No abstract

Aim-To determine the consequences of renal calcification in preterm infants. Methods-A cohort of 11 preterm babies was studied at the age of 4 to 5 years. They had had renal calcification as neonates. Seventeen matched controls were also studied. Each child had a renal ultrasound scan, a calcium load test, and a desmopressin test for renal concentrating ability (RCA). The study group also had glomerular filtration rate (GFR) estimated, using the height:creatinine ratio, and tubular phosphate reabsorption, without phosphate load, per glomerular filtration rate (Tp/GFR) calculated. Results-In the study group the median GFR was 61 ml/min/1.73m 2 (range 46-79 ml/min/1.73m2 ) and the median calculated Tp/GFR SD score was −0.94 (range −2.8-0.68). Five children out of the study group had ultrasonic evidence of renal calcification. There was no significant diVerence between the two groups in renal size, calciuria, before or after calcium load, or RCA. Eight children (three patients, five controls) had an abnormal calcium load test. The RCA of the children in the study and control groups combined was below that of published values, with a median calculated SD score −0.71 (95% CI −1.21 to −0.23). Conclusions-There was evidence of renal dysfunction in children who had been born preterm. Renal calcification detected in the neonatal period does not seem to be a major predisposing factor for the abnormalities of renal function subsequently observed in these infants. (Arch Dis Child 1997;76:F185-F189)

Investigations linking sudden infant death syndrome (SIDS) and type II intrauterine growth retardation (IUGR) have thus far failed due in part to technical limitations. Recently developed stereological methods for the unbiased estimation of total nephron number in the human kidney are capable of detecting deviations from normal values of greater than 10%. We compared the total number of nephrons in the kidneys of 24 SIDS victims with those from 16 controls with the same age range. Mean nephron number was significantly (P < 0.001) reduced in ex-IUGR SIDS cases (birthweight under the 10th centile, n = 9, mean number 635,000, range 327,000-1,010,000) in comparison with controls (903,000, 740,000-1,060,000). A similarly significant (P < 0.01) reduction in the "normal birthweight" SIDS group (birthweight over 10th centile, n = 15, 690,000, 361,000-1,040,000) was found. This hitherto unreported renal developmental arrest may be only one manifestation of a general, somatic developmental defect, reflecting adverse intrauterine conditions; other organ systems, similarly critical to homeostasis may be comparably affected. The findings, although not proposed as direct cause of SIDS, may represent a potential explanation for the recognized association of IUGR and SIDS, and provide--we believe--the first quantitative evidence of intrauterine growth retardation in, at least a number of, children of average birthweight.

We studied 13 children subjected to elective tonsillectomy, 6 of whom (study patients) received supplemental intravenous isotonic saline during and after operation, and 7 of whom (controls) did not. Clinical and biochemical evidence of hypovolaemia was present in the control but not in the study patients. Plasma antidiuretic hormone (ADH) and urine osmolality were higher in controls (p less than 0.005 and p less than 0.05 respectively). Plasma sodium concentration and osmolality were similar in the two groups. We conclude that hypovolaemia is the principal stimulus to ADH release following surgery and that, in addition to replacement of observed losses of blood and other fluids by fluids of appropriate composition, hypovolaemia should be prevented by the administration of maintenance quantities of isotonic fluid, rather than exacerbated by fluid restriction, in patients in whom oral fluid intake is interrupted for more than a brief period. Hypotonic and sodium free fluids should be avoided because of the risk of hyponatraemia.