Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomerular hemodynamics were studied, by micropuncture, in Munich-Wistar rats submitted to 24-hour unilateral ureteral ligation (UUL). Glomerular capillary pressure (PG), intratubular pressure (PT) and pressure in the first-order peritubular capillaries (EAP) were measured with a servonulling device. Single nephron filtration fraction (SNIFF) was calculated fmom arterial and peritubular blood protein concentration. SNGFR was both measured by conventional micropuncture techniques and calculated from efferent arteriole blood flow (EABF) and SNFF. Afferent arteriole blood flow (AABF) and resistance of afferent (Ra) and efferent (Re) arterioles were calculated. Measurements were repeated 1 to 2 hours after the release of the ureter. Sham-operated rats were used as control. UUL caused a marked increase in Ra (from 4.9 +/- [SD] 2.4 to 12.7 +/- 5.1 dynes/sec/cm-5). The fall in SNGFR (from 111.9 +/- [SD] 23.9 to 34.4 +/- 23.1 nl/min/kg body wt) was secondary to a decrease in both PG and AABF. A further increase in Ra (16.0 +/- 6.7 dynes.sec.cm-5) occurred after releasing the ureter. SNGFR, however, was unaltered (33.7 +/- 16.6 nl/min/kg body wt) since PG decreased parallel to PT, but AABF did not significantly change. Conclusion. Ureteral obstruction determines, in 24 hours, a marked cortical ischemia that is not promptly reversed by ureteral release.
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PMID:Effects of 24-hour unilateral ureteral obstruction on glomerular hemodynamics in rat kidney. 48 Jul 81

In the last few years, we have focused our research effort on the magnetic resonance spectroscopic (NMR) studies of organ transplantation in the rat. P-31 NMR was employed to study changes in high-energy phosphates, intracellular pH in vivo of transplanted kidneys either during normal function, while undergoing the rejection process or subjected to other insults (e.g. ischemia, cyclosporine nephrotoxicity, urinary obstruction) which may also cause graft dysfunction. Nuclear magnetic resonance (NMR) parameters, specifically relative peak areas and intracellular pH, accurately distinguished among the different causes of graft dysfunction. Ureteral obstruction was clearly identified by elevations in the phosphodiester/urine phosphate peak. Ischemia and rejection were both associated with increases in inorganic phosphates and phosphomonesters and decreases in the beta-phosphate peak of adenosine triphosphate but were distinguishable from each other by differences in intracellular pH which was normal in rejected allografts (7.33 +/- 0.07, n = 3) and low in ischemic allografts (7.00 +/- 0.05, n = 3, p less than 0.05). Grafts insulted with cyclosporine toxicity were not distinguishable from normal allografts by any of the parameters studied. To determine the temporal relationship of NMR changes in allograft rejection, similar studies were performed serially in a group of rejecting (R) kidneys (n = 7) and compared with a control group of nonrejecting (NR) kidneys (n = 7). Major decrease in adenosine triphosphate (ATP) with increases in Pi and a marked increase in the Pi/ATP ratio were noted in the R allografts over time. The R allografts could be completely segregated from the NR allografts on the basis of the Pi/ATP ratio by day 7. These data suggest that 31P NMR spectroscopy may have potential clinical application in differentiating among the causes of graft failure of human renal allografts.
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PMID:Magnetic resonance study of renal transplantation. 262 44

31P NMR spectroscopy was used to study renal allografts in rats subjected to allograft rejection, cyclosporine toxicity, ischemia, and ureteral obstruction. Parameters of relative peak areas and intracellular pH were accurately distinguished among the different causes of graft dysfunction. Ureteral obstruction was clearly identified by elevations in the phosphodiester/urine phosphate peak. Ischemia and rejection were both associated with increases in inorganic phosphates and phosphomonesters and decreases in the beta-phosphate peak of adenosine triphosphate but were distinguishable from each other by differences in intracellular pH which was normal in rejected allografts (7.33 +/- 0.07, n = 3) but low in ischemic allografts (7.00 +/- 0.05, n = 3, P less than 0.05). Grafts insulted with cyclosporine toxicity were not distinguishable from normal allografts by any of the parameters studied. These data suggest that 31P NMR spectroscopy may have potential clinical application in differentiating among the causes of graft failure of human renal allografts.
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PMID:31P nuclear magnetic resonance study of acute renal dysfunction in rat kidney transplants. 331 20

Ureteral obstruction can have a variety of causes intrinsic or extrinsic to the kidney. The effects of obstruction are examined from the perspectives of duration, severity, totality, and the presence of complicating factors. There is a difference in the postobstructive pathophysiology depending on whether one or both ureters were obstructed. Atrial natriuretic peptide may be important in postobstructive diuresis, and preliminary evidence suggests a role for it as protection against nephron ischemia in acute obstruction. The potential for recovery of renal function after relief of obstruction depends on the duration and degree of obstruction, the condition of the contralateral kidney, and the presence or absence of infection. Ability to acidify the urine to pH < 6.0 preoperatively may be a good predictor of the recovery potential of an obstructed kidney. Urine concentrations of lysosomal enzymes such as N-acetylglucosaminidase also may be useful for this purpose, as may measurement of creatinine clearance in urine obtained from a nephrostomy tube.
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PMID:The pathophysiology of ureteral obstruction. 851 34

Ureteric obstruction is a common complication following kidney transplantation ranging from 2% to 5% after one year and till 9% after five years post-transplantation. It hinders the return to good renal function and in certain cases leads to the organ loss or patient mortality. Technical factors and ureteric ischemia are the most important causes. The authors report their experience with kidney transplantation and 6 cases of ureter obstruction with a global incidence of 5.5%. We discuss the aetiology, the management and the treatment for this complication emphasizing the importance of either color Doppler ultrasound for the diagnosis or percutaneous nephrostomy for the radiological establishment of the blocked level as well as the first choice of treatment. In order to reduce the morbidity and mortality for this complication early and aggressive treatment is advocated.
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PMID:[Ureteral obstruction in the kidney transplant patient]. 856 Mar 50

Ureteral obstruction secondary to ischemia is the most common urologic complication of kidney transplantation. Although endoscopic management has shown satisfactory short-term success rates, surgical repair is considered the definitive therapy. To our knowledge, this procedure has been performed only through open surgery. We present a minimally invasive approach for reconstruction of a ureteral stricture in a renal transplant patient using the Da Vinci robotic system.
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PMID:Case report: robot-assisted laparoscopic pyeloureterostomy in a transplanted kidney with ureteral stricture. 1642 29

Animal models are essential tools to understand the mechanisms underlying the development and progression of renal disease and to study potential therapeutic approaches. Recently, interventional models suitable to induce acute and chronic kidney disease in the mouse have become a focus of interest due to the wide availability of genetically engineered mouse lines. These models differ by their damaging mechanism (cell toxicity, immune mechanisms, surgical renal mass reduction, ischemia, hypertension, ureter obstruction etc.), functional and histomorphological phenotype and disease evolution. The susceptibility to a damaging mechanism often depends on strain and gender. The C57BL/6 strain, the most commonly used genetic background of transgenic mice, appears to be relatively resistant against developing glomerulosclerosis, proteinuria and hypertension. This review serves to provide a comprehensive overview of interventional mouse models of acute and chronic kidney disease.
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PMID:Non-Transgenic Mouse Models of Kidney Disease. 2721 80