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

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

Warm ischemia is a potential problem during the harvesting of cadaveric kidneys for transplantation purposes. This ischemia can cause impaired renal function following transplantation. The purpose of our study was to determine whether the beta-adrenergic blocking agent propranolol was effective in improving renal function after ischemia. Dog kidneys were subjected to 30 minutes of warm ischemia followed by hypothermic pulsatile preservation for 24 hours. The kidneys then were autotransplanted with immediate contralateral nephrectomy. In this model only 50% of the untreated control group survived. Three different protocols using propranolol were tested. Administration of propranolol to dogs before the ischemic period, or installation of propranolol into the renal artery at the start of the ischemia, or addition of propranolol to the preservation perfusate lessened the severity of acute tubular necrosis and resulted in 100% long-term survival. Although the mechanism was not investigated, it has been suggested that propranolol is acting through its blockade of beta-mediated renin release and/or through its so-called membrane-stabilizing effect.
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PMID:Protective effect of propranolol in the treatment of ischemically damaged canine kidneys prior to transplantation. 35 13

We measured indices of the renin-aldosterone system and body-fluid spaces in 11 adolescents who had received a renal transplant after removal of their own diseased kidneys. None had hypervolemia but 6 had hypertension. Renal angiography revealed greater than 50% luminal occlusion by allograft renal-artery stenosis (RAS) in only the 3 patients who had severe hypertension refractory to conventional medical therapy. Excessive peripheral plasma renin activity (PRA) distinguished these patients from those who had less severe stenosis or normal angiogram, and diuretic stimulation heightened the PRA differences. We conclude that significant allograft RAS does not necessarily act like a typical single-kidney Goldblatt model until after volume depletion. Our findings indicate that peripheral PRA values can be used to assess the degree of graft ischemia clinically. This permits early identification of patients who have severe RAS that probably will be difficult to control medically, and, therefore, should be followed closely with a view of reconstructive vascular surgery before further deterioration of renal function.
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PMID:Allograft renal-artery stenosis: increased peripheral plasma renin activity as an early indicator of uncontrollable hypertension. 36 8

Renovascular hypertension can result from renal artery lesions involving the main renal artery, or its branches. It is generally felt that the elevation of blood pressure results from excessive systemic vasoconstriction secondary to enhanced renin secretion by one or part of one kidney. Renin secretion is enhanced because of constriction of the renal artery and resultant intrarenal ischemia. Clinically patients cannot be distinguished from those with essential hypertension and diagnosis must be made with arteriography although urography and isotope renography may suggest the diagnosis. Surgical cure can be predicted if differential renal vein renin ratios lateralize but a non-lateralizing study does not necessarily mean that surgery will fail. In properly selected patients, surgical results are excellent.
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PMID:Renovascular hypertension: pathophysiology, diagnosis, and treatment. 37 21

Examination of patients with acute embologenic arterial occlusion yielded data testifying to activation of the renin-angiotensin-aldosterone system both in the ischemic and in the postischemic periods. Direct dependence of the activation of the renin-angiotensin-aldosterone system on the degree of tissue ischemia and duration of the ischemic period of up to 2 days was revealed. The development of secondary hyperaldosteronism in patients with embolism of the major vessels stipulated the expediency of using aldosterone antagonists in patients with most marked ischemic changes in the tissues as well as when the ischemic period lasted more than 6 hours.
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PMID:[Renin-angiotensin-aldosterone system in acute embologenic arterial obstruction]. 43 Sep 58

To evaluate the effect of prostaglandin inhibition on the renal blood flow of the ischemic kidney, we administered indomethacin to 10 anesthetized dogs with renal artery stenosis and contralateral nephrectomy. Following the operation to produce renal ischemia, there was an increase of blood pressure associated with an increase of renin and the prostaglandins F1 (PGF1), and E (PGE). The administration of indomethacin to the intact, normotensive animals caused the anticipated decrease of prostaglandin E, renin, and renal blood flow. However, in the hypertensive dogs, indomethacin caused a paradoxical 45 per cent increase in the renal blood flow, despite a 44 per cent decrease of prostaglandin E. PGF1, PGE, renin, and erythropoietin exhibited the anticipated decreased levels. The study suggests that prostaglandins may not be the sole important factor in the regulation of renal blood flow in the presence of ischemia. Other important factors likely include the renin-sensitive angiotensin, the adrenergic, and the kallikrein-kinin systems.
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PMID:Paradoxical increase of renal blood flow in anesthetized hypertensive dog treated with indomethacin. 48

Severe renin-mediated hypertension was noted in 2 children as a result of selective renal damage from vesicoureteral reflux during the early years of life. In each case the reflux had been corrected successfully long before hypertension developed. In 1 case the late damage involved only 1 kidney and nephrectomy resulted in immediate relief of the hypertension. In the second case, even though both kidneys showed segmental scarring from calicectasis and chronic pyelonephritis, removal of the atrophied lower pole of 1 kidney made hypertension amenable to medical treatment and reduced excessive renin output to a fraction of the original high levels. The mechanism of renin-mediated hypertension in kidneys with segmental scars of chronic pyelonephritis is believed to be ischemia of the relatively normal renal cortex in proximity to areas of interstitial fibrosis, within which are tortuous interlobular and smaller arterioles with severe intimal thickening. Hypertrophy of normal renal segment occurs in young patients with segmental chronic pyelonephritis. To accommodate this enlargement the original calix develops an extension or elongation readily distinguishable from other dilated calices.
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PMID:Malignant hypertension in children secondary to chronic pyelonephritis: laboratory and radiologic indications for partial or total nephrectomy. 61 6

Activation of the renin-angiotensin system has been implicated as one of the mechanisms involved in acute renal failure. Support of this hypothesis was forwarded by the finding that propranolol, a blocker of renin release, reduced the deleterious effect of ischemia on kidney function. The hypothesis was tested further in these experiments by studying renal blood flow after ischemic injury to rat kidneys with and without propranolol proection. Miniature electromagnetic flow probes measured blood flow after 70 min of total renal artery occlusion. Although brief infusion of propranolol reduced the degree of acute renal failure, it had no effect on renal blood reflow. The data do not support the hypothesis that the renin-angiotensin system plays a role in acute renal failure. Other explanations for the protective effect of propranolol are suggested.
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PMID:Propranolol protection in acute renal failure. 64 Aug 2

Some chronic renal failure patients maintained on dialysis have uncontrollable hypertension. Those with elevated renin levels require bilateral nephrectomies prior to kidney transplant to avoid nephrosclerosis. The morbidity and mortality from surgical nephrectomies are high. In 2 such patients we embolized the renal arteries with gelfoam and successfully occluded all the major vessels. One patient became normotensive. The second remained hypertensive and had increased renin levels, probably on the basis of ischemia. Subsequent surgical nephrectomies demonstrated completely occluded segmental branches but only focal areas of infarction. Collateral blood supply determines the success of the procedure.
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PMID:Gelfoam embolization of the kidneys for treatment of malignant hypertension. 66 23


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