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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension. 83 Apr 37

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

Oliguric ARF occurred in 0.5% of battle casualties who reached the field medical care system and raised their mortality expectancy from less than 5% to nearly 90%, due primarily to fluid volume overload and/or myocardial potassium intoxication. For their effective treatment the Renal Insufficiency Center with laboratory and a Brigham-Kolff rotating drum dialyzer began operations in 1952, as depicted in a videotape prepared for this presentation from motion picture footage filmed in early 1953. Our Surgical Research Team's major findings relevant to ARF were: (1) Renal function was depressed in most battle casualties in proportion to the severity of their wounds and blood loss. (2) Among the more severely wounded some developed nonoliguric; others, oliguric ARF. (3) Oliguria lasted from 3 days to 3 weeks without a discernible peak frequency of beginning diuresis at 10 days. (4) During oliguria, posttraumatic catabolism greatly accelerated extracellular accumulations of nitrogen, potassium, phosphate, and hydrogen ion with rapid, concurrent clinical deterioration. (5) Dialysis "on indication" produced an oscillating clinical and chemical course. (6) ARF was then revealed as a wasting disease complicated by infections, poor wound healing until diuresis occurred, anemia and bleeding, and hypertension during dialyses and in early diuresis. (7) The overall mortality rate was reduced.
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PMID:Acute renal failure during the Korean War. 150 54

Mineral balance studies were performed in 61 sick preterm infants given parenteral fluids only. Their gestational ages varied from 24 to 35 weeks, and 50 required mechanical ventilation. Two consecutive balance studies were performed; the first from admission to 48 hours in all babies given maintenance fluids of 10% Dextrose, and the second from 48 hours to 7 days in those babies given intravenous feeding (IVN). At the beginning and end of each balance period, the baby was weighed and an arterial blood sample taken for blood gases, electrolyte, urea, creatinine and protein determinations. During the balance period all urine was collected and analysed for electrolyte, urea, and creatinine composition, and all fluid intake was recorded. The balance of a mineral was calculated as the difference between parenteral intake and urine output. Infants requiring IVN were allocated alternatively to regimen X or regimen Y, which had the same calcium content of 9.5 mmol/L, but different phosphate contents, regimen X containing 7.3 mmol/L and regimen Y 11.6 mmol/L. In those infants requiring prolonged IVN, 12-24 hour balance studies were performed at weekly intervals after day 10. 1. Phosphate deficiency developed in infants given regimen X, who had higher urine calcium excretion, lower percentage calcium retention and lower plasma phosphate levels than those given regimen Y. These differences were apparent by day 7 and persisted after day 10. In infants given regimen Y, mean calcium retention from admission to day 7 was 3.9 mmol/kg, and after day 10 was 0.9 mmol/kg/day. 2. In the first 48 hours, urine output and creatinine clearance varied widely and were lower in infants with higher oxygen requirements at 48 hours. Ten babies had severe oliguria with outputs less than 10 mL/kg/day. Creatinine clearance was directly related to gestational age, mean arterial blood pressure, and plasma protein concentrations on admission. After 48 hours, urine output and creatinine clearance increased considerably. 3. In the first 48 hours, metabolic acidosis was produced by increased plasma non-protein metabolisable acid concentrations, which were associated with low creatinine clearances, and were thought to be due to lactic acid accumulation in response to decreased tissue perfusion. At 7 days, metabolic acidosis was of similar severity but was produced by decreased plasma non-metabolisable base concentrations, caused by increased urine loss of net base, and not directly by IVN.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mineral balance studies in sick preterm intravenously fed infants during the first week after birth. A guide to fluid therapy. 251 60

The result of this study shows that a simple phosphate buffered sucrose solution (PBS) is better than hyperosmolar citrate (HOC) solution in the flush perfusion and hypothermic storage of canine kidneys for 72 hr prior to autotransplantation with immediate contralateral nephrectomy. The peroperative measurement of postreperfusion renal blood flow revealed a significant reduction after 60 min in kidneys preserved with HOC solution. All grafts and animals in the PBS group (5/5) survived with primary renal function compared with one in the HOC group (1/5), which functioned after a period of oliguria. The early serum creatinine and urea levels were significantly lower in the PBS group, with a return to normal range within two weeks. This is reflected in higher inulin clearances and a more rapid recovery of proximal tubular function in the PBS animals, which also demonstrated a more rapid return of loop function and the ability to concentrate urine.
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PMID:Improved 72-hour renal preservation with phosphate-buffered sucrose. 265 11

Acute toxic nephropathy was produced in 6 healthy goats by injecting intravenously 1% uranyl nitrate (UN) (15 mg/kg body weight). The early painful clinical signs simulating shock progressed with subnormal temperature, slow-shallow respiration and arrhythmic pulse followed by death due to respiratory failure within 96 to 120 hr. All the affected goats had normocytic normochromic anemia, leucocytosis, neutrophilia with left shift eosinopenia, decreased monocytes and presence of 1-2% reticulocytes in the peripheral blood smears. On blood chemical analysis, a uniform and continuous rise was seen in serum creatinine with a concomitant daily increase of serum urea and uric acid. Simultaneous analysis of urine indicated polyuria leading to oliguria, acidic pH, albuminuria, glycosuria with presence of neutrophils, RBC's, epithelial and fatty casts, increase of triple phosphate, and cystine crystals reflecting acute damage of kidneys in the affected goats.
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PMID:Clinico-biochemical studies on acute toxic nephropathy in goats due to uranyl nitrate. 271 8

The timing and circumstances of changes in renal energetics during the gradual induction of haemorrhagic hypotension were studied in anaesthetised rats by phosphorus-31 nuclear magnetic resonance. Animals were bled at a constant rate of 0.1 ml/min via the femoral artery. Whenever changes in renal energetics were seen, a similar pattern was observed. A decrease in adenosine triphosphate occurred rapidly and was always associated with accumulation of inorganic phosphate and tissue acidosis. Profound oliguria, reflecting a markedly decreased rate of glomerular filtration preceded the changes in metabolite levels. Such a fall in glomerular filtration rate and consequently in the energy requirement for tubular reabsorption could be viewed as a mechanism by which energy demands of the kidney are reduced before a critical limitation of energy supply is reached. During uncomplicated haemorrhage in Wistar rats, mean arterial pressures as low as 25-40 mm Hg were reached before changes in renal energetics developed. In contrast, spontaneously hypertensive rates subjected to uncomplicated haemorrhage, and Wistar rats subjected to haemorrhage during concurrent stimulation of the ipsilateral sciatic nerve, developed changes in renal energetics at higher and more variable blood pressures and in response to the withdrawal of lesser but more variable quantities of blood. The sudden onset and severe degree of energy depletion at varying blood pressures during bleeding and its more ready occurrence in animals in which sympathetic nervous activity could be expected to be increased, suggests that sudden renal vasoconstriction is responsible for the unpredictable occurrence of tubular ischaemia in haemorrhagic hypotension.
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PMID:Timing of the onset of changes in renal energetics in relation to blood pressure and glomerular filtration in haemorrhagic hypotension in the rat. 291 61

In male Wistar rats, renal adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH were measured by 31phosphorus nuclear magnetic resonance (31P NMR) and correlated with renal function before, during, and for one hour after a period of 30 to 40 minutes hemorrhagic hypotension. In animals which suffered no change in these metabolites during hypotension, retransfusion immediately restored normal renal function. When metabolite changes were observed during hypotension, they occurred suddenly with severe ATP depletion, Pi accumulation, and intracellular acidosis occurring almost concurrently. Metabolic changes of this magnitude were always associated with renal dysfunction in the post-hypotensive period, which occurred even when the period of biochemical change was only 10 to 15 minutes. The abnormalities in post-hypotensive renal function resemble the pattern of change seen in human acute tubular necrosis (ATN): depressed glomerular filtration rate (GFR), urine output varying from polyuria to oliguria, decreased urine to plasma inulin ratio, increased urinary sodium concentration, increased fractional excretion of sodium, and increased fractional excretion of potassium. It is postulated that changes in renal cellular energy status during hemorrhagic hypotension distinguish pre-renal failure from early or incipient ATN.
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PMID:Acute renal failure in hemorrhagic hypotension: cellular energetics and renal function. 378 80

In order to determine the prevalence of rhabdomyolysis-associated acute renal failure (RM-ARF) and assess the effect of oliguria on biochemical features in this condition, 127 cases of ARF seen over 18 months were reviewed. Eleven cases of RM-ARF were seen, a prevalence of 8.6% of all cases of ARF. There were ten males and one female (age range 15-72 years) with precipitating events being trauma in three, coma in two, infection in two and other causes in five. Ten had concurrent clinical or historical evidence of dehydration, two had mild hypokalemia, and one abused alcohol. Serum and urine myoglobin by radioimmunoassay were greater than 800 ng/l in all cases tested. False negative tests for urine myoglobin by o-tolidine reaction after (NH4)2SO4 extraction occurred in four cases. Despite attempted forced saline diuresis and urinary alkalinisation, seven became oliguric and required dialysis for 12-81 days. Initially (pre-dialysis) oliguric patients had significantly higher maximum serum levels of potassium, phosphate, and rate of rise of creatinine, significantly lower trough levels of calcium, and no significant difference in peak creatine phosphokinase or uric acid levels than non-oliguric patients. Two subjects developed recovery phase hypercalcemia, four required fasciotomy for compartment syndromes, three sustained permanent nerve damage, and three required limb amputation. Ten survived, with a mean creatinine clearance of 96 ml/min after nine to 30 months. RM-ARF is common, may be clinically occult and show false negative urine myoglobin tests. Hyperkalemia, hyperphosphatemia, and hypocalcemia are more common in oliguric than in non-oliguric RM-ARF, but both have a good prognosis with appropriate medical and surgical management.
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PMID:Rhabdomyolysis and acute renal failure. 386 39

The acute tumor lysis syndrome occurs rarely in nonhematologic malignancies. This patient, a 34-year-old woman with metastatic medulloblastoma, was receiving palliative radiotherapy for a rapidly expanding abdominopelvic mass. After a total of 300 rad, the patient developed the biochemical hallmarks of the acute tumor lysis syndrome, hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. This was complicated by oliguria from hyperuricemic acute renal failure. The patient responded well to hydration, alkaline diuresis, phosphate and potassium binders, and allopurinol. The potential for acute tumor lysis syndrome should be anticipated when treating metastatic medulloblastoma.
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PMID:Acute tumor lysis syndrome with metastatic medulloblastoma. A case report. 619 3


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