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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparison was made between the excretion urogram and the radio-isotope renogram in 35 patients with uretero-sigmoid anastomosis. A good correlation was obtained between the 2 tests in the presence of radiographic evidence of (a) hydronephrosis, (b) poor renal function and (c) absent function. Renographic evidence of mild impairment of secretory function and of delayed excretion was associated with a significant number of normal excretion urograms and in a few instances there was later progression to severe renal impairment or hydronephrosis. Hydro-ureter associated with a normal renogram carried a good functional prognosis. Renography is recommended in the long-term supervision of patients with uretero-sigmoid anastomosis.
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PMID:Renography in the assessment of patients with uretero-sigmoid diversion. 91 40

Formation of nephrons from primitive mesenchyme in fetal kidneys is induced by ureteric buds. Nephron induction is closely coordinated with branching morphogenesis of the ureteric bud. Having previously shown that branching of the primitive ureter is associated with de novo synthesis of chondroitin sulfate proteoglycan and release of free heparan sulfate glycosaminoglycan chains, we asked whether glycosaminoglycans influence nephron development. Fetal mouse kidneys were incubated in organ cultures containing heparan sulfate, heparin, chondroitin sulfate, or hyaluronate. After 48 hr the number of nephrons at each developmental stage was enumerated by light microscopic analysis of serial tissue sections. Kidneys incubated in heparin or in heparan sulfate contained up to 10-fold fewer nephrons than did kidneys incubated in control conditions or in chondroitin sulfate or hyaluronic acid. Maturation of nephrons, however, was unaffected. Inhibition of nephron development was associated with binding of labeled heparin to primitive mesenchyme and altered tissue distribution of fibronectin. Branching morphogenesis was impaired in kidneys exposed to heparin but not to heparan sulfate or to de-N-sulfated, N-acetylated heparin. The capacity of glycosaminoglycans to inhibit nephron formation depended on sugar composition and O-sulfation but not GAG chain size or charge density. Thus, heparan sulfate may have the capacity to specifically control formation of nephrons in fetal metanephric kidneys in vitro.
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PMID:Heparin and heparan sulfate delimit nephron formation in fetal metanephric kidneys. 214 Jan 4

The study was carried out to determine the proximal tubular length, surface area and length of peritubular capillaries and the nephron numbers in kidneys with chronic nephropathy and varying increase in the cortical interstitial volume. Kidneys of pigs with varying chronic obstructive nephropathy were used for the experiments. Two subgroups of ureter-obstructed kidneys were defined arbitrarily according to the volume of cortical interstitium. One subgroup (I) comprised kidneys with a volume fraction of cortical interstitium less than 30% (mean 17.2%; mean of controls 9.7%). The other subgroup (II) consisted of kidneys with severe chronic nephropathy and with a volume fraction of interstitium more than 30% (mean 44.5%). Proximal tubular length and length and surface area of peritubular capillaries were assessed by conventional morphometric techniques on 1 micron thick sections of plastic embedded material. Nephron numbers were determined by a stereological method for counting glomeruli. The results demonstrated that proximal tubular length and capillary dimensions were significantly reduced in subgroup II, whereas no significant changes were observed in subgroup I. The mean number of glomeruli was not significantly different from control values in any of the subgroups. The results are in line with observations from previous quantitative analyses of proximal tubular cross-sections indicating that proximal tubular dimensions become reduced mainly at advanced stages of chronic nephropathy. The results also indicate that shortening of individual tubules rather than loss of entire nephrons is responsible for the observed reduction in total length of proximal tubules. Finally, the present observations suggest that reduced dimensions of the cortical capillary network may have pathogenetic significance for ongoing proximal tubular atrophy in chronic renal disease.
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PMID:Dimensional changes of proximal tubules and cortical capillaries in chronic obstructive renal disease. A light microscopic morphometric analysis. 309 58

The role of the kidney tubules in the renal formation of erythropoietin is incompletely understood. Therefore, the capability to produce erythropoietin in response to hypoxia was studied in rats with tubular lesions. Nephron damage was induced in two different ways. First, rats were treated with the nephrotoxic aminoglycoside gentamicin (67.5 mg/kg and day) for 14 days. The animals were then subjected to simulated altitude (6,800 m) for 6 h. The resulting plasma erythropoietin concentration was significantly lower (0.5 IU/ml) than in saline treated control rats exposed to hypoxia (1.0 IU/ml). Second, unilateral hydronephrosis was induced by ureteral ligation. The contralateral kidney was removed immediately before the animals were exposed to simulated altitude for 6 h. The plasma erythropoietin concentration in the ureter-ligated rats did not increase above the value (0.3 IU/ml) in hypoxia exposed anephric rats. These results indicate that the production of erythropoietin is reduced following tubular injury. Tubule cells may directly produce the hormone or interfere with the O2-sensing mechanisms controlling its synthesis. The latter hypothesis would seem to be supported by our failure to demonstrate in vitro erythropoietin production by the two established kidney tubule cell lines, LLC-PK1 and PK-15.
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PMID:Lowered plasma erythropoietin in hypoxic rats with kidney tubule lesions. 319 83

The risk of developing renal papillary necrosis or cancer of the renal pelvis, ureter or bladder associated with consumption of either phenacetin or paracetamol was calculated from data acquired by questionnaire from 381 cases and 808 controls. The risk of renal papillary necrosis was increased nearly 20-fold by consumption of phenacetin, which also increased the risk for cancer of the renal pelvis and bladder but not for ureteric cancer. By contrast, we were unable to substantiate an increased risk from paracetamol consumption for renal papillary necrosis or any of these cancers although there was a suggestion of an association with cancer of the ureter.
Nephron 1988
PMID:Does paracetamol cause urothelial cancer or renal papillary necrosis? 341 44

Hepatocytes were isolated from rats following bilateral nephrectomy, ureter ligation or sham operation under sodium pentobarbital (Nembutal) anesthesia to investigate the potential role of energy charge and redox state for the gluconeogenetic ability of liver cells. Ketogenesis from l-serine, sodium pyruvate or dihydroxyacetone was significantly higher in hepatocytes of acutely uremic rats indicating higher concentration of reducing equivalents in the mitochondria. During incubation, the mitochondrial redox state characterized by beta-hydroxybutyrate/acetoacetate ratio moved into direction of reduction in all experimental groups, whereas cytosolic redox state characterized by lactate/pyruvate ratio shifted to the oxidative state indicating lack of cytosolic reducing equivalents. Hepatocyte ATP and oxoglutarate production of ureter-ligated rats were significantly higher compared with binephrectomized or sham-operated animals independent of the substrates used. Simultaneously, energy charge showed values higher than 0.85 only in hepatocytes of ureter-ligated animals indicating high energy supply for energy requiring processes. We conclude that hepatic gluconeogenesis and ketogenesis of acutely uremic rats are limited by a lack of cytosolic reducing equivalents independent of cell energy supply.
Nephron 1985
PMID:Role of energy charge and redox state for hepatocyte gluconeogenesis of acutely uremic rats. 400 Mar 49

Hepatocytes isolated from the livers of starved, sham-operated, bilaterally nephrectomised and ureter-ligated rats as well as rats with ischaemic acute renal failure were used for a comparative study of the effects of different hormones on gluconeogenesis. In all tested groups dibutyryl-3':5'-adenosine monophosphate inhibits glucose synthesis from pyruvate whereas this process is not affected by glucagon and only slightly activated by adrenalin. In contrast, gluconeogenesis from dihydroxyacetone was stimulated by all three hormones at the expense of the conversion of dihydroxyacetone to lactate. In the presence of l-serine adrenalin, glucagon and dibutyryl cAMP also stimulate glucose synthesis, which is more marked in bilaterally nephrectomised and ureter-ligated animals. In half of the experiments with bilaterally nephrectomised rats (group BN 2), lack of sensitivity of hepatocytes to all tested hormones on gluconeogenesis from serine or dihydroxyacetone was observed. The beta-adrenergic antagonist propranolol reduced the stimulatory effect of adrenalin on glucose synthesis from serine and abolished the influence of catecholamines in the presence of dihydroxyacetone and pyruvate. This suggests that both alpha- and beta-receptors are involved in the activation of hepatic gluconeogenesis. Insulin and parathyroid hormone did not change the rate of glucose synthesis in any of the experimental groups.
Nephron 1982
PMID:Effect of hormones on hepatocyte gluconeogenesis in different models of acute uraemia. 629 38

Carbohydrate metabolism in salivary glands of acutely uremic rats was investigated. In the submandibular glands there was an increase of total carbohydrate and glycogen content 24 and 48 h following binephrectomy or ureter ligation. In contrast, lactate concentration was significantly lower. Similar alterations of carbohydrate metabolism could not be observed in sublingual or parotid glands of acutely uremic rats.
Nephron 1983
PMID:Carbohydrate metabolism of salivary glands of acutely uremic rats. 664 99

Liver cells were prepared from untreated controls, rats with various models of acute uraemia (uranyl nitrate-treated, bilaterally nephrectomised and ureter-ligated rats, rats with acute ischaemic renal failure) and sham-operated animals. Hepatocyte glucose output, pyruvate utilisation and lactate production were determined in the presence of Krebs-Ringer bicarbonate buffer with different pH values (7.1, 7.4, 7.6) using pyruvate, dihydroxyacetone, serine and fructose as substrates. In the presence of pyruvate and dihydroxyacetone a significant increase of glucose production in hepatocytes from bilaterally nephrectomised and ureter-ligated rats was observed. However, pyruvate-generated glucose production in the hepatocytes of uranyl nitrate-treated animals was unchanged, while a diminished glucose output was seen in the presence of dihydroxyacetone. A marked increase in glucose and lactate production in the presence of serine was observed in the hepatocytes of uranyl nitrate-treated, ureter-ligated and binephrectomised rats. However, lactate production from dihydroxyacetone in the liver cells of uranyl nitrate-treated animals was inhibited. In contrast to other types of uraemia, in acute ischaemic renal failure there is significantly lower hepatocyte glucose production using pyruvate as a substrate, but unchanged glucose generation from dihydroxyacetone or serine.
Nephron 1982
PMID:The gluconeogenetic ability of hepatocytes in various types of acute uraemia. 681 Jan 92

As the nephron population diminishes and azotemia develops, each remaining nephron adapts and increases its function by as much as 80%. To determine whether this adaption is permanent or transient, a rat model utilizing one remnant kidney and one normal control kidney was used. In stage one, immediately after ligation of the ureter to the control kidney, the glomerular filtration rate in the remnant kidney was 0.185 cm3/min. 1 week after ligation of the ureter to the control kidney, the glomerular filtration rate in the remnant kidney had increased to 0.336 cm3/min (stage two), and 2 weeks later, after removal of the obstruction to the control kidney, the glomerular filtration rate in the remnant kidney was 0.155 cm3/min (stage three), p less than 0.01.
Nephron 1982
PMID:Reversible uremia and its effect on the glomerular filtration rate. 716 10


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