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Journal ArticleDOI

Spurious hypercreatininemia: 28 neonatal foals (2000–2008)

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TLDR
Creatinine decreased by >50% within the initial 24 hours of standard neonatal therapy and was within the reference interval in all but 1 foal within 72 hours of hospitalization.
Abstract
Objectives – To (1) determine the occurrence of spurious hypercreatininemia in a population of hospitalized foals <2 days old, (2) assess the resolution of the hypercreatininemia, and (3) determine its association with survival in these foals. Design – Retrospective case series. Setting – 2 Referral hospitals. Animals – Foals 442 μmol/L (>5.0 mg/dL) from 2 referral hospitals. Interventions – None. Measurements and Main Results – The medical records of 33 foals were reviewed. Twenty-eight had spurious hypercreatininemia and 5 had acute renal failure. Admission creatinine was not significantly different between the 2 groups (mean [standard deviation]). The creatinine was 1,202 μmol/L (663 μmol/L) (13.6 mg/dL [7.5 mg/dL]) versus 1,185 μmol/L (787 μmol/L) (13.4 mg/dL [8.9 mg/d]) (P=0.96) in each group, respectively, though BUN at the time of hospital admission was significantly higher for acute renal failure foals (P=0.009). In the spurious group, serum creatinine at admission decreased to 504 μmol/L (380 μmol/L) (5.7 mg/dL [4.3 mg/dL]) by 24 hours, and to 159 μmol/L (80 μmol/L) (1.8 mg/dL [0.9 mg/dL]) at 48 hours, and to 115 μmol/L (44 μmol/L) (1.3 mg/dL [0.5 mg/dL]) at 72 hours. Twenty-three of 28 foals with spurious hypercreatininemia survived to hospital discharge and there was no difference in mean admission creatinine between survivors (1176 μmol/L [628 μmol/L]) (13.3 mg/dL [7.1 mg/dL]) and nonsurvivors (1308 μmol/L [857 μmol/L]) (14.8 mg/dL [9.7 mg/dL]) (P=0.67). Twenty of 28 foals had clinical signs suggestive of neonatal encephalopathy. Conclusion – Creatinine decreased by >50% within the initial 24 hours of standard neonatal therapy and was within the reference interval in all but 1 foal within 72 hours of hospitalization. The diagnosis of neonatal encephalopathy was common in these foals.

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Disorders of Foals

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References
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Journal ArticleDOI

Why do newborn infants have a high plasma creatinine

TL;DR: The riddle of the high Pcr levels in term and particularly in preterm newborns seems to be solved, as the results in the newborn rabbits showed an unexpected underestimation of the Ccr vis-a-vis Cin, which means, as is explained at length in the “Discussion” of this article, that the pre term newborn infant reabsorbs creatinine along the renal tubule.
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High-Risk Pregnancy

TL;DR: It is shown that despite many obstacles, most pregnancies, at least when measured in terms of perinatal mortality, can be considered a success.
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Evaluation of renal functions in asphyxiated newborns.

TL;DR: Renal function tests, calculated renal indices using timed urine collections and excretion of beta2-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) were monitored in asphyxiated babies and clinical markers of asphyxia were better predictors of adverse outcome than renal function tests.
Journal ArticleDOI

Neonatal organ system injury in acute birth asphyxia sufficient to result in neonatal encephalopathy.

TL;DR: Using common diagnostic tests as markers of acute asphyxial injury, it is noted that multiple organs suffer damage during an acute intrapartum asphyxia event sufficient to result in a neonatal encephalopathy.
Journal ArticleDOI

Clinical Pathology of the Foal

TL;DR: The neonatal foal is in a period of transition between fetal and extrauterine life; thus, the clinicopathologic findings in this period often reflect the in utero environment and results need to be interpreted with reference to the physical examination findings of the foal.
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