Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic renal disease (IRD) is defined as a clinically important reduction in glomerular filtration rate or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents itself in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. Eleven to 14% of end-stage renal disease (ESRD) cases are attributable to chronic IRD. A high percentage of patients entering ESRD programs are hypertensive. Many patients with a presumed diagnosis of hypertensive nephrosclerosis actually have undiagnosed ischemic nephropathy as the etiology of their ESRD. It is important for the clinician to identify IRD, because IRD is a potentially reversible cause of chronic renal failure in a hypertensive patient. Atherosclerotic renal artery disease is common among patients with coronary artery disease and aortic and peripheral vascular disease. Atherosclerotic renal artery disease is a progressive disorder, and its progression is associated with loss of renal mass and functioning. A decrease in glomerular filtration rate sufficient to cause an elevation of the serum creatinine concentration requires injury to both kidneys. Consequently, IRD can arise from one of two main clinical situations: bilateral hemodynamically significant renal artery stenosis leading to bilateral renal ischemia; and hemodynamically significant renal artery stenosis in a solitary functioning kidney, or in a kidney that is providing the majority of a patient's glomerular filtration. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function, or a delay in progression to ESRD. There are six major clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed upon poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. Noninvasive testing modalities that have been used recently include the angiotensin converting enzyme inhibitor renal scan, duplex Doppler sonography, magnetic resonance angiography, and the spiral computed tomography. Treatment methods include percutaneous transluminal angioplasty, endovascular stenting, and surgical revascularization. The results of treatment for preservation of renal function have been encouraging, with stabilization or improvement in renal function observed in a significant proportion of cases.
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PMID:Ischemic renal disease: an emerging cause of chronic renal failure and end-stage renal disease. 943 40

Diabetes mellitus is associated with alterations in a number of key metabolic pathways. Despite theoretical concerns, clinically significant alterations in the pharmacokinetic properties of commonly prescribed drugs are relatively uncommon. Indeed, dose adjustment is rarely required in the setting of well controlled diabetes mellitus. However, significant alterations in drug handling may occur in the context of poor metabolic control or in the presence of complications such as nephropathy. Metformin use may be complicated by lactic acidosis. Fortunately, this is a rare occurrence providing that the agent is not used in circumstances in which it is contraindicated. Indeed, the risk of death from metformin-related lactic acidosis is similar in magnitude to the risk of death related to hypoglycaemia in sulphonylurea-treated patients. The novel hypoglycaemic agent troglitazone may be associated with abnormalities in liver function in approximately 2% of patients. Discontinuation of treatment is followed by normalisation of liver enzyme levels. Current prescribing information recommends frequent monitoring of liver function tests and immediate cessation of therapy if abnormalities develop. In addition to disturbances in intermediary metabolism, diabetes mellitus may also lead to chronic microvascular and marcovascular complications. Thus, in addition to the use of drugs for the control of blood glucose, patients with diabetes mellitus are likely to be prescribed medication for associated conditions such as cardiovascular disease. Such medication includes the ACE inhibitors which are contraindicated in patients with bilateral renal artery stenosis. This complication may be theoretically more common in patients with diabetes mellitus because of accelerated atherosclerosis. However, in clinical practice this is an uncommon occurrence in the absence of clinical features that should alert the treating clinician that an individual patient might be at high risk. Although caution should also be used with beta-blocker therapy in patients with diabetes mellitus, current evidence suggests that, like ACE inhibitors, these drugs may be particularly useful in this patient group.
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PMID:Drug administration in patients with diabetes mellitus. Safety considerations. 963 89

To test the utility of endoprosthetic treatment for ostial renal artery stenosis, and to examine blood pressure and its treatment, serum creatinine, and restenosis rate, 44 ostial renal stent placements were performed in 30 patients with concomitant coronary artery disease, arterial hypertension, and the indication for angiotensin converting enzyme (ACE) therapy. There was a marked decrease in systolic and diastolic blood pressure (163+/-30 to 145+/-17 and 93+/-18 to 83+/-10 mm Hg; P < 0.008) with a decrease in number of medication (3.2+/-0.9 to 2.8+/-1.0; P = 0.005). In 5 out of 8 patients not receiving an ACE inhibitor, this drug could be added. Serum creatinine changed from 1.46+/-0.7 mg/dl to 1.39+/-0.58 mg/dl (P = ns). Three patients showed restenosis (12.5%). Ostial stenting lowers blood pressure, decreases antihypertensive drugs and increases medication flexibility.
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PMID:Ostial renal artery stent placement for atherosclerotic renal artery stenosis in patients with coronary artery disease. 973 43

Losartan-induced acute renal failure may occur in patients sensitive to reduced renal plasma flow. Such patients include those with bilateral renal artery stenosis, severe congestive heart failure, and severe sodium and volume depletion because their renal function is often angiotensin-dependent. Theoretically, both ACE inhibitors and losartan could adversely affect renal function in such sensitive patients. The ELITE trial showed a 10.5% incidence of losartan-induced renal dysfunction in elderly patients with congestive heart failure with no known underlying renal dysfunction, an incidence identical to that for captopril. A review of the literature revealed no controlled trials that specifically address whether losartan can be used as an alternative in patients in whom renal dysfunction associated with losartan have been published and an additional case report was identified from a local adverse drug reaction monitoring program. There were two cases of patients who developed renal dysfunction while receiving ACE inhibitors and then losartan. We found only one published case in which losartan was used without deterioration in renal function in patients who developed renal dysfunction while taking an ACE inhibitor, although underreporting of such cases would be expected. There was one case of renal dysfunction with losartan after a lack of renal dysfunction while the patient was taking an ACE inhibitor. The remaining three reports are of patients who developed renal dysfunction while taking losartan with no antecedent ACE inhibitor use. All case reports describe renal deterioration that was reversible upon discontinuation of the inciting agent, whether an ACE inhibitor or losartan. All but two patients (personal communication, Barbara Cadario) had underlying renal pathology. Although there is a paucity of published literature and the clinical experience of some may suggest otherwise, there is currently no evidence (with the exception of 1 case report) to suggest that losartan is any better tolerated than ACE inhibitors from the standpoint of renal toxicity. Available evidence suggests that this is equally true in patients with and without underlying renal dysfunction. Furthermore, case reports suggest that, as with ACE inhibitors, losartan should be avoided in patients with bilateral renal artery stenosis and in patients with unilateral renal artery stenosis in a solitary kidney. In patients with underlying renal dysfunction, regardless of whether they tolerate ACE inhibitors, losartan may be used if deemed necessary. Renal function should be monitored and losartan should be stopped if evidence of renal dysfunction becomes apparent, since several case reports and a randomized trial suggest that losartan may cause the same negative renal effects as ACE inhibitors.
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PMID:Losartan as an alternative to ACE inhibitors in patients with renal dysfunction. 979 3

HLA-DNA typing using PCR-SSOP and PCR-DCP methods was performed in 85 patients with Takayasu arteritis and 492 healthy controls who had been typed for HLA by serological method. Frequencies of HLA-B52 (B*5201) and B39 (B*3901 and B*3902) were significantly increased in the patients. Frequency of HLA-DRB1*1502 was also increased but it was suggested to be a reflection of its linkage disequilibrium with B52. Association of HLA-B52 and B39 with seven clinical manifestations--pulmonary infarction, ischemic heart disease, aortic regurgitation, systemic hypertension, renal artery stenosis, cerebrovascular disease, and visual disturbance--in 132 HLA-typed patients with Takayasu arteritis was studied. In HLA-B52 positive TA patients, aortic regurgitation (vs B52(-)-B39(+), OR=3.8, P<0.05, vs B52(-)-B39(-), OR=5.49, P<0.001), ischemic heart disease (vs B52(-)-B39(+), OR=12.05, P<0.05, vs B52(-)-B39(-), OR=2.85, P<0.05), and pulmonary infarction (vs B52(-)-B39(+), OR=5.74, P<0.03) were found to be significantly prevalent. On the other hand, in HLA-B39 positive TA patients, frequency of renal artery stenosis was significantly increased (vs B52(+)-B39(-), OR=12.14, P<0.001, vs B52(-)-B39(-), OR=5.21, P<0.03). These observations have suggested that HLA-B52 molecule and B39 molecule would contribute to different clinical manifestations by binding different antigenic peptides to cause inflammations. Thus HLA-B molecule may play an important role in pathogenesis or determining clinical manifestations of Takayasu arteritis.
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PMID:Association of clinical manifestations with HLA-B alleles in Takayasu arteritis. 995 11

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.
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PMID:[Antihypertensive therapy in diabetes mellitus]. 1006 31

Recent advances have increased the value of radionuclide renography in evaluating the patient with suspected disease of the genitourinary tract. The use of the consensus process to help standardize procedures and recommend interpretative criteria provides guidance for the nuclear medicine practitioner, serves as a basis to improve the standard of practice, and facilitates pooling of data from different centers. This review draws on the consensus criteria to present a personal approach to radionuclide renography with a particular emphasis on diuresis renography and the detection of renovascular hypertension. Patients are encouraged to come well hydrated and void immediately prior to the study. Our standard radiopharmaceutical is 99mTc mercaptoacetyltriglycine (MAG3). Routine quantitative indices include a MAG3 clearance, whole kidney and cortical (parenchymal) regions of interest, measurements of relative uptake, time to peak height (Tmax), 20 min/max count ratio, residual urine volume and a T(1/2) in patients undergoing diuresis renography. A 1-minute image of the injection site is obtained at the conclusion of the study to check for infiltration because infiltration can invalidate a plasma sample clearance and alter the renogram curve. A postvoid image of the kidneys and bladder is obtained to calculate residual urine volume and to better evaluate drainage from the collecting system. In patients undergoing diuresis renography, the T(1/2) is calculated using a region of interest around the activity in the dilated collecting system. A prolonged T(1/2), however, should never be the sole criterion for diagnosing the presence of obstruction; the T(1/2) must be interpreted in the context of the sequential images, total and individual kidney function, other quantitative indices and available diagnostic studies. The goal of ACE inhibitor renography is to detect renovascular hypertension, not renal artery stenosis. Patients with a positive study have a high probability of cure or amelioration of the hypertension following revascularization. In patients with azotemia or in patients with a small, poorly functioning kidney, the test result is often indeterminate (intermediate probability) with an abnormal baseline study that does not change following ACE inhibition. In patients with normal renal function, the test is highly accurate. To avoid unrealistic expectations on the part of the referring physician, it is often helpful to explain the likely differences in test results in these two-patient populations prior to the study.
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PMID:Radionuclide renography: a personal approach. 1032 24

Comprehensive evaluation of renal transplants has been important in differential diagnosis of medical and surgical complications in the early post-transplantation period and in the long-term follow-up. If performed well, it yields excellent functional and good anatomic information about the graft that can be effectively used in the patient. That includes selection of patients for biopsy and for various drug regimens. This is true especially in patients with anuric acute tubular necrosis (ATN) and in patients with developing chronic rejection. Improving indices of renal function (effective renal plasma flow, uptake of tubular tracers) can indicate resolution of tubular injury (ATN) while there is still no improvement in plasma creatinine. In patients with chronic rejection, plasma creatinine increases only after approximately 30% of renal function is lost due to graft fibrosis. Early recognition of this condition could permit treatment and delay of retransplantation. The protocol recommended at the Copenhagen meeting includes a flow study, scintigram of the kidneys, prevoid and postvoid bladder image, injection site image (quality control), time/activity curves of the graft and bladder, and quantitative data of perfusion, function, and tracer transit. The flow study obtained during the initial transit of the bolus through the graft could be performed either with 99mTc mercaptoacetyltriglycine, or 99mTc diethylenetriaminepentaacetate (DTPA). Quantitative analysis of perfusion facilitates interpretation of the study during the early post-transplantation period. ATN, common in cadaver transplants, typically shows adequate perfusion. The function phase should include images and time/activity curves. Images alone are insufficient. Quantitative data such as clearance or other indices of function and indices of tracer transit are essential for correct interpretation of the results. Normal images and normal graft function reliably exclude clinically important complications. A single scintigram demonstrating prolonged tracer transit with decreased function cannot separate acute rejection and ATN. On serial studies, decline in function and poor perfusion are indicative of acute rejection. A normally appearing scintigram without cortical retention, but with low function, is consistent with chronic rejection. Pharmacological intervention to exclude obstruction (diuretic renogram) or hemodynamically significant renal artery stenosis (angiotensin converting enzyme challenge) should be used whenever indicated.
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PMID:Report of the Radionuclides in Nephrourology Committee for evaluation of transplanted kidney (review of techniques). 1032 28

Assessment of intrarenal doppler signals is of particular importance in screening for renal artery stenosis. We studied the effect of acute ACE-inhibition (1,25 mg enalaprilate i.v.) on intrarenal resistive indices in 10 hypertensive patients with unilateral renal artery stenosis versus 10 patients with essential hypertension. Any changes limited to poststenotic vessels could possibly improve the diagnostic value of duplex sonography. After ACE-inhibition a significant fall of the intrarenal Resistive Index occurred in both patient groups. In cases of unilateral renal artery stenosis we saw a tendency to an increased side difference of the Resistive Index due to a greater fall on the poststenotic side. Therefore a clear advantage of duplex scanning after acute ACE-inhibition due to a limited effect of enalaprilate on poststenotic vessels was not found. The results suggest that the vascular resistance and not only the degree of renal artery stenosis is of significance for the characteristics of the doppler signal.
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PMID:Effect of acute intravenous ace-inhibition on the intrarenal doppler flow characteristics in hypertensive patients with and without unilateral renal artery stenosis. 1097 62

Atherosclerotic renal artery stenosis typically occurs in high-risk patients with coexistent vascular disease elsewhere. Patients with atherosclerotic renal artery stenosis may develop progressive renal failure but have a much higher risk of dying of stroke or myocardial infarction than of progressing to endstage renal disease. Recent controlled trials comparing medication to revascularization have shown that only a minority of such patients can expect hypertension cure, whereas trials designed to document the ability of revascularization to prevent progressive renal failure are not yet available. Revascularization should be undertaken in patients with atherosclerotic renal artery stenosis and resistant hypertension or heart failure, and probably in those with rapidly deteriorating renal function or an increase in plasma creatinine levels during angiotensin converting enzyme inhibition. With or without revascularization, medical therapy using antihypertensive agents, statins, and aspirin is necessary in almost all cases.
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PMID:Atherosclerotic renal artery stenosis: surgery, percutaneous transluminal angioplasty, or medical therapy? 1099 25


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