摘要:

A potent adenosine A, receptor antagonist, FR-113453, was tested for its preventive effect on glycerol-induced acute renal failure in rats. First, the optimum timing of FR-113453 administration was studied. Oral FR-113453 (100 mg/kg) given 1 h before or 5–10 min after glycerol injection produced a significant reduction of the serum creatinine at 24 h (4.3±0.8 mg/dL [vehicle] vs. 1.4±0.4 mg/dL [FR-113453], and 4.7±1.1 mg/dL vs. 1.3±0.6 mg/dL, respectively, p<0.001). However, when FR-113453 was given 2 h after glycerol injection, the serum creatinine did not improve. Creatinine clearance at 24 h after the induction of acute renal failure was significantly better in rats given FR-113453 (100 mg/kg) 1 h before glycerol than in rats given vehicle alone (0.08±0.08 mL/min vs. 0.01±0.02 mL/min), (p<0.01). The kidney weight was lower and less severe histologic changes were observed at 24 h in the FR-113453-treated group. Renal blood flow (measured using85Sr microspheres) did not change at 24 h after glycerol injection (3.0±0.9 mL/min/g [vehicle] vs. 3.6±0.9 mL/minig [FR-113453]), but renal vascular resistance was significantly reduced by FR-113453 (47.9±37.9 vs. 26.4±5.2 mm Hg/mL/min/g, p<0.05). Beta-ATP levels (measured by3IP-magnetic resonance spectroscopy) were reduced in glycerol-induced acute renal failure, with no difference between the vehicle and FR-113453-treated groups. These results demonstrate that FR-113453 ameliorates glycerol-induced acute renal failure when administered before or just after glycerol injection, indicating that adenosine has a very important role in the induction of acute renal failure by glycerol.

ISSN:0886-022X    

DOI:10.3109/08860229309065565

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Previously we have shown that the amount of protein in a dietary regimen prior to the induction of renal ischemia will significantly affect the degree of postischemic acute renal failure (Andrews PM, Bates SB: Kidney Int 30:299–303, 1986). The present investigation was undertaken to determine what effect dietary protein regimen has on the histopathology of renal ischemia. Rats were pair-fed for 2 weeks on either 0% or 5% (restricted), 20% (normal), or 60% (high) purified protein isocaloric diets. Ischemia was induced by 45 min of renal pedicle clamping. Light and electron microscopic evaluation of kidney morphology immediately following renal ischemia (prior to blood reflow) revealed that the extent of morphological damage to cells lining proximal convoluted tubules and the thick ascending segments of Henle's loop increased with increasing concentration of dietary protein. However, all dietary protein groups also exhibited heterogeneity in the extent of damage to different nephrons within the same kidney.

ISSN:0886-022X    

DOI:10.3109/08860229309065566

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

The angiotensin I-converting enzyme (ACE) activity was measured in urine, serum, and tissues from rats with carbon tetrachloride (CCl4)-induced acute renal failure on days 1, 2, 3, and 7 after CCl4administration. Serum ACE increased on days 1 to 3. Heart, lung, small intestine, brain, and testis ACE decreased, whereas kidney and liver ACE remained unchanged. Urine ACE activity increased from day 1 to day 3. Our data suggest that the increase in serum ACE may be secondary to the ACE release from the damaged tissues, and that the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of damage to the proximal tubule.

ISSN:0886-022X    

DOI:10.3109/08860229309065567

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

In order to understand the mechanism of acute renal failure frequently observed in severe acute pancreatitis, renal microcirculation and renal hemodynamics were investigated during experimental acute pancreatitis in dogs induced by autologous bile and trypsin mixture into the pancreatic duct. Renal tissue blood flow (hydrogen gas clearance method), renal arterial blood flow, and cardiac output (transonic blood flow meter) were each measured for 5 h after induction of pancreatitis. The effect on renal hemodynamics of a new synthesized protease inhibitor—E-3123; 4-(2-succinimidoethylthio)phenyl-4-quanidinobenzoate methane sulfonate—intraveneously infused at the rate of 3 mg/kg/h was also investigated. The mean blood pressure and pulse pressure decreased after induction of pancreatitis. Renal microcirculation and renal artery blood flow decreased during the experiment. However, in dogs with treated by E-3123, renal microcirculation was preserved during the first hour of the experiment and decreased gradually afterward, but it was significantly higher than that of the dogs without E-3123 during 3--5 h. The mean blood pressure and pulse pressure were preserved nearly at preoperative levels during the experimental period. We concluded that renal microcirculation decreased concomitantly with a deterioration of acute pancreatitis, and that the new pancreatic protease inhibitor E-3123 may have some beneficial effect to improve renal hemodynamics in the early period of acute pancreatitis.

ISSN:0886-022X    

DOI:10.3109/08860229309065568

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

We obstructed renal lymph drainage from a single kidney in diabetic rats who had received 65 mg/kg streptozotocin 6 months prior to the study. Lymphatic obstruction led to a progressive fall in systematic blood pressure from a mean arterial pressure of 101±5 (SEM) mm Hg (n = 7) to 62±4 mm Hg (n = 5) (p<. 02) after 1.5 h. No change was seen in a sham-operated animal. Despite the decline in systemic blood pressure there was no significant change in the GFR of either kidney. Sodium excretion increased significantly in the experimental kidney. There was no change in the urinary excretion of cyclic GMP from either kidney, and plasma levels of atrial natriuretic peptide (ANP) did not change (55±21 pg/mL pre- to 64±18 postobstruction). The results are consistent with a systemic vasodilatation after lymphatic obstruction. The mechanism of this response is still under investigation, but apparently it does not involve ANP.

ISSN:0886-022X    

DOI:10.3109/08860229309065569

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Oxygen-based free radicals produced by the enzyme xanthine oxidase may be involved in postischemic reperfusion injury. To determine whether oxypurinol, a xanthine oxidase inhibitor and the major metabolite of allopurinol, attenuates renal ischemic reperfusion injury, and, if so, to determine its most effective dose, oxypurinol 2.5, 5, 10 or 20 mg/kg BW was infused 20 min prior to 20 min of complete renal ischemia in uniephrectomized rats. Animals treated with 5 mg/kg BW oxypurinol had significantly higher creatinine clearances on the first and second days postischemia than did untreated animals.In other animals given either buffered saline or oxypurinol at 5 mg/kg BW i.v. 20 min before ischemia, the inulin clearance (Cln) returned to near-control values within 1 h after ischemia. At 24 h there was a secondary decline in the C1nin animals receiving buffered saline, whereas in the animals treated with oxypurinol, this decline was less evident. In animals given oxypurinol at 5 mg/kg BW 40 min after ischemia, the Clnwas significantly greater than in those receiving buffered saline. No changes in renal blood flow or renal vascular resistance were observed, suggesting that the effect of oxypurinol was not hemodynamically mediated.Analysis of plasma hypoxanthine, xanthine, uric acid and oxypurinol levels by high-pressure liquid chromatography revealed that in the absence of oxypurinol, a significant increase in uric acid production occurred between 20 and 170 min after the period of ischemia. In the presence of oxypurinol, there was a marked reduction in the rate of production of uric acid for the first 3 h postischemia.

ISSN:0886-022X    

DOI:10.3109/08860229309065570

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

We investigated the plasma concentrations of thyroid hormones in 27 patients with acute renal failure. Both the mean free T3, 1.17±0.74(SD) pmol/L (range 0.5–2.9 pmol/L) and total T3 plasma concentrations, 0.43±0.14 nmol/L (range 0.3–0.7 nmol/L) were reduced compared to the normal range (3.3–8.2 pmol/L and 1.0–3.0 nmol/L, respectively). In all 15 patients with plasma creatinine>3.33 mg/dL (295μmol/L), the mean FT3 was 0.92 pmol/L and the plasma concentrations have all been<1.5 pmol/L. There was a weak correlation between the plasma creatinine and the plasma concentrations of TT3 (x = 0.38, p = 0.049). Similarly, both plasma free T4 and total T4 were also reduced in the patients compared to the normal range: mean free T4 5.91±3.68 pmol/L, range 1.0–13.1 pmol/L, and total T4 47.80±29.31 nmol/L, range 5–99 nmol/L; normal range 9.4–25.0 pmol/L and 50–160 nmol/L, respectively. There was no difference between the ranges in either plasma TSH, patients 1.19±1.25 mU/L, range 0.1–4.9 mU/L, vs. control range 0.3–6.0 mU/L; and TBG, patients 19.05 mg/L±3.69, range 11.0–26.9 mg/L, controls range 13.0–30.0 mg/L. Thus we have determined that patients in the early phase of ARF have consistently reduced plasma concentrations of both free and total T3, and reduced concentrations of free and total T4; and that the reduction of TT3 is dependent upon the plasma creatinine level.

ISSN:0886-022X    

DOI:10.3109/08860229309065571

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Ten patients, mean age 51.50±3.03 years, with degenerative rheumatism on NSAID treatment without any sign of renal desease, and 11 control subjects, mean age 43.50±1.51 years, were studied. NSAID treatment was of 11.30±5.60 weeks duration in average, with ibuprofen, naproxen, or indomethacin. Urinary excretion of three specific renal tubular enzymes—AAP: alanine-amino-peptidase, GGT:γ-glutamyl-transpeptidase, andβ-NAG:β-N-acetyl-glucosaminidase, were determined in 8-h overnight urine samples, as well as GFR creatinine clearancel 1.73 m2, urinary volume/8 h, specific gravity of the urine, proteinuria and glucosuria. In the group treated with NSAIDs, urinary excretion of the enzymes was significantly higher than in the control group—AAP: 1414.20±317.60, 864.20±94.42, p<0.00001; GGT: 8034.6±1378.55, 5095.64±614.40, p<0.00001, andβ-NAG: 1644.60±299.97, 964.82±142.00, p<0.00001. Patients on NSAID treatment showed abnormal urinary excretion of AAP in 7/10 cases, of GGT in 6/10, and ofβ-NAG in 7/10 cases. Duration of the treatment did not correlate with the urinary excretion of the enzymes. Age was in correlation with the urinary excretion of the enzymes only in the control group, r = 0.52, p<0.005 for AAP, r = -0.43, p<0.02 for GGT, and r = -0.23, p<0.05 forβ-NAG. Our results suggest that after long-term administration of NSAIDs, toxic renal tubular involvement is frequent, that urinary excretion of three specific renal tubular enzymes could be a suitable tracer of the toxic effects of the drugs at the cellular level, and that prolonged cellular injury could lead toward progressive renal damage, with a rather“silent”clinical picture.

ISSN:0886-022X    

DOI:10.3109/08860229309065572

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

A total of 1784 children suffering from acute nonobstructive anuric renal failure requiring dialysis were studied in the Pediatrics Nephrology unit of Institute of Postgraduate Medicine and Research, Dhaka, Bangladesh, for the 10-year period 1981--1990. The patients were divided into two groups: Group I, the majority of the children (94.5%), presented with acute renal failure without evidence of hemolysis and were labeled as acute ischemic renal failure (AIRF), and the remaining 5.5% of the children with acute renal failure (ARF) showing features of severe hemolysis were labeled as hemolytic uremic syndrome (Group II.) The children of group I had mean age 4 (0.5--10) years, mean period of anuria 5 (2--13) days, and had mean serum creatinine 701±267.98μmol/L. The overall mortality in this group was 89%. Children in Group II had mean age 2 (0.2--6) years, mean duration of anuria 3 (2--5) days, and mean serum creatinine level 500±100μmol/L. The mortality rate in this group was 15%. In spite of some differences between the two groups the difference in the mortality rate between the two groups was significant (p<0.001). It is concluded that AIRF in children bears a much poorer prognosis compared to that of ARF due to HUS.

ISSN:0886-022X    

DOI:10.3109/08860229309065573

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor

摘要:

Previous studies suggest a role for renal vasoconstriction in the pathogenesis of radiocontrast-induced nephropathy (RCIN). A renal vasodilator such as dopamine may be protective. However, the effect of dopamine on renal blood flow (RBF) in patients with chronic renal failure (CRF) is controversial. Patients with CRF of diabetic (DM) or nondiabetic (NDM) origin were hydrated with 0.45% NaCl intravenously at 100 mL/h for 12 h and then randomized to either 0.45% NaCl IV at 100 mL/h (Group 1) or dopamine IV at 2μg/kg/min in 0.45% NaCl at 100 mL/h for 2 h during and after cardiac catheterization. Mean arterial pressure (MAP), cardiac output (CO), and RBF were measured at baseline (t = 0), after 5 min of vehicle (Group 1) or dopamine (Group 2) but before ionic radiocontrast (t = 5 min), after ventriculogram (t = 15 min), and after coronary angiography (t = 65 min). Serum creatinine (SCr) was measured at baseline and 24 and 48 h after cardiac catheterization. RCIN was defined as a 25% increase of SCrabove baseline 48 h after cardiac catheterization. Baseline characteristics demonstrated the groups to be equivalent in age, SCr, creatinine clearance, CO, MAP, RBF, and radiocontrast dose administered. The incidence of RCIN was not different between Group 1 and Group2 (Group 1, 6 of 15 patients; Group 2, 5 of 15 patients). Dopamine infusion was associated with a significant increase in RBF at 5 min (Group 1, 110±13%; Group 2, 193±40% at t = 5, p<. 05). RBF remained elevated throughout the catheterization in Group 2. Within Group 2, RBF tended to rise only in those patients who subsequently developed RCIN (RCIN, 92±40 mL/min; No RCIN, 203±24 mL/min, p<. 05 at baseline); at t = 65: RCIN 530±242%; No RCIN, 184±38%, p<. 05. All the patients in the dopamine group who developed RCIN had diabetes mellitus. The patients with DM had lower baseline RBF than the patients with NDM, despite equivalent baseline renal function. The dopamine-stimulated increase in RBF was seen exclusively in the patients with DM. In conclusion, dopamine does not prevent RCIN in patients with CRF despite a significant renal vasodilatory effect. The renal vasodiliatory effect of low-dose dopamine in patients with CRF is heterogeneous, occurring only in patients with DM. Patients who subsequently developed RCIN had lower baseline RBF and the greatest rise in RBF with dopamine. Patients with DM and CRF have lower RBF and higher filtration fraction than NDM patients with equivalent SCrand creatinine clearance. These phenomena are functional (rather than fixed), as evidenced by the renal vasodilatory response to low-dose dopamine.

ISSN:0886-022X    

DOI:10.3109/08860229309065574

出版商:Taylor&Francis    

年代:1993

数据来源: Taylor