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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l 10 ml/kg). Either 2 or 4--6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mm Hg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra- rather than intra-renal mechanisms.
Clin Sci Mol Med 1978 Sep
PMID:Renal vasoconstriction in glycerol-induced acute renal failure. Studies in the isolated perfused rat kidney. 69

1. Acute renal failure was induced in female Sprague-Dawley rats by the subcutaneous injection of glycerol. 2. Four groups of rats were studied; all animals received a glycerol challenge. Group A (control) were sham-operated only, group B received an infusion of sodium chloride solution (150 mmol/l; saline) for 24 h, group C received an infusion containing prostaglandin E2 (PGE2, 1.7 micronmol/l) in saline and group D a solution containing PGE2 (3.4 micronmol/l) in saline. 3. All rats were killed 48 h after glycerol challenge. The degree of renal impairment was assessed by serum creatinine concentration, which did not differ in sham-operated animals and the group receiving saline alone. The group of rats receiving the lower dose dose of PGE2 has a significantly lower mean serum creatinine concentration than the saline-infused control rats (P less than 0.0025). Creatinine concentration was further lowered by the higher dose of PGE2 but there was not a significant difference in the number of rats showing severe tubular necrosis histologically. 4. The study demonstrates that intravenous infusion of prostaglandin E2 has a protective influence on glycerol-induced renal failure in the rat; the protection afforded may be due to the vasodilator effect of PGE2 and/or an effect on glomerular permeability.
Clin Sci Mol Med 1978 Nov
PMID:Protective effect of prostaglandin [PGE2] and in glycerol-induced acute renal failure in rats. 72 5

1. In rats deprived of food and water for 24 h acute renal failure was produced by the intramuscular injection of glycerol. Eight hours later plasma urea concentration had increased threefold despite a small rise in urine volume. Plasma concentrations of renin and renin substrate were elevated. 2. When saralasin, a competitive antagonist of angiotensin II, was infused for 8 h after glycerol injection, urine volume and plasma urea were similar to values in rats that had received an infusion of saline. 3. Administration of rat serum (4.5 ml h-1 kg-1) for 4 h suppressed plasma renin concentrations, but plasma urea increased to the same extent as in rats without serum. 4. When saralasin and serum were infused at the same time, urine volume, urine osmolality and solute excretion increased and the rise of plasma urea was diminished. 5. Saralasin has a protective effect against glycerol-induced acute renal failure only when volume is replaced concomitantly.
Clin Sci Mol Med 1978 May
PMID:Effect of saralasin and serum in myohaemoglobinuric acute renal failure of rats. 75 Jan 57

1. Acute renal failure was produced in rats by intramuscular injection of glycerol. Subsequently, changes in the concentrations of renin and of angiotensin II in plasma and the renin content of the kidneys were followed. 2. at 4 and 8 h after glycerol administration, plasma renin and angiotensin II had increased two to three-fold; they remained elevated for 48 h and then returned towards normal. At 7 days, the values were still slightly raised. 3. At 4 and 8 h after glycerol injection, kidney renin had decreased but it had increased after 24 and 48 h. 4. Passive immunization with angiotensin II antibodies, given at the time of glycerol injection and 2 and 4 h afterwards, prevented the development of acute renal failure. When angiotensin II antiserum was administered later (8, 10 and 12 h after glycerol) it had no effect. 5. Stimulation of the renin-angiotensin system may be involved in the pathogenesis of the early phase of acute renal failure.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The renin-angiotensin system in acute renal failure of rats. 105 77

1. High plasma immunoreactive calcitonin concentrations were observed in ten of eleven patients with acute renal failure, particularly in the oliguric phase. 2. Immunoreactive calcitonin decreased progressively with time, independently of recovery of renal function. 3. Radioimmunoassay curves obtained with serial dilutions of plasma from these patients were parallel to or superimposed upon those obtained with calcitonin standards.
Clin Sci Mol Med 1975 Oct
PMID:Increased plasma calcitonin in early acute renal failure. 119 89

1. Acute renal failure was induced in conscious rate by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE2) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.
Clin Sci Mol Med 1975 Nov
PMID:The effect of indomethacin and prostaglandin (PGE2) on renal failure due to glycerol in saline-loaded rats. 119 9

It is now well documented that some enteric bacteria which cause diarrhoeal and/or dysenteric disease produce, at high levels, one or more of a family of protein toxins referred to as Shiga toxin and Shiga-like toxins (SLTs; alternatively called verocytotoxins or VTs). Within the past few years, there have been considerable advancements made in our understanding of the biochemistry and molecular biology of Shiga toxin and SLTs. However, the precise role of the toxins in mediating colonic disease, as well as their contribution to the development of extra-intestinal sequelae (e.g. the haemolytic uraemic syndrome and neurological disorders), remain less clear. In this MicroReview, we will briefly summarize recent progress in Shiga toxin- and SLT-related research and present evidence supporting the concept that these toxins contribute to pathogenesis by directly damaging vascular endothelial cells, thereby disrupting the homeostatic properties of these cells. We will also discuss data which suggest that toxin-mediated damage in the kidney may not be limited to glomerular endothelial cells but may include tubular epithelial cells. Thus, the role of the toxins in renal disease may not be limited to the glomeruli, as was initially hypothesized when the association of infection with toxin-producing strains and the development of acute renal failure was established.
Mol Microbiol 1991 Aug
PMID:The pathogenic mechanisms of Shiga toxin and the Shiga-like toxins. 176 67

The administration of anticancer platinum derivatives such as cisplatin, or aminoglycoside antibiotics is frequently associated with tubular necrosis which can eventually lead to acute renal failure. Previously, we have shown that renal tissue injury induced by these drugs elicits a process of tissue repair involving the stimulation of cell proliferation. The present study was undertaken to examine the morphological alterations and the proliferative response resulting from tobramycin administration to animals previously challenged with the platinum derivatives cisplatin and carboplatin. Female Sprague-Dawley rats were treated i.p. with cisplatin (8 mg/kg delivered in four daily injections) or carboplatin (40 mg/kg given in one injection) and sacrificed 21 or 60 days after drug administration. Tobramycin was administered i.p. twice a day at a daily dose of 10 mg/kg over the ten days preceding sacrifice. At 1 h before sacrifice, each animal received i.p. 200 microCi of [3H] thymidine for the measurement of DNA synthesis and cell proliferation (determined by histoautoradiography). Successive treatments with cisplatin and tobramycin appeared to produce an increase in the severity of histopathological alterations such as tubular necrosis and cystic degeneration. Moreover, cisplatin pretreatment dramatically increased the severity of tobramycin-induced lysosomal phospholipidosis. Histopathological alterations were followed by an important proliferative response partly associated with tubular regeneration but also due to fibroblastic proliferation which led to peritubular fibrosis. Surprisingly, the additive effect of cisplatin and tobramycin on renal injury became particularly striking with increasing time intervals between treatments. In contrast, successive treatments with carboplatin and tobramycin did not cause significative changes of the degree of renal injury, compared with either drug given alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Renal tissue injury and proliferative response after successive treatments with anticancer platinum derivatives and tobramycin. 198 Jul 61

The sequence of 1416 base-pairs of the P22 PL operon was determined, linking a continuous sequence from PL through abc2. P22 mutants bearing deletions in the sequenced region were constructed and tested for their phenotypes. Plasmids were constructed to express PL operon genes singly and in combination from Plac UV5. Two previously known genes, 17 and c3, are located within this sequence. In addition, three new genes have been identified: ral, kil and arf. Genes ral and c3 are homologous, as well as functionally analogous, to lambda ral and cIII, respectively. P22 kil, like lambda kil, kills the host cell when it is expressed. The two kil genes, although analogous in cell killing and map location, have no apparent sequence homology. The functions of the P22 and lambda kil genes are unknown; however, P22 kil is essential for lytic growth in the absence of abc. Gene arf (accessory recombination function) is located just upstream from erf; it is essential for P22 growth in the absence of kil or other genes upstream in PL. The growth defect of P22 bearing a deletion that removes arf is complemented by expression of either arf or the lambda red genes from plasmids. Sequences that include the stop codon for gene 17 may form a small stem-loop structure and are nearly identical to lambda sequences that contain the stop codon for ssb, which is near lambda tL 2b. Plasmids that include the P22 structure negatively regulate kil gene expression in cis.
J Mol Biol 1989 May 05
PMID:Genetic structure of the bacteriophage P22 PL operon. 273 22

An unusual cytoplasmic accumulation of glycogen within the distal tubular epithelium of the kidney was produced by subcutaneouse administration of a single dose of HgCl2 (4 mg/kg body weight), used to induce acute renal failure. Since the plasma immune-reactive insulin was increased while plasma and urine glucose levels remained normal, it was concluded that activation of glycogen synthase might have lead to this effect. Furthermore, the accumulated glycogen was considered to contribute to the protection of distal tubular cells against HgCl2-induced injury, since oxidative energy metabolism was severely depressed after HgCl2 administration.
Virchows Arch B Cell Pathol Incl Mol Pathol 1980
PMID:Glycogen deposition in distal tubular cells during HgCl2 induced acute renal failure. 610 39


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