Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enhanced-MR imaging in combination with ultrasmall superparamagnetic iron oxide (USPIO) was used in the glycerol-induced model of acute renal failure (ARF) in the rabbit to detect renal perfusion abnormalities. A control group (n = 5) and an ARF group (n = 5) were studied after intramuscular injection of glycerol (10 ml/kg) with T2-weighted spin-echo sequence at 1.5 T and a 27 mumol/kg IV dose of iron. The signal intensity (SI) was quantified in the cortex, the outer medulla (OM), and the inner medulla (IM). In control rabbits, the maximum SI decrease after USPIO injection was in the OM (76% +/- 3.6), as this is the region of maximal vascular density, then in the IM (73.4% +/- 2.9). In the glycerol group, SI loss in the OM (61% +/- 12.6) and the IM (45.2% +/- 16.24) was significant less than in the control group (p < .05). Pathology results showed fibrinous thrombus in the efferent arterioles and congestive aspect of the vasa recta in the medulla. We argue that a reduced medullary concentration of USPIO in the renal failure group is indicative of medullary hypoperfusion.
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PMID:USPIO-enhanced MR imaging of glycerol-induced acute renal failure in the rabbit. 773 65

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 46-year-old man with cardiac failure and statues epileptics]. 794 26

Uremic encephalopathy is a complication of renal failure that reflects stresses exerted by as yet poorly defined uremic toxins. All cells respond to stresses by undergoing the "heat shock" response. Although urea kinetics and creatinine concentration are routinely used to assess dialysis adequacy, the roles of urea and creatinine as uremic toxins remain controversial. To investigate their potential roles in uremic encephalopathy, cultured human neuroblastoma cells (SK-N-SH) were exposed to 0.5 to 14 mg/dL creatinine, or to 20 to 200 mg/dL urea, or to mannitol, NaCl, or glycerol at equivalent osmolalities for 30 min to 48 h, and the induction of Hsp72 (heat shock) protein was used as a marker of cell stress. Although creatinine failed to elicit a heat shock response, urea in clinically relevant concentrations (40 to 200 mg/dL) induced it at 30 min. The response peaked at 10 h and returned to zero by 48 h. Cells exposed to equivalent osmolalities of mannitol, NaCl, or glycerol failed to exhibit this response. Protein extracts from cells exposed to urea showed significant carbamylation that increased as a function of time. These results demonstrate: (1) that urea is neurotoxic in vitro and that creatinine is not: (2) that the insult urea causes is not simply the result of hypertonicity; but rather (3) that urea, via breakdown to cyanate and ammonium ions, may cause cell stress because of its ability to cause carbamylation of cellular proteins. The cells attenuation of the heat shock response after 10 h of exposure to urea suggests that they can adapt to the presence of urea or carbamylation. This may explain, in part, why the same degree of azotemia causes fewer neurological symptoms in patients with chronic as opposed to acute renal failure.
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PMID:Urea induces the heat shock response in human neuroblastoma cells. 878 97

A 36-year-old male presented with headache, vomiting, and gait disturbance. Examination found marked anemia, renal failure, markedly choked disks, and hypertensive encephalopathy. Magnetic resonance imaging demonstrated diffuse swelling of the brainstem and cerebellum, and obstructive hydrocephalus. Treatment with steroid, glycerol, and antihypertensive drugs resulted in a slow decrease in the brain swelling and cerebral edema. However, hydrocephalus and intracranial hypertension persisted, requiring a shunt operation. Hypertensive encephalopathy is usually improved by the treatment of hypertension, but shunt operation may be required to treat exacerbated intracranial pressure associated with obstructive hydrocephalus.
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PMID:Malignant hypertension associated with obstructive hydrocephalus--case report. 909 27

Heme oxygenase (HO) is the rate limiting enzyme in the degradation of heme, and its isozyme, HO-1, may protect against tissue injury. One posited mechanism is the degradation of heme released from destabilized heme proteins. We demonstrate that HO-1 is a critical protectant against acute heme protein-induced toxicity in vivo. In the glycerol model of heme protein toxicity-one characterized by myolysis, hemolysis, and kidney damage-HO-1 is rapidly induced in the kidney of HO-1 +/+ mice as the latter sustain mild, reversible renal insufficiency without mortality. In stark contrast, after this insult, HO-1 -/- mice exhibit fulminant, irreversible renal failure and 100% mortality; HO-1 -/- mice do not express HO-1, and evince an eightfold increment in kidney heme content as compared to HO-1 +/+ mice. We also demonstrate directly the critical dependency on HO-1 in protecting against a specific heme protein, namely, hemoglobin: doses of hemoglobin which exert no nephrotoxicity or mortality in HO-1 +/+ mice, however, precipitate rapidly developing, acute renal failure and marked mortality in HO-1 -/- mice. We conclude that the induction of HO-1 is an indispensable response in protecting against acute heme protein toxicity in vivo.
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PMID:The indispensability of heme oxygenase-1 in protecting against acute heme protein-induced toxicity in vivo. 1079 59

Increased circulating growth hormone (GH) levels and aberrant response to different stimuli characterize both type 1 diabetes mellitus and chronic uremia and are associated with severe retinal, kidney and heart complications. Combined kidney and pancreas transplantation is a therapy that restores the endogenous, closed-loop, insulin secretion in diabetes and cure uremia. To evaluate if combined transplantation can restore a normal secretion and response of GH to growth hormone releasing hormone (GH-RH), we studied four groups of subjects: (1) seven type 1 diabetic patients with end-stage renal failure who had received pancreas and kidney transplantation (KPTx); (2) six diabetic uremic subjects, candidates for combined transplantation (IDDUP); (3) nine patients with chronic uveitis on immunosuppressive therapy comparable to pancreas recipients, six of whom treated only with prednisone (UVEST), while three (4) were treated with both prednisone and cyclosporin (UVESTCY). All subjects underwent a GH-RH test (50 microg intravenously, i.v., at 13:00 h). Serum insulin levels were significantly higher in IDDUP compared to UVEST (P=0.05) both at baseline and post GH-RH stimulus, while were similar to KPTx (P=0.2) and UVESTCY (P=0.7). In contrast, plasma free fatty acids were similar in all groups. In IDDUP baseline plasma glycerol was higher than in KPTx (P=0.04) and UVEST (P=0.02) and similar to UVESTCY (P=0.36); glycerol concentration did not change after GH-RH (P=0.08). Before and after GH-RH, serum GH levels tended to be higher in IDDUP (P=0.5) and KPTx (P=0.2) compared to UVEST and UVESTCY. Our results indicate that: 1) kidney-pancreas transplantation does not normalize the GH response to GH-RH; 2) GH abnormalities are not due either to the chronic immunosuppressive therapy or to the insulin effect on GH release; 3) GH abnormalities are probably secondary to functional and/or organic complications of the hypothalamus and/or pituitary as a sequela of diabetes mellitus.
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PMID:Persistence of anomalies in the growth hormone-releasing hormone-stimulated growth hormone response in diabetic-uremic patients after combined kidney-pancreas transplantation. 1083 Feb 43

Rhabdomyolysis may account for about 10% of all cases of acute renal failure (ARF). This study was performed to explore the protective influence of proanthocyanidins from seeds of grape in an experimental model of myoglobinuric ARF. Rats were injected with 50% glycerol (8 mL/kg, im) followed immediately and daily in the next three days by ip proanthocyanidins (20 mg/kg) or saline. After 96 h rats were sacrificed and kidney morphology, kidney cortex peptidase activities, and malondialdehyde (MDA) content were determined. A moderate renal failure was produced by glycerol injection with blood urea of 31.8+/-11.0 vs. 7.68+/-0.24 m mol/L, and serum creatinine of 153. +/-38.2 vs. 39.6+/-9.0 micromol/L, in glycerol-induced ARF vs. control rats, respectively. Rats that received proanthocyanidins in addition to glycerol had significantly lower (p < 0.01) blood urea and serum creatinine levels compared to those receiving glycerol alone. These functional differences between the glycerol and glycerol plus proanthocianidins groups were also confirmed histologically. Kidney cortex dipeptidylpeptidase IV (DPP IV) activity was not significantly changed in glycerol-induced ARF, however, markedly increased after proanthocyanidins treatment. Kidney cortex malondialdehyde content was found significantly increased in glycerol-induced ARF over control level, and was markedly reduced by proanthocyanidin treatment. Taken together, these results provide strong evidence for the protective role of proanthocyanidins from seeds of grape in glycerol-induced ARF. The effect is probably due to the antioxidant activity of proanthocyanidins and to increased expression of kidney cortex DPP IV with effective degradation of TNF-alpha. This may provide therapeutic opportunities of preventing and/or treating myoglobinuric ARF in humans.
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PMID:Reversal of experimental myoglobinuric acute renal failure with bioflavonoids from seeds of grape. 1084 37

The effect of glycerol-induced acute renal failure on P-glycoprotein expression and function was evaluated in rats. The in vivo function of P-glycoprotein was evaluated by measuring renal secretory and biliary clearance and brain distribution of rhodamine 123 (Rho-123), a P-glycoprotein substrate, under a steady-state plasma concentration. In acute renal failure rats, the P-glycoprotein level increased 2.5-fold in the kidney, but not in the liver and brain. In contrast, P-glycoprotein function in these tissues was suppressed. Interestingly, not only the renal but also the biliary clearance of Rho-123 was correlated with the glomerular filtration rate. In Caco-2 cells, plasma from renal failure rats exhibited a greater inhibitory effect on P-glycoprotein-mediated transport of Rho-123 than did plasma from control rats. In conclusion, P-glycoprotein function was systemically suppressed in acute renal failure, even though the level of P-glycoprotein remained unchanged or rather increased. This may be due to the accumulation of some endogenous P-glycoprotein substrates/modulators in the plasma in disease states.
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PMID:Expression and function of P-glycoprotein in rats with glycerol-induced acute renal failure. 1104 Mar 53

Administration of glycerol produces acute renal failure (ARF) accompanied by profound vasoconstriction. It was hypothesized that impaired arachidonic acid metabolism may contribute to the vasoconstriction through alteration of renal eicosanoids or endothelin-1 or angiotensin II stimulation of renal oxygenases. Arachidonic acid (5, 10, 25 microg) in the control kidney produced increases in perfusion pressure of 15 +/- 9, 18 +/- 8, and 43 +/- 18 mm Hg, respectively. These responses were increased 1.5-fold in glycerol-induced renal failure (p < 0.01). Indomethacin (10 microM), the cyclooxygenase inhibitor, converted arachidonic acid vasoconstriction to epoxide-mediated vasodilator responses, which were unchanged in ARF. In ARF, 5,8,11,14-eicosatetraynoic acid (10 microM), the all-purpose inhibitor of arachidonic acid metabolism; indomethacin (10 microM), a cyclooxygenase inhibitor; 5,8,11-eicosatriyenoic acid (2.5 microM), the 5- and 12-lipoxygenase inhibitor; or aminobenzotriazole (50 mM), the cytochrome P-450 monooxygenase inhibitor, markedly attenuated arachidonic acid-induced vasoconstriction by 73 +/- 11% (p < 0.01), 89 +/- 1% (p < 0.01), 62 +/- 11% (p < 0.01), and 82 +/- 2% (p < 0.01), respectively. In ARF, angiotensin II-induced vasoconstriction was amplified by 67% (p < 0.01). Eicosatetraynoic acid, eicosatriyenoic acid, and aminobenzotriazole reduced these responses by 33 +/- 6% (p < 0.05), 53 +/- 6% (p < 0.01), and 52 +/- 11% (p < 0.05), respectively. Vasoconstriction by endothelin-1 was unchanged in ARF (24 +/- 17%). However, indomethacin attenuated endothelin-1 vasoconstriction by 41 +/- 11% (p < 0.05), whereas eicosatriyenoic acid and aminobenzotriazole were without effect. These data suggest that the increased renal vascular reactivity in ARF in response to arachidonic acid involves a relatively greater production of cyclooxygenase metabolites than monoxygenase- or lipoxygenase-derived eicosanoid metabolites. Furthermore, increased angiotensin II vasoconstriction is predominantly through lipoxygenase and monoxygenase metabolic pathways, whereas for endothelin-1, increased cyclooxygenase-derived vasoconstrictor metabolites play a significant role in its amplified vasoconstrictor effect in glycerol-induced ARF.
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PMID:Contribution of renal oxygenases to glycerol-induced acute renal failure in the rat. 1202 77

Oxygen metabolites play an important role in renal injury during myoglobinuric acute renal failure (ARF). This study was designed to determine the protective influence of N-acetylcysteine (NAC), a hydroxyl radical scavenger, and treatment in an experimental model of myoglobinuric-ARF induced by intramuscular injection of hypertonic glycerol in rats. The rats were randomly distributed into five groups: Group 0 (n = 10), was assigned to receive 2mL saline (0,9%) intraperitoneally (ip); Group 1 (n = 10), NAC ip in a dose of 0 mg/100 g of body weight 30 min before the intramuscular (im) injection of 50% glycerol (10 mg/kg); Group 2 (n = 10), received saline 0,9% ip in a equivalent volume of NAC in Group I before the im injection of glycerol; Group 3 (n = 10), received NAC ip in a dose of 10 mg/100 g after im injection of glycerol; Group 4 (n = 10), saline 0,9% ip in a equivalent volume of NAC of the Group 3 after im administration of glycerol. After 24 h rats were sacrificed and kidney morphology and renal function were determined. A severe renal failure was produced by glycerol injection in the Groups 1, 2, 3, and 4, with significant tubular proximal necrosis and cast formation, and creatinine and urea concentrations were elevated in these groups without significant differences among groups, but Group 0 where the values were significantly lower. The results of this study suggests that ip administration of NAC in rats before or after glycerol injection do not confer protection against impairment of renal function under these conditions in this model of myoglobinuric-ARF.
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PMID:Effects of N-acetylcysteine on myoglobinuric-acute renal failure in rats. 1247 95


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