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)

Three patients with right renal tumors extending into the inferior vena cava underwent ligation of the left renal vein coincident with right nephrectomy and en bloc resection of the vena cava. Two patients exhibited no postoperative renal dysfunction while the third demonstrated renal dysfunction which cleared by 9 days postoperatively. Features of the temporary renal dysfunction included proteinuria, elevated serum creatinine levels, oliguria, hypertension, elevated peripheral venous renin level, as well as radiographic evidence of swelling the kidney. The collateral venous drainage of the left kidney makes it possible to ligate the main vein of a solitary kidney with survival of the patient. However, postoperative temporary renal dysfunction may occur and a plan to deal with this problem should be fromulated.
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PMID:Ligation of the renal vein in the solitary kidney: effects on renal function. 111 94

The renin-aldosterone system and plasma insulin were studied in 19 patients with familial Mediterranean fever (FMF). Their relationships to serum potassium level at rest and before and after oral glucose loading are described. An interesting finding is the occurrence of hyperkalemia in the absence of oliguria, in the advanced stages of renal failure. No differences were found in the activity of the renin-angiotensin-aldosterone system to explain these variations in serum potassium found in some of the patients. The response of the renin-aldosterone system to glucose loading showed no abnormality, and the regular relationship between serum potassium, plasma renin activity (PRA), aldosterone, insulin, and plasma pH is maintained. Levels of insulin, potassium, and bicarbonate in serum or plasma pH were found similar in FMF patients with normal renal function with and without proteinuria. Further decrease in renal function due to the progression of the underlying disease is manifested by an increase in FENa+ and FEK+ and a hyperchloremic metabolic acidosis, as is the case in other patients with chronic renal failure.
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PMID:Normal renin-aldosterone-insulin and potassium interrelationship in FMF patients and amyloid nephropathy. 146 7

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.
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PMID:Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release. 183 31

A total of 29 patients with severe hemorrhagic fever associated with the renal syndrome were studied for impact of extracorporeal hemodialysis on the activity of the renin-aldosterone system (RAS), plasma vasopressin and osmolality and the levels of the major osmotically active agents, as well as the circadian urine output and blood pressures. In patients with oliguria there was a significant activation of RAS, an increase in plasma vasopressin ad osmolality due to the increment of the urea in presence of hyponatremia. Hemodialysis led to a temporary normalization of plasma aldosterone and vasopressin levels and a decrease in blood pressure. No significant changes were documented in the activity of the plasma renin and circadian urinary output. A direct correlation was established between the plasma osmolality and the levels of vasopressin. In patients with polyuria developed in presence of hypernatremic hyperosmia plasma vasopressin elevated and aldosterone dropped.
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PMID:[The effect of hemodialysis on the vasopressin level and on the renin-aldosterone system in patients with hemorrhagic fever with renal syndrome]. 197 Sep 14

Recombinant interleukin-2 (rIL-2) is a new promising treatment for cancer, but is associated with severe renal toxicity. This study is the first to analyse the renal effects of rIL-2 in children. Twenty-one cycles of continuous rIL-2 infusion were studied in 15 patients; mean age was 6.9 years and average weight 18.9 kg. Interstitial fluid retention and oliguria (baseline, 1.7 ml/kg per hour; nadir, 0.5 mg/kg per hour) were associated with hypotension (baseline, 101/56 mm Hg; nadir, 85/43 mm Hg) and decreased intravascular volume (plasma renin activity increased x 10). Weight gain (+7.9%) was observed in 13 cycles whereas weight loss (-6.3%) was shown in 8 cycles because of digestive and cutaneous losses, mainly in the youngest patients. This prerenal azotaemia was characterized by a decrease in creatinine clearance (from 101 to 36 ml/min per 1.73 m2) and a low fractional excretion of sodium (FENa) (from 0.70% to 0.09%). Hypotension and hypovolaemia needed vascular filling (n = 12), dopamine (n = 7) and interruption of rIL-2 (n = 2). Most abnormalities occurred as early as day 2 of therapy and were always reversible after a short period with sodium leakage (diuresis = 2.2 ml/kg per hour, FENa = 2.01%). Hypophosphataemia was associated with low urinary excretion of phosphorus, suggesting an increased uptake of inorganic phosphorus by rapidly proliferating lymphoid cells.
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PMID:Renal effects of continuous infusion of recombinant interleukin-2 in children. 202 34

Brain serotonin depletion induced by peripheral parachlorophenylalanine (pCPA) is frequently used to evaluate the role of the central serotoninergic system in the regulation of a number of physiological functions, including the secretion of renin by the kidney. We found that due to the treatments applied in the protocol used for the investigation of pCPA effect on renin and vasopressin secretion in rats (300 mg/kg i.p. 64 and 40 h before sacrifice) renal injury was induced as well. Typical changes indicating acute renal failure were observed--an initial polyuria, natriuresis and body mass loss, succeeded by oliguria, decreased glomerular filtration rate, and salt and creatinine retention. Morphological changes in the glomeruli included a thickening of the basal membranes, a confluence and a reduced number of podocyte pedicles. A slight to moderate granular degeneration was observed in epithelial cells of the proximal convoluted tubule, combined with mitochondrial changes--an increase in number, matrix disorganization, and myelin degeneration. In conclusion, the renal function changes after i.p. pCPA may be due not to brain serotonin depletion-alone, but also to nephrotoxic effect.
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PMID:Nephrotoxic effect of the specific brain serotonin depletor para-chlorophenylalanine. 215 5

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)
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PMID:Neurologic complications of captopril treatment of neonatal hypertension. 264 19

Five patients with hepatorenal syndrome were treated with the orally active angiotensin-converting enzyme inhibitor captopril (25 or 50 mg 6 hourly) for up to 48 hours. Only one patient showed a significant increase in urinary sodium concentration (from less than 10 to 70 mmol/liter), but without associated diuresis; renal function continued to deteriorate in all patients with persistent oliguria and rising serum creatinine. The outcome was uniformly fatal. These results suggest that in the hepatorenal syndrome, captopril in standard dosage is without benefit, and provide further evidence that the changes in the renin-angiotensin system are probably secondary to reduced renal perfusion from some other cause.
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PMID:Captopril in the hepatorenal syndrome. 299 80

Seven patients with Bartter's syndrome were investigated before and after 3 months' treatment by enalapril. Serum potassium rose from 2.4 +/- 0.5 to 3.9 +/- 0.6 mmol/L. In all patients, serum magnesium rose and bicarbonate fell. Hormonal changes were as suspected: a further stimulation of renin and a decline in aldosterone. The BP sensitivity to angiotensin II normalized in the five patients in whom the test was performed. Clearance studies during maximal water diuresis, performed in four patients, were compatible with a high proximal fractional tubular sodium reabsorption and a relatively low distal fractional sodium reabsorption. Fractional free water excretion after furosemide was also low, confirming the concept of a primary sodium reabsorption defect in the furosemide-insensitive part of the nephron in Bartter's syndrome. The only consistent change after enalapril was a further decline in distal fractional sodium reabsorption. Initiation of therapy produced a BP fall in each subject. Clinical important hypotension associated with oliguria was seen twice, but these reactions were short-lasting. The BP rose to pretreatment values within 72 hours, despite continuation of converting-enzyme inhibition. Renal function recovered, though a moderate fall in function persisted. No other side effects were noticed. We conclude that converting-enzyme inhibition improves the potassium metabolism of patients with Bartter's syndrome, without ameliorating the abnormal renal sodium handling.
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PMID:Correction of hypokalemia in Bartter's syndrome by enalapril. 303 96

We investigated the association between plasma catecholamines and the renal response to nonhypotensive sepsis. Arterial plasma catecholamines were measured in 16 sheep, before and 24 h after surgical induction of peritonitis. Animals were volume loaded with lactated Ringer's solution (8 L/24 h) before and after surgery; non became hypotensive. For analysis, animals were retrospectively divided into those with increased serum creatinine after 24 h of sepsis (group 1, n = 8) and those without (group 2, n = 8). Group 1 showed increased cardiac index and decreased systemic vascular resistance typical of severe sepsis, with decreased glomerular filtration rate (GFR), oliguria, sodium retention, increased plasma renin activity (PRA), decreased urinary kallikrein excretion, and increased urinary 6-keto-prostaglandin-F1 alpha excretion. Group 2 showed insignificant hemodynamic disturbance, and no significant renal response. Plasma catecholamines were equal in both groups at baseline. In group 1, there were uniform increases after 24 h in plasma norepinephrine (474 +/- 115 to 1183 +/- 158 [SEM] pg/ml; p less than .01) and plasma epinephrine (108 +/- 8 to 309 +/- 70 pg/ml; p less than .05). In group 2, neither plasma norepinephrine (343 +/- 59 to 330 +/- 56 pg/ml) nor plasma epinephrine (116 +/- 16 to 116 +/- 13 pg/ml) changed significantly. Plasma norepinephrine correlated inversely with GFR; plasma epinephrine correlated with PRA. The sympathetic nervous system may be involved in the renal response to nonhypotensive sepsis, both directly and via effects on other vasoactive hormone systems.
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PMID:Association between renal and sympathetic responses to nonhypotensive systemic sepsis. 316 6


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