFR after UN administration and if maintenance of SNGFR was due to tubular cell cytoprotection or suppression of the tubuloglomerular feedback. Administration of 0.65 ng of UN into the early proximal tubule was associated with a decrease in distal SNGFR (SNGFRD)from 29±2 to 24±2 nL/min (p<. 05) and late proximal SNGFR (SNGFRLP) from 37±2 to 26±2 nL/min, and APR from 14±1 to 10±1 nL/min. Systemic administration of glycine (20 g/dL, 1.4 mL/h) was associated with significant increases in SNGFRDand SNGFRLP, and APR (38±3,44±3, and 15±2 nL/min). UN administration did not affect APR or SNGFR in glycine-treated rats. These findings demonstrate that glycine prevents UN-induced decreases in SNGFR through a cytoprotective effect on proximal tubular cells.
ISSN:0886-022X
DOI:10.3109/08860229409044851
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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