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)

A woman pregnant with her second child was given sulfisoxazole (Gantrisin) during her eighth month of pregnancy for a urinary tract infection. Her 34-week-old male infant was stillborn with hydrops fetalis and severe anemia. The mother was found to be glucose-6-phosphate-dehydrogenase (G-6-PDH) deficient. Ingestion of the drug which is known to produce hemolysis in G-6-PDH-deficient people may have compromised the male infant by creating an abundance of bilirubin via massive hemolysis and also retarding its elimnation by competing with bilirubin for albumin-binding sites. This case identifies a newly recognized danger in the use of sulfonzmides in the third trimester of pregnancy.
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PMID:Hydrops fetalis and stillbirth in a male glucose-6-phosphate dehydrogenase-deficient fetus possibly due to maternal ingestion of sulfisoxazole; a case report. 499 90

Nephropathy may develop in patients with type 1 diabetes because poor glycemic control produces effects that eventually lead to glomerular scarring and renal failure. The worse and more prolonged the hyperglycemia, the greater the risk of diabetic nephropathy. In patients with type 2 diabetes, hyperglycemia, as well as insulin resistance and generalized vascular disease, is involved in the pathogenesis of nephropathy. The glomerular changes of early diabetic nephropathy can be identified only by renal biopsy or by testing for microalbuminuria. Once macroalbuminuria occurs (albumin excretion rate, > 300 mg/day), usually after type 1 diabetes has been present for 10 to 15 postpubertal years, end-stage renal disease is almost inevitable. However, aggressive control of hypertension in diabetic patients without microalbuminuria helps avoid nephropathy, and tight glycemic control in those with microalbuminuria can avoid or delay its onset. Even when macroalbuminuria is present, treatment can prolong renal function. Aggressive antihypertensive therapy, especially with ACE inhibitors, can reduce renal decline by half. Avoiding circumstances that may damage the kidneys (e.g., use of radiocontrast materials or nephrotoxic drugs, dehydration, hyperlipidemia, urinary tract infection, buildup of AGEs) is critical. Some treatment methods are controversial (dietary protein restriction) or still under investigation (use of injected or oral heparin) but may help delay renal transplantation or dialysis.
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PMID:Dealing with diabetic nephropathy. 1002 5

We investigated angiotensin converting enzyme gene (ACE I/D) polymorphism as a risk for progressive renal damage in congenital uropathies. The ACE I/D genotype was determined in 196 Caucasian patients with congenital uropathies and 163 individuals with no clinical or sonographic evidence of any urological malformations. The study group included patients with ureteropelvic junction obstruction (n=49), primary obstructive megaureter (n=19), primary vesicoureteral reflux (VUR) (n=67), and posterior urethral valves (n=27). Thirty-four patients were excluded because of additional diseases or insufficient follow-up. There was no difference in the ACE I/D distribution between children with uropathies and normal controls (II 16%, ID 56%. DD 28% vs. II 26%, ID 50%, DD 24%). Renal lesions were found in 99 of 162 children by ultrasonography, intravenous pyelography, and nuclear scans. In these children there was significant over-representation of the DD genotype (II 11%, ID 53%, DD 36%) compared with normals (P<0.005, X2=14.9) or with patients with uropathies but no renal lesions (II 23%, ID 62%, DD 15%, P<0.005, X2=14.9). Because ACE I/D has been linked with progressive deterioration of renal function, we evaluated a subset of patients with initially normal kidneys who developed radiographic renal lesions (n=28). Among these patients there was an even greater over-representation of the DD genotype (II 0%, ID 43%, DD 57%, P<0.001, X2=22.6) compared with patients with uropathies but no radiographic lesions. Multivariate analysis revealed that the DD genotype is a risk factor for parenchymal destruction, which was independent of time of diagnosis, surgical intervention, or urinary tract infection. This finding was particularly relevant in patients with VUR who constituted the majority with initially normal kidneys who developed radiographic damage (22/28). Indeed, the odds ratio of developing parenchymal damage with VUR was significantly increased if the individual had the DD genotype (4.2, 95% confidence interval 1.4-13.0). In conclusion the ACE I/D gene polymorphism is a risk factor for renal parenchymal damage in patients with congenital urological abnormalities and appears particularly relevant in children with VUR, where it is an independent predisposing factor.
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PMID:ACE I/D gene polymorphism predicts renal damage in congenital uropathies. 1045 81

We experienced a Duchenne muscular dystrophy (DMD) patient with severe congestive heart failure (CHF) successfully treated with milrinone. He had been diagnosed as having CHF since 24 years of age when he began to have mechanical ventilation with a nasal mask at home. Although angiotensin converting enzyme (ACE) inhibitor was effective for his CHF, cardiac function worsened year by year. Respiratory infection triggered the exacerbation of CHF at the end of 1997 (27 years old). On admission to our hospital on January 7, 1998, PaO2 was 48 mmHg and cardiothoracic ratio (CTR) was 62%. Both ventricles were dilated and ventricular wall motility was markedly reduced on ultrasonocardiography. Ejection fraction of the left ventricle (LVEF) was 5%. Serum brain natriuretic peptide (BNP) was 760 pg/ml. Continuous intravenous infusion of milrinone was started on January 8 at the rate of 0.25-0.35 microgram/kg/min. His general condition improved and LVEF increased up to 15% on January 27. No serious side effects were observed. Even after milrinone withdrawal, his cardiac condition remained stable until the end of February 1998. Temporary deteriorated CHF due to urinary tract infection was successfully treated by chemotherapy and milrinone. Subsequently he was discharged on March 13 and could stay in his home for 7 weeks uneventfully with milrinone infusion therapy. When he was readmitted to the hospital for evaluation of CHF on April 30, CTR was 44%, LVEF was 20% and BNP was 44 pg/ml. CHF is one of the life threatening complications for DMD. Although catecholamine is a well utilized agent for advanced CHF, it has limited effect in DMD, because beta receptors are down-regulated due to long-lasting cardiac dysfunction. Increased heart rate and arrhytmia are also serious problems during catecholamine therapy. Milrinone is a type III phosphodiesterase inhibitor having inotropic and vasodilatic actions with modest increase of heart rate and little torelance. Milrinone is probably effective in improving CHF of DMD and has less side effects as compared to catecholamine. We concluded that milrinone might improve quality of lives of DMD patients with advanced CHF, although further cumultative studies are necessary to confirm its effectiveness and safety.
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PMID:[Effective milrinone therapy to a Duchenne muscular dystrophy patient with advanced congestive heart failure]. 1050 90

The prevalence of vesico-ureteric reflux in the general population is unknown, but it is increased in risk groups, such as children with symptomatic urinary tract infection, schoolgirls with asymptomatic bacteriuria, first-degree relatives of patients with reflux and children with prenatal dilatation of their upper urinary tract. Children and adults with pyelonephritic renal scarring are at risk of serious long-term complications, e.g. hypertension and renal failure. Modern paediatric care, with early detection and treatment of urinary tract infections and reflux during childhood and adolescence, may improve long-term prognosis. In the adult patient with established pyelonephritic renal scarring, careful control of hypertension may retard the rate of progression, and angiotensin converting enzyme inhibitors may have renal protective properties.
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PMID:Vesico-ureteric reflux: occurrence and long-term risks. 1058 68

We present a 77-year-old male with moderate chronic renal insufficiency from diabetic nephropathy who developed severe metabolic acidosis and life threatening hyperkalemia on treatment with regular dose of trimethoprim-sulfamethoxazole (TMP-SMZ) for urinary tract infection. The metabolic acidosis and hyperkalemia resolved upon appropriate medical intervention and discontinuation of TMP-SMZ. While hyperkalemia has commonly been reported with high dose of TMP-SMZ, severe metabolic acidosis is quite uncommon with regular dose TMP-SMZ. We emphasize that patients with renal tubular acidosis (RTA), renal insufficiency, aldosterone deficiency, old age with reduced renal mass and function, and angiotensin converting enzyme (ACE)-inhibitor therapy are at high risk of developing these severe and potentially life threatening complications.
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PMID:Life threatening hyperkalemia and acidosis secondary to trimethoprim-sulfamethoxazole treatment. 1173 Feb 76

We report a rare case of essential mixed cryoglobulinemia type II with membrano-proliferative glomerulonephritis (MPGN) type I in which HCV was not found. Long-term history of palindromic rheumatism, skin leukocytoclastic vasculitis attacks and micro-normocytic anemia preceded the appearance of cryoglobulinemia. Cryoprecipitate consisted of monoclonal IgMk-RF and polyclonal IgG (essential mixed type II). The newly appreciated cryoglobulinemia was associated with Coombs positive hemolytic anemia. The MPGN in this case had a benign course and responded to complex simple therapies including prevention of exposure to cold, low antigen content diet, treatment of provoking factors such as UTI, and maximal dose of ACE inhibitor. Responsiveness of skin vasculitis to colchicine therapy was restored after a two-month colchicine withdrawal period and therefore corticosteroid and immunosuppressive therapy was postponed.
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PMID:Essential mixed cryoglobulinemia type II. 1687 Jan 5

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest congenital cystic renal disease. Factors such as hypertension, urinary tract infection, hematuria, and proteinuria may affect the progression to chronic renal failure in ADPKD patients. Therapeutic interventions, such as the use of angiotensin converting enzyme inhibitors (ACEI) or diet modification, may impact the natural progression of the disease. We aim in this study to review a registry of ADPKD patients in order to compare the slow and fast progressors and identify possible predictors of progression and interventions that slow the progression of this disease. Sheffield Kidney Institute (SKI), one of the largest kidney institutes in Northern Europe, has registered a large number of ADPKD patients since 1981. SKI's computer network contains a wide range of information on these patients. We selected 94 adult polycystic patients from the SKI for retrospective analysis of factors affecting progression to chronic renal failure. Patients who doubled their s. creatinine in < or = 36 months were considered fast progressors (FP), while those who doubled their s. creatinine in > 36 months were regarded as slow progressors (SP). There were 70 patients in the FP group and 24 patients in the SP group. A third group of 137 patients consisted of non-progressors (NP) who had stable s. creatinine levels during the same period. We found that the incidence of hypertension, UTI, macroscopic and microscopic hematuria, and overt proteinuria in the FP group was higher than in the SP and NP groups. Modification of some factors, such as hypertension and UTI, may decrease the rate of the deterioration of renal function.
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PMID:Retrospective analysis of factors affecting the progression of chronic renal failure in adult polycystic kidney disease. 1718 85

Urinary tract infection is a common bacterial disease that presents during childhood and may lead to renal scarring. Several studies have shown a strong association between the angiotensin converting enzyme (ACE) deletion polymorphism and renal scarring in children with vesicoureteric reflux (VUR). The purpose of this study was to investigate the possible correlation between the ACE deletion polymorphism and renal scarring in 186 children with urinary tract infection (UTI), of whom 90 were renal scar positive and 96 were renal scar negative. The control group consisted of 129 children with no UTI. Renal scars were diagnosed by means of (99m)Tc-dimercapto-succinic acid scans, and ACE genotypes were determined as II, ID, and DD by PCR analyses. The ACE genotype distribution was 10% II, 67% ID, and 23% DD in the renal scar-positive group, 18% IotaIota, 42% ID, and 40% DD in the renal scar-negative group, and 22% II, 47% ID, and 31% DD in the control group. No correlation was found between the DD genotype and renal scar formation in children with UTI. The same results were obtained following strafication of the patients by VUR and age of the first urinary tract infection. In conclusion, the results of this study suggest that the DD genotype is not an independent risk factor for renal scarring in children with UTI.
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PMID:ACE gene insertion/deletion polymorphism and renal scarring in children with urinary tract infections. 1960 95

In 2011 several articles seemed significant for the practice of general medicine. Diagnosis of hypertension needs several measurements and may need 24-hour ambulatory blood pressure monitoring. Glycosylated hemoglobin is a reliable tool to diagnose diabetes mellitus. The ABCD2 score with neurological imaging help the triage of transient ischemic attacks. Pulmonary embolism can be treated as outpatient for low risk patients. Gluten-free diet may be tried in irritable bowel syndrome. Nitrofurantoin is a reasonable alternative for simple urinary tract infection in women, but antibiotics are not needed after drainage of an uncomplicated skin abscess. Subclinical thyroid dysfunction is a risk factor of osteoporosis in older men. Sequential use of MMSE and ACE scores is a promising approach to assess medical decision-making capacity.
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PMID:[2011 findings from literature on general internal ambulatory medicine]. 2236 76


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