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

Urinary renin activity (URA) was measured by radioimmunoassay in sequential studies of 5 patients with acute renal failure (ARF) and in 13 normal volunteers. URA was elevated during the oliguric phase of ARF and fell to low levels prior to resolution of oliguria. Plasma renin activity (PRA) varied approximately in response to changes in intravascular volume status. In normal volunteers, the very low URA values did not change following furosemide-induced increases in PRA. A simple, rapid, and accurate method is described for the measurement of URA in humans by radioimmunoassay of angiotensin I generated during incubation of urine with homologous plasma substrate. The urinary enzyme exhibited the same properties as purified human renal renin and the incubation product appeared identical to angiotensin I standard. Renin activity in urine was directly proportional to enzyme concentration and no evidence was obtained for interference from other proteolytic activities or from inhibitors or promoters of renin in urine.
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PMID:Measurement of urinary renin activity by radioimmunoassay: sequential studies in acute renal failure in man. 64 43

1. The haemodynamic and hormonal responses of four patients with acute post-surgical oliguria (urine output < 0.5 mL/kg per h) were measured in response to the renin inhibitor enalkiren. Enalkiren was infused at 0.01 up to 0.1 mg/kg per h for up to 4 h. 2. Enalkiren infusion was associated with a progressive fall in blood pressure, clinically significant in three of the four patients. Systemic vascular resistance fell in proportion to blood pressure fall. Cardiac output and pulse rate remained unchanged. Effective renal plasma flow rose in all four cases (236 +/- 19 to 327 +/- 38). There was no change in urine flow rate, or urinary sodium excretion. 3. Plasma renin activity (ng angiotensin I/mL per h) fell from 1.9 +/- 0.5 to 0.02 +/- 0.01 (P < 0.04), plasma angiotensin II (pg/mL) fell from 104 +/- 93 to 7.7 +/- 1.5, and plasma aldosterone (ng/dL) fell from 32 +/- 8 to 21 +/- 9 (P = 0.03) at the highest infusion dose. 4. Enalkiren inhibited plasma renin activity with reduced plasma angiotensin II and aldosterone concentrations. This was associated with vasodilation, reduced blood pressure and maintained cardiac output. There was no beneficial effect on renal function in these patients with post-surgical oliguria.
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PMID:Haemodynamic, renal and hormonal responses to enalkiren in four patients with post-surgical oliguria. 803 72

A 49-year-old woman was admitted with fatigue, dyspnoea, pretibial oedema and decreased daily urination. Seven years ago she was treated with doxorubicin, bleomycin, vinblastine and dacarbazine, alternating with mechlorethamine, vincristine, procarbazine and prednisone and 80 Gy abdominal radiotherapy for Hodgkin's disease. Two years later, malignant hypertension was diagnosed. Angiotensin-2 antagonist and beta-blocker treatment was given. After increased serum creatinine levels were determined, renal angiography was performed and total obstruction in the left renal artery and near total obstruction in the right side was observed. She was admitted to our clinic with oliguria, and acute renal failure was diagnosed. Balloon angioplasty and stent implantation was performed to the right renal artery. After a polyuric period, serum creatinine reduced to near normal levels. Angiotensin-2 antagonist treatment worsened the course in this patient. Patients with resistant hypertension occurring years after abdominal radiotherapy should be evaluated for renal artery stenosis.
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PMID:Bilateral renal artery stenosis after abdominal radiotherapy for Hodgkin's disease. 1471 1

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17