Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PGI2, or prostacyclin, and PGE2 are major derivatives of arachidonic acid. Arachidonic acid is converted by the cyclooxygenase enzyme to intermediate prostaglandin endoperoxides which are then enzymatically converted to PGI2 and PGE2 as well as to thromboxane A2 and PGF2 alpha. Aspirin and other nonsteroidal anti-inflammatory drugs inhibit the cyclooxygenase enzyme thereby reducing the amount of PGE2 and PGI2 produced. In the kidney, major stimuli of prostaglandin synthesis include vasoconstrictor hormones such as angiotensin II, vasopressin, endothelin and norepinephrine. Renal PGI2 and PGE2 synthesis is also increased after renal ischemia, immune injury to the kidney, and with renal parenchymal disease. Renal prostaglandin production also increases with severe arteriosclerotic cardiovascular disease, congestive heart failure, and severe hepatic disease. The increment of renal prostaglandin synthesis is important since PGI2 and PGE2 act as modulators of renal ischemia and vasoconstriction. The modulatory action leads to a negative feedback loop through which PGE2 and PGI2 and renal blood vessels in glomeruli reduce the vasoconstrictor action of the agonist, such as angiotensin II or norepinephrine. Nonsteroidal anti-inflammatory drugs can have nephrotoxic effects if they are used in clinical situations in which renal prostaglandin synthesis has increased compensatorily. In other words, the administration of indomethacin or other prostaglandin inhibitory drugs will reduce renal blood flow and glomerular filtration rate in patients with congestive heart failure, significant hepatic disease, or renal ischemia and vasoconstriction. PGI2 and PGE2 may have additional beneficial effects within the kidney in addition to being vasodilatory.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1989 Nov
PMID:Prostaglandin I2 and the kidney. 251 64

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The experimental discovery of the pathophysiological relationship between renal artery stenosis and arterial hypertension was historically reported (1934) before the clinical description of the disease in human patients (1950). The experimental model explains the relation between renal ischemia, renal endocrine activation, and morphological alterations of the homo and contralateral kidneys. In particular, the experimental model improves the understanding of the evolution of renovascular disease. In human patients, renal artery stenosis does not always lead to clinical disease. Because of the frequency of arterial hypertension, there is not always a clear relationship between hypertension and renal insufficiency or renal artery stenosis. Therefore a complete diagnosis of renal endocrine and exocrine function is needed to understand this relation before deciding on the therapeutic approach. This diagnosis is made by exploration of the renal renin-angiotensin axis, its pharmacological blockade and the response of the excretory function. This approach corresponds to the clinical description of the evolution of the disease; the peripheral and renal vein renin assays; the pressure and scintigraphic response to converting enzyme inhibition and renal morphological definition by echography and CT scan. This pathological approach permits a rational choice of the therapeutic indication: non-intervention, specific medical treatment, endovascular or surgical revascularization or nephrectomy.
J Mal Vasc 1994
PMID:[Is in depth diagnosis important in renal artery stenosis?]. 815 92

Atherosclerotic disease is the most common pathologic condition of renal artery stenosis, which typically compromises the ostium or the proximal 1-2 cm of renal arteries and is also usually present in the abdominal aorta. Fibromuscular dysplasia is the second most common cause of renal artery stenosis (RAS) which usually involves the distal two-third of the main renal artery with bed-like stenosis alternating with small fusiform or saccular aneurysms. Magnetic Resonance Angiography (MRA) was initially performed without contrast media injection using two- or three-dimensional Time-of-Flight (TOF) or Phase-Contrast (PC) techniques. Sensitivity and specificity of non-enhanced MRA in detection of proximal RAS are comprised between 53%-100% and 47%-97% respectively (table I). Main limitations of non-enhanced MRA are the long acquisition time, i.e. 5-8 min, the short field of view with lack of kidney visualization and major artifacts. Recent improvements allowed a three-dimensional acquisition during a single breath-hold (18-23 sec), associated to a bolus injection of a gadolinium chelate demonstrating a lack of nephrotoxicity. 3D gadolinium-enhanced ultrafast gradient-echo MRA techniques (3D enhanced-MRA) requires a precise technique. Firstly, kidney localization and morphologic imaging is performed before a 3D MRA data acquisition without injection (fig. 1). Secondly two successive 3D MRA sequences are performed synchronized with the gadolinium chelate bolus injection: the first acquisition corresponds to the arterial enhancement (fig. 4) and the second one to the venous enhancement. At last, a three-dimensional phase contrast could also be performed. After data acquisition, image post-processing is performed including image subtraction, maximum intensity projection (MIP) and reformation images of each renal artery, the abdominal aorta and its main branches (fig. 2, 3). The normal findings, pitfalls and anatomic variation are explained in detail. Particularly, when 3D enhanced MR angiography shows a normal artery, it is considered to be normal. It is also important to be aware of the existence of accessory or aberrant renal arteries that are well diagnosed by 3D enhanced MRA in 75% to 100% of the cases (fig. 2). 3D enhanced-MR angiography present several advantages in comparison to nonenhanced MRA: 1) a great field-of-view (30-36 cm) could be used allowing visualization of the abdominal aorta as well as its main branches; 2) the fast acquisition time allows an arterial imaging followed by a venous enhancement; 3) the kidneys are analyzed: kidney length, cortical thickness, corticomedullary differentiation and renal enhancement are well evaluated; 4) an accurate sensitivity and specificity in detection of proximal RAS comprised between 88%-100% and 71%-100% respectively (table II). Because a severe RAS (i.e. degree of stenosis > 50%) may cause renal ischemia leading to a blood pressure elevation that is often difficult to control with medical therapy, imaging has to assess the severity of RAS. MRA assessment of hemodynamic significance of RAS can be further refined by considering additional factors (fig. 4): arterial stop of signal, post stenotic dilatation, delayed renal enhancement and functional changes in the renal parenchyma (i.e. reduced kidney length and parenchymal thickness, loss of corticomedullary differentiation) (fig. 1). Precise evaluation of degree of stenosis requires the development of dedicated software such as MARACAS (MAgnetic Resonance Angiography Computer ASsisted analysis) software (fig. 5). In conclusions, 3D enhanced MRA allows an accurate diagnosis of proximal RAS, mainly due to atherosclerosis, without the risks associated with nephrotoxic contrast agents, ionizing radiation or arterial catheterization.
J Mal Vasc 2000 Dec
PMID:[Diagnosis of renal artery stenosis with magnetic resonance angiography and stenosis quantification]. 1114 91

We report a case of a 76-year-old woman with isolated unilateral Raynaud phenomenon revealing giant-cell arteritis with diffuse arterial lesions and bilateral renal artery stenosis. Doppler ultrasonography showed bilateral stenosis of the subclavian and axillary arteries. Angio-CT PET enlightened diffuse arterial lesions, mainly involving the aorta and the brachial and femoral arteries as well as bilateral renal ostial stenosis with right kidney ischemia. Diagnosis of giant-cell arteritis was made on the temporal artery biopsy. Corticosteroid therapy led to rapid clinical and radiological improvement. Clinical manifestations of giant-cell arteritis may be atypical. Diffuse arterial disease may exist in the absence of cephalic symptoms or significant inflammatory biological features. Ostial renal artery stenosis may induce potentially threatening renal ischemia.
J Mal Vasc 2015 May
PMID:[Unilateral isolated Raynaud's phenomenon leading to diagnosis of multifocal giant-cell arteritis complicated with renal ischemia]. 2579 Sep