PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24362637-2 2014 Of 332 patients who received an ACE inhibitor as inpatients at our institution from 1 January 2010 to 1 July 2012, 20 patients had a doubling of serum creatinine (SCr) within 72 h after initiation or dose uptitration of an ACE inhibitor (AKI group). Creatinine 151-161 angiotensin I converting enzyme Homo sapiens 32-35 25232564-0 2014 Rates and predictors of ACE inhibitor discontinuation subsequent to elevated serum creatinine: a retrospective cohort study. Creatinine 83-93 angiotensin I converting enzyme Homo sapiens 24-27 25232564-1 2014 OBJECTIVES: ACE inhibitors (ACEI) are underutilised despite cardiovascular benefits, in part due to concerns of known transient elevations in serum creatinine (SCr) after initiation. Creatinine 148-158 angiotensin I converting enzyme Homo sapiens 12-15 22739771-8 2013 ACE rs4267385 was associated with older clinical coronary disease onset (P=0.008) and hypertension (P=0.013) onset, increased plasma creatinine (P=0.01), yet greater mortality (P=0.044). Creatinine 133-143 angiotensin I converting enzyme Homo sapiens 0-3 24157497-7 2013 Compared with placebo, only ACE inhibitors significantly reduced the doubling of serum creatinine levels (odds ratio 0.58, 95% credible interval 0.32 to 0.90), and only beta blockers showed a significant difference in mortality (odds ratio 7.13, 95% credible interval 1.37 to 41.39). Creatinine 87-97 angiotensin I converting enzyme Homo sapiens 28-31 21317676-16 2011 Logistic regression identified cyanosis, coadministration of furosemide, and baseline estimated creatinine clearance as independent risk factors for any degree of angiotensin-converting enzyme inhibitor-associated acute kidney injury (p < .05). Creatinine 96-106 angiotensin I converting enzyme Homo sapiens 163-192 22982912-5 2012 A significant correlation was found between the ACE mRNA gene expression and the mean blood pressure, serum creatinine, blood urea nitrogen and 24-h urinary protein. Creatinine 108-118 angiotensin I converting enzyme Homo sapiens 48-51 26105881-7 2013 In pregnancy, plasma ACE levels were related to protein/creatinine (r=0.29, P=0.036, n=54). Creatinine 56-66 angiotensin I converting enzyme Homo sapiens 21-24 21976404-11 2012 Significant positive correlations were found between serum ACE level and serum creatinine and 24 h proteinuria (p = 0.03, 0.009, respectively). Creatinine 79-89 angiotensin I converting enzyme Homo sapiens 59-62 21103678-6 2010 Considering admission SOFA score and trend of renal function (measured by daily renal SOFA scores, with daily measure of serum creatinine and diuresis), we hypothesize that ACE polymorphisms could influence in the trend of renal function in ICU patients. Creatinine 127-137 angiotensin I converting enzyme Homo sapiens 173-176 22783291-4 2011 Major reasons for non-use of ACE inhibitors/ARBs were hyperkalemia and elevated serum creatinine level. Creatinine 86-96 angiotensin I converting enzyme Homo sapiens 29-32 20104936-5 2010 The reasons for this include physician concerns regarding patient age and limited life expectancy and potential complications of ACE inhibitor or ARB use, specifically an increase in creatinine levels and hyperkalaemia. Creatinine 183-193 angiotensin I converting enzyme Homo sapiens 129-132 17903694-10 2007 Creatinine clearance also interacted with the relationship between the ACE I/D polymorphism and LVH (beta, 0.12; P = .037), although less strongly, and the other way around. Creatinine 0-10 angiotensin I converting enzyme Homo sapiens 71-74 23148146-7 2010 A modest decrease in estimated glomerular filtration rate (eGFR) and increase in creatinine often occurs with ACE inhibitors or ARBs. Creatinine 81-91 angiotensin I converting enzyme Homo sapiens 110-113 18284535-10 2008 At the 4-year follow-up, the magnitude of declines of the above four renal parameters was significantly higher in subjects with the ACE D allele than in the non-D-allele carriers (P = .01, .01, .04, and .01 for creatinine, CG CrCl, Jelliffe CrCl, and MDRD GFR, respectively). Creatinine 211-221 angiotensin I converting enzyme Homo sapiens 132-135 18371537-10 2008 ACE/ACE2 ratio correlated positively with values for mean blood pressure, fasting blood glucose, serum creatinine, proteinuria, and hemoglobin A(1c) and inversely with estimated glomerular filtration rate (P < 0.001). Creatinine 103-113 angiotensin I converting enzyme Homo sapiens 0-3 18068386-10 2008 Among people with an abnormal albumin/creatinine ratio (11%), 59% received an ACE inhibitor/ARB. Creatinine 38-48 angiotensin I converting enzyme Homo sapiens 78-81 16685140-5 2006 Serum creatinine level increased from 1.34 +/- 0.20 to 1.53 +/- 0.27 mg/dl in the ACE inhibitor group and from 1.33 +/- 0.18 to 1.45 +/- 0.19 mg/dl in the control group (p < 0.001). Creatinine 6-16 angiotensin I converting enzyme Homo sapiens 82-85 17066218-5 2006 The usual laboratory tests must include calculation of the creatinine clearance, which is indispensable for dosage adjustment of certain drugs (ACE inhibitors, digoxin, spironolactone). Creatinine 59-69 angiotensin I converting enzyme Homo sapiens 144-147 18035185-11 2007 In hypertensive patients with type 2 diabetes and microalbuminuria, combination ACE-inhibitor/ARB therapy resulted in better BP control than either agent alone (mean difference, 11.2 mm Hg systolic [P = 0.002], 5.9 mm Hg diastolic [P = 0.003]), as well as greater reductions in microalbuminuria (mean difference in albumin:creatinine ratio, 34%; P = 0.04). Creatinine 323-333 angiotensin I converting enzyme Homo sapiens 80-83 17699280-10 2006 The serum creatinine concentration increased from 3.02 +/- 0.27 to 3.38 +/- 0.49 mg/dl (candesartan plus ACE inhibitor group) versus 3.00 +/- 0.37 to 4.48 +/- 0.57 mg/dl (ACE inhibitor group; P < 0.01) at year 3. Creatinine 10-20 angiotensin I converting enzyme Homo sapiens 171-174 16544182-5 2006 After the induction of ACE-I in this patient, the rate of regression of renal function was significantly reduced and his serum creatinine was maintained at almost the same level for 18 months. Creatinine 127-137 angiotensin I converting enzyme Homo sapiens 23-26 16194413-0 2005 [Can angiotensin-converting enzyme inhibitor be used in chronic kidney disease patients with serum creatinine level greater than 266 micromol/L?]. Creatinine 99-109 angiotensin I converting enzyme Homo sapiens 5-34 16338452-7 2005 FINDINGS: Comparisons of ACE inhibitors or ARBs with other antihypertensive drugs yielded a relative risk of 0.71 (95% CI 0.49-1.04) for doubling of creatinine and a small benefit on end-stage renal disease (relative risk 0.87, 0.75-0.99). Creatinine 149-159 angiotensin I converting enzyme Homo sapiens 25-28 16245436-9 2005 This should probably be undertaken in RAS patients with rapidly deteriorating renal function, refractory hypertension and in whom plasma creatinine concentration has increased by >20% during one month long administration of angiotensin-converting enzyme inhibitor. Creatinine 137-147 angiotensin I converting enzyme Homo sapiens 227-256 15848522-10 2005 Significantly higher creatinine concentrations were found among recipients with II genotype compared to the combined group of ID and DD among patients not treated with ACE inhibitors, but not among those receiving ACE I after kidney transplantation. Creatinine 21-31 angiotensin I converting enzyme Homo sapiens 168-171 15482412-8 2004 Patients with creatinine > or = 1.6 mg dL(-1) were likely to discontinue ACE inhibitors because of renal dysfunction (HR: 4.7; 95% CI: 1.5-12.7) and hyperkalaemia (HR: 10.9; 95% CI: 3.1-39.0). Creatinine 14-24 angiotensin I converting enzyme Homo sapiens 76-79 16362602-11 2005 In 10 patients with a rise in serum creatinine on recent introduction of ACE inhibition, 2 had evidence of RAS on renal arteriography. Creatinine 36-46 angiotensin I converting enzyme Homo sapiens 73-76 16078597-5 2005 After administration of ACE inhibitors in doses lowering arterial pressure not higher than 130/80 mm Hg and statins reducing serum cholesterol nitric residues stopped accumulating while serum creatinine went down after 5 months of the combined treatment. Creatinine 192-202 angiotensin I converting enzyme Homo sapiens 24-27 15489090-8 2004 Although ACE inhibitor users with creatinine clearances > or =60 ml/min had lower 12-month mortality (OR 0.72, 95% CI 0.48 to 0.99), ACE inhibitor users with clearances <60 ml/min did not (OR 1.21, 95% CI 0.97 to 1.51). Creatinine 34-44 angiotensin I converting enzyme Homo sapiens 9-12 15369420-12 2004 However, a combination of the ARB plus the ACE inhibitor produced both a significant reduction in urinary protein excretion beyond that seen with either agent alone and a significantly greater protection against progression to doubling of serum creatinine or ESRD. Creatinine 245-255 angiotensin I converting enzyme Homo sapiens 43-46 15168387-7 2004 Conversely, serum creatinine levels decreased significantly faster in patients administered an ACE inhibitor/ATII blocker than in those without therapy (P < 0.01). Creatinine 18-28 angiotensin I converting enzyme Homo sapiens 95-98 15289383-9 2004 ACE inhibitor prescription was associated with lower crude 1-year mortality (33.0% versus 42.1%, P<0.001), lower risk of death after adjustment (RR 0.86, 95% CI 0.82 to 0.90), and lower mortality regardless of patient gender, age, race, or serum creatinine level. Creatinine 249-259 angiotensin I converting enzyme Homo sapiens 0-3 14673630-5 2004 In children with chronic allograft dysfunction ( n=8), treatment with ACE-I stabilized graft function, with improvement in creatinine clearance in 50% ( p<0.01). Creatinine 123-133 angiotensin I converting enzyme Homo sapiens 70-73 15198481-10 2004 In patients with severe ARAS, ACE inhibitor use, calcium channel blocker use and diuretic use were shown to correlate significantly with serum creatinine levels after controlling for potential confounding factors. Creatinine 143-153 angiotensin I converting enzyme Homo sapiens 30-33 15017529-6 2004 A strong association exists between acute increases in serum creatinine of up to 30% to 35% after initiating ACE inhibitor therapy and long-term preservation of renal function. Creatinine 61-71 angiotensin I converting enzyme Homo sapiens 109-112 15017529-9 2004 Thus, withdrawal of an ACE inhibitor in such patients should occur only when the rise in creatinine exceeds this threshold over a shorter period of time or hyperkalemia develops, ie, serum potassium level of 5.6 mmol/L or greater. Creatinine 89-99 angiotensin I converting enzyme Homo sapiens 23-26 12753883-1 2003 Many clinicians are uncomfortable about using angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (AT(1)-blockers) to treat patients with renal disease because of concerns about increasing serum creatinine levels. Creatinine 233-243 angiotensin I converting enzyme Homo sapiens 46-75 14569094-4 2003 In a Cox proportional hazards model corrected for other risk factors, the D allele (ACE/ID) was associated with time to doubling of s-creatinine/ESRD (rate ratio, 1.81 per allele; 95% confidence interval, 1.09 to 3.03; P = 0.02). Creatinine 134-144 angiotensin I converting enzyme Homo sapiens 84-87 14579936-7 2003 CONCLUSION: Withdrawal of ACE inhibitor causes the deterioration of renal function in patients with the II or DI genotypes, high proteinuria after the withdrawal, and high serum creatinine level at the withdrawal, which probably causes the rebound increase in serum ACE activity. Creatinine 178-188 angiotensin I converting enzyme Homo sapiens 26-29 14579936-7 2003 CONCLUSION: Withdrawal of ACE inhibitor causes the deterioration of renal function in patients with the II or DI genotypes, high proteinuria after the withdrawal, and high serum creatinine level at the withdrawal, which probably causes the rebound increase in serum ACE activity. Creatinine 178-188 angiotensin I converting enzyme Homo sapiens 266-269 12753883-1 2003 Many clinicians are uncomfortable about using angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (AT(1)-blockers) to treat patients with renal disease because of concerns about increasing serum creatinine levels. Creatinine 233-243 angiotensin I converting enzyme Homo sapiens 77-80 12704481-7 2003 Multivariate predictors of ACE inhibitor usage were serum creatinine, male sex, peripheral edema and increasing serum glucose. Creatinine 58-68 angiotensin I converting enzyme Homo sapiens 27-30 12133029-1 2002 PURPOSE: To determine the association between the early rise in serum creatinine levels associated with the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) and the long-term renoprotective properties of these drugs in patients with chronic renal insufficiency. Creatinine 70-80 angiotensin I converting enzyme Homo sapiens 146-149 12610747-5 2003 RESULTS: Among patients receiving ACE inhibitors, serum creatinine levels increased in 22% of participants who were dispensed calcium antagonists, and in 31% of other patients (P=0.005). Creatinine 56-66 angiotensin I converting enzyme Homo sapiens 34-37 12133029-4 2002 In fact, patients who have the most advanced renal insufficiency at baseline are the ones who show the maximum slowing of the disease progression, but these patients are also more likely to show an early rise in serum creatinine levels after ACE inhibitor therapy. Creatinine 218-228 angiotensin I converting enzyme Homo sapiens 242-245 12133029-26 2002 Patients with chronic renal insufficiency (serum creatinine>1.5 mg/dL) who received therapy with ACE inhibitors had about a five times higher risk of developing hyperkalemia than those with normal renal function, whereas presence of heart failure increased the risk of hyperkalemia by about three times over those without heart failure. Creatinine 49-59 angiotensin I converting enzyme Homo sapiens 100-103 12133029-7 2002 One of the main reasons for this underutilization of ACE inhibitors in patients with heart failure is the underlying renal insufficiency or the rise in serum creatinine level after initiation of therapy with an ACE inhibitor. Creatinine 158-168 angiotensin I converting enzyme Homo sapiens 53-56 12133029-28 2002 CONCLUSION: The authors conclude that, in patients with renal insufficiency (serum creatinine>1.4 mg/dL) treated with ACE inhibitors, there is a strong association between early (within the first 2 months) and moderate (not exceeding 30% over baseline) rise in serum creatinine and slowing of the renal disease progression in the long run. Creatinine 83-93 angiotensin I converting enzyme Homo sapiens 121-124 12133029-28 2002 CONCLUSION: The authors conclude that, in patients with renal insufficiency (serum creatinine>1.4 mg/dL) treated with ACE inhibitors, there is a strong association between early (within the first 2 months) and moderate (not exceeding 30% over baseline) rise in serum creatinine and slowing of the renal disease progression in the long run. Creatinine 270-280 angiotensin I converting enzyme Homo sapiens 121-124 12133029-7 2002 One of the main reasons for this underutilization of ACE inhibitors in patients with heart failure is the underlying renal insufficiency or the rise in serum creatinine level after initiation of therapy with an ACE inhibitor. Creatinine 158-168 angiotensin I converting enzyme Homo sapiens 211-214 12133029-17 2002 RESULTS: Patients with preexisting chronic renal insufficiency who achieved their blood pressure control goals were likely to demonstrate an early rise in serum creatinine levels, approximately 25% above the baseline (approximately 1.7 mg/dL) after initiation of ACE inhibitor or ARB therapy. Creatinine 161-171 angiotensin I converting enzyme Homo sapiens 263-266 12133029-25 2002 Serum creatinine levels in these patients sharply increased (by approximately 75% above baseline) in the 2 weeks after the initiation of therapy with an ACE inhibitor, followed by an even sharper increase (another approximately 150%) during the subsequent 2 weeks. Creatinine 6-16 angiotensin I converting enzyme Homo sapiens 153-156 11532109-6 2001 The Cox proportional hazards analysis was used to assess the relationship between changes in urine protein excretion during follow-up and the effect of ACE inhibitors on the time to doubling of baseline serum creatinine values or onset of end-stage renal disease. Creatinine 209-219 angiotensin I converting enzyme Homo sapiens 152-155 11687678-7 2001 After injection of the ACE inhibitor, patients with elevated creatinine levels showed low renal medullary enhancement regardless of the presence of renal artery stenosis (RAS). Creatinine 61-71 angiotensin I converting enzyme Homo sapiens 23-26 11687678-8 2001 However, in patients with creatinine less than 2 mg/dL, medullary enhancement ratios after injection of the ACE inhibitor were consistently lower in patients with RAS of 50% or greater than in those without stenosis (P = .02 to .08). Creatinine 26-36 angiotensin I converting enzyme Homo sapiens 108-111 12003699-7 2002 Therefore, as of this writing, all patients with type 2 diabetes and no evidence of nephropathy, ie, proteinuria and an elevated creatinine > 1.5 mg/dL, should be placed on an ACE inhibitor for cardiovascular risk reduction. Creatinine 129-139 angiotensin I converting enzyme Homo sapiens 179-182 11544438-4 2001 RESULTS: ACE (D) and AGT (A/A) genotypes were associated with poorer chronic renal transplant function and more rapid chronic progression, defined as an increase of serum creatinine level with time. Creatinine 171-181 angiotensin I converting enzyme Homo sapiens 9-12 11453706-8 2001 After adjustment for patient and study characteristics at baseline and changes in systolic blood pressure and urinary protein excretion during follow-up, relative risks in the ACE inhibitor group were 0.69 (CI, 0.51 to 0.94) for end-stage renal disease and 0.70 (CI, 0.55 to 0.88) for the combined outcome of doubling of the baseline serum creatinine concentration or end-stage renal disease. Creatinine 340-350 angiotensin I converting enzyme Homo sapiens 176-179 11431175-8 2001 Multivariate analysis using age; sex; duration of diabetes; glycemic, blood pressure, and lipid level control; serum creatinine level; and presence of the ACE D allele showed that presence of the D allele (P = 0.03; odds ratio, 1.8; confidence interval, 1.1 to 3.1) and serum creatinine level (P = 0.0007) were independent risk factors for macroangiopathy. Creatinine 276-286 angiotensin I converting enzyme Homo sapiens 155-158 11422818-6 2001 After renal Tx, the ACE II genotype (p = 0.024, chi-square test) and the presence of the I allele (p=0.033, chi-square test) were associated with a favorable slope of 1/creatinine. Creatinine 169-179 angiotensin I converting enzyme Homo sapiens 20-23 10999979-9 2000 In stratified models, the receipt of an ACE inhibitor was associated with a 37% (16%-52%) lower mortality for patients who had poor renal function (serum creatinine level,<265 micromol/L [<3 mg/dL]) and a 16% (8%-23%) lower mortality for patients who had better renal function. Creatinine 154-164 angiotensin I converting enzyme Homo sapiens 40-43 11431902-5 2001 Four months after the administration of an ACE-inhibitor, the urinary protein decreased to 0.04 g while the serum creatinine level increased to 1.5 mg/dl. Creatinine 114-124 angiotensin I converting enzyme Homo sapiens 43-46 11325074-6 2001 Systolic and diastolic blood pressure were significantly reduced from 150/90 +/- 15/11 mmHg to 130/75 +/- 11/9 mmHg (ACE) and the levels of serum creatinine were increased significantly from 1.8 +/- 0.3 to 2.0 +/- 0.4 mg/dl (ACE). Creatinine 146-156 angiotensin I converting enzyme Homo sapiens 225-228 10999979-12 2000 Use of aspirin therapy may attenuate the benefit of ACE inhibitors in patients with high serum creatinine levels; therefore, further studies are needed to determine whether treatment with aspirin, alternative antiplatelet agents, or anticoagulation is indicated for these patients. Creatinine 95-105 angiotensin I converting enzyme Homo sapiens 52-55 10739792-6 2000 In seven trials of subjects with overt proteinuria and renal insufficiency from a variety of causes (30% diabetes, 70% nondiabetes), the relative risk for doubling of serum creatinine concentration or developing end-stage renal disease was 0.60 (95% CI, 0.49 to 0.73) for individuals treated with an ACE inhibitor compared with placebo. Creatinine 173-183 angiotensin I converting enzyme Homo sapiens 300-303 10724055-0 2000 Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern? Creatinine 71-81 angiotensin I converting enzyme Homo sapiens 0-29 10078892-10 1999 By comparison, ACE inhibition conferred meaningful clinical benefit among those whose creatinine was < or = 1.9 mg/dL. Creatinine 86-96 angiotensin I converting enzyme Homo sapiens 15-18 11229627-5 2000 Our study suggests that the addition of verapamil to ACE inhibitors can reverse ACE-induced increase in creatinine levels in elderly hypertensive patients in whom this side effect is observed. Creatinine 104-114 angiotensin I converting enzyme Homo sapiens 53-56 11229627-5 2000 Our study suggests that the addition of verapamil to ACE inhibitors can reverse ACE-induced increase in creatinine levels in elderly hypertensive patients in whom this side effect is observed. Creatinine 104-114 angiotensin I converting enzyme Homo sapiens 80-83 10539812-6 1999 Family physicians expressed more concern over the risks of ACE inhibitors in patients with blood pressure of 100/70 mm Hg or serum creatinine of 2.0 mg/dL and were less likely to prescribe an ACE inhibitor in these settings. Creatinine 131-141 angiotensin I converting enzyme Homo sapiens 59-62 10951856-0 1999 [Effect of ACE-inhibitors on changes in creatinine in the blood-- introduction]. Creatinine 40-50 angiotensin I converting enzyme Homo sapiens 11-14 10437863-1 1999 BACKGROUND: Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study has already shown that in patients with chronic nephropathies and proteinuria of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition reduced the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) found in controls on placebo plus conventional antihypertensives. Creatinine 328-338 angiotensin I converting enzyme Homo sapiens 178-207 10437863-1 1999 BACKGROUND: Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study has already shown that in patients with chronic nephropathies and proteinuria of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition reduced the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) found in controls on placebo plus conventional antihypertensives. Creatinine 328-338 angiotensin I converting enzyme Homo sapiens 209-212 10619572-3 1999 The ability of ACE inhibitors to stabilize renal function is not attenuated by more severe renal insufficiency, but greater caution with these drugs is necessary, as there may be drug accumulation and a greater propensity for an increase in serum potassium and creatinine levels. Creatinine 261-271 angiotensin I converting enzyme Homo sapiens 15-18 9649959-12 1998 A specific renal protective effect of ACE-inhibitors in diabetic nephropathy has been demonstrated in IDDM patients with moderately reduced kidney function (s-creatinine > 133 mumol/l) while the data conflict with NIDDM patients. Creatinine 159-169 angiotensin I converting enzyme Homo sapiens 38-41 9551410-6 1998 Angiotensin converting enzyme inhibition induced a significant reduction in MABP, albuminuria and kidney function in all three groups (II/ID/DD; P < 0.05): (1) MABP (mean +/- SD) 12 +/- 7/5 +/- 7/8 +/- 9 mm Hg (ANOVA, P = 0.02); (2) albuminuria [mean (95% CI)] 61 (34 to 77)/22 (3 to 37)/31 (13 to 46) %, (ANOVA, P < 0.01); and (3) increasing serum creatinine [mean (95% CI)] 8 (4 to 12)/9 (3 to 16)/8 (0 to 16) % (ANOVA, NS), respectively. Creatinine 355-365 angiotensin I converting enzyme Homo sapiens 0-29 10100072-7 1999 Although serum angiotensin converting enzyme activity was higher in the deletion/deletion than in the other two genotypes (insertion/insertion 9.7 +/- 0.7, insertion/deletion 10.7 +/- 0.9, deletion/deletion 14.0 +/- 2.4 IU/I; P < 0.05), other factors of the renin-angiotensin system, including blood pressure and serum creatinine levels, were not different among the three groups. Creatinine 322-332 angiotensin I converting enzyme Homo sapiens 15-44 9148377-4 1997 In the recently completed trial of angiotensin converting enzyme (ACE) inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death independent of their effect on systemic blood pressure. Creatinine 201-211 angiotensin I converting enzyme Homo sapiens 35-64 9491949-6 1998 Multivariate analysis suggested no change in the prescribing biases previously observed; ACE inhibitor use was related to lower ejection fraction, lower serum creatinine, documentation of left ventricular systolic function, younger patient age, prescription of any diuretic drug, and nonprescription of alternate vasodilators and calcium blockers. Creatinine 159-169 angiotensin I converting enzyme Homo sapiens 89-92 9425858-9 1997 On multivariate logistic regression modeling, the following key clinical variables were positively related to the prescription of ACE inhibitors: low ejection fraction, dyspnea and orthopnea, normal creatinine levels, high diastolic blood pressure, cardiomegaly, and increasing age. Creatinine 199-209 angiotensin I converting enzyme Homo sapiens 130-133 9211022-3 1997 Relatively few patients with left ventricular systolic dysfunction and a serum creatinine > or = 2 mg/dl receive an ACE inhibitor in clinical practice. Creatinine 79-89 angiotensin I converting enzyme Homo sapiens 119-122 9148377-4 1997 In the recently completed trial of angiotensin converting enzyme (ACE) inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death independent of their effect on systemic blood pressure. Creatinine 201-211 angiotensin I converting enzyme Homo sapiens 66-69 9148377-4 1997 In the recently completed trial of angiotensin converting enzyme (ACE) inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death independent of their effect on systemic blood pressure. Creatinine 201-211 angiotensin I converting enzyme Homo sapiens 107-110 9040425-1 1997 Normalization of blood pressure--and use of an ACE inhibitor or AT1-receptor blocker for patients with abnormal albumin or creatinine levels--can prevent or significantly slow the rate of progression toward end-stage renal disease. Creatinine 123-133 angiotensin I converting enzyme Homo sapiens 47-50 34294186-9 2022 Angiotensin-converting enzyme inhibitors were used by 48% of patients and their use was associated with creatinine clearance <90 ml/min (p = 0.007), as was Fontan completion at an older age (p = 0.007). Creatinine 104-114 angiotensin I converting enzyme Homo sapiens 0-29 8800625-8 1996 The available results from large-scale studies suggest that abnormalities in kidney function (namely an increase in serum creatinine) are observed in 0.9 to 2.4% of patients with MI who, nevertheless, experience some benefit from treatment with ACE inhibitors. Creatinine 122-132 angiotensin I converting enzyme Homo sapiens 245-248 8659493-3 1996 We observed three patients with hereditary glomerulonephritis with plasma creatinine concentrations ranging from 1.7 to 2.0 mg/dL who were treated with angiotensin-converting enzyme inhibitors (ACEIs) for 3.5 to 6 years. Creatinine 74-84 angiotensin I converting enzyme Homo sapiens 152-181 8659493-4 1996 Angiotensin-converting enzyme inhibitor therapy was accompanied by a decrease in the mean arterial pressure (MAP) from 115 +/- 10 mm Hg to 93 +/- 2 mm Hg (+/- SD), a decrease in the mean urinary protein/creatinine ratio from 2,910 +/- 1,720 mg/g to 391 +/- 355 mg/g, and stabilization of the decline of creatinine clearance with time in two of the three patients. Creatinine 203-213 angiotensin I converting enzyme Homo sapiens 0-29 8659493-4 1996 Angiotensin-converting enzyme inhibitor therapy was accompanied by a decrease in the mean arterial pressure (MAP) from 115 +/- 10 mm Hg to 93 +/- 2 mm Hg (+/- SD), a decrease in the mean urinary protein/creatinine ratio from 2,910 +/- 1,720 mg/g to 391 +/- 355 mg/g, and stabilization of the decline of creatinine clearance with time in two of the three patients. Creatinine 303-313 angiotensin I converting enzyme Homo sapiens 0-29 8452322-0 1993 Long-term stabilizing effect of angiotensin-converting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type II diabetic patients. Creatinine 83-93 angiotensin I converting enzyme Homo sapiens 32-61 8452322-16 1993 CONCLUSIONS: In normotensive patients with diabetes mellitus type II, the institution of angiotensin-converting enzyme inhibition during early stages of diabetic nephropathy results in long-term stabilization of plasma creatinine levels and of the degree of urinary loss of albumin. Creatinine 219-229 angiotensin I converting enzyme Homo sapiens 89-118 1893640-5 1991 Side effects believed to be related to the pharmacologic action of ACE inhibitors as a class include symptomatic hypotension, which occurred at a relatively low rate with benazepril, and hyperkalemia and elevation of serum creatinine, which occurred to the same extent with benazepril as has been noted with other ACE inhibitors. Creatinine 223-233 angiotensin I converting enzyme Homo sapiens 67-70 1706805-7 1990 Nevertheless, there was a significant correlation between the decline in arterial pressure and fall in creatinine clearance induced by ACE inhibition (r = 0.65, p less than 0.05), with evidence that drug accumulation may potentiate hypotension and renal impairment should arterial pressure be reduced below the threshold for renal autoregulation. Creatinine 103-113 angiotensin I converting enzyme Homo sapiens 135-138 2345591-4 1990 Median serum creatinine levels in the ACE group rose acutely from 2.33 to 2.7 mg/dl after 1 month of therapy and remained stable thereafter. Creatinine 13-23 angiotensin I converting enzyme Homo sapiens 38-41 8707068-5 1996 For hypertension control and renal protection, start ACE inhibitors when serum creatinine is less than 2 mg/dl. Creatinine 79-89 angiotensin I converting enzyme Homo sapiens 53-56 8761013-7 1996 In addition, multiple regression analysis with a forward elimination procedure showed that only the ACE genotype was associated with RI of arcuate arteries (R2 = 0.24, p < 0.01) among the parameters of sex, age, IDDM duration, body mass index, HbA1c, plasma glucose levels, serum levels of total cholesterol and creatinine, urinary albumin excretion index, mean blood pressure and ACE genotype. Creatinine 315-325 angiotensin I converting enzyme Homo sapiens 100-103 8749676-6 1995 In the recently completed trial of ACE inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death. Creatinine 169-179 angiotensin I converting enzyme Homo sapiens 35-38 8749676-6 1995 In the recently completed trial of ACE inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death. Creatinine 169-179 angiotensin I converting enzyme Homo sapiens 75-78 7845322-7 1994 An asymptomatic increase in serum creatinine in patients administered ACE inhibitors should raise the possibility of RAS; however, more common renal diseases should be considered. Creatinine 34-44 angiotensin I converting enzyme Homo sapiens 70-73 1546024-9 1992 Elevation in the serum creatinine level of a patient taking an angiotensin-converting enzyme (ACE) inhibitor suggests bilateral renovascular hypertension. Creatinine 23-33 angiotensin I converting enzyme Homo sapiens 63-92 1546024-9 1992 Elevation in the serum creatinine level of a patient taking an angiotensin-converting enzyme (ACE) inhibitor suggests bilateral renovascular hypertension. Creatinine 23-33 angiotensin I converting enzyme Homo sapiens 94-97 33973994-6 2021 RESULTS: Urinary ACE activity was significantly higher in patients with SCD than in healthy children (median 0.01; range 0.00-0.07 vs median 0.00; range 0.00-0.01 mU/mL creatinine, p < 0.001. Creatinine 169-179 angiotensin I converting enzyme Homo sapiens 17-20 34645988-0 2022 Urinary albumin-to-creatinine ratio and the risk of first stroke in Chinese hypertensive patients treated with angiotensin-converting enzyme inhibitors. Creatinine 19-29 angiotensin I converting enzyme Homo sapiens 111-140 32981368-1 2020 Multiple clinical guidelines recommend an ACE (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker (ARB) in patients with elevated albuminuria, which can be measured through urine albumin-to-creatinine ratio (ACR), protein-to-creatinine ratio, or dipstick. Creatinine 215-225 angiotensin I converting enzyme Homo sapiens 42-45 2644824-4 1989 Moreover, the decline in the reciprocal of serum creatinine over time observed during triple drug therapy was arrested during therapy with the ACE inhibitor. Creatinine 49-59 angiotensin I converting enzyme Homo sapiens 143-146 2527539-6 1989 There was a significant correlation between ACE inhibition at 24 h and creatinine clearance (CrCL). Creatinine 71-81 angiotensin I converting enzyme Homo sapiens 44-47 3672075-5 1987 In high risk patients it is therefore recommended that serum creatinine be checked after initiating therapy with an ACE inhibitor. Creatinine 61-71 angiotensin I converting enzyme Homo sapiens 116-119 32981368-1 2020 Multiple clinical guidelines recommend an ACE (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker (ARB) in patients with elevated albuminuria, which can be measured through urine albumin-to-creatinine ratio (ACR), protein-to-creatinine ratio, or dipstick. Creatinine 215-225 angiotensin I converting enzyme Homo sapiens 47-76 32981368-1 2020 Multiple clinical guidelines recommend an ACE (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker (ARB) in patients with elevated albuminuria, which can be measured through urine albumin-to-creatinine ratio (ACR), protein-to-creatinine ratio, or dipstick. Creatinine 250-260 angiotensin I converting enzyme Homo sapiens 42-45 32981368-5 2020 We applied similar methods to investigate the association of protein-to-creatinine ratio and dipstick measurement results with the prescription of ACE inhibitor/ARB. Creatinine 72-82 angiotensin I converting enzyme Homo sapiens 147-150 32226931-9 2020 Treatment with ACE inhibitors or ARBs plus TGs resulted in significantly greater reductions in serum creatinine (SCr) compared with ACE inhibitors or ARBs alone (MD: -9.87; 95% CI: -13.76, -5.97). Creatinine 101-111 angiotensin I converting enzyme Homo sapiens 15-18 31303349-12 2020 LIMITATIONS: Creatinine results were not blinded, making it possible that ACE-inhibitor/placebo dosing was influenced by creatinine level. Creatinine 13-23 angiotensin I converting enzyme Homo sapiens 74-77 31303349-12 2020 LIMITATIONS: Creatinine results were not blinded, making it possible that ACE-inhibitor/placebo dosing was influenced by creatinine level. Creatinine 121-131 angiotensin I converting enzyme Homo sapiens 74-77 31719297-8 2019 ACE inhibitors protected carriers of alleles that supposedly decrease serum ACE levels (rs1800764-T, rs4291-A, Alu II) regarding creatinine clearance variations (P <0.005), but carriers of Alu DD (P <0.02), rs1800764-C (P <0.05), or rs4291-AT (P <0.04) showed better blood pressure lowering effects. Creatinine 129-139 angiotensin I converting enzyme Homo sapiens 0-3 31719297-8 2019 ACE inhibitors protected carriers of alleles that supposedly decrease serum ACE levels (rs1800764-T, rs4291-A, Alu II) regarding creatinine clearance variations (P <0.005), but carriers of Alu DD (P <0.02), rs1800764-C (P <0.05), or rs4291-AT (P <0.04) showed better blood pressure lowering effects. Creatinine 129-139 angiotensin I converting enzyme Homo sapiens 76-79 31719297-11 2019 Interpretation & conclusions: Pharmacological response of blood pressure and creatinine clearance to ACE inhibitors and statins may be genetically mediated. Creatinine 77-87 angiotensin I converting enzyme Homo sapiens 101-104 27546928-0 2016 Pharmacogenetic effects of angiotensin-converting enzyme inhibitors over age-related urea and creatinine variations in patients with dementia due to Alzheimer disease. Creatinine 94-104 angiotensin I converting enzyme Homo sapiens 27-56 30571562-0 2019 Acute Increases in Serum Creatinine After Starting Angiotensin-Converting Enzyme Inhibitor-Based Therapy and Effects of its Continuation on Major Clinical Outcomes in Type 2 Diabetes Mellitus. Creatinine 25-35 angiotensin I converting enzyme Homo sapiens 51-80 30571562-1 2019 Discontinuation of angiotensin-converting enzyme (ACE) inhibitor is recommended if patients experience >=30% acute increase in serum creatinine after starting this therapy. Creatinine 136-146 angiotensin I converting enzyme Homo sapiens 19-48 30571562-1 2019 Discontinuation of angiotensin-converting enzyme (ACE) inhibitor is recommended if patients experience >=30% acute increase in serum creatinine after starting this therapy. Creatinine 136-146 angiotensin I converting enzyme Homo sapiens 50-53 29794446-9 2018 Both ACE inhibitors and ARBs reduced the risk of doubling of the serum creatinine level (0.60, 0.39-0.91 for ACE inhibitors; 0.75, 0.64-0.88 for ARBs), and subgroup analyses for patients with macroalbuminuria or microalbuminuria showed similar results. Creatinine 71-81 angiotensin I converting enzyme Homo sapiens 5-8 29794446-9 2018 Both ACE inhibitors and ARBs reduced the risk of doubling of the serum creatinine level (0.60, 0.39-0.91 for ACE inhibitors; 0.75, 0.64-0.88 for ARBs), and subgroup analyses for patients with macroalbuminuria or microalbuminuria showed similar results. Creatinine 71-81 angiotensin I converting enzyme Homo sapiens 109-112 27269276-2 2017 The widespread use of ACE inhibitors has been associated with several notable adverse effects such as hyperkalemia and an increased serum creatinine. Creatinine 138-148 angiotensin I converting enzyme Homo sapiens 22-25 28344754-5 2017 A significant reduction in ACR was observed after 6 mo treatment with ACE inhibitor irrespective of whether DN patients were micro-albuminuric (>= 30 and < 300 mg/g creatinine) or macro-albuminuric (>= 300 mg/g creatinine) at the time of enrollment. Creatinine 171-181 angiotensin I converting enzyme Homo sapiens 70-73 28344754-5 2017 A significant reduction in ACR was observed after 6 mo treatment with ACE inhibitor irrespective of whether DN patients were micro-albuminuric (>= 30 and < 300 mg/g creatinine) or macro-albuminuric (>= 300 mg/g creatinine) at the time of enrollment. Creatinine 220-230 angiotensin I converting enzyme Homo sapiens 70-73 31144454-2 2019 After chromatographic separation on an ACE Excel 2 AQ column, high abundant creatinine and uric acid and the other low abundant purines were sequentially detected by ultraviolet and quadrupole time-of-flight mass spectrometry within a single run. Creatinine 76-86 angiotensin I converting enzyme Homo sapiens 39-42 26000752-7 2015 RESULTS: ACE I/D polymorphism was found to be associated with acute rejection (AR) in genotypes DD+ID versus II (OR = 1.62, 95% CI = 1.14-2.29) and with serum creatinine concentration after renal transplantation in genotypes DD versus ID (WMD = 13.12, 95% CI = 8.09-18.16). Creatinine 159-169 angiotensin I converting enzyme Homo sapiens 9-12 25878372-4 2015 The study aims to compare ACE inhibitors and ARBs in terms of delaying or preventing the progression of diabetic nephropathy, association between blood pressure (B.P) and urinary albumin and also B.P and serum creatinine with ACE inhibitor and ARB, know the percentage of hyperkalemia in patients of diabetic nephropathy receiving ACE inhibitor or ARB. Creatinine 210-220 angiotensin I converting enzyme Homo sapiens 226-229 25878372-4 2015 The study aims to compare ACE inhibitors and ARBs in terms of delaying or preventing the progression of diabetic nephropathy, association between blood pressure (B.P) and urinary albumin and also B.P and serum creatinine with ACE inhibitor and ARB, know the percentage of hyperkalemia in patients of diabetic nephropathy receiving ACE inhibitor or ARB. Creatinine 210-220 angiotensin I converting enzyme Homo sapiens 226-229