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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the influence of hypertension on human glomerulonephritis, 200 biopsies from 74 patients with Iga nephropathy were examined. Chosen for this study were 28 hypertensive patients and 46 normotensive subjects during an observation period of 3.84 +/- 2.17 years, which extended from the first to the last biopsy. In a comprehensive analysis, the following findings were observed: Glomerular sclerosis was analyzed semiquantitatively and estimated as "glomerular index" (GI). Interstitial volume (IV) was determined by the point-counting method. Mesangial electron dense deposits (MDD) and arteriolar hyaline change (HC) were also analyzed semiquantitatively. Arterial fibroelastic intimal thickening was analyzed morphometrically and estimated as the luminal "occlusive rate" (OR). These morphological parameters including their serial changes were compared between the hypertensives and the normotensives. The serial changes in GI and IV from the first to the last biopsy were significantly greater in the hypertensives than in the normotensives. Both OR and HC, including their serial changes, were significantly higher in the hypertensive subjects. In the study of MDD and its serial changes, no difference was apparent between the two groups. In the study of OR and HC, there was no correlation observed with GI. Our observations show that hypertension accelerates the progression of both glomerular and vascular sclerosis in case of human glomerulonephritis and suggests that this acceleration cannot only be explained by ischemia-related factors resulting from vascular sclerosis.
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PMID:Hypertension-related aggravation of Iga nephropathy: a statistical approach. 321 69

We performed a multicenter study to investigate the problem of cadaver kidney transplants that never achieve function, or that recover after a period of delayed function, and we used multivariate techniques to model the results. Sixty-nine patients who received cadaver kidney transplants that never functioned (NF) were compared with 69 kidney recipients with early graft function (EF), and 69 with delayed but recovering graft function (DF), matched for transplant hospital and time. The results were analyzed using an unconditional logistic regression model. Risk factors for never-function transplants compared to immediate-function transplants were as follows: previous failed transplant, no polyclonal antilymphocyte globulin (ALG) prophylaxis, increasing anastomosis time, decreasing donor blood pressure, and prior transfusions in first but not subsequent transplant recipients. When technical failures were excluded, 88% of NF grafts displayed severe rejection, suggesting that rejection in a poorly functioning kidney is the principal cause of the NF outcome. Risk factors for delayed function compared to immediate function were these: increasing anastomosis time, no ALG, increasing total cold ischemia time, duration of end-stage renal disease (ESRD), and male sex. Thus ischemic and immunologic risk factors contributed to the DF and NF outcomes. This study suggests that efforts to reduce the delayed and never-function outcomes should be directed to the use of ALG prophylaxis and to the reduction of cold ischemia and anastomosis times, particularly in recipients who have lost a previous transplant.
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PMID:Factors influencing early renal function in cadaver kidney transplants. A case-control study. 327 40

Tissue damage as a consequence of ischemia is a major medical problem in an industrialized society. Whereas the conventional view has attributed this injury process to ischemia itself, recent studies have found that a variable, but often substantial proportion of the injury is caused by toxic oxygen metabolites that are generated from xanthine oxidase at the time of reperfusion. This mechanism was first identified and characterized in a model of moderately mild partial vascular occlusion in the feline small intestine. Strikingly similar mechanisms have been subsequently confirmed as the basis for ischemia/reperfusion injury in the stomach, pancreas, liver, skin, skeletal muscle, heart, lung, kidney and central nervous system. The potential for clinical application of this concept is related primarily to that proportion of the total post-ischemic injury that is due to this reperfusion mechanism, set against the proportion due to ischemia itself. Ironically, in clinical cases of intestinal ischemia the reperfusion component appears to be proportionately small, and the potential for treatment of ischemic bowel disease is correspondingly limited. On the other hand, there is reason to expect that the ablation of free radical-mediated reperfusion injury, something that can be readily achieved through non-toxic means, may provide substantial benefit for the treatment of ischemic renal disease, myocardial infarction, stroke, cardiac arrest, and of organs preserved for transplantation.
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PMID:Free radical-mediated reperfusion injury: a selective review. 330 76

Patients with diabetes mellitus and coronary artery disease are thought to have painless myocardial ischemia more often than patients without diabetes. We studied 50 consecutive patients with diabetes and 50 consecutive patients without diabetes, all with ischemia, on exercise thallium scintigraphy to show the reliability of angina as a marker for exertional ischemia. The two groups had similar clinical characteristics, treadmill test results, and extent of infarction and ischemia, but only 14 [corrected] patients with diabetes compared with 34 [corrected] patients without diabetes had angina during exertional ischemia. In diabetic patients the extent of retinopathy, nephropathy, or peripheral neuropathy was similar in patients with and without angina. Angina is an unreliable index of myocardial ischemia in diabetic patients with coronary artery disease. Given the increased cardiac morbidity and mortality in such patients, periodic objective assessments of the extent of ischemia are warranted.
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PMID:Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: assessment by exercise thallium scintigraphy. 334 50

A marked defect in renal concentration ability associated with hypoxic lesions in the medullary thick ascending limb (mTAL) characterizes the isolated rat kidney perfused with cell-free solutions. Addition of erythrocytes to the perfusion medium, a maneuver known to eliminate signs of hypoxic cellular injury to mTALs, greatly improved renal concentrating ability. When indomethacin was given to kidneys perfused with erythrocyte-enriched medium, concentrating ability was further improved by the drug to an average U/Posm of 2.45 +/- 0.81, and medullary cellular structure remained normal in appearance. Since renal hypoperfusion predisposes to acute renal failure from non-steroidal antiinflammatory drugs (NSAIDs) and medullary ischemia might play a role in chronic analgesic nephropathy, a synergism between NSAIDs and medullary hypoxia was evaluated in the isolated perfused rat kidney. Indomethacin and naproxen added to the perfusion medium (at 10(-4) and 5 X 10(-4) M, respectively) effectively depressed prostaglandin E2 (PGE2) production by the isolated kidney but did not improve its concentrating ability when perfused with cell-free medium. Quantitation of hypoxic injury to mTALs, regularly observed in this model, indicated that both indomethacin and naproxen increased the extent and severity of damage in the deeper, most hypoxic portions of the inner stripe. Addition of PGE2 to cell-free perfusate reduced the extent of hypoxic damage to the mTAL. These results suggest that in medullary hypoxia, prostaglandins protect mTAL cells by either vasodilatation or reduction in active transtubular transport. NASAIDs, by suppressing prostaglandin production, could predispose the renal medulla to hypoxic injury.
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PMID:Inhibition of prostaglandin synthesis in rat kidney perfused with and without erythrocytes: implication for analgesic nephropathy. 346 23

Cyclosporine (CSA) is a new immunosuppressant which has selectivity for the immune system and is without systemic side effects at therapeutic doses. In contrast to the cytotoxic class of immunosuppressants, no myelotoxic, teratogenic, mutagenic, or carcinogenic effects were observed. Nevertheless, overdosage may lead to renal dysfunction, which occurs mainly in rats, and often complicates its clinical use. The experimental data also showed that significant nephrotoxicity was only caused under specific conditions at therapeutic doses. These conditions included ischemia, heminephrectomy, concomitant administration of nephrotoxic drugs, and/or genetic predisposition. Thus, concomitant renal damage is a prerequisite in order to obtain overt nephrotoxicity at therapeutic CSA doses. Since these conditions cannot be avoided in patients, nephrotoxicity often occurs at therapeutic doses in man. The rat might be a suitable experimental model of CSA nephropathy displaying similar morphologic and functional changes as observed in man. This model also allows further investigations on the pathogenic mechanisms which are elusive at the present time.
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PMID:Cyclosporine nephrotoxicity. 352 Jul 82

Cross-sectional studies of renal function in man indicate there is a progressive decline with age after the age of 40 years. The blood vessels, glomeruli, tubules and interstitium are all potential sites of primary involvement in the aging process as well as for renal disease. Regardless of the anatomic structure initially affected, most chronic renal conditions evolve with destruction of the entire nephron. Whether the observed decrease in renal function associated with aging is the result of intervening pathologic processes, e.g. ischemia (vascular obliteration) or infection, or is the result of a more insidious involutional process, it has generated much discussion but few answers. The purpose of this report is to review the descriptive studies documenting the changes in renal morphology and physiology with age and to focus on what is known about the mechanisms involved in these losses of renal substances and function.
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PMID:Anatomic and physiologic age changes in the kidney. 354 73

Glomerular responses to angiotensin II (AII), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium-mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile responses to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.
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PMID:Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. 354 13

Concentrations of plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable metabolite of prostacyclin, were measured by radioimmunoassay before and after 3 min of induced ischemia in 45 diabetics and 23 controls matched for age. In the 45 diabetics, 15 had no vascular complications (group I), 10 had a macroangiopathy (group II), 10 had a microangiopathy (group III) and 10 had both macroangiopathy and microangiopathy (group IV). Plasma levels of 6-keto-PGF1 alpha before forearm ischemia were significantly lower in group IV diabetics than in non-diabetic controls (188 +/- 17 pg/ml and 245 +/- 14 pg/ml, respectively). After 3 min of ischemia, plasma 6-keto-PGF1 alpha concentrations were increased in control subjects by 34% and by 21% in group I diabetics. In group III diabetics as well as diabetics with atherosclerotic vascular lesions (groups II and IV), no significant change was observed after 3 min of ischemia. These results suggest that impaired vessel wall prostacyclin production may to some extent be responsible for the development of diabetic retinopathy and nephropathy as well as atherosclerotic vascular complications.
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PMID:Prostacyclin production reduced in diabetics with vascular complications. 384 Aug 49

Experimental and clinical evidence are summarized that support the hypothesis that enhanced transmission of systemic hypertension to the adapted glomerulus in the setting of reduced nephron mass may be responsible for accelerated vascular and glomerular damage in the hypertensive stage of parenchymal renal disease in man. In experimental models of hypertension associated with reduced renal mass, the kidney appears to be damaged directly by transmission of pressure rather than primarily through vasoconstriction and ischemia. When hypertension is combined with models of glomerular disease, vascular and glomerular injury are aggravated. It is proposed that adaptive glomerular hemodynamic alterations which occur in parenchymal renal disease magnify the transmission of increased pressure and flows when hypertension supervenes. Accelerated vascular and glomerular damage and functional deterioration result. According to this hypothesis, control of systemic hypertension and minimization of hydraulic stress on the diseased glomerulus become critical to the management of chronic renal disease and the prevention of progressive renal insufficiency.
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PMID:Treatment of hypertension in renal disease. 388 4


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