enalapril and Acute-Kidney-Injury

The case of a 19 year old patient with Takayasu arteritis with exclusive involvement of the abdominal aorta and without involvement of the renal arteries who presented severe arterial hypertension during the acute phase of the disease is referred. The administration of a dose of 20 mg of enalapril maleate was followed in less than 24 hours by lameness of the lower limbs and acute oligoanuric renal failure, both of which were reversible after discontinuation of the drug. During the inflammatory phase of the disease, treatment with high doses of prednisone was effective in the control of the general symptoms and the biologic parameters of inflammation. Surgical revascularization was successfully carried out 5 months after diagnosis. Two years later the patient continues to be normotense and asymptomatic.

Topics: Acute Kidney Injury; Adult; Enalapril; Female; Humans; Takayasu Arteritis

Oligohydramnios and neonatal renal failure is reported in a premature infant whose mother had used enalapril in weeks 32-35 of her pregnancy. The infant recovered adequate renal function after peritoneal dialysis. Review of the literature supports our view that angiotensin-converting enzyme inhibitors should not be used in pregnancy; if they are, both mother and fetus should be monitored with extreme care.

Topics: Acute Kidney Injury; Enalapril; Female; Humans; Hypertension; Infant, Newborn; Male; Pregnancy; Pregnancy Complications, Cardiovascular

Angiotensin-converting enzyme (ACE) inhibitors are clearly effective treatment for all stages of hypertension. Since the introduction of captopril in 1981, numerous ACE inhibitors have been synthesized and are under investigation. Their exact antihypertensive mechanism of action remains unclear. Part of their effect may be mediated by vasodilator prostaglandins. Early studies with as much as 1,000 mg a day captopril demonstrated the agent's ability to reduce blood pressure, but only 10 percent of the severely hypertensive patients were controlled with monotherapy. Subsequent studies have demonstrated that patients with mild to moderate hypertension can be controlled with ACE inhibitor alone, although there is a tendency for the very low doses to lose their effect with time. Black patients are less readily controlled with monotherapy. Captopril has now been demonstrated to be effective in the hypertension of scleroderma and has reversed scleroderma renal crisis. ACE inhibitors are also effective for the treatment of severe congestive heart failure.

Topics: Acute Kidney Injury; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Captopril; Clinical Trials as Topic; Dipeptides; Enalapril; Heart Failure; Humans; Hypertension; Proline; Racial Groups; Teprotide; Time Factors

The purpose of this study was to investigate the effectiveness and safety of enalapril in elderly people. A double-blind, randomized, placebo-controlled trial was carried out in 32 subjects aged from 75 to 97 years (mean: 86 years) with blood pressure values equal or superior to 160/90 mmHg. After 8 weeks of treatment with enalapril in doses of 20 to 40 mg/day, the systolic pressure was lowered from 190 +/- 16 to 151 +/- 19 mmHg (P less than 0.0001) and the diastolic pressure from 102 +/- 7 to 85 +/- 11 mmHg (P less than 0.0001). Systolic and diastolic pressures were also significantly reduced in subjects under placebo (from 183 +/- 16 to 165 +/- 21 mmHg, P less than 0.001; and from 101 +/- 9 to 91 +/- 13 mmHg, P less than 0.001, respectively), but the degree of reduction was significantly superior with enalapril (systolic: 39 +/- 25 vs 18 +/- 19 mmHg, P less than 0.005; diastolic: 17 +/- 13 vs 11 +/- 12, P less than 0.001); blood pressure was inferior to 160/90 mmHg in 67% of the subjects treated, as against 35% of those under placebo. Two patients under enalapril died: one on the 27th, the other on the 47th day of treatment. No relation could be established between these deaths and the drug, and this figure of 2 is not significantly different for the number of deaths expected over the same period in a population of that age-group. Among the patients under placebo, one had pulmonary embolism on the 34th day and another had a sudden increase in blood pressure on the 6th day, requiring discontinuation of treatment. It is concluded that enalapril administered alone is effective and well tolerated. Long-term studies are needed to find out whether this angiotensin-converting enzyme inhibitor is superior to a diuretic as initial treatment of arterial hypertension.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Clinical Trials as Topic; Creatinine; Double-Blind Method; Enalapril; Female; Heart Rate; Humans; Hypertension; Kidney; Male; Renin

Angiotensin-converting enzyme (ACE) inhibitors are clearly effective treatment for all stages of hypertension. Since the introduction of captopril in 1981, numerous ACE inhibitors have been synthesized and are under investigation. Their exact antihypertensive mechanism of action remains unclear. Part of their effect may be mediated by vasodilator prostaglandins. Early studies with as much as 1,000 mg a day captopril demonstrated the agent's ability to reduce blood pressure, but only 10 percent of the severely hypertensive patients were controlled with monotherapy. Subsequent studies have demonstrated that patients with mild to moderate hypertension can be controlled with ACE inhibitor alone, although there is a tendency for the very low doses to lose their effect with time. Black patients are less readily controlled with monotherapy. Captopril has now been demonstrated to be effective in the hypertension of scleroderma and has reversed scleroderma renal crisis. ACE inhibitors are also effective for the treatment of severe congestive heart failure.

Topics: Acute Kidney Injury; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Captopril; Clinical Trials as Topic; Dipeptides; Enalapril; Heart Failure; Humans; Hypertension; Proline; Racial Groups; Teprotide; Time Factors

The renal effects of long-term antihypertensive treatment with enalapril were evaluated in 34 subjects (age, 53 yr; range, 27 to 65) with mild, uncomplicated hypertension. After receiving placebo for 4 wk, subjects were randomly assigned to groups receiving incremental doses of enalapril (10, 20, or 40 mg/day for 4 wk each) in a single morning dose or two divided doses, or of placebo. One subject who received enalapril developed acute renal failure by the end of the study. There was no evidence of glomerular or tubular damage in the other subjects; as measured by 24-hr urinary protein excretion, urinary activity of N-acetyl-beta-D-glucosaminidase, and uric acid clearance. During treatment with enalapril, renal plasma flow (measured with 131I-iodohippurate sodium) and glomerular filtration rate increased by 12.1% and 6.8%. Changes in renal plasma flow correlated inversely with age and final mean arterial pressure and correlated positively with initial plasma renin activity of subjects. Except for an occasional idiosyncratic adverse reaction, enalapril is a safe and effective antihypertensive drug with the unique ability to increase renal function despite a fall in renal perfusion pressure.

Topics: Acute Kidney Injury; Adult; Aged; Blood Pressure; Dipeptides; Drug Evaluation; Enalapril; Female; Glomerular Filtration Rate; Humans; Hypertension; Male; Middle Aged; Random Allocation; Renal Circulation

Targeted therapy with anaplastic lymphoma kinase inhibitor alectinib has become standard therapy for selected patients with non-small cell lung carcinoma. Few data are available on the renal effects of alectinib. We report on a case of acute kidney injury in a patient using alectinib for less than 2 weeks and on serum sodium and creatinine during long-term use of alectinib.. A 70-year-old Asian woman was diagnosed with metastasized non-small cell lung carcinoma (cT4N3M1c, stage IV) with echinoderm microtubule-associated protein-like 4 and anaplastic lymphoma kinase gene rearrangement and received alectinib, in two daily doses of 600 mg. Eleven days after the initiation of therapy, she was seen at the emergency department with acute kidney injury. Renal biopsy showed lesions in the proximal tubular epithelial cells. Nine days after alectinib cessation, renal function recovered quickly and reintroduction of alectinib in a reduced dose was tolerated, while withholding metformin, enalapril, and naproxen. In seven other patients, data on estimated glomerular filtration rate showed decreased kidney function at 3 months with stabilization at 6 months. Serum sodium at 3 months increased during alectinib treatment and increased further at 6 months.. Our data suggest direct or indirect toxic (proximal) tubulopathy due to alectinib with a good prognosis after cessation. Adverse acute renal effects of alectinib may be prevented by avoiding other medication influencing renal hemodynamics, in particular nonsteroidal anti-inflammatory drugs. Without these co-medications, alectinib could be reintroduced in our patient.

Topics: Acute Kidney Injury; Aged; Anaplastic Lymphoma Kinase; Anti-Inflammatory Agents; Antineoplastic Agents; Carbazoles; Carcinoma, Non-Small-Cell Lung; Creatinine; Enalapril; Female; Humans; Kidney; Lung Neoplasms; Metformin; Microtubule-Associated Proteins; Naproxen; Piperidines; Protein Kinase Inhibitors; Sodium

Acute renal failure (ARF) is a clinical critical syndrome with rapid and severe decline of renal function. Complications of ARF, especially its cardiac complications (cardiorenal syndrome type 3, CRS-3), are the main causes of death in patients with ARF. However, the shortage and limited efficacy of therapeutic drugs make it significant to establish new large-scale drug screening models. Based on the Nitroreductase/Metronidazole (NTR/MTZ) cell ablation system, we constructed a

Topics: Acute Kidney Injury; Animals; Animals, Genetically Modified; Cardio-Renal Syndrome; Cardiovascular Diseases; Digoxin; Disease Models, Animal; Drug Evaluation, Preclinical; Enalapril; Epithelial Cells; Humans; Kidney Tubules; Larva; Metronidazole; Regional Blood Flow; Thioctic Acid; Treatment Outcome; Zebrafish

Anticoagulant-related nephropathy (ARN), that was described in humans first as warfarin-related nephropathy, is characterized by acute kidney injury and red blood cell (RBC) tubular casts in the kidney. 5/6 nephrectomy (5/7NE) rats treated with warfarin or dabigatran show changes in kidney function and morphology that are similar to human disease. The role of glomerular filtration rate (GFR) in the pathogenesis of ARN is not clear. The aim of these studies was to elucidate the role of GFR in the pathogenesis of dabigatran-induced ARN in 5/6NE rats.. 5/6NE rats were treated per os with 150 mg/kg/day dabigatran alone or with drugs that lower (enalapril, 1.5 mg/kg/day) or increase (albuterol, 4.0 mg/kg/day) GFR for 7 days. Changes in coagulation and kidney function were recorded daily. Kidney morphology was evaluated on day 7 after the treatment.. Dabigatran resulted in activated partial thromboplastin time increase that was not affected by GFR-modifying drugs. Blood pressure was significantly lower in 5/6NE rats treated with enalapril and dabigatran as compared to dabigatran alone. The GFR was decreased by 35% in enalapril/dabigatran- and increased by 26% in albuterol/dabigatran-treated animals. There were no changes in serum creatinine, hematuria or urinary kidney injury molecule (KIM-1) levels when GFR-modifying drugs were added to dabigatran. All dabigatran-treated animals had RBC casts in the kidney regardless of the GFR modification.. GFR does not play a significant role in the dabigatran-induced acute kidney injury in 5/6 nephrectomy model in rats. Based in these data, modification of GFR in patients with ARN is not warranted.

Topics: Acute Kidney Injury; Albuterol; Animals; Antihypertensive Agents; Antithrombins; Bronchodilator Agents; Dabigatran; Disease Models, Animal; Enalapril; Glomerular Filtration Rate; Male; Nephrectomy; Rats; Rats, Sprague-Dawley

Acute kidney injury (AKI) frequently complicates major surgery and can be associated with hypertension and progress to chronic kidney disease, but reports on blood pressure normalization in AKI are conflicting. In the present study, we investigated the effects of an angiotensin-converting enzyme inhibitor, enalapril, and a soluble epoxide hydrolase inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea (TPPU), on renal inflammation, fibrosis, and glomerulosclerosis in a mouse model of ischemia-reperfusion injury (IRI)-induced AKI. Male CD1 mice underwent unilateral IRI for 35 min. Blood pressure was measured by tail cuff, and mesangial matrix expansion was quantified on methenamine silver-stained sections. Renal perfusion was assessed by functional MRI in vehicle- and TPPU-treated mice. Immunohistochemistry was performed to study the severity of AKI and inflammation. Leukocyte subsets were analyzed by flow cytometry, and proinflammatory cytokines were analyzed by quantitative PCR. Plasma and tissue levels of TPPU and lipid mediators were analyzed by liquid chromatography mass spectrometry. IRI resulted in a blood pressure increase of 20 mmHg in the vehicle-treated group. TPPU and enalapril normalized blood pressure and reduced mesangial matrix expansion. However, inflammation and progressive renal fibrosis were severe in all groups. TPPU further reduced renal perfusion on

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Blood Pressure; Disease Models, Animal; Disease Progression; Enalapril; Enzyme Inhibitors; Epoxide Hydrolases; Fibrosis; Glomerular Mesangium; Glomerulonephritis; Hypertension; Male; Mice; Phenylurea Compounds; Piperidines; Reperfusion Injury

Renin-angiotensin-aldosterone system inhibitors have proven clinical benefit in management of patients with heart failure with reduced ejection fraction. However, there are no guidelines to manage decline in kidney function that occurs with initiation and titration of renin-angiotensin-aldosterone system agents during management of heart failure. We discuss the complex interplay of kidney function and heart failure in the presence of renin-angiotensin-aldosterone system agents and suggest a clinical algorithm for management of acute decline in kidney function.

Topics: Acute Kidney Injury; Enalapril; Glomerular Filtration Rate; Heart Failure; Humans; Mineralocorticoid Receptor Antagonists; Renin-Angiotensin System; Stroke Volume

Though acute kidney injury (AKI) is often multifactorial, investigators are now emphasizing the specific contribution of nephrotoxins. This study examines the epidemiology of nephrotoxin exposure and nephrotoxin-associated AKI among children undergoing congenital heart surgery (CHS).. This is a retrospective cohort study of children admitted following CHS between June 1, 2014, and September 30, 2014. Nephrotoxins were defined according to the Nephrotoxic Injury Negated by Just-in-time-Action (NINJA) collaborative; high nephrotoxin exposure was defined as receipt of ≥ 3 nephrotoxins concurrently. AKI was diagnosed according to KDIGO creatinine criteria. Severe AKI was defined as KDIGO stage ≥ 2. Poisson models were used to compute adjusted relative risk (aRR) of high nephrotoxin exposure for AKI.. One hundred fifty-four children (median age 20.4 months, IQR 2.3-59.5) were included. One hundred thirty-one (85.1%) received at least one nephrotoxin; 32 (20.8%) received ≥ 3 nephrotoxins. The most commonly administered medications were ketorolac (n = 74, 48.1%), aspirin (n = 62, 40.3%), ibuprofen (n = 51, 33.1%), vancomycin (n = 39, 25.3%), piperacillin/tazobactam (n = 35, 22.7%), and enalapril (n = 14, 9.1%). AKI occurred more commonly in those exposed to ≥ 3 nephrotoxins (62.5 vs. 50.8%); this was not statistically significant after adjusting for confounders (aRR = 1.2, 95% CI 0.9-1.7). Severe AKI was similar between those with and without high nephrotoxin exposure (21.9 vs. 19.7%, p = 0.78).. Nephrotoxin use is common following pediatric CHS. While we found no association between high nephrotoxin exposure and AKI, this may be related to the multifactorial nature of AKI in this population. For many common nephrotoxins, less injurious agents exist and nephrotoxin exposure may represent a modifiable risk factor for AKI.

Topics: Acute Kidney Injury; Adolescent; Aspirin; Cardiac Surgical Procedures; Child; Child, Preschool; Critical Illness; Enalapril; Female; Heart Defects, Congenital; Humans; Ibuprofen; Infant; Ketorolac; Male; Piperacillin, Tazobactam Drug Combination; Postoperative Complications; Retrospective Studies; Vancomycin

Renin lineage cells (RLCs) serve as a progenitor cell reservoir during nephrogenesis and after renal injury. The maintenance mechanisms of the RLC pool are still poorly understood. Since RLCs were also identified as a progenitor cell population in bone marrow we first considered that these may be their source in the kidney. However, transplantation experiments in adult mice demonstrated that bone marrow-derived cells do not give rise to RLCs in the kidney indicating their non-hematopoietic origin. Therefore we tested whether RLCs develop in the kidney through neogenesis (de novo differentiation) from cells that have never expressed renin before. We used a murine model to track neogenesis of RLCs by flow cytometry, histochemistry, and intravital kidney imaging. During nephrogenesis RLCs first appear at e14, form a distinct population at e16, and expand to reach a steady state level of 8-10% of all kidney cells in adulthood. De novo differentiated RLCs persist as a clearly detectable population through embryogenesis until at least eight months after birth. Pharmacologic stimulation of renin production with enalapril or glomerular injury induced the rate of RLC neogenesis in the adult mouse kidney by 14% or more than three-fold, respectively. Thus, the renal RLC niche is constantly filled by local de novo differentiation. This process could be stimulated consequently representing a new potential target to beneficially influence repair and regeneration after kidney injury.

Topics: Acute Kidney Injury; Animals; Biopsy; Bone Marrow Cells; Bone Marrow Transplantation; Cell Differentiation; Cell Lineage; Enalapril; Glomerular Mesangium; Humans; Lipopolysaccharides; Mesangial Cells; Mice; Mice, Inbred C57BL; Mice, Transgenic; Models, Animal; Regeneration; Renin; Stem Cells

Background There is very little evidence relating to the association of herbal medicine with diarrhea and the development of acute kidney injury (AKI). This study reports a case of diarrhea-induced AKI, possibly related to an individual ingesting copious amounts of homemade mixed fruit and herb puree. Case presentation A 45-year-old Thai man with diabetes had diarrhea for 2 days, as a result of taking high amounts of a puree made up of eight mixed fruits and herbs over a 3-day period. He developed dehydration and stage 2 AKI, with a doubling of his serum creatinine. He had been receiving enalapril, as a prescribed medication, over one year. After he stopped taking both the puree and enalapril, and received fluid replacement therapy, within a week his serum creatinine had gradually decreased. The combination of puree, enalapril and AKI may also have induced hyperkalemia in this patient. Furthermore, the patient developed hyperphosphatemia due to his worsening kidney function, exacerbated by regularly taking some dietary supplements containing high levels of phosphate. His serum levels of potassium and phosphate returned to normal within a week, once the patient stopped both the puree and all dietary supplements, and had begun receiving treatment for hyperkalemia. Results The mixed fruit and herb puree taken by this man may have led to his diarrhea due to its effect; particularly if the patient was taking a high concentration of such a drink. Both the puree and enalapril are likely to attenuate the progression of kidney function. The causal relationship between the puree and AKI was probable (5 scores) assessed by the modified Naranjo algorithm. This is the first case report, as far as the authors are aware, relating the drinking of a mixed fruit and herbal puree to diarrhea and AKI in a patient with diabetes. Conclusions This case can alert health care providers to the possibility that herbal medicine could induce diarrhea and develop acute kidney injury.

Topics: Acute Kidney Injury; Diabetes Mellitus; Diabetic Nephropathies; Diarrhea; Dietary Supplements; Enalapril; Fruit; Humans; Male; Middle Aged; Phytotherapy; Plant Preparations

The use of angiotensin converting enzyme (ACE) inhibitors in combination with diuretics is a common strategy used for the treatment of patients affected by heart failure. An infant affected by initial congestive cardiac failure, after starting the treatment with enalapril in association with furosemide, developed acute kidney injury (AKI). No underlying renal disease or renal artery stenosis was found. He recovered from kidney injury after the therapy was suspended, thus suggesting that the drug combination is responsible for the onset of the adverse reaction. The present case report, the appraisal of the current knowledge on the onset of AKI and the analysis of available pharmacovigilance databases indicate that particular caution should be exercised when infants affected by heart failure are treated with the enalapril and furosemide combination therapy. Moreover, we strongly suggest an up-to-date revision of the ACE-inhibitor dosing guidelines in pediatric patients to define unambiguously the safe upper limits of this class of drugs.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Diuretics; Drug Interactions; Drug Therapy, Combination; Enalapril; Furosemide; Heart Failure; Heart Septal Defects, Ventricular; Humans; Infant; Male

Oxidative stress-induced PARP activation has been recognized to be a main factor in the pathogenesis of cisplatin-induced nephrotoxicity. Accumulating literature has revealed that ACE inhibitors may exert beneficial effect in several disease models via preventing PARP activation. Based on this hypothesis, we have evaluated the renoprotective effect of enalapril, an ACE inhibitor, and its underlying mechanism(s) in cisplatin-induced renal injury in rats. Male Albino Wistar rats were orally administered normal saline or enalapril (10, 20 and 40 mg/kg) for 10 days. Nephrotoxicity was induced by a single dose of cisplatin (8 mg/kg; i.p.) on the 7th day. The animals were thereafter sacrificed on the 11th day and both the kidneys were excised and processed for biochemical, histopathological, molecular, and immunohistochemical studies. Enalapril (40 mg/kg) significantly prevented cisplatin-induced renal dysfunction. In comparison to cisplatin-treated group, the elevation of BUN and creatinine levels was significantly less in this group. This improvement in kidney injury markers was well substantiated with reduced PARP expression along with phosphorylation of MAPKs including JNK/ERK/p38. Enalapril, in a dose-dependent fashion, attenuated cisplatin-induced oxidative stress as evidenced by augmented GSH, SOD and catalase activities, reduced TBARS and oxidative DNA damage (8-OHDG), and Nox-4 protein expression. Moreover, enalapril dose dependently inhibited cisplatin-induced inflammation (NF-κB/IKK-β/IL-6/Cox-2/TNF-α expressions), apoptosis (increased Bcl-2 and reduced p53, cytochrome c, Bax and caspase-3 expressions, and TUNEL/DAPI positivity) and preserved the structural integrity of the kidney. Thus, enalapril attenuated cisplatin-induced renal injury via inhibiting PARP activation and subsequent MAPKs/TNF-α/NF-κB mediated inflammatory and apoptotic response.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Animals; Antineoplastic Agents; Cisplatin; Enalapril; Kidney; Oxidative Stress; Poly(ADP-ribose) Polymerase Inhibitors; Rats; Rats, Wistar

Dose adjustment for certain drugs is required in patients with reduced renal function to avoid toxicity as many drugs are eliminated by the kidneys. The aim of this study was to assess whether appropriate dosage adjustments were made in hospitalized patients with renal impairment.. A prospective cross-sectional study was carried out in the internal medicine wards of Tikur Anbessa Specialized Hospital. All patients with creatinine clearance ≤ 59 ml/min admitted to hospital between April and July, 2013 were included in the analysis. Data regarding serum creatinine level, age, sex and prescribed drugs and their dosage was collected from the patients' medical records. Serum creatinine level ≥ 1.2 mg/dL was used as a cutoff point in pre-selection of patients. The estimated creatinine clearance was calculated using the Cockcroft- Gault (CG) equation. Guideline for Drug prescribing in renal failure provided by the American College of Physicians was used as the standard for dose adjustment.. Nine percent (73/810) of medical admissions were found to have renal impairment (CrCl  ≤ 59 ml/min). There were 372 prescription entries for 73 patients with renal impairment. Dose adjustment was required in 31 % (115/372) of prescription entries and fifty eight (51 %) prescription entries requiring dose adjustment were found to be inappropriate. Of 73 patients, 54 patient received ≥ 1 drug that required dose adjustment (median 2; range 1-6). Fifteen (28 %) patients had all of their drugs appropriately adjusted while twenty two (41 %) patients had some drugs appropriately adjusted, and seventeen (31 %) of patients had no drugs appropriately adjusted. No patients were documented to have received dialysis.. The findings indicate that dosing errors were common among hospitalized patients with renal impairment. Improving the quality of drug prescription in patients with renal impairment could be of importance for improving the quality of care.

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Aged, 80 and over; Allopurinol; Anti-Arrhythmia Agents; Anti-Bacterial Agents; Anti-Ulcer Agents; Antifungal Agents; Antihypertensive Agents; Ceftazidime; Cimetidine; Creatinine; Cross-Sectional Studies; Digoxin; Diuretics; Drug Dosage Calculations; Drug Prescriptions; Enalapril; Ethiopia; Female; Fluconazole; Gout Suppressants; Hospitalization; Humans; Male; Medication Errors; Middle Aged; Pharmaceutical Preparations; Prospective Studies; Renal Insufficiency, Chronic; Severity of Illness Index; Spironolactone; Trimethoprim, Sulfamethoxazole Drug Combination; Vancomycin; Young Adult

This retrospective study aimed to compare systolic and diastolic blood pressures between patients with acute kidney injury (AKI) after initiation of angiotensin-converting enzyme (ACE) inhibitor therapy and those of patients who do not experience AKI after ACE inhibitor therapy. 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). These cases were matched one to four by age and gender to patients who received an ACE inhibitor but did not have a doubling of SCr (control group). The patients in the AKI group had a significantly greater decrease in systolic and diastolic blood pressures before their AKI than the control group. Pediatric patients who experience ACE inhibitor-associated AKI have a significantly greater decrease in blood pressure than patients who do not experience ACE inhibitor-associated AKI. The authors suggest that the risk and benefits of ACE inhibitor use be stringently evaluated before initiation of therapy.

Topics: Acute Kidney Injury; Adolescent; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Captopril; Cardiovascular Diseases; Case-Control Studies; Child; Child, Preschool; Creatinine; Enalapril; Female; Humans; Hypotension; Infant; Male; Retrospective Studies

Less than 10% of the patients with systemic scleroderma develop renal crisis, i.e. acute renal failure and severe hypertension in most cases. Kidney biopsy shows hypertensive arteriolar changes. This complication was lethal until treatment with captopril was introduced in 1976. Since that time the survival of the patients has improved. If treatment is started early, further deteoriation of the kidney may be prevented.

Topics: Acute Kidney Injury; Antihypertensive Agents; Enalapril; Humans; Hypertension; Male; Middle Aged; Renal Dialysis; Scleroderma, Diffuse

Angiotensin converting enzyme inhibitors have been used in the neonatal population for both cardiac and renal diseases. Past reports have described deleterious renal and neurological consequences as a result of these drugs. This report describes two infants receiving enalapril for different indications who suffered renal impairments, likely a result of concomitant diuretic use. These cases demonstrate the risks associated with ACE inhibitor use and the importance of vigilant monitoring when using these medications.

Topics: Acute Kidney Injury; Anal Canal; Angiotensin-Converting Enzyme Inhibitors; Enalapril; Esophagus; Heart Defects, Congenital; Heart Septal Defects, Atrial; Humans; Infant; Kidney; Limb Deformities, Congenital; Male; Spine; Trachea; Transposition of Great Vessels

Topics: Acute Kidney Injury; Adenocarcinoma; Aged; Biphenyl Compounds; Disease Progression; Diuretics; Doxazosin; Drug Therapy, Combination; Enalapril; Furosemide; Glomerulonephritis, IGA; Humans; Irbesartan; Male; Methylprednisolone; Nocturia; Prednisone; Prostatic Neoplasms; Remission Induction; Renal Dialysis; Tetrazoles

Topics: Acute Kidney Injury; Antihypertensive Agents; Biopsy; Child; Diagnosis, Differential; Enalapril; Follow-Up Studies; Hemolytic-Uremic Syndrome; Humans; Hypertension, Renal; Hypertrophy, Left Ventricular; Kidney; Propranolol; Purpura, Thrombotic Thrombocytopenic; Radionuclide Imaging; Renal Dialysis; Severity of Illness Index; Technetium Tc 99m Dimercaptosuccinic Acid; Time Factors; Treatment Outcome

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Child; Enalapril; Etanercept; Familial Mediterranean Fever; Glomerulonephritis; Humans; Immunoglobulin G; Male; Receptors, Tumor Necrosis Factor; Tumor Necrosis Factor-alpha

Sepsis-related acute kidney injury (AKI) is the leading cause of AKI in intensive care units. Endotoxin is a primary initiator of inflammatory and hemodynamic consequences of sepsis and is associated with experimental AKI. The present study was undertaken to further examine the role of the endothelium, specifically prostacyclin (PGI(2)), in the pathogenesis of endotoxemia-related AKI. A low dose of endotoxin (LPS, 1 mg/kg) in wild-type (WT) mice was associated with stable glomerular filtration rate (GFR) (164.0 +/- 16.7 vs. 173.3 +/- 6.7 microl/min, P = not significant) as urinary excretion of 6-keto-PGF(1alpha), the major metabolite of PGI(2), increased. When cyclooxygenase inhibition with indomethacin abolished this rise in 6-keto-PGF(1alpha), the same low dose of LPS significantly decreased GFR (110.7 +/- 12.1 vs. 173.3 +/- 6.7 microl/min, P < 0.05). The same dose of indomethacin did not alter GFR in WT mice. To further study the role of PGI(2) in endotoxemia, renal-specific PGI synthase (PGIs) transgenic (Tg) mice were developed that had increased PGIs expression only in the kidney and increased urinary 6-keto-PGF(1alpha). These Tg mice, however, demonstrated endotoxemia-related AKI with low-dose LPS (1 mg/kg) (GFR: 12.6 +/- 3.9 vs. 196.5 +/- 21.0 microl/min P < 0.01), which did not alter GFR in WT mice (164.0 +/- 16.7 vs. 173.3 +/- 6.7 microl/min, P = not significant). An elevation in renal cAMP, however, suggested an activation of the PGI(2)-cAMP-renin system in these Tg mice. Moreover, angiotensin-converting enzyme inhibition afforded protection against endotoxin-related AKI in these Tg mice. Thus endothelial PGIs-mediated PGI(2), as previously shown with endothelial nitric oxide synthase-mediated nitric oxide, contributes to renal protection against endotoxemia-related AKI. This effect may be overridden by excessive activation of the renin-angiotensin system in renal-specific PGIs Tg mice.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Cyclooxygenase Inhibitors; Cytochrome P-450 Enzyme System; Enalapril; Endothelium; Endotoxemia; Endotoxins; Epoprostenol; Escherichia coli Infections; Glomerular Filtration Rate; Indomethacin; Intramolecular Oxidoreductases; Kidney; Lipopolysaccharides; Male; Mice; Mice, Transgenic; Prostaglandin-Endoperoxide Synthases; Regional Blood Flow

Ischemia-reperfusion-induced acute renal failure (ARF) is associated with a high mortality in patients with hypertension and with an unfavorable outcome of kidney transplants from marginal donors.. The influence of allopurinol and enalapril on urinary nitrate/nitrite (UNOx), glomerular filtration rate, plasma and urinary sodium, and hemodynamic parameters was examined in spontaneously hypertensive rats (SHR) with ARF.. ARF was induced by right-kidney removal and clamping the left renal artery for 40 min in 50 male 26-week-old SHR weighing 300 +/- 23 g. The rats were randomly allocated to five groups: (1) sham operated; (2) ARF; (3) ARF after pretreatment with 40 mg/kg allopurinol; (4) ARF after pretreatment with 40 mg/kg enalapril, and (5) ARF after pretreatment with 40 mg/kg allopurinol and 40 mg/kg enalapril. Creatinine clearance, UNOx (Griess reaction), cardiac output (dye dilution technique), mean arterial blood pressure, and renal blood flow were measured 24 h after reperfusion. Total vascular resistance and renal vascular resistance were calculated and compared between the groups.. A nonsignificant decrease was found in both daily UNOx excretion and creatinine clearance when pretreated ARF groups and the ARF group without pretreatment were compared (p > 0.05). Significantly lower plasma sodium values (139.5 +/- 4.86 mmol/l) in the allopurinol-pretreated ARF group were found than in the ARF group without pretreatment, in the ARF group pretreated with enalapril, and in the sham SHR group (p = 0.029). The urinary sodium loss was greater in the enalapril-pretreated than in the allopurinol-pretreated ARF group (p = 0.047). Allopurinol and/or enalapril pretreatment decreased total vascular resistance (p = 0.003) in comparison with the sham SHR group.. Neither allopurinol nor enalapril nor both were protective against ischemia-reperfusion injury in SHR, nor altered glomerular filtration rate and UNOx in a favorable direction.

Topics: Acute Kidney Injury; Allopurinol; Animals; Antihypertensive Agents; Antimetabolites; Drug Combinations; Enalapril; Male; Nitrates; Nitrites; Rats; Rats, Inbred SHR; Reperfusion Injury; Sodium; Treatment Outcome

A 67 year old woman developed acute renal failure with serum potassium 9.4 mmol/l requiring emergency dialysis after seven days of diarrhoea while taking an ACE inhibitor for vascular disease. Review of the literature, the British National Formulary, and the patient information leaflets for each of the 11 ACE inhibitors currently marketed in the UK suggests that this potentially life threatening complication of ACE inhibition is not yet widely recognised.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Diarrhea; Enalapril; Female; Humans; Hyperkalemia

Parathyroid hormone-related protein (PTHrP), a mitogenic factor for renal cells, is overexpressed in acute renal failure (ARF). Recent data support an association between PTHrP and the renin-angiotensin system in the damaged kidney. The effects of angiotensin II (Ang II) inhibitors (quinapril, enalapril, and/or losartan) on PTHrP and the PTH1 receptor (PTH1R) expression in rats with either folic acid (FA)- or gentamicin-induced ARF were analyzed. The decreased renal function and the PTHrP upregulation and PTH1R downregulation induced by the nephrotoxins were inhibited by the Ang II blockers. In tubuloepithelial cells NRK-52E, the rapid (10 min) increase in PTHrP mRNA by FA, associated with a perinuclear relocalization of Ang II/AT1 receptor, was inhibited by losartan but not candesartan, which traps Ang II receptors at the cell surface. Maximal PTHrP protein overexpression by FA (at 24 to 72 h)-or by exogenous Ang II-was abolished by both Ang II antagonists. PTHrP upregulation by FA was preceded by increased extracellular signal-regulated kinase (ERK) phosphorylation and inhibited by the ERK inhibitor PD098059. FA also activated cAMP response element-binding (CREB) protein, and this was prevented by losartan in these cells. Moreover, PTHrP mRNA overexpression by either FA or Ang II occurred in NRK 52E that were transfected with a CREB construct but not the dominant-negative CREB133 construct. These findings demonstrate that the decreased renal function and PTHrP overexpression in nephrotoxin-damaged kidney depends on renin-angiotensin system. In this setting, intracellular Ang II/AT1 receptor recycling seems to be related to PTHrP induction through ERK and CREB activation in tubuloepithelial cells.

Topics: Acute Kidney Injury; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Cell Line; Enalapril; Folic Acid; Gentamicins; Kidney; Kidney Tubules; Losartan; Male; Parathyroid Hormone-Related Protein; Quinapril; Rats; Rats, Wistar; Receptor, Parathyroid Hormone, Type 1; Renin-Angiotensin System; Tetrahydroisoquinolines

ACE inhibitors are commonly used drugs in the management of adult hypertension. However their use in pregnant women can have serious effects on the fetus. In this manuscript we report a case of fatal neonatal renal failure associated with maternal intake of enalapril during third trimester and review the related literature.. The index case was born to a mother with PIH which was treated with enalapril (5 mg) once a day for 21 days prior to delivery in addition to other anti-hypertensives. Temporally, use of enalapril was associated with the onset of oligohydramnios. The neonate presented with intrauterine growth retardation, hydrops and oliguric renal failure, which did not respond to furosemide, peritoneal dialysis and exchange transfusion. Autopsy showed macroscopically and microscopically normal kidneys.. Use of ACE inhibitors during pregnancy should be avoided.

Topics: Acute Kidney Injury; Adult; Angiotensin-Converting Enzyme Inhibitors; Diagnosis, Differential; Enalapril; Fatal Outcome; Female; Humans; Hypertension; Infant, Newborn; Male; Pregnancy; Pregnancy Complications, Cardiovascular

A 60 year old male patient having systemic scleroderma and normotensive scleroderma renal crisis was admitted in our hospital. He presented polyarticular, esophagic, lung and skin compromise. Before admission he had been treated with high doses of corticosteroids. We believe corticosteroids led to the worsening of renal damage with renal failure, microangiopathic hemolytic anemia without high blood pressure. The 10% of these cases have normal blood pressure. The patient was treated with enalapril and hemodialysis. There was no favourable response to this treatment and he died seven days after admission.

Topics: Acute Kidney Injury; Adrenal Cortex Hormones; Anemia, Hemolytic; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Enalapril; Fatal Outcome; Humans; Male; Middle Aged; Renal Dialysis; Scleroderma, Systemic

A full-term baby boy developed congestive cardiac failure secondary to left-to-right shunts. He developed acute renal failure following the administration of oral enalapril given for the treatment of cardiac failure. There was no underlying renal disease or renal artery stenosis. He required three peritoneal dialyses, following which he recovered from the renal failure.

Topics: Acute Kidney Injury; Antihypertensive Agents; Enalapril; Heart Defects, Congenital; Heart Failure; Humans; Infant, Newborn; Male; Peritoneal Dialysis

Renal artery stenosis may present as acute pulmonary oedema and be misinterpreted as congestive heart failure. ACE inhibitors and angiotensin-II antagonists are widely used among patients with congestive heart failure and hypertension.. The authors present a patient with congestive heart failure caused by a combination of coronary heart disease and bilateral renal artery stenosis. The patient developed acute kidney failure secondary to ACE inhibitor and angiotensin II antagonist treatment.. Mechanisms behind pulmonary oedema secondary to renovascular hypertension are discussed.. Revascularisation is the treatment of choice for this patient category.

Topics: Acute Kidney Injury; Adult; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Diagnosis, Differential; Enalapril; Heart Failure; Humans; Hypertension; Hypertension, Renovascular; Male; Pulmonary Edema; Renal Artery Obstruction

Acute renal failure is a well-known complication in patients with renal artery stenosis during treatment with ACE inhibitor. Renal artery thrombosis after withdrawal of ACE inhibitor has not been reported previously.. We describe a patient with acute renal failure with an unexpected course.. A 67-year-old man was admitted with acute anuric renal failure during treatment with hydrochlorothiazide and enalapril. His blood pressure was 165/60 mm Hg. Renal ultrasound was normal. After initial rehydration and dialysis, diuresis resumed until a sudden unexpected anuric renal failure recurred on day 12. Angiography disclosed bilateral renal artery occlusion. The right renal artery was successfully opened and a stenosis was blocked and stented, and brisk diuresis ensued. Two days later hypertension accelerated, and a new invasive procedure on day 24 succeeded in opening, blocking and stenting a proximal stenosis in the left artery; a mobile thrombus was located behind the stenosis and successfully treated with intraarterial thrombolysis. Blood pressure rapidly normalized, and serum creatinine was normal on visits 1.5 and 4 months later.. General aspects and prevention of acute renal failure during ACE inhibitor therapy are discussed. Acute renal thrombosis after withdrawal of ACE inhibitor in patients with stimulated renin angiotensin system and significant renal artery stenosis may be causally related to the antifibrinolytic effects of angiotensin II and aldosterone. Endovascular reconstruction of renal artery occlusion may completely restore the kidney function.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Diuretics; Enalapril; Humans; Hydrochlorothiazide; Male; Radiography; Renal Artery Obstruction; Renin-Angiotensin System; Sodium Chloride Symporter Inhibitors

A reduction in glomerular filtration rate (GFR) is a primary characteristic of ischemic acute renal failure. The present study was undertaken to examine the roles of angiotensin II, tubuloglomerular-feedback (TGF) mechanism, and tubular obstruction for the GFR reduction in the post-ischemic kidney. Renal ischemia was induced by occlusion of the bilateral renal arteries for 60 min, and renal function was examined at 2 and 24 h after the onset of reflow. After the end of 2-h reflow, the GFR was not significantly changed, but the urine flow increased significantly. On the other hand, at the end of 24-h reflow, the GFR and urine flow decreased markedly along with increased filtration fraction. The renal blood flow significantly decreased at 24 h, but not 2 h, after reflow, which was accompanied by increased total renal vascular resistance. Furosemide infusion (1 mg/min/kg) after 24 h of reflow prevented the reduction in GFR and filtration fraction without no changes in renal blood flow and total renal vascular resistance. Pretreatment of enalapril and losartan did not prevent the reduction in GFR, indicating that angiotensin II was not involved. In morphological examinations, tubular obstruction was seen in the proximal and distal tubules of kidneys both at 2 and 24 h after the onset of reflow. In two rabbits subjected to 48 h of reflow, the tubular obstruction was not observed, despite GFR remained depressed. These results suggest that the late reduction in GFR in postischemic kidneys is not mediated by angiotensin II, but is mediated, at least in part, by the TGF mechanism. The tubular obstruction may be not prerequisite for the GFR reduction in rabbits.

Topics: Acute Kidney Injury; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Biomarkers; Creatinine; Enalapril; Female; Glomerular Filtration Rate; Ischemia; Kidney; Kidney Tubules; Losartan; Male; Rabbits; Renal Circulation; Urodynamics

Renal failure in multiple myeloma can be precipitated during hemodynamic perturbances of renal blood flow, as seen secondary to volume depletion, radiocontrast dye, and nonsteroidal anti-inflammatory agents. We report two cases of acute renal failure that developed suddenly after initiation of angiotensin-converting enzyme (ACE) inhibitor, both with biopsy-proven cast nephropathy. ACE inhibitors may contribute to the intratubular light chain cast formation and acute "myeloma kidney" in susceptible patients.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Back Pain; Captopril; Diabetes Mellitus, Type 1; Enalapril; Humans; Hypertension; Male; Multiple Myeloma

Successful bilateral renal revascularization was performed 24 days after the development of angiotensin converting enzyme-inhibitor-induced bilateral renal artery thrombosis and anuric acute renal failure in a patient with Takayasu's arteritis. Excellent results were obtained after an unusually long ischemic time for a patient with active-phase disease. The outcome suggests that aggressive surgical revascularization can benefit patients with renal failure caused by renal arterial occlusion during the active phase of Takayasu's arteritis.

Topics: Acute Kidney Injury; Adult; Angiotensin-Converting Enzyme Inhibitors; Anuria; Collateral Circulation; Enalapril; Female; Humans; Radiography; Renal Artery Obstruction; Takayasu Arteritis; Thrombosis

Topics: Acute Kidney Injury; Anti-Inflammatory Agents, Non-Steroidal; Antihypertensive Agents; Diabetes Mellitus, Type 1; Diuretics; Electrocardiography; Enalapril; Female; Humans; Hyperkalemia; Ibuprofen; Middle Aged; Spironolactone

The endothelial vasoconstrictor endothelin (ET) can induce acute renal failure when fibrinolysis and vasodilatory prostanoids (PGs) are inhibited. This study compares therapeutic agents preventing ET-induced acute renal failure in anesthetized female pigs. We investigated the effect of four ET boli (1.5 microg/kg, i.v.) after pretreatment with indomethacin (2 mg/kg) and epsilon-aminocaproicacid (100 + 50 mg/kg) alone (controls, group 1) or during additional nifedipine (10 microg/kg/h; group 2), hirudin (0.5 mg/kg; group 3), or enalapril (2 x 0.15 mg; group 4) on coagulation, PGs, and renal function. The ET-induced blood pressure increase was lower in groups 2 to 4 (lowest in group 3, P < 0.05). PG synthesis was blocked in all groups. The initial hypercoagulability (controls) resulted in disseminated intravascular coagulation that was prevented by hirudin and was attenuated in groups 2 and 4. At the end of the experiment, creatinine clearance was significantly (P < 0.05) decreased. The recovery of renal function two hours after the last ET bolus was most pronounced in the hirudin group. All therapeutic drugs attenuated ET-induced impairment of renal function. Hirudin seems to be the most potent protective drug. Prevention of further ET release evoked by ET-mediated secretion of thrombin might explain this. These results suggest three important pathways for ET's hemodynamic and renal effects.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antithrombins; Blood Pressure; Calcium Channel Blockers; Creatinine; Disease Models, Animal; Enalapril; Endothelins; Female; Hirudins; Indomethacin; Nifedipine; Renal Circulation; Swine; Vasoconstrictor Agents

Rapid degradation of renal function may occur in patients given drug regimens combining a converting enzyme inhibitor, a diuretic and a nonsteroidal anti-inflammatory drug.. A patient given flecainide and an enalapril /hydrochlorothiazide combination in a well-tolerated long-term regimen suddenly developed acute renal failure when a nonsteroidal anti-inflammatory drug was introduced leading to an overdose of the anti-arrhythmic drug.. A poor understanding of the elimination routes for anti-arrhythmic drugs and the risks involved when combined with nonsteroidal anti-inflammatory drugs modifying glomerular hemodynamics can lead to dangerous prescriptions and life-threatening situations in patients on multiple drug regimens.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Anti-Inflammatory Agents, Non-Steroidal; Antihypertensive Agents; Atrial Fibrillation; Diuretics; Drug Interactions; Drug Therapy, Combination; Electrocardiography; Enalapril; Flecainide; Heart Block; Humans; Hydrochlorothiazide; Hypertension; Iatrogenic Disease; Indomethacin; Male; Periarthritis; Sodium Chloride Symporter Inhibitors

Acute renal failure and hyperkalemia due to angiotensin-converting enzyme inhibitors have been described in diabetic patients with other predisposing conditions. The case reported here involves a patient with type 1 diabetes mellitus, microalbuminuria and normal renal function who was treated with enalapril. Two years after initiation of this therapy, at a time when glycemic control was poor, he presented with symptomatic hyperkalemia and impaired renal function accompanied by hyporeninemic hypoaldosteronism. This case illustrates that reversible impairment of renal function and hyperkalemia can present after 2 years of treatment with angiotensin-converting enzyme inhibitors in patients with precipitating factors.

Topics: Acute Kidney Injury; Adult; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Enalapril; Humans; Hyperkalemia; Hypertension; Hypoaldosteronism; Male; Precipitating Factors

Based on 2 case presentations - acute renal failure (ARF) due to myeloma kidney and due to angiotensin-converting enzyme inhibitor administration in the presence of transplant artery stenosis - new aspects in the pathogenesis of ARF are presented and discussed. The multifactorial pathogenesis of ARF includes (a) a disturbance of glomerular microcirculation (afferent and perhaps mesangial constriction, inadequate efferent dilatation); (b) a disturbance of medullary microcirculation (medullary capillary congestion) attributed to a combination of endothelial damage and tubular dilatation; (c) tubular cell damage which, though rarely in humans justifying the term 'acute tubular necrosis', promotes both backleak of glomerular filtrate and shedding of brush border vesicles; (d) the latter promotes tubular obstruction by casts which consist of Tamm-Horsfall protein and brush border components. Once ARF is established, repair processes set in which appear to depend on growth factors such as epidermal growth factor and insulin-like growth factor 1, of which there is a relative shortage in established ARF. Experimental therapeutic approaches focus on the restitution of microcirculation (endothelin receptor antagonists, atriopeptins), interference with cast formation (integrin receptor blockers), and the promotion of recovery by growth factors.

Topics: Acute Kidney Injury; Aged; Angioplasty, Balloon; Angiotensin-Converting Enzyme Inhibitors; Antineoplastic Agents; Arteriosclerosis; Enalapril; Female; Glomerular Filtration Rate; Humans; Kidney; Kidney Glomerulus; Kidney Neoplasms; Kidney Transplantation; Male; Multiple Myeloma; Postoperative Complications; Renal Circulation

Topics: Acute Kidney Injury; Adult; Angiotensin-Converting Enzyme Inhibitors; Anuria; Cesarean Section; Enalapril; Female; Humans; Hypertension; Infant, Newborn; Iodine Radioisotopes; Kidney; Peptidyl-Dipeptidase A; Peritoneal Dialysis; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Trimester, Third; Prenatal Exposure Delayed Effects; Radionuclide Imaging; Technetium Tc 99m Pentetate

A 35-year-old nephrotic man developed acute renal failure with serum creatinine to 1543 micromol/l after a month of therapy with enalapril. Renal biopsy demonstrated minimal glomerular changes with fusion of podocytes, tubular necrosis with regeneration of tubular epithelial cells, interstitial edema with focal interstitial fibrosis, and interstitial infiltration with neutrophils, eosinophils, plasma cells and mononuclear cells. Three hemodialyses were performed in the patient during the oliguric phase of the disease. Renal function was restored after withdrawal of enalapril and initiation of steroid therapy. Steroids also contributed to the improvement of the nephrotic syndrome and proteinuria decreased from maximal ranges of 27 g/l to 2.2 g/l after six months of the follow-up. Similar cases were previously described associated with captopril treatment, but not with enalapril.

Topics: Acute Kidney Injury; Adult; Cyclophosphamide; Enalapril; Humans; Kidney; Kidney Tubules; Male; Methylprednisolone; Microscopy, Electron; Nephrosis, Lipoid; Prednisone

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Captopril; Child, Preschool; Down Syndrome; Enalapril; Female; Heart Failure; Humans; Infant; Male

Topics: Acute Disease; Acute Kidney Injury; Anti-Bacterial Agents; Antihypertensive Agents; Enalapril; Erythromycin; Glomerulonephritis, IGA; Humans; Hypertension; Male; Middle Aged; Nephritis, Interstitial

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Aortic Coarctation; Enalapril; Heart Failure; Humans; Male; Middle Aged

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Bicarbonates; Diabetes Mellitus, Type 1; Diabetic Angiopathies; Diuresis; Enalapril; Female; Gemfibrozil; Humans; Hyperlipidemias; Hypertension; Hypolipidemic Agents; Rhabdomyolysis

Topics: Acute Kidney Injury; Aged; Enalapril; Female; Humans

We report a patient with reversible acute oligoanuric renal failure. Intravenous mannitol 25% was infused to treat intracranial edema, during chronic administration of ACE inhibitors for arterial hypertension. Serum creatinine level rose to 5.6 mg/dl from a previous value of 1.2 mg/dl. Measured and calculated serum osmolalities were 310 and 280 mosm/kg respectively. We postulate that the association of afferent arteriolar constriction due to mannitol induced tubulo-glomerular imbalance and efferent dilatation due to ACE inhibitors provoked a sharp reduction in glomerular filtration rate. Alternatively, mannitol infusion may have caused tubular cell swelling with luminal obstruction.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Diuretics, Osmotic; Drug Therapy, Combination; Enalapril; Humans; Male; Mannitol; Middle Aged

Treatment of hypertension with enalapril in a preterm infant is described. Enalapril is a new converting enzyme blocker with a longer plasma half-life and less side effects than captopril. Oral administration of enalapril 0.1 mg/kg caused severe hypotension and renal failure in a preterm infant. We recommend an oral starting dose of 0.01 mg/kg in preterm infants and extremely close monitoring of infants receiving the first dose of enalapril.

Topics: Acute Kidney Injury; Antihypertensive Agents; Dose-Response Relationship, Drug; Drug Administration Schedule; Enalapril; Humans; Hypotension; Infant, Newborn; Infant, Premature, Diseases; Male

BACKGROUND. Exposure of pregnant women to angiotensin converting enzyme inhibitor may have side effects on the fetus or newborn, mainly oligoamnios and impaired renal function. CASE REPORT N zero 1. A 34 year-old woman was given enalapril from the onset of her pregnancy because of hypertension from the age of 18 years. Oligoamnios was diagnosed in the fetus on gestational week 28; enalapril was then replaced by nifedipine but this drug was badly tolerated so that the woman was again given enalapril 8 days later. The baby (1700 g) was born by cesarean section at gestational week 34 because of acute distress syndrome; he developed hypotension, anuria, generalized oedema and was placed in intensive care. Treatment included ventilation, sympathomimetic agents, and diuretics. An exchange-transfusion followed by peritoneal dialysis was performed a few hours later. Renal function returned to normal between the 3rd and 5th day. Unilateral kidney hypoplasia was diagnosed at the age of 2 years. CASE N zero 2. A 24 year-old woman was given enalapril at the third trimester of a twin pregnancy. Delivery was full term at 37 weeks. The first baby, a boy weighing 2610 g, suffered from hypoglycemia and vomiting followed by hypotension and oliguria that required exchange-transfusion and repeated peritoneal dialysis. This boy has developed moderate chronic renal failure and hypertension. The second baby, a girl weighing 2,165 g, suffered from respiratory distress syndrome followed by hypotension and oliguria, but her renal function returned to normal within a few days. CONCLUSIONS. The use of angiotension converting enzyme inhibitor by pregnant women places the fetus at severe risk: treatment with this type of drug should be stopped as soon as pregnancy is confirmed.

Topics: Acute Kidney Injury; Adult; Blood Pressure; Enalapril; Female; Humans; Infant, Newborn; Male; Maternal-Fetal Exchange; Oligohydramnios; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects

In a tertiary referral centre 63 patients underwent 67 treatment periods with enalapril. The median age was 5.4 months. All children had signs of heart failure: congestive cardiac failure with breathlessness at rest was present in 88%. Haemodynamic groups were left-to-right shunt (n = 15), impaired ventricular function (n = 14), after cardiac surgery (n = 23), valvar regurgitation (n = 12), and hypertension (n = 3). Serial clinical, radiological, and laboratory data were used to judge outcome. The mean (SD) maximal dose was 0.30 (0.21) mg/kg/day. Thirty nine (58%) patients improved, 20 (30%) showed no improvement, and eight (12%) had side effects requiring discontinuation of enalapril. Renal failure in eight patients was related to young age, low weight, and left-to-right shunt group. Three patients died in congestive heart failure with renal failure. Enalapril was clinically safe and effective for children with cardiac failure secondary to ventricular impairment, valvar regurgitation, or after cardiac surgery. Renal failure was a problem in young infants with left-to-right shunts.

Topics: Acute Kidney Injury; Adolescent; Blood Pressure; Child; Child, Preschool; Drug Administration Schedule; Enalapril; Endocardial Cushion Defects; Heart Diseases; Heart Failure; Humans; Infant; Infant, Newborn; Vascular Resistance

Topics: Acrylates; Acute Kidney Injury; Angiotensin I; Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Captopril; Cough; Dogs; Enalapril; Female; Glomerular Filtration Rate; Imidazoles; Male; Renal Circulation; Thiophenes

When administered to a 45-year-old woman who was ill with severe hypertension, combined enalapril and hydrochlorothiazide therapy resulted in acute renal failure, leading to a successful search for renal artery stenosis. Acute renal failure as an adverse reaction to enalapril therapy occurs in approximately 20% of patients with secondary hypertension from renovascular disease. On the other hand, in a group of essential hypertensives this occurs at a rate of approximately 0.2%. Thus, a likelihood ratio of 100 is produced, and given the prevalence of renovascular hypertension of approximately 2% in all hypertensives, a posterior probability of 0.67 can be calculated. The occurrence of this adverse effect should indicate that a diagnostic work-up to rule out renovascular hypertension in such patients should be pursued. The sensitivity and specificity of this "test" are 0.20 and 0.998, respectively. This illustrates that the mathematic aids in decision theory need not be applied solely to those more traditional aspects of diagnostic testing, but may be useful in other situations as well.

Topics: Acute Kidney Injury; Enalapril; Female; Humans; Hydrochlorothiazide; Hypertension, Renovascular; Middle Aged; Uremia

Topics: Acute Kidney Injury; Enalapril; Humans; Male; Middle Aged

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Diuretics; Drug Synergism; Enalapril; Humans; Hypertension, Renal; Male; Nephrosclerosis

Topics: Acute Kidney Injury; Enalapril; Humans; Hypertension; Male

The Authors describe a clinical case of a patient affected by arterial hypertension of severe degree (IV grade OMS) that during therapy with ACE inhibitors and diuretics developed acute renal failure that reversed after stopping treatment. The clinical course was quite similar to acute renal failure induced by ACE inhibitors and diuretics in patient with bilateral renal artery stenosis. In interpreting the pathogenesis, the Authors suppose, beside a reductions of effective plasma flow, the coexistence of hyalinosis of renal arterioles. They underline the necessity of monitoring renal function at least in the first weeks of therapy when a treatment with ACE inhibitors and diuretics is started especially in patients with hypertension of high degree and/or reduced renal function.

Topics: Acute Kidney Injury; Adult; Angiotensin-Converting Enzyme Inhibitors; Chlorthalidone; Diuretics; Enalapril; Humans; Hypertension; Kidney Function Tests; Male; Renal Artery Obstruction

Five patients (median age 63 years) with severe crescentic glomerulonephritis had acute renal failure (median plasma creatinine 930, range 690-1390). Following induction of immunosuppressive treatment all patients achieved recovery of adequate renal function (median creatinine 440, range 290-570 mumol/l). After 3-6 months of continuous remission, all patients, despite stable renal function developed increasing proteinuria (median 4.4 g/24 h, range 3.2-6.1), and enalapril (5-20 mg per day) was substituted or introduced as antihypertensive therapy. Immunosuppression was not altered. After 1 year, renal function remained stable in four patients and plasma creatinine increased initially in one patient before becoming stable: proteinuria was reduced substantially in all patients to a median of 0.8 g/24 h, range 0.2-1.3). Patients with severe crescentic glomerulonephritis may develop persistent or increasing proteinuria despite successful treatment of acute disease. We have used enalapril to reduce proteinuria and maintain function in such patients.

Topics: Acute Kidney Injury; Aged; Antihypertensive Agents; Creatinine; Drug Therapy, Combination; Enalapril; Glomerulonephritis; Humans; Immunosuppressive Agents; Middle Aged; Proteinuria

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Drug Therapy, Combination; Enalapril; Glomerular Filtration Rate; Humans; Kidney

Topics: Acute Kidney Injury; Enalapril; Heart Failure; Humans; Hypotension; Male; Middle Aged

In 1986, the Committee on Safety of Medicines published a report suggesting that enalapril may have an adverse effect on renal function. The prescription event monitoring scheme subsequently published figures on adverse drug reactions and mortality for patients treated with enalapril. They concluded that enalapril did not have an adverse effect on renal function and survival. Similar data were not available for captopril, as the drug was marketed before prescription event monitoring had been developed. In the Department of Health and Social Security (DHSS) Hypertension Care Computing Project (DHCCP), 368 hypertensive patients treated with captopril and 371 treated with enalapril were followed for an average of 3.1 and 1.6 years, respectively. Thirty-two patients died; none had renal failure as an underlying cause of death. The death rate was similar in both drug groups, at 17.5 (enalapril) and 24.0 (captopril) per 1000 patient-years. The present report shows that, for patients treated for high blood pressure, the relative risk of mortality with captopril compared with enalapril was 1.37, an insignificant difference (95% confidence interval 0.63, 2.98).

Topics: Acute Kidney Injury; Captopril; Enalapril; Female; Humans; Hypertension; Male; Middle Aged; Product Surveillance, Postmarketing; Survival Rate; United Kingdom

Acute deterioration of renal function occurred shortly after the angiotensin-converting enzyme (ACE) inhibitor, enalapril, was administered to two renal transplant patients who were also receiving cyclosporine. Renal function recovered completely in both cases upon discontinuation of enalapril. Neither patient had evidence of transplant artery stenosis or chronic rejection, conditions known to predispose to renal failure during ACE inhibitor therapy. The possibility that afferent vasoconstriction induced by cyclosporine may have predisposed these patients to renal failure from enalapril is discussed.

Topics: Acute Kidney Injury; Adult; Cyclosporins; Enalapril; Female; Graft Rejection; Humans; Kidney Transplantation; Male; Renal Circulation; Vasoconstriction

Ten daily injections of gentamicin, 40 mg/kg/d intraperitoneal (IP), produced a marked reduction in the glomerular capillary ultrafiltration coefficient (Kf) of virgin female Munich-Wistar rats without eliciting significant reductions in glomerular filtration rate (GFR) or single nephron (SN)GFR. A similar gentamicin-induced decrease in Kf was seen in midterm pregnant (day 12) rats and the normal gestational increase in GFR and SNGFR was blunted by gentamicin. Concomitant converting enzyme inhibition (CEI) (MK 421, 50 mg/L drinking water) completely prevented the gentamicin-induced decrease in Kf in virgin females, thus confirming that the gentamicin-induced decline in Kf is mediated by angiotensin II (ANG II). These studies indicate that pregnancy neither exacerbates nor ameliorates gentamicin-induced glomerulotoxicity and also that glomerular ANG II responsivity is not diminished in midterm pregnant rats.

Topics: Acute Kidney Injury; Animals; Enalapril; Female; Gentamicins; Glomerular Filtration Rate; Hematocrit; Pregnancy; Pregnancy, Animal; Rats; Renal Circulation; Vascular Resistance

Activation of the renin angiotensin system is important in the development of accelerated hypertension and progression to acute renal failure in scleroderma and undifferentiated connective tissue disease. Inhibition of angiotensin-converting enzyme activity may effectively control blood pressure and ameliorate renal insufficiency. To our knowledge, we describe the first reversal of dialysis-dependent renal insufficiency by enalapril maleate and recovery and maintenance of near-normal renal function in a patient suffering from undifferentiated connective tissue disease with sclerodermatous features. The pathophysiologic mechanisms and long-term treatment implications with angiotensin-converting enzyme inhibitors in this setting are discussed.

Topics: Acute Kidney Injury; Adult; Captopril; Connective Tissue Diseases; Enalapril; Female; Humans; Hypertension; Renin-Angiotensin System

Persistent anuria was diagnosed in a neonate born to a mother whose pregnancy was complicated by severe hypertension and systemic lupus erythematosus. Severe maternal hypertension necessitated the use of a battery of antihypertensive medications that included enalapril, an angiotensin converting enzyme inhibitor. The role of enalapril in neonatal renal failure is discussed.

Topics: Acute Kidney Injury; Antihypertensive Agents; Anuria; Drug Therapy, Combination; Enalapril; Female; Humans; Hyaline Membrane Disease; Hypertension; Infant, Newborn; Kidney; Lupus Erythematosus, Systemic; Male; Pregnancy; Pregnancy Complications

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Enalapril; Female; Humans; Hyperkalemia; Lisinopril; Male; Middle Aged

Topics: Acute Kidney Injury; Adult; Enalapril; Female; Humans; Infant, Newborn; Pre-Eclampsia; Pregnancy

The influence of the renin-angiotensin system on renal hemodynamics, tubular pressure and tubulo-glomerular feedback was investigated with the angiotensin converting enzyme inhibitor MK 421 (enalapril), in uninephrectomized rats with and without ischemia-induced acute renal failure. In animals with normal renal function proximal tubular pressure and tubulo-glomerular feedback response were lowered by enalapril long-term treatment, whereas glomerular filtration rate and renal blood flow were not influenced by the drug. After 45 and 70 minutes ischemia there was no difference between treated and untreated animals in the severely impaired glomerular filtration rate. Renal blood flow remained unaffected by the treatment. The histological damage due to ischemia (tubular casts, tubular necrosis and medullary capillary congestion) was not influenced by enalapril. As tubulo-glomerular feedback had been significantly inhibited during renin-angiotensin inhibition, its importance in mediating acute renal failure remains doubtful; other factors such as tubular obstruction and medullary congestion may be crucial.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Animals; Enalapril; Feedback; Female; Hemodynamics; Ischemia; Kidney Glomerulus; Kidney Tubules; Rats; Rats, Inbred Strains; Renal Artery Obstruction; Renal Circulation; Thrombosis

The pharmacokinetics of lisinopril was studied after administration of single and multiple doses of 5 mg to hypertensive patients with normal and impaired renal function. In patients with severe renal failure the peak concentrations were higher, the decline in serum concentration was slower and the time to peak concentration was extended. Accumulation of lisinopril was highly correlated with the creatinine clearance. The effective half-life was doubled and tripled in patients with mild and severe renal impairment, respectively, as compared to patients with a normal renal function. Lisinopril lowered blood pressure in all three groups over 24 h. It is suggested that smaller doses of lisinopril should be administered to patients with severe renal failure.

Topics: Acute Kidney Injury; Administration, Oral; Adult; Aged; Blood Pressure; Creatinine; Drug Administration Schedule; Enalapril; Female; Glomerular Filtration Rate; Half-Life; Humans; Hypertension; Intestinal Absorption; Lisinopril; Male; Middle Aged; Time Factors

Deterioration in renal function after the use of angiotensin converting-enzyme inhibitors may be the first clue to the presence of bilateral renal arterial stenosis. In order to avoid serious threat to the patient, early detection of the insidious decline in renal function is necessary and depends on routine biochemical monitoring after the initiation of therapy. Six cases are described here, to illustrate the very real danger of this class of drugs in this chemical setting; the grave risk of their combination with potassium-sparing diuretic agents is highlighted.

Topics: Acute Kidney Injury; Aged; Captopril; Creatinine; Enalapril; Female; Humans; Hypertension; Male; Middle Aged; Renal Artery Obstruction; Smoking

The possibility that enalapril might damage renal function was investigated in 1098 deaths recorded in a prescription-event monitoring study. Case notes for 913 patients were examined. In seventy five there was a rise in the urea or creatinine concentration of 50% or more above pretreatment values. Enalapril appeared to have contributed to a decline in renal function and subsequent death in 10 of these patients. Several characteristics were identified among these patients, including old age, the use of high dose or potassium sparing diuretics, and pre-existing renal disease. Adding a non-steroidal anti-inflammatory drug was also associated with a deterioration in patients with previously stable renal function. No death was encountered of a patient with uncomplicated hypertension. Enalapril infrequently contributed to a substantial decline in renal function in certain vulnerable patients, especially those receiving other drugs known to be capable of adversely affecting renal function. Awareness of the characteristics of these patients and of their concomitant treatment may serve to reduce the risk.

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Diuretics; Drug Therapy, Combination; Enalapril; Female; Humans; Male; Middle Aged; Product Surveillance, Postmarketing

In 3 patients with severe cardiac failure high dose therapy with the ACE inhibitor enalapril was instituted during a state of extracellular volume depletion. Severe arterial hypotension with reversible renal insufficiency developed in all the patients. In two the hypovolemia was induced by diuretic treatment and in one by an acute infection with diarrhea. The latter patient also developed life-threatening hyperkalemia with cardiac arrest since he was also receiving spironolactone and potassium supplements. These cases demonstrate that ACE inhibitors should not be instituted during extracellular volume depletion and their initial dosage should be low. The dangerous combination of ACE inhibitors with spironolactone and potassium supplements should be avoided wherever possible.

Topics: Acute Kidney Injury; Drug Interactions; Enalapril; Heart Failure; Humans; Hypotension; Male; Middle Aged; Potassium; Spironolactone; Water-Electrolyte Imbalance

Topics: Acute Kidney Injury; Aged; Drug Therapy, Combination; Enalapril; Female; Heart Failure; Humans; Male; Middle Aged

Three patients are described in whom haemodynamic collapse and acute renal failure occurred following intercurrent gastrointestinal fluid loss during treatment with an angiotensin converting-enzyme inhibitor. The possible consequences of blockade of the formation of angiotensin II during fluid loss are discussed.

Topics: Acute Kidney Injury; Aged; Angiotensin-Converting Enzyme Inhibitors; Captopril; Dehydration; Diarrhea; Enalapril; Hemodynamics; Humans; Male; Middle Aged

The case of vasomotor parenchymal acute renal failure is reported in a patient a few days after the initiation of treatment by Enalapril which is a new converting enzyme inhibitor. No renal artery stenosis could be demonstrated, which is in contrast with the numerous cases reported up to now. However the helping roles of an incomplete obstruction by a peri-aneurysmal retroperitoneal sclerosis, of prolonged anterior treatment with flurbiprofen and of simultaneous administration of furosemide may be discussed.

Topics: Acute Kidney Injury; Drug Therapy, Combination; Enalapril; Flurbiprofen; Furosemide; Humans; Male; Middle Aged; Propionates; Retroperitoneal Fibrosis

A 46 years old patient with IgA nephritis developed an acute renal failure due to enalapril, without renal artery abnormality. A similar impairment of renal function was found during an acute test with 50 mg Captopril.

Topics: Acute Kidney Injury; Aldosterone; Blood Pressure; Captopril; Enalapril; Glomerular Filtration Rate; Glomerulonephritis, IGA; Humans; Male; Middle Aged; Renal Circulation

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Enalapril; Female; Humans; Male; Middle Aged

Topics: Acute Kidney Injury; Aged; Diuretics; Enalapril; Humans; Hypertension, Renovascular; Male

Acute reversible renal failure with hyperkalemia developed in a 42-year-old woman during treatment of heart failure and hypertension with high doses of enalapril and diuretics. Creatinine clearance fell as low as 9 ml/min. Renal-artery stenosis and prerenal renal failure were excluded. Reduction in blood pressure in conjunction with reduced renal perfusion in heart failure can make glomerular filtration angiotensin dependent. Interruption of angiotensin II formation in this situation triggers off functional renal insufficiency.

Topics: Acute Kidney Injury; Adult; Drug Therapy, Combination; Enalapril; Female; Heart Failure; Humans; Hypokalemia; Inulin; Kidney Function Tests; p-Aminohippuric Acid; Spironolactone

A patient with scleroderma renal crisis is described. At presentation he had severe hypertension, deteriorating renal function, microangiopathic haemolytic anaemia, and elevated levels of renin, aldosterone and noradrenaline. Enalapril controlled blood pressure, stabilized renal function, lowered aldosterone and noradrenaline levels, and improved peripheral circulation. It appears that converting-enzyme inhibitors can favourably alter the outlook of this otherwise fatal disorder.

Topics: Acute Kidney Injury; Enalapril; Humans; Hypertension, Renal; Male; Middle Aged; Scleroderma, Systemic

A patient with congestive heart failure and moderate renal insufficiency developed severe reversible non-oliguric renal failure while on frusemide and enalapril. Renal failure developed when enalapril was given in the presence of pronounced sodium depletion. When positive sodium balance was restored the plasma creatinine concentration began to fall while angiotensin converting enzyme inhibition remained effective and blood pressure was stable. These observations suggest that the degree of sodium depletion plays an important role in the tendency for angiotensin converting enzyme inhibitors to induce renal failure in patients with congestive heart failure and moderate renal insufficiency. Restoration of a positive sodium balance promotes the recovery of renal function after the combined administration of angiotensin converting enzyme inhibitors and diuretics.

Topics: Acute Kidney Injury; Aged; Drug Therapy, Combination; Enalapril; Furosemide; Heart Failure; Humans; Male; Sodium

Renal function was measured sequentially in 32 patients with proven renovascular hypertension who were treated with the oral angiotensin converting enzyme inhibitor captopril. Renal function was assessed by serial measurement of serum creatinine. Six patients showed acute rises in serum creatinine concentration compatible with acute renal failure. Acute renal failure was confined to those patients with stenosis to a solitary kidney (transplant or native, occurring in 3 of 8 patients) or bilateral renal artery stenosis (occurring in 3 of 13 patients). No rise in serum creatinine concentration was observed in 11 patients with unilateral renal artery stenosis during long-term angiotensin converting enzyme inhibitor therapy. Acute renal failure during angiotensin converting enzyme inhibitor therapy was not related to the degree of blood pressure fall or the plasma angiotensin II level. Eleven patients with renovascular hypertension were followed prospectively with estimation of renal function by 99mTc-diethylenetriaminepentaacetic acid (DTPA) clearance (determined by computer analysis of scintillation camera renography). In six patients with unilateral renal artery stenosis, total 99mTc-DTPA clearance and serum creatinine level remained constant following angiotensin converting enzyme inhibitor therapy, while in five patients with bilateral renal artery stenosis 99mTc-DTPA clearance fell from 40 +/- 9 to 27 +/- 5 ml/min (p less than 0.05). Split renal function studies revealed that 99mTc-DTPA clearance fell in most kidneys with stenosed arteries during angiotensin converting enzyme inhibition, including the stenosed kidney from patients with unilateral renal artery stenosis (16 stenosed kidneys studied; change in Tc-DTPA clearance, -7.5 +/- 2.7 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Kidney Injury; Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Captopril; Creatinine; Enalapril; Female; Humans; Hypertension, Renovascular; Male; Prospective Studies

Although converting-enzyme inhibition is of established value in the management of patients with severe chronic congestive heart failure, troublesome adverse reactions occur frequently during the course of treatment and may cause physicians to interrupt effective therapy. The three most common adverse reactions that are seen in patients with heart failure following treatment with captopril and enalapril (symptomatic hypotension, functional renal insufficiency, hyperkalaemia) are predictable consequences of interfering with the homeostatic functions of the renin-angiotensin system, which evolved millions of years ago to preserve life in sodium-depleted states. It is not surprising, therefore, that these untoward effects can be prevented or reversed by increasing the dietary intake of salt or reducing the dose of concomitantly administered diuretics; their occurrence rarely requires discontinuation of drug therapy. Recognition of this link between sodium balance and the adverse effects of converting-enzyme inhibition is important, because most patients with severe heart failure who experience such untoward reactions can nevertheless be expected to improve clinically during long-term therapy, if effective treatment is not interrupted.

Topics: Acute Kidney Injury; Angiotensin-Converting Enzyme Inhibitors; Captopril; Enalapril; Heart Failure; Humans; Hyperkalemia; Hypotension; Sodium Chloride

Topics: Acute Kidney Injury; Aged; Enalapril; Female; Furosemide; Heart Failure; Humans; Male

Topics: Acute Kidney Injury; Antihypertensive Agents; Dipeptides; Enalapril; Glomerulonephritis; Glomerulosclerosis, Focal Segmental; Humans; Hypertension, Renovascular; Male; Middle Aged; Renal Artery Obstruction

Worldwide experience with captopril and enalapril showed that angiotensin-converting enzyme (ACE) inhibitor monotherapy in hypertensive patients rarely caused renal dysfunction. The ACE inhibitors in combination with potent vasodilating drugs and diuretics may produce sudden systemic normotension or hypotension that may impair glomerular filtration at reduced renal perfusion pressure. Reversible renal insufficiency developed during the 13th week of hydrochlorothiazide-enalapril-alpha methyldopa therapy in patient 1 and during the 6th week of hydrochlorothiazide-enalapril treatment in patient 2. Systemic hypotension in patient 1 and routine biochemical monitoring in patient 2 was the first clue of renal insufficiency. Renal angiography was normal in both patients. Renal insufficiency resolved after stopping all drugs temporarily and did not recur on other antihypertensive drug regimens. These data suggested the importance of systemic arterial blood pressure as the best clinical determinant of renal function in hypertensive patients receiving an ACE inhibitor in combination with other antihypertensive agents.

Topics: Acute Kidney Injury; Captopril; Enalapril; Female; Humans; Hydrochlorothiazide; Hypertension; Hypertension, Renovascular; Kidney Diseases; Male; Middle Aged; Oligopeptides; Teprotide

In this case we are reporting on a patient suffering from malignant renovascular hypertension and chronic renal failure due to occlusion of both renal arteries. The acute renal insufficiency after Captopril and later on after Enalapril treatment was fully reversible. We believe that the acute reversible renal insufficiency was caused by the blockage of glomerular autoregulation depending on Angiotensin II.

Topics: Acute Kidney Injury; Aged; Angiotensin II; Antihypertensive Agents; Captopril; Dipeptides; Drug Therapy, Combination; Enalapril; Furosemide; Humans; Hypertension, Renovascular; Male; Proline; Renin-Angiotensin System

Topics: Acute Kidney Injury; Captopril; Child; Dipeptides; Enalapril; Female; Humans; Hypertension; Proline