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)

In the course of a 19-d study of renal function in five ultramarathon runners, before, during and after a 90 km race, one runner developed transient oliguria with renal tubular dysfunction and anuria during and immediately after the race. Other features of the renal failure were an 84-fold increase in urine beta 2-microglobulin excretion (from 0.19 to 16.0 micrograms.min-1) and a much smaller increase in urine total protein excretion (from 0.07 to 0.18 mg.min-1) during the post-race period. Post-race creatinine clearance remained below pre-race levels throughout the study, varying between 42.8 and 72.9 ml.min-1, in contrast to the post-race 49% increase in the remaining runners (from 138.1 +/- 12.9 to 205.5 +/- 59.9 ml.min-1). Osmolal clearance also remained low (0.31 to 0.98 ml.min-1) compared with the pre-race values (1.46 +/- 0.02 ml.min-1), as did the urine flow rates (0.11 to 0.18 ml.min-1) compared with the pre-race values (0.34 +/- 0.02 ml.min-1). This renal dysfunction persisted despite the patient receiving 2 l of intravenous fluids immediately after the race and probably resulted from fluid restriction during the race. There was full recovery of renal function 1 yr later when the subject again ran the Comrades Marathon.
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PMID:Transient oliguria with renal tubular dysfunction after a 90 km running race. 228 52

The relationship of renal and central nervous system injury was prospectively evaluated in 120 asphyxiated infants. Renal evaluation findings were considered abnormal if there was oliguria (urine output less than 1 ml/kg/hr), which was designated transient if present in the first 24 hours only and persistent if present for at least 36 hours, or if the urinary beta 2-microglobulin concentration from first-void urine was elevated: (1) Thirteen infants had persistent oliguria; the urinary beta 2-microglobulin level was elevated in all. The six term infants had clinical signs consistent with hypoxic-ischemic encephalopathy (HIE); all six had ultrasonographic abnormalities. The outcome was poor (i.e., death or long-term neurologic deficits) in five of six infants. The seven preterm infants with persistent oliguria had clinical evidence of HIE, and three infants had intraventricular hemorrhage; all seven infants died. (2) Fifteen infants had transient oliguria (beta 2-microglobulin level was elevated in eight infants). Two of the eight term infants had evidence for HIE; the cranial ultrasound scan was normal in all. At follow-up, seven term infants are normal and one is abnormal. Six of the seven preterm infants with transient oliguria had clinical evidence of HIE; three infants had intraventricular hemorrhage. Three infants died, and the four survivors are normal at follow-up. (3) Ninety-two infants had normal urine output. Of the 22 term infants, two developed signs of HIE, and the ultrasound scan was abnormal in three infants. Of the 70 preterm infants, eight (11%) had clinical signs consistent with HIE, the ultrasound scan was abnormal in 20 of 64 (31%) infants scanned, and 14 (20%) infants died. Most of the followed infants are normal. Thus oliguria was significantly associated with clinical signs of HIE, including seizures, death (specifically in the premature infant), and long-term neurologic deficits. These data suggest that oliguria in the perinatal period is a sensitive indicator of infants at risk for long-term neurologic deficits.
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PMID:Renal injury in the asphyxiated newborn infant: relationship to neurologic outcome. 305 34

Urinary concentrations of beta 2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary beta 2-microglobulin concentrations in healthy infants averaged 1.34 +/- 1.34 mg/L (mean +/- SD) in first voided specimens and 1.32 +/- 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 +/- 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 +/- 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring beta 2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary beta 2-microglobulin levels were not (1) related to gestational age; low beta 2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary beta 2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of beta 2-microglobulin; urinary and serum beta 2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary beta 2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal injury in sick newborn infants: a prospective evaluation using urinary beta 2-microglobulin concentrations. 327 95