Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphocreatine (PCr) is a critical intracellular energy reservoir used in the regeneration of ATP. The aim of this study was to determine the efficacy of exogenously added PCr on preservation of renal function in an in vitro model. The renal artery and ureter of a rat were cannulated and the kidney was subjected to 45 min of normothermic in vivo ischemia. The kidneys were then perfused ex vivo with either a Krebs-bicarbonate solution (Krebs) or a Krebs solution containing 3 mM PCr or an osmotically balanced solution containing 3 mM PCr. Our results indicate that the perfusion of kidneys subjected to 45 min of warm ischemia with solutions containing PCr resulted in significant improvements in GFR, RPF, and V, FRNa and FRH2O compared to KREBS alone. This suggests that the important factor in preservation of kidney function after an initial ischemic insult may be the addition of PCr rather that the electrolyte solution used.
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PMID:Amelioration of renal ischemic injury by phosphocreatine. 192 64

In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.
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PMID:Renal corticomedullary metabolite gradients during graded arterial occlusion: a localized 31P magnetic resonance spectroscopy study. 195 32

We examined the effects of dietary deficiency of vitamin E and selenium on the ischemia-reperfusion model of renal injury in the rat. Deficient diets imposed for six weeks on three-week-old weanling rats led to no significant differences in body weights, serum creatinine, GFR, RBF, TmPAH or urinary total protein excretory rates prior to ischemia. Twenty-four hours after one hour of ischemia, animals on the deficient diet demonstrated more markedly impaired GFR, RBF, TmPAH and urine to plasma creatinine concentrations and an increased renal failure index. Tubular damage was more severe injury in the deficient animals. Lipid peroxidation, 15 minutes after the release of the ischemic clamp, was increased in the deficient animals. We confirmed the effects of our dietary manipulation in impairing the oxidant scavenging system in the deficient animals since glutathione peroxidase activity was reduced to less than 5% in the basal state, and this striking reduction persisted following ischemia. Plasma vitamin E concentrations were also markedly depressed in the deficient diets. This dietary deficiency also worsened the course of acute renal injury and was accompanied by 50% mortality compared to 0% mortality in the control animals. Thus, dietary deficiency of vitamin E and selenium led to greater structural and functional renal impairment and increased lipid peroxidation following ischemia. These data provide support for the role of reactive oxygen species in mediating ischemia-reperfusion injury.
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PMID:Dietary deficiency of antioxidants exacerbates ischemic injury in the rat kidney. 207 54

The effects of two different H2-receptor antagonists, cimetidine and famotidine, on the acute renal failure induced by 20 min of renal artery occlusion and gentamicin (240mg/kg BW, s. c., for 3 days) were investigated in Sprague-Dawley rats. The animals were treated with either cimetidine (80 or 160 mg/kg BW) or famotidine (4 or 8 mg/kg BW) mixed in the drinking water for 7 days. The low dose of cimetidine and famotidine did not alter the renal function in the absence of renal trauma. However, the high dose of cimetidine or famotidine decreased the GFR by 32% and 22%, whereas RPFR increased by 46% and 62%, and % FENa by 92% and 558%, respectively. The data for the renal function obtained 24 hrs after 20 min of renal ischemia demonstrated a decrease of 54% in GFR, a decrease of 47% in RPFR and an increase of 370% in %FENa over the non-ischemic control values (p less than 0.05). Cimetidine (80 mg/kg BW) or famotidine (4 mg/kg BW) did not modify the recovery of renal function following the ischemic insult, showing 55% and 539% decreases in GFR, 74% and 101% increases in RPFR, and 393% and 461% increases in %FENa over the non-ischemic control rats, respectively. Famotidine reduced the decrease in RPFR significantly during the recovery period following ischemia. In the gentamicin study, gentamicin treatment was found to lower the renal function significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Do the H2-receptor antagonists, cimetidine and famotidine, modify the degree of renal recovery following renal insult? 225 Apr 7

The influence of the hematocrit (Hct) on the trapping of red blood cells (RBC) in the renal microvasculature and its effect on the long-term outcome following unilateral ischemia were investigated in the rat. The results showed that an increase in the duration of ischemia increased the RBC trapping, as measured by 51Cr-labeled erythrocytes, in a dose-dependent manner. At normal Hct (46%) the period of ischemia producing half-maximum RBC trapping was 45 minutes, whereas after hemodilution (Hct = 31%) or hemoconcentration (Hct = 60%) the corresponding periods were 80 and 25 minutes, respectively. Regarding the long-term outcome, 45 minutes of ischemia with a normal Hct was associated with a marked decrease in kidney weight, GFR and urine osmolarity after four weeks of recovery, which could be prevented to a large extent by hemodilution. Conversely, with hemoconcentration there was severe damage after only 25 minutes of ischemia. It is suggested that these long-term effects are attributable to RBC trapping in the microvasculature of the outer medulla, which may cause added ischemia in this area of the kidney. It is also suggested that cortical atrophy is secondary to the medullary injury, and is brought about to avoid extensive water and salt losses.
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PMID:Red cell trapping after ischemia and long-term kidney damage. Influence of hematocrit. 234 22

Sprague-Dawley rats received infusions of 55-microns microspheres (groups 1 and 3) or dextrose (groups 2 and 4) into both renal arteries. Groups 1 and 2 rats were studied over 7 mo. In group 1 rats renal embolization increased the mean arterial pressure (group 1, 140 +/- 4 mmHg; group 2, 118 +/- 2 mmHg) without reducing the glomerular filtration rate (GFR; group 1, 4.69 +/- 0.16 ml/min; group 2, 4.57 +/- 0.22 ml/min). Micropuncture studies showed that systemic hypertension was accompanied by an increase in the glomerular capillary pressure of functioning nephrons in group 1 rats. Morphological studies showed that renal embolization caused both glomerular ischemia (group 1, 11.8 +/- 1.9% of glomeruli; group 2, 0.1 +/- 0.1% of glomeruli) and glomerular segmental sclerosis (group 1, 15.0 +/- 1.0% of glomeruli; group 2, 3.3 +/- 0.2% of glomeruli). Groups 3 and 4 rats were studied over 2 mo. Renal embolization again increased the mean arterial pressure without reducing the GFR in group 3 rats. Morphological studies showed that at 2 mo renal embolization caused glomerular ischemia without glomerular segmental sclerosis. These studies show that focal glomerular ischemia can cause systemic and glomerular capillary hypertension in the absence of a reduction in the GFR. They further show that focal glomerular ischemia can cause progressive sclerotic injury in the remaining, nonischemic portion of the glomerular population.
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PMID:Hypertension and progressive glomerular injury caused by focal glomerular ischemia. 238 5

The present experimental study investigates whether the atrial natriuretic factor (ANF) is able to prevent the nephrotoxic effects of cyclosporine infused after 30 min of warm renal ischemia in the rat. At 2 hr after the end of ischemia, the glomerular filtration rate was improved by an ANF infusion: 390 +/- 19 microliters/min/100 g versus 298.3 +/- 31 microliters/min/100 g in ANF and saline-infused rats, respectively (P less than 0.05). Intravenous CsA infusion at a dose of 2.5 mg/kg/day produced a more pronounced fall in GFR when compared with the control: 205.4 +/- 19.7 microliters/min/100 g versus 298.3 +/- 31 microliters/min/100 g in CsA and saline, respectively (P less than 0.05). In contrast, a synthetic rat atriopeptin III (0.5 microgram/kg/min) infusion after ischemia given together with CsA prevented its deleterious effects upon GFR: 316 +/- 22 microliters/min/100 g versus 205.4 +/- 19 microliters/min/100 g in ANF/CsA versus CsA alone (P less than 0.001). Moreover, the natriuretic ANF effects remained unaffected by high plasma CsA peak levels: indeed, other parameters of renal function--urinary flow, urinary sodium concentration and excretion rates, and urinary sodium reabsorption and fractional excretion rates, were significantly increased in ANF alone or CsA/ANF groups. These preliminary results suggest that ANF may be useful in renal transplantation or in the management of patients given large doses of CsA (liver or heart transplant) since, despite nephrotoxic CsA levels (greater than 1500 ng/ml), ANF provides an improved GFR and tubular function after ischemia.
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PMID:Prevention of acute cyclosporine nephrotoxicity by atrial natriuretic factor after ischemia in the rat. 252 54

This experimental study in dogs was designed to investigate whether maximal loading produces atrial natriuretic factor (ANF) release and whether this physiological peptide is involved in the improvement of the early renal function recovery after acute ischemia. The experimental protocol included a renal artery occlusion for 45 min in uninephrectomized dogs and the measurement of various parameters of renal function over 2-hr period after declamping. There were 3 experimental groups. In the control group (I) (n = 10), the dogs received, after ischemia, an isotonic saline solution infusion at a rate of 0.2 ml/kg/min. In group II, (n = 10) the animals underwent acute volemic expansion (1 ml/kg/min) with whole blood (hematocrit approximately equal to 25%) during the ischemic period, and after declamping, an isotonic saline infusion (NaCl 0.9%) infusion at the same rate as in the control group. In group III, (n = 8) the dogs only received NaCl 0.9% (0.2 ml/kg/min) before ischemia and alpha human ANF (3.6 ng/kg/min) dissolved in saline after ischemia and during the 2 hr of the renal recovery period. Volemic expansion induced a highly significant increase of the cardiac filling pressures concomitant with a prompt but transient 5-6-fold increase in ANF levels (357 +/- 92 pg/ml versus 60 +/- 4.1 pg/ml in controls at the time of declamping [P less than 0.05]). With these higher plasma ANF levels in overloaded animals, we observed, 2 hr after declamping, considerably improved renal function recovery in terms of glomerular filtration rate--37.5% +/- 8.7 versus 11.8 +/- 3.9%; urinary sodium excretion rate--53.89 mu eq/min versus 5.36 +/- 1.2 mu eq/min (P less than 0.01); total Na reabsorption rate--1.2 +/- 0.23 meq/min versus 0.28 +/- 0.09 meq/min (P less than 0.01) (group II vs. controls, respectively). A 1-28 alpha ANF infusion after the ischemic insult allowed a comparable but more significant improved recovery of renal function--indeed, 2 hr after declamping, the GFR reached 73.7 +/- 14% of the preoperative GFR values. The urinary sodium excretion rate was 15-fold higher than in controls, and the total and fractional sodium reabsorption rates followed a similar increase. These beneficial effects of ANF were obtained with low doses of synthetic ANF (3.6 ng/kg/min) inducing plasma levels slightly higher (120 pg/ml) than in controls and comparable to the levels reached in the overloading group. In addition, maximal loading or ANF infusion produces an inhibition of the aldosterone rise occurring after the ischemic insult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that atrial natriuretic factor is the humoral factor by which volume loading or mannitol infusion produces an improved renal function after acute ischemia. An experimental study in dogs. 252 2

These data indicate that chronic administration of CGS-12970 to renal allograft recipients maintains renal allograft function. These effects are probably due to selective inhibition of local tissue TXA2 production. These data also suggest that elevations in renal allograft tissue prostacyclin production may be secondary to ischemia since improving renal blood flow and GFR with selective thromboxane synthesis inhibitors leads to normalization of renal prostacyclin synthesis. The possible utility of using CGS-12970 as an adjunct therapy in human renal allotransplantation should be strongly considered.
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PMID:Thromboxane synthesis inhibition and renal allograft function. 265 85

Renal ischemia and reperfusion have been shown to be associated with an enhanced renal lipid peroxidation. Because glutathione (GSH) serves to protect cells from oxidative stress, the role of GSH in renal ischemia was investigated. The content of renal GSH in the rat declined to 40% of control values during 35 min of renal artery occlusion. Renal GSH levels only partially recovered after 120 min of blood reflow. To assess the significance of this effect, renal GSH levels were altered before occlusion of the renal artery. Rats were treated with either buthionine sulfoximine (BSO) or glutathione monoethylester (GSH-ester) to lower or elevate, respectively, renal GSH levels. The ischemia-induced changes in renal ATP, ADP, and AMP after 35 min of ischemia and 90 min of blood reflow were not affected by prior alteration of renal GSH levels. The ischemia-induced decrease in the respiratory control of isolated cortex mitochondria was also unaffected. In control animals, ischemia of 35 min increased urine flow rate 3.2-fold and decreased GFR to 29% of normal values during the reflow period. Similar changes occurred in kidneys with a depleted GSH level. In kidneys with an elevated GSH, however, both urine flow rate and GFR were decreased to values 50 and 3% of normal, respectively. Morphological analysis demonstrated that ischemia produced an enhanced degree of damage with an increase in cast formation in kidneys pretreated with GSH-ester; however, the ester also produced morphological changes in nonischemic kidneys. The severity of ischemic damage was similar in kidneys with a lower GSH content when compared with controls. We conclude that renal GSH is depleted by ischemia but depletion of renal GSH with BSO before ischemia has no effect on ischemic-induced damage to the kidney. However, ischemic-induced renal dysfunction is enhanced when GSH is elevated with glutathione monoethylester before ischemia.
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PMID:Effect of an altered glutathione content on renal ischemic injury. 318 64


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