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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The existence of a clear relationship between renal ischemia and hypertension has been widely documented by Harry Goldblatt and his colleagues. In their original papers they showed that gross and persistent elevation of systolic blood pressure could be produced in dogs by clamping both renal artery, or one if the other kidney had been removed. If renal arteries constriction was not too severe, a stable hypertension unaccompanied by more than mild renal impairment was produced. Subsequently, Goldblatt showed that, with severe constriction, retinal changes, arteriolar impairment and left ventricular hypertension could occur. Goldblatt has remained steadily of the opinion that essential hypertension in man is similarly due to renal ischemia occasioned either by stenosis of a main artery, or by organic changes in the smaller renal arteries down to the size of the different glomerular arteries. At first sight, it might seem like a simple matter to correctly identify the chain of events that begins with renal artery constriction and ends with persistent hypertension. Observing that a link was missing in this chain of events, Goldblatt hypothesised that the link was a humoral mechanism. Tigersted and Bergman showed that renin was the missing link. Renal ischemia as cause of hypertension in dogs opened a new chapter in the connection between kidney circulation and blood pressure elevation. This quite unexpected connection is one of the most challenging issues today and clearly demonstrates that the development of Goldblatt's ideas on renal circulation is still important and has by no means ended. Goldblatt, in his epistemologic approach to hypertension scientific challenges, realised that ideas are the building blocks of science: not flights of fancy, not notions sculpted in snow, but enduring concepts. Goldblatt's lasting ideas are more than a function of time and place: they have inherent qualities that have survived up to the present day.
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PMID:[Historical Archives of Italian Nephrology. Goldblatt, kidney and hypertension: three steps in the history of nephrology]. 1463 67

Hypertension is a common problem in patients with autosomal dominant polycystic kidney disease affecting both renal and patient survival. Activation of the renin-angiotensin-aldosterone system due to cyst expansion and local renal ischemia has been proposed to play an important role in the development of hypertension in autosomal dominant polycystic kidney disease. Left ventricular hypertrophy, a major cardiovascular risk factor, is also common in patients with autosomal dominant polycystic kidney disease. Both hypertension and the activation of the renin-angiotensin-aldosterone system play a role in the development of left ventricular hypertrophy in these patients. Prospective randomized results indicate that aggressive control of blood pressure is important for the optimal reversal of left ventricular hypertrophy, thereby diminishing a major risk factor for cardiovascular morbidity and mortality of patients with autosomal dominant polycystic kidney disease. There is also substantial epidemiological support for aggressive control of blood pressure in slowing renal disease progression in autosomal dominant polycystic kidney disease patients. Blockade of the renin-angiotensin-aldosterone system should be the initial approach in the treatment of hypertension in these patients.
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PMID:Hypertension and left ventricular hypertrophy in autosomal dominant polycystic kidney disease. 1515 83

Unilateral renal ischemia for 40 min in rat results in increased fibronectin (FN) expression in proximal tubular cells. This study examines the role of 24 h of blood reperfusion and the role of the renin-angiotensin system (RAS) on these results. Rats were submitted to 40 min of unilateral renal ischemia followed by 24 h of blood reperfusion. Renal function was assayed by clearance measurement in metabolic cages. Intracellular ATP and calcium were determined in proximal tubules. The expression and abundance of FN were investigated by reverse transcription-polymerase chain reaction, ELISA and Western blot either in isolated proximal tubules or cortex homogenates from control, ischemic and ischemic with reperfusion rats. Matrix metalloproteases (MMPs) activity was also measured. Losartan effects on renal function and on the abundance of FN and the MMPs activity in cortical homogenates were also measured. The renal function remained altered after 24 h of reperfusion in untreated and losartan-treated ischemic rats. On the other hand, the abundance of FN is increased after reperfusion both in isolated proximal tubules and total cortex homogenates and the same pattern was observed in the MMPs activity. Twenty-four h of blood reperfusion presented FN-mRNA signals similar to control ones. Losartan pretreated-rats presented diminished FN abundance in homogenates of cortex tissue from ischemic rats with or without reperfusion. Similar results were observed in the MMPs-activity. These results suggest that angiotensin II acting via the AT1 receptor plays a role in the development of tubulointersticial fibrosis after ischemia-reperfusion by activation of intrarenal RAS from the injured kidney.
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PMID:Losartan reverses fibrotic changes in cortical renal tissue induced by ischemia or ischemia-reperfusion without changes in renal function. 1522 98

In healthy subjects, arterial pressure reduction or renal ischemia produces renal artery dilatation through autoregulation and tubuloglomerular feedback (TuGF). Patients with decompensated cirrhosis have reduced kidney perfusion pressure but show renal vasoconstriction instead of autoregulation-mediated vasodilation. This study investigates the consequences of kidney autoregulation loss on renal perfusion, glomerular filtration rate, and tubular handling of electrolytes in both compensated and ascitic nonazotemic cirrhotic patients. Forty-two consecutive patients with diuretic-free liver cirrhosis (32 with preascitic and 10 with ascitic disease) and 10 controls were submitted to the following determinations: (a) basal plasma renin activity and aldosterone levels; (b) endogenous dopaminergic activity measured as incremental aldosterone responses during metoclopramide administration; and (c) renal clearances of sodium, potassium, inulin, para-aminohippurate and lithium. Compared with the other groups, ascitic patients showed lower renal plasma flow (P < 0.01) and lithium clearance (P < 0.05), a higher filtration fraction (P < 0.01), and secondary aldosteronism. Controls and preascitic patients displayed tubuloglomerular feedback (the mechanism increasing the glomerular filtration rate when a reduced sodium load reaches the distal tubule), as demonstrated by negative correlations between fractional excretion of lithium (an expression of fractional delivery of sodium to the distal nephron) and glomerular filtration rate (respectively, r = -0.73, P < 0.03, and r = -0.48, P < 0.01). Conversely, patients with ascites showed a positive correlation between lithium fractional excretion and glomerular filtration rate (r = 0.64, P < 0.05). Reduction in renal perfusion, increased filtration fraction, and TuGF derangement, as found in decompensated patients, are indicative of prevalent postglomerular arteriolar vasoconstriction, with ensuing stimulation of proximal tubular sodium reabsorption.
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PMID:Loss of tubuloglomerular feedback in decompensated liver cirrhosis: physiopathological implications. 1590 75

With the widespread use of non-invasive diagnostic tools, such as abodminal ultrasound and computerized tomography, renal cysts are diagnosed with increasing frequency. In patients 50 years or older, simple renal cysts of various size may be found in nearly one third. Increasing frequency with age is clearly demonstrated. Two thirds of simple renal cysts are 2 cm or less in diameter. The average renal cyst needs about 10 years to reach 2 cm in size. Simple renal cysts (category I according to Bosniak classification) usually are asymptomatic, produce no harm to the kidney and require no treatment once diagnosed. However, an occasional eypanding cyst causes progressive obstruction to caliceal and pelvic outflow. There is a possible association between renal cysts and arterial hypertension. Renal cysts may produce segmental renal ischemia, and in turn activate the renin angiotensin system. Percutaneous cyst aspiration or surgical cyst removal could cause a fall in blood pressure. Bosniak suggested a classification in an attempt to sort out the different cases into nonsurgical (category I and II), and surgical ones (category III and IV). Borderline between cystic lesions type II and III is not clear-cut, but Bosniak type IV lesions are clearly cystic renal cell carcinoma.
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PMID:[Simple renal cysts]. 1591 25

In addition to the long-term renal complications, previous studies suggested that after acute renal failure (ARF), rats manifest an increased pressor response to an overnight infusion of ANG II. The present study tested whether recovery from ARF results in alterations in sensitivity to the peripheral vasculature. ARF was induced in Sprague-Dawley rats by 45 min of bilateral renal ischemia and reperfusion. Animals were allowed to recover renal structure and function for 5-8 wk, after which the acute pressor responses to ANG II were evaluated either in vivo in in situ skeletal muscle arterioles or in isolated gracilis muscle arteries in vitro. Baseline arterial pressure was not different in ARF rats vs. sham-operated controls, although ARF rats exhibited an enhanced pressor response to bolus ANG II infusion compared with control rats. Steady-state plasma ANG II concentration and plasma renin activity were similar between ARF and control rats. Constrictor reactivity of in situ cremasteric arterioles from ARF rats was enhanced in response to increasing concentrations of ANG II; however, no difference was observed in arteriolar responses to elevated PO2, norepinephrine, acetylcholine, or sodium nitroprusside. Isolated gracilis muscle arteries from ARF rats also showed increased vasoconstriction in response to ANG II but not norepinephrine. In conclusion, recovery from ischemic ARF is not associated with hypertension but is associated with increased arteriolar constrictor reactivity to ANG II. Although the mechanisms of this altered responsiveness are unclear, such changes may relate, in part, to cardiovascular complications in patients with ARF and/or after renal transplant.
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PMID:Enhanced skeletal muscle arteriolar reactivity to ANG II after recovery from ischemic acute renal failure. 1609 26

The association between hypertension and chronic renal disease is well known. The pathogenesis of hypertension in patients with chronic kidney disease (CKD) is complex and multifactorial, which may explain why it is resistant to treatment. The traditional paradigm is that hypertension in CKD is due either to an excess of intravascular volume (volume dependent) or to excessive activation of the renin-angiotensin system in relation to the state of sodium/volume balance (renin-dependent hypertension). This review focuses on the importance of less established mechanisms, such as increased activity of the sympathetic nervous system, increased endothelin production, decreased availability of endothelium-derived vasodilators and structural changes of the arteries, renal ischemia, and sleep apnea.
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PMID:Hypertension in renal parenchymal disease: why is it so resistant to treatment? 1652 45

Atherosclerotic renovascular disease is a combination of renal artery stenosis and renal ischemia. Blood pressure does not rise until the stenosis is 60% or greater. Disease of both large and small blood vessels is often accompanied by the loss of glomerular filtration rate. Activation of the renin-angiotensin-aldosterone system leads to vasoconstriction and salt retention. Risk factors for atherosclerotic renovascular disease include long-standing hypertension, diabetes, smoking and dyslipidemia. The prevalence of the condition in patients with hypertension resistant to two medications is 20%. As yet, there is no single ideal screening test or evidence-based recommended screening algorithm. Magnetic resonance angiography and computed tomography angiography are noninvasive and have high sensitivity and specificity, but also have high costs associated with them. The captopril renal scan has low sensitivity and specificity in people with renal disease (the population most likely to require the test). Doppler ultrasonography has high sensitivity and specificity in experienced hands, and the renal resistance index, which can easily be added to this test, can identify those with microvascular disease who may not benefit from revascularization. The best determinant of patient outcome is not the degree of renal artery stenosis but the degree of renal parenchymal disease. To date, renal revascularization has not been associated with improved renal survival compared with medical treatment alone. Today, the approach to atherosclerotic renovascular disease is determined by the patient's blood pressure and renal function; possibly, in the future, it will be determined by the result of the renal resistance index as part of a screening algorithm. If the blood pressure is uncontrollable or the renal function is deteriorating, the patient should be considered for renal revascularization initially, with a percutaneous endovascular stent. The management of hypertension involves the use of combinations of antihypertensive agents at doses sufficient to control blood pressure. Medical management also includes aggressive lipid-lowering therapy.
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PMID:Atherosclerotic renovascular disease. 1675 19

A case report in the journal Pediatric Nephrology describes a 15-month-old girl with the syndrome of hypertension and hyponatremia (HH syndrome) due to underlying unilateral renal artery stenosis. This syndrome is typically associated with hypokalemia and severe volume depletion and sometimes proteinuria, all of which, along with hypertension and hyponatremia, are usually corrected by resolution of the underlying renal ischemia. Gross and probably sudden activation of the renin-angiotensin system in response to renal ischemia is central to the pathophysiology although the cardiac atrial and B-type natriuretic peptides probably contribute also. Initial control of the severe hypertension may, in some cases, require careful volume repletion prior to introduction of blockade of the renin-angiotensin system in order to avoid first-dose hypotension, after which correction of the underlying renal ischemia is required. Whereas the syndrome has rarely been reported in children, it is possible that, as in adults, this reflects its lack of recognition by clinicians. The HH syndrome due to unilateral renal ischemia in children may be much more common than we think.
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PMID:Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children--more common than we think? 1677 97

Nonsteroidal antiinflammatory drugs (NSAIDs) have potentially important renal adverse effects. With regard to renal adverse effects there is no indication of significant differences between conventional NSAIDs and selective COX-2 inhibitors. Their nephrotoxicity has been well documented. Many of the renal abnormalities that are encountered as a result of NSAIDs use can be attributed to the inhibition of prostaglandins synthesis. The release of prostaglandins is particulary importent in high-risk patients, including patients with severe heart disease, liver disease, preexisting renal disease, elderly and patients with volume depletion. The common complication of NSAID use is retention of sodium and edema formation due to increased reabsorption of sodium and water in the loop of Henle and hyperkalemie due to diminished renin secretion. Nonsteroidal antiiflammatory drugs can induce two different forms of acute renal failure. Decreased prostaglandin synthesis can lead to reversible renal ischemia and hemodynamically-mediated acute renal failure. Second form of acute renal failure is acute interstitial nephritis. This type of interstitial nephritis is often accompanied by nephrotic syndrome due to minimal change disease. Nephrotic syndrome after NSAIDs treatments may be also associated with membranous nephropathy. Another complication of NSAIDs treatment is modest rise of systemic blood pressure in some hypertensive patients due to increase in renal and systemic vascular resistence. In patients consuming excessive amount of NSAIDs over a prolonged period of years papillary necrosis can occur. Exposure to large quantities of NSAIDs can probably induce in some patients chronic renal insufficiency.
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PMID:[Nonsteroidal antiinflammatory drugs and the kidney]. 1696 9


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