Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a patient presenting rapid deterioration of renal function due to primary cholesterol atheroembolism. The patient was 75-year-old hypertensive male and was admitted to a hospital because of rt. hemiplegia which developed 2 weeks earlier. On admission, his blood pressure was 200/100 mmHg and serum creatinine level was 2.9 mg/dl with urinalysis 1+ both for protein and hematuria. 2 weeks later, an angiotensin converting enzyme inhibitor (ACE inhibitor, delapril 15 mg/day) was given to control high blood pressure. Immediately after this medication, his renal failure rapidly progressed with a fall in blood pressure (110/60 mmHg) and oliguria (100 ml/day). Although he was transferred to our hospital and was treated with hemodialysis, he died of an attack of acute myocardial infarction in a week. At post-mortem examination, microscopic findings of the kidney disclosed numerous occlusions of medium-sized artery by cholesterol emboli. These emboli were also observed in other organs, but not so prominent as in the kidney. The coronary arteries exhibited severe sclerosis. In this presented case, acute deterioration of renal function was caused by ACE-inhibitor, although which was administered in a volume depleted condition. Therefore, further study would be necessary whether or not ACE-inhibitors predispose the patients with this disease to acute renal failure.
 ...
PMID:[A case of renal failure due to primary cholesterol atheroembolism]. 187 61

In two cases with drug-related hyperkalemia, potassium homeostasis, causes, symptoms and therapy are discussed. Iatrogenic and therefore avoidable hyperkalemia occurs most often when potassium, ACE-inhibitors, nonsteroidal antiinflammatory drugs or potassium-sparing diuretics are administered in patients with impaired renal function or diabetes mellitus. The emergency treatment in patients with severe hyperkalemia consists of intravenous calcium injections, infusion of glucose with insulin and, more recently, salbutamol. With acidotic patients administration of sodium-bicarbonate can be tried. Ion-exchange drugs and furosemide have a more delayed effect. With oliguria and anuria hemodialysis is often necessary.
 ...
PMID:[Hyperkalemia]. 199

The occurrence of neurologic abnormalities is described in a series of nine infants with chronic hypertension, in whom antihypertensive therapy decreased BP markedly and for a prolonged period, although to levels often within the normal range. All infants had mean systolic BPs greater than 113 mm Hg and elevated renin values to a mean of 134 +/- 128 ng/mL/h. Antihypertensive therapy, such as captopril, an inhibitor of angiotensin I-converting enzyme, consistently lowered the systolic BP by 20% from baseline per dose. However, the nine infants exhibited a total of 17 episodes of striking decreases in systolic BP of greater than 40% from baseline; the markedly decreased systolic BP values were usually within the normal range for corrected age. Seven of the 17 episodes were characterized by marked decrease in systolic BP, ie, decreased by 57% +/- 10%, and were prolonged, ie, remained at the lower values for 17 +/- 6 hours despite therapeutic interventions. These seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/h) and neurologic abnormalities (ie, seizures). In the remaining ten episodes, the systolic BP decreased by 50% +/- 8%, but the decreases were relatively brief, ie, remained at the lower values for 2.8 +/- 2 hours. These briefer episodes were not accompanied by renal or neurologic signs. These data indicate a particular vulnerability of the cerebral and renal circulation in premature infants with chronic hypertension to decreases in systolic BP to levels that would otherwise be considered in the normal range. The findings suggest that adaptive responses in both cerebral and renal blood flow are altered by chronic hypertension in such infants.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Neurologic complications of captopril treatment of neonatal hypertension. 264 19

We have examined the acute renal failure that occurs after uranyl nitrate administration in the rat and the specific effects of pretreatment of rats with angiotensin converting enzyme inhibitor (CEI), plasma volume expansion (PVE) after uranyl nitrate, and a combination of these treatments. We utilized a combination of micropuncture measurements of glomerular hemodynamics, cage studies, and histologic examination of renal tissue to evaluate the degree of acute renal failure in all groups studied. Uranyl nitrate (UN) (25 mg/kg body wt) administration caused a reduction in the nephron filtration rate (SNGFR) (39.4 +/- 1.6 to 24.8 +/- 2.9 nl X min-1 X g kidney wt-1, P less than 0.02) as a result of a major decrease in the glomerular ultrafiltration coefficient (LpA) from control values (greater than or equal to 0.085 +/- 0.008 to 0.035 +/- 0.007 nl X sec-1 X mm Hg-1 X g kidney wt-1, P less than 0.01). Treatments with CEI, PVE, and the combination of CEI and PVE in rats receiving UN restored 0.38 +/- LpA to normal values (greater than 0.061 +/- 0.009, 0.091 +/- 0.020, and 0.138 +/- 0.020 nl X sec-1 X mm Hg-1 X g kidney wt-1, respectively). Cage studies revealed that CEI treatment prevented oliguria and resulted in major volume losses and reduction in weight. However, rats died after a similar period after UN, but probably by different mechanisms. Analysis of renal ultrastructure revealed equivalent tubular damage in all experimental groups. Alterations in LpA after UN are functional in nature and are potentially preventable and reversible by a combination of treatments with CEI and PVE.
 ...
PMID:Functional basis for the glomerular alterations in uranyl nitrate acute renal failure. 300 41

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.
 ...
PMID:[Fetal and neonatal effects of maternal treatment with angiotensin converting enzyme inhibitor]. 795 36

The therapeutic effects of angiotensin converting enzyme inhibitor, lisinopril, on puromycin aminonucleoside (PAN)-induced nephrosis were investigated using unilaterally nephrectomized rats. Lisinopril showed potent dual effects on PAN nephrosis. Lisinopril treatment (50 mg/l in drinking water) from day 5 or day 9 reduced urinary protein excretion and suppressed the development of glomerular sclerosis at 8 weeks after PAN injection (150 mg/kg, i.p.), indicating a therapeutic effect on the nephrosis. Recovery of decreased anionic charge sites on the glomerular basement membrane was involved, at least in part, in the therapeutic action of lisinopril against proteinuria. On the other hand, oliguria and progressive azotemia derived from continuous deterioration of the renal function was induced if the treatment of lisinopril was started on the same day as PAN injection. The renal dysfunction induced by simultaneous administration of lisinopril with PAN could be abolished by combination dosing with sarcosine, an angiotensin II (AII)-receptor agonist. These results indicate that lisinopril treatment attenuates proteinuria by ameliorating the anionic charge barrier on the glomerular basement membrane and that it also protects against the development of chronic renal disease with segmental glomerular sclerosis, although AII depletion during the acute nephrotic stage exacerbates the renal damage in PAN nephrosis of unilaterally nephrectomized rats.
 ...
PMID:Dual effects of lisinopril on puromycin aminonucleoside nephrosis in unilaterally nephrectomized rats. 916 71

Since the introduction of angiotensin converting enzyme-inhibitors (ACE-inhibitors) in the 1980's, more than 50 cases of foetotoxic effects ascribed to intrauterine exposure to inhibitors have been published. Among the most commonly reported effects are: Hypotension, renal dysplasia, anuria/oliguria, oligohydramios, intrauterine growth retardation, pulmonary hypoplasia, unclosed ductus arteriosus, incomplete ossification of the skull, intrauterine og neonatal death. Recent animal studies have confirmed that intrauterine or neonatal exposure to ACE-inhibitors or the AT1-receptor antagonist losartan can cause death and serious, irreversible organ damage. These effects are similar to the complications previously reported in humans. Animal studies suggest that the foetotoxic actions are most common after exposure during the last trimester. However, due to the severity of these complications, the use of ACE-inhibitors and AT1-receptor antagonists should be avoided throughout pregnancy and in women who are breast feeding.
 ...
PMID:[Teratogenic effects of ACE-inhibitors and angiotensin II receptor antagonists]. 952 Jun 13

The healthy term, and particularly the premature infant, is born with a very low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and include hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal septicemia. Other causes include the administration of angiotensin converting enzyme inhibitors, indomethacin and tolazoline. The most-important factors governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avoidance of severe iatrogenic complications. The immediate treatment is of particular importance in VMNP, i.e., prerenal ischemic ARF, and consists of correcting abnormalities in fluid homeostasis and reduction of the complications of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypertension). In severe and prolonged (established) ARF, temporary dialysis therapy may be indicated. Prerenal ARF with oliguria or anuria warrants immediate volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria and CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARF. In most other conditions, the therapeutic effect of FM is limited to a transient increase in urine flow, without improving basic renal function. The special conditions of the maturing kidney have to be appreciated in order to protect babies from undue renal injury. With the increasing knowledge of the mechanisms governing the development of ARF, progress has been made in the development of new treatment modalities. For example theophylline, calcium antagonists, ATP-MgCl2, thyroxine, and a variety of cytokines may in the near future be used to prevent or ameliorate VMNP and/or recently established ARF. With a combination of time-honored and new therapeutic strategies, there may well be a brighter future for neonates with vasomotor, prerenal, ischemic ARF.
 ...
PMID:The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy. 1075 64

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
 ...
PMID:[Heart failure in acute myocardial infarction]. 1200 71

Despite major advances in nutritional support, membrane technology and dialytic techniques, the mortality of patients with acute renal failure (ARF) who require dialysis is still almost 50% (1). Increased patient age and co-morbidity confer a poorer prognosis, and the condition is certainly commoner in this patient group. Hence, one study showed that the age-related annual incidence of ARF increased from 17 per million in adults under 50 years to 949 per million in the 80-89 age group (2). Over 60% of cases of ARF ultimately result from renal hypoperfusion and consequent intra-renal ischaemic damage, which leads to acute tubular necrosis (ATN) (3). Ischaemic ARF may thus result from a diversity of systemic and intra-renal circulatory stresses including acute losses of blood and extra-cellular fluids, from low cardiac output states such as following ischaemic or toxic myocardial damage, and even from drug-induced renal perfusion shutdown (ACE inhibitors, non-steroidal anti-inflammatory agents). Many cases of ARF have a multi-factorial aetiology (e.g. post-surgical sepsis with hypovolaemia, hypotension and injudicious antibiotic use), and these patients, who often have other organ failure, fit into the poorer prognostic category. A large number of patients with ischaemic ARF pass through a phase of potentially reversible pre-renal oliguria; early recognition and prompt, appropriate treatment of these pre-renal factors can prevent progression to established ARF, with the genuine prospect of improved patient morbidity and mortality, and this is the main scope of this article. Early diagnosis in other patients with ARF, such as those with acute inflammatory renal disease (e.g. vasculitis) or urinary tract obstruction, will allow appropriate prompt treatment and the possibility for reversal of the ARF. The following account, which is composed of personal experience, that of colleagues, and the literature (1,4), is not intended to provide a comprehensive guide to the management of ARF, but seeks to highlight important common pitfalls and fundamental principles in the recognition and subsequent preventive treatment of these patients.
 ...
PMID:Early management and prevention of acute renal failure. 1237 20


1 2 Next >>