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

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
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PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

Oliguria is common in critically ill patients and may result from prerenal, renal, and postrenal causes. Oliguria also frequently develops in patients with normal concentrations of blood urea nitrogen and creatinine. Most of these patients do not develop renal failure. The authors prospectively studied 100 patients admitted to the ICU to determine the etiology of oliguria in these patients. Eighteen patients (18%) developed oliguria (less than 0.33 ml.kg-1.h-1 X 2 h). Seven and eleven patients were felt on clinical assessment to be hypovolemic or normovolemic, respectively. Compared with the hypovolemic patients, the normovolemic oliguric patients had significantly lower serum osmolalities (278 +/- 3 vs. 290 +/- 5 mOsm/kg H2O) and serum sodium concentrations (138 +/- 3 vs. 132 +/- 1 mEq/l). In addition, normovolemic patients had significantly higher urine sodium concentrations (83 +/- 12 vs. 13 +/- 2 mEq/l), fractional excretion of sodium (1.14 +/- 0.2 vs. 0.15 +/- 0.03), and renal failure indices (1.5 +/- 0.3 vs. 0.21 +/- 0.04). ADH concentrations in six hypovolemic and six normovolemic patients were increased in both groups but not significantly different. The hypovolemic patients increased their urine output from 17 +/- 2 ml/h to greater than 0.5 ml.kg-1.h-1 following a 500-ml bolus of normal saline. The normovolemic oliguric patients remained oliguric following the saline bolus (13 +/- 2 to 19 +/- 3 ml/h). The authors conclude that oliguria is common in critically ill patients and results from renal hypoperfusion and ADH excess.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oliguria in patients with normal renal function. 239 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

A case is reported of acute renal failure occurring after prolonged abdominal aortic bypass surgery in an overweight 69-year-old male patient. Preoperative serum creatinine concentration was normal. Surgery lasted for 6 h, and infrarenal aortic cross-clamping 2 1/2 h. The patient complained of important lumbar pain immediately after the operation. In the same time, oliguria and acute renal failure also developed (creatinine: 464 mumol.l-1; urea: 13 mmol.l-1). Rhabdomyolysis caused by the kidney-bridge was confirmed by the elevated blood creatine phosphokinase levels (16,000 IU.l-1 on the second postoperative day). A 99 m-Technetium methylene-diphosphonate imaging on the 10th postoperative day exhibited diffuse fixation in the paravertebral lumbar and thoracic muscles, extending from Th8 to L3. The acute renal failure regressed completely after haemodialysis.
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PMID:[Peroperative rhabdomyolysis caused by compression of a kidney-bridge. Value of muscular scintigraphy]. 253 65

102 children with acute gastroenteritis were thought by the admitting junior doctors to be 5% or more dehydrated. As judged by subsequent weight recovery in hospital, the main indicators of mild to moderate dehydration were decreased peripheral perfusion, deep breathing, decreased skin turgor, high urea, low pH, and a large base deficit; a history of increased thirst was just short of statistical significance. Dehydration was not indicated by a history of oliguria, by the presence of restlessness or lethargy, sunken eyes, dry mouth, or a sunken fontanelle or by the absence of tears. Clinical signs of dehydration became apparent at 3-4% rather than 5% dehydration. The degree of dehydration was overestimated by a mean of 3.2%; this caused unnecessary hospital admissions and overtreatment with intravenous fluid.
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PMID:Clinical signs of dehydration in children. 257 63

Although a wide variety of disease processes can result in a failure of renal excretory function, the vast majority of cases with "acute renal failure" (ARF) are due to the syndrome of acute tubular necrosis (ATN). The syndrome is usually initiated by an acute injury to the proximal renal tubular epithelial cells by ischemic or nephrotoxic events. This is followed by progressive and often rapid increases in the concentration of blood urea nitrogen (BUN) and serum creatinine. In the average case, the failure of renal excretory function persists for 1 to 3 weeks, to be followed by recovery. Oliguria (urine volume less than 400 ml) is present in about half of the patients. The pathogenesis of the retention of nitrogenous waste in human ATN is the subject of controversy, but the balance of data in most patients suggests that the predominant mechanism is a profound secondary vasoconstriction in response to tubular cell injury. This may represent a teleologically appropriate response to prevent catastrophic losses of fluid that would occur, if the normally high rates of glomerular filtration continued, in the face of reduced tubular reabsorptive capacity. The mechanisms by which the tubular cell injury is communicated to the vasculature, and the mediators of the hemodynamic changes, remain to be established. The differential diagnosis in a patient with ARF, usually involves exclusion of an obstruction to the urinary tract as an initial step. The next step is to differentiate the patients with ATN from those who have renal hypoperfusion in response to events in the systemic circulation, but who otherwise have functionally and structurally intact kidneys, i.e., prerenal ARF. The kidneys of patients with prerenal ARF exhibit the normal renal response to an acute reduction in renal blood flow and glomerular filtration rate (GFR). This consists of avid reabsorption of the filtered salt and H2O, so that a small amount of concentrated and NaCl-poor urine is elaborated. The tubular cell injury in ATN syndromes prevents this response from maximally occurring, so that the urine is isosmotic and relatively rich in NaCl.
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PMID:Acute renal failure. 264 37

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

Renal function in the newborn infant varies with conceptual age and should be evaluated in this context. Very preterm infants less than 34 weeks' conceptual age have reduced GFR and tubular immaturity in the handling of filtered solutes when compared to term infants. Premature infants between 34 and 37 weeks' conceptual age undergo rapid maturation of renal function similar to term infants, with establishment of glomerulotubular balance early in the postnatal period. ARF in neonates differs from that seen in older children and adults in that ischemic (e.g., hypoxic) insults and congenital malformations constitute the major pathophysiologic mechanisms responsible for clinically observed oliguria and azotemia. Principles of conservative management are similar to those used in older children except for the greatly increased insensible water loss requirements of the very preterm and premature infant. Technical advances have added peritoneal dialysis and CAVH to the therapeutic regimen for persistent ARF or life-threatening complications of reduced renal function.
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PMID:Renal function and renal failure in the newborn. 265 61

In order to evaluate the clinical usefulness of serum and urinary beta 2 microglobulin (beta 2-m) determination as a marker of renal damage following perinatal asphyxia, twenty asphyxiated and twenty healthy full term newborns were studied. Renal function was monitored on the first and third day after birth by traditional tests such as creatinine (Cr), endogenous creatinine clearance (Ccr), and fractional Na excretion (FeNa), as well as by serum and urinary beta 2 microglobulin. The value of different tests for the diagnosis of oliguria and of acute renal failure was determined. Eleven asphyxiated neonates developed oliguria and five ARF in contrast to none of the controls. Both traditional tests of renal function, and determinations of beta 2-m with the exception of serum beta 2-m, were significantly different (p less than 0.01) between controls and asphyxiated neonates. When stratified analysis was performed, only serum cr, urinary beta 2-m/cr ratio, and Fe beta 2-m were able to discriminate oliguria from preserved diuresis on the first day of life. For ARF, only Ccr and Fe beta 2-m were different, again on the first day of life. Urinary beta 2-m/creatinine ratio and Fe beta 2-m appear to be more sensitive and specific for the early detection of proximal tubular renal dysfunction following perinatal asphyxia than usual tests of renal function.
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PMID:Beta-2-microglobulin in the assessment of renal function in full term newborns following perinatal asphyxia. 269 47

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


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