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Objective To study whether furosemide infusion in early-onset acute kidney injury (AKI) in critically ill children would be associated with a reduced proportion of patients progressing to the higher stage (Injury or Failure) as compared to placebo. Method A double-blind, placebo-controlled, randomized pilot trial was conducted. The authors enrolled children aged 1-mo (corrected) to 12-y, who were diagnosed with AKI ("risk" stage) using pediatric-Risk, Injury, Failure, Loss, End stage kidney disease (p-RIFLE) criteria, and achieved immediate resuscitation goals within 24 h of admission. Participants received either furosemide (0.05 to 0.4 mg/kg/h) or placebo (5%-dextrose) infusion. The primary outcome was the proportion of patients progressing to a higher stage (injury or failure). Secondary outcomes were (i) need for renal replacement therapy, (ii) the effect on neutrophil gelatinase-associated lipocalin (urine and blood), (iii) fluid balance, (iv) adverse effects, (v) time to achieve renal recovery, (vi) duration of hospital stay and mechanical ventilation, and (vii) all-cause 28-d mortality.Results The trial was stopped for futility, and data were analyzed on an intention-to-treat basis (furosemide-group: n = 38; placebo-group: n = 37). No significant difference was noted in the progression of AKI to a higher stage between furosemide and placebo groups (10.5% vs. 21.6%; relative risk = 0.49, 95% CI 0.16 to 1.48) (p = 0.22). There were no differences in the secondary outcomes between the study groups. All-cause 28-d mortality was similar between the groups (10.5% vs. 10.8%). No trial-related severe adverse events occurred. Conclusions Furosemide infusion in early-onset AKI did not reduce the progression to a higher stage of AKI. A future trial with large sample size is warranted.

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A 3-month-old female infant, born to non-consanguineous parents at 36 weeks of gestation with a birthweight of 2.5 kg, presented with complaints of poor feeding and lethargy of 3 days duration and recurrent apnoeic episodes for 1 day. At presentation, she had apnoea and hypotensive shock, requiring resuscitation with endotracheal intubation, mechanical ventilation, multiple crystalloid boluses followed by epinephrine and norepinephrine infusions. Hypoglycaemia was noted at presentation needing dextrose boluses and infusion. On examination, the baby had sinus bradycardia (68 beats per minute) and hypothermia (33.5 C). Wide-open anterior fontanelle, coarse facies, microcephaly (head circumference 34 cm (À6.29z)), and generalised pitting oedema were remarkable. There was no neck swelling. Anthropometry showed severe underweight (weight 2.5 kg (À4.29z)), severe stunting (height 45 cm (À5.67z)), and no wasting (weight for height 0.49z), suggestive of significant failure to thrive. A detailed neurological examination revealed generalised hypotonia. The examination of other systems was non-contributory. Empirical intravenous antibiotics (cefotaxime and amikacin) were started for suspected sepsis. Investigations revealed microcytic hypochromic anaemia (haemoglobin 72 g/L (normal range: 105-140 g/L)), leucocytosis (white blood cells = 25.2 Â 10 9 /L (normal range: 6.0-14.0 Â 10 9 /L)), and thrombocytosis (platelet count = 662 Â 10 9 /L (normal range: 150-400 Â 10 9 /L)) and hypoalbuminaemia (serum albumin DiscussionMC is a condition with high mortality. 1 The guidelines for the management of MC in children are not well established. 2 MC in Key Points1 Oral levothyroxine is effective in myxoedema crisis with shock. 2 Treatment with intravenous hydrocortisone (or suitable steroids) should precede levothyroxine to avoid cortisol deficiency which can lead to worsening of shock. 3 Thyroid nodules may not be clinically palpable in infants. However, they can be found on imaging (neck ultrasonography).

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