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H. Narchi. Paediatric Department, Sandwell General Hospital, West Bromwich B71 4HJ, UK

Aim: To compare the incidence of renal tract anomalies diagnosed following foetal renal dilatation detected incidentally in late pregnancy with that detected during the recommended 20 week scan.

Material and Methods: A routine 20 week scan was carried out on a cohort of 4992 pregnant women. Fetuses with renal dilatation were rescanned at 28 weeks and those with persistent dilatation constituted group A. Group B consisted of fetuses with renal tract dilatation diagnosed on incidental third trimester scan. Postnatal investigations were performed according to a well defined protocol and the incidence of diagnosed renal tract anomalies detected was compared between both groups.

Results: In group A (44 infants) there was one infant with vesico-ureteric reflux (VUR) and another with a unilateral pelvi-ureteric junction obstruction. In group B (12 infants, of whom eight had an earlier normal scan at 20 weeks), two infants had VUR, one had renal dysplasia, and one had posterior urethral valve with absent right kidney. The incidence rate for VUR was 16.16 times higher (95% CI 0.80 to 953.9) when dilatation was diagnosed in the third trimester compared with the 20 week scan.

Conclusion: The 20 week scan may not be the best time to detect renal tract abnormalities and may be falsely reassuring. During any scan in the third trimester, even with a prior normal 20 week scan, renal tract dilatation should be looked for as its presence at that stage is more likely to be associated with renal tract anomalies.


M. Z. Mughal, J. Eelloo, S. Sibartie, S. A. Roberts, M. Maresh, C. P. Sibley, J. E. Adams. Central Manchester and Manchester Children’s Hospitals and the University of Manchester, Manchester, UK

Background: Offspring of diabetic rats have reduced urinary calcium and magnesium excretion compared with offspring of controls; these differences persisted up to 16 weeks after birth, a time equivalent to young adulthood in humans.

Aims: We tested the hypothesis that urinary calcium and magnesium excretion would be lower in children born to mothers with insulin dependent diabetes mellitus (ChIDDM) as compared with those born to non-diabetic mothers.

Methods: Concentrations of calcium, magnesium, sodium, and creatinine were measured in first void spot urine samples collected from 45 (28 male; median age 9.6 years) ChIDDM and in 127 (58 male; median age 11.3) controls. Analysis of covariance was used to test for differences in urinary calcium:creatinine ratios (UCa:Cr), magnesium: creatinine ratios (UMg:Cr), and log sodium:creatinine ratios (logUNa:Cr) between controls and ChIDDM after allowing for the effects of sex and age.

Results: UCa:Cr (difference −0.10, 95% CI −0.19 to −0.01; p 0.033) and UMg:Cr (difference −0.15, 95% CI −0.22 to −0.08; p<0.0001) were lower in ChIDDM compared with control subjects. However, logUNa:Cr did not differ between ChIDDM and control subjects (difference −0.14, 95% CI −0.33 to 0.05; p 0.14). The daily estimated intake of magnesium, sodium, and protein expressed as mg/kg per day, were all significantly higher in ChIDDM compared with controls. In ChIDDM, UCa:Cr and UMg:Cr were not related to mothers’ diabetic control.

Conclusions: Results of this study provide the first evidence that in humans, as in rats, there is modification of renal Ca and Mg handling in ChIDDM, which persists well into childhood.


S. C. Waller1, D. Ridout2, T. Cantor3, L. Rees1. 1Nephro-Urology, Institute of Child Health and Great Ormond Street Hospital for Children, London, UK; 2Paediatric Epidemiology and Biostatistics, Institute of Child Health, London, UK; 3Scantibodies Laboratory Inc., Santee, California, US

Background: In paediatric CRF optimal PTH levels that minimise renal osteodystrophy and maximise growth are unknown; we aim for normal range PTH levels. Currently used “intact” immunoradiometric (iIRMA) PTH assays cross react with long carboxyl-terminal PTH fragments (C-PTH), which antagonise the biological actions of 1-84PTH. The introduction of an assay (CAP-PTH) that is specific for 1-84PTH, enables estimation of the agonist (1-84PTH) to antagonist (C-PTH) ratio. In adults this ratio may be predictive of bone turnover; it may, therefore, also be relevant to growth.

Aims: To investigate the relationship between PTH, the 1-84PTH:C-PTH ratio and growth in children with CRF.

Method: 194 patients, median (range) age 9.9 years (0.3–17.1) were recruited: 168 with a GFR <60 mls/min/1.73 m2 (including 41 transplanted patients), 19 on peritoneal and 7 on haemodialysis. Over a median (range) period of 1.1 (0.5–1.7) years, children attended five (3–15) clinics at which iIRMA PTH and CAP-PTH were assayed, height measured, and height standard deviation score (Ht SDS) was calculated.

Results: Overall mean PTH levels were within the normal range (NR) for both assays; CAP-PTH 28.5 pg/mL (NR 5-39), iIRMA 45.1 pg/mL (NR 14–66). The patients grew normally (change in Ht SDS per year (ΔHt SDS) 0.01). Those with normal range PTH levels grew significantly better than those with raised PTH levels (p = 0.018). Normal range PTH was associated with a higher 1-84PTH:C-PTH ratio (p 0.01). There was a weak correlation between the ΔHt SDS and the 1-84PTH:C-PTH ratio (r 0.2, p 0.01). This relationship was emphasised by splitting the patients into tertiles by their ratio; the third of patients with the highest ratio grew better than those with the lowest ratio (p 0.033).

Conclusion: Normal range PTH levels are appropriate in children with CRF. C-PTH may be of clinical significance.


T. Anbu, T. Kemp, K. O’Donnell, M. A. Lewis, N. Plant, N. Webb, M. G. Bradbury. Royal Manchester Children’s Hospital UK

Background: Recombinant erythropoietin is more effective at correcting anaemia if body iron stores are replete. Oral iron can be inadequate, necessitating intravenous therapy.

Aims: To quantify the adverse events following 870 doses of Venofer given as 90 min intravenous infusion as day case or during haemodialysis compared with 50 doses given as 3 min rapid infusion in outpatients or during haemodialysis.

Method: Data were collected prospectively in a large UK centre as part of an anaemia treatment protocol.

Results: Four adverse events were seen following 870 90 min infusions. Three children developed abdominal pain while receiving infusions of 5, 6.7, and 7 mg/kg. These were subsequently decreased to 3, 4.4, and 5 mg/kg, respectively. No further abdominal pain was reported. One child developed worsening of his hypertension and dilated cardiomyopathy 2–3 weeks after receiving the iron. The patient had frequent previous admissions for hypertension and it is unlikely that this was due to the intravenous iron. Four adverse events were seen following the 50 3 min infusions. Two transient metallic taste (one associated with nausea), one child vomited, and one child developed diarrhoea 24 h post-dose that may not have been related to the iron. The 90 min infusion is associated with fewer adverse events (p<0.001). The 3 min infusion saves £8 per dose in disposables and the significant cost of a day case bed in the outpatient treated children and reduces the time absent from school.

Conclusion: Intravenous iron given as a 90 min infusion is safe, and well tolerated. A 3 min infusion is associated with an increased number of adverse events but reduces cost and days absent from school.


M. F. Riordan, V. Garg, G. Thulin, M. Kashgarian, N. J. Siegel. Departments of Pediatrics and Pathology, Yale University, School of Medicine, New Haven, Connecticut, 06511, USA

Introduction: Over expression of HSP72 or HSP25 augments recovery of cellular polarity in injured renal epithelial cells. To evaluate the relationship between heat shock response and recovery from ATP depletion, HSP72 and HSP25 were differentially inhibited using transcription factor decoy or short interference RNA (siRNA).

Method: Pre-transcriptional heat shock inhibition was achieved using double stranded, circular, heat shock transcription factor decoy oligonucleotides. Post transcriptional inhibition was provided by siRNA targeted at an inducible porcine HSP72 gene. Porcine proximal renal tubular cells were injured for 2 h by incubation with substrate deplete media and antimycin A. Cells were allowed to recover for 4 h prior to harvest. HSP expression was assessed by western blotting; alterations in polarity were quantified by NaK ATPase solubility. Cell viability was assessed by live dead assay.

Results: Scrambled controls for both the decoy and the siRNA failed to significantly alter HSP expression. Decoy reduced the induction of HSP72 from 85% to 10% above baseline; HSP25 fell in parallel (30–3%). Decoy resulted in augmented injury, with a 55% increase in NaK ATPase solubility. In contrast siRNA completely ablated the injury induced rise in HSP72; reducing expression to 40% below baseline. HSP25 levels were not significantly changed. Increased HSP72 inhibition resulted in exacerbated loss of polarity, NaK ATPase solubility increasing 103%. Cell viability was unchanged as a consequence of treatment with decoy; quantification of viability was complicated in the siRNA treated group due to marked loss of adhesion.

Conclusion: Inhibiting the induction of HSP in response to ATP depletion delays recovery of cellular polarity, an essential prerequisite for restitution of tubular function. The severity of cellular impairment increased in proportion to the degree of HSP72 inhibition. Cells treated with siRNA were unable to compensate for HSP72 loss by mounting an augmented HSP25 response; suggesting discreet function or the absence of feedback control.


S. D. Marks, M. J. Dillon, G. Hamilton, R. H. Lord, S. E. Stephens, K. Tullus. Department of Paediatric Nephrology, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, London WC1N 3JH, UK

Aims: To evaluate the mortality, morbidity, and outcomes of young children undergoing complex revascularisation and/or autotransplantation procedures for severe bilateral renovascular hypertension in a tertiary and quaternary paediatric nephrology service over the past 2.5 years.

Methods: Patients were identified through searches in the paediatric nephrology database at Great Ormond Street Hospital for Children.

Results: Five children (three female) aged 0.9–7.6 (median 5.3) years had revascularisation and/or autotransplantation procedures performed by a paediatric transplant and a vascular surgeon between May 2001 and September 2003. All patients survived with a follow up period of 0.2–2.5 (median 1.4) years. Out of three patients with mid-aortic syndrome, two had previous abdominal malignancies. All patients had evidence of left ventricular hypertrophy and three had failed angioplasty attempts. The technical aspects of the surgery were complex with three revascularisations performed using a trouser graft placed end to side onto the aorta and the limbs were anastomosed end to end onto the spatulated renal arteries. The youngest patient who pre-operatively had hypertensive encephalopathy with a maximal systolic blood pressure of 300 mm Hg underwent left renal transposition and right renal autotransplantation. In the remaining patient, the gastroduodenal artery was mobilised and anastomosed end to end onto the right renal artery and the splenic artery was anastomosed end to end onto two spatulated left renal arteries. All patients were admitted post-operatively to the paediatric intensive care unit. Two patients developed acute renal failure secondary to acute tubular necrosis, which resolved spontaneously without dialysis and all patients now have stable plasma creatinine levels. Patients were on maximal doses of 3–7 (median 5) antihypertensive agents pre-operatively and are now normotensive on 0–5 (median 2) agents post-operatively.

Conclusions: Revascularisation and/or autotransplantation procedures provide excellent results for young children with severe bilateral renovascular disease.


M. F. Riordan, S. A. Wang, G. Thulin, M. Kashgarian, K. L. Behar, N. J. Siegel. Departments of Pediatrics, Pathology and Magnetic Resonance Research, Yale University, School of Medicine, New Haven, Connecticut, 06511, USA

Introduction: Renal ischaemia is associated with a rapid fall in cellular ATP levels in vivo. Following ischaemia mitochondria change from being ATP producers to avid ATP consumers—using the reversible ATP synthase (also known as the F1F0 ATPase) in an attempt to maintain membrane potential. Changes in the expression and distribution of this proton pump were observed in an in vivo model of renal ischaemia.

Method: Male Sprague-Dawley rats (n 28) underwent 45 min bilateral renal artery occlusion. Kidneys were removed at reflow intervals of 15 min, 2, 6, and 24 h. Non-ischaemic kidneys were obtained from sham operated rats. Aliquots of renal cortex underwent homogenisation in protein and mitochondrial extraction buffers to allow comparison of expression between total and mitochondrial protein fractions. F1F0 ATPase expression was assessed by western blotting using an antibody to the F1 subunit.

Results: Consistent baseline expression of F1 ATPase was detected in sham operated rats and protein levels were comparable at each of the time points. Total cortical F1 ATPase levels increased by 46% of control values at 2 h of reperfusion, remained elevated at 6 h, but fell to less than 40% of control levels at 24 h. Mitochondrial isolates demonstrated a fall in F1 ATPase to 25% of control levels by 2 h of reflow; gradually returning to normal by 24 h reflow.

Conclusion: Mitochondrial levels of renal cortical F1F0 ATPase decrease following ischaemic renal injury. Potential factors underlying reciprocal changes in total F1ATPase levels include decreased cytosolic degradation of mobilised protein or extra-mitochondrial synthesis. Recovery of mitochondrial F1 ATPase levels is associated with a marked fall in total cortical F1 ATPase; possible explanations include altered compartmentalisation, phosphorylation, or degradation. Changes in mitochondrial F1F0 ATPase level may be important in determining the direction in which the F1F0 ATPase exerts its pivotal dual role in regulating cellular energetics in extremis.


R. Coward, S. Cross, R. Smith, P. Mathieson, M. Saleem. Academic Renal unit, University of Bristol

Podocytes are essential for maintaining the integrity of the glomerular filtration barrier, however, studying the normal properties of these cells has proven difficult due to a lack of differentiated cell models. We have developed a unique conditionally immortalised human podocyte cell line (

) and have studied its characteristics during development from a de-differentiated phenotype at 33°C to a differentiated phenotype that occurs after 14 days at 37°C. Additionally we have compared how the differentiated cell behaves under culture conditions that mimic the normal physiological milleu (human AB plasma), compared with human nephrotic conditions (FSGS, SLE, and IgA nephropathy plasma). We have convincing evidence from western blotting and immunofluorescence that normal plasma enables nephrin, and CD2AP to assume a peripheral plasma membrane location and nephrin to be up regulated within 48 h of exposure. Furthermore normal plasma can “rescue” the cytoplasmic location of nephrin that is induced with nephrotic plasma.

We have also explored if podocytes are able to produce cytokines de novo and if these are modulated by development, disease states, or the standard nephrotic syndrome therapy dexamethasone (Dex) (10−5 M). Using cytometric bead array technology we have found in vitro that within 24 h podocytes produce IL 6 and IL 8 under the influence of normal human plasma but the cytokines IL 1β, IL 2, IL 4, IL 10, IL 12, TNFα, and IFNγ are undetectable. Developmentally IL 6 and IL 8 are maximally expressed early in differentiation (day 2–3). Nephrotic disease plasma has no significant effect on the amount of cytokine produced within 48 h of exposure, but Dex selectively down regulates IL 6 (mean 39%) in all samples (n 9) over 48 h (p 0.02). This suggests that normal human plasma contains factor(s) that are able to maintain nephrin and CD2AP at the periphery of the podocyte; podocytes are able to produce IL 6 and IL 8 that may be important in their development; and IL 6 is down regulated by therapeutic doses of Dex after 48 h that may be important mechanistically in its action in glomerular disease.


J. Hegarty3, J. Adams4, M. Z. Mughal2, N. J. A. Webb1. Departments of Paediatric Nephrology1 and Paediatrics2, Central Manchester and Manchester Children’s Hospitals; 3Department of Nephrology, Hope Hospital, Salford; 4Department of Diagnostic Imaging, University of Manchester

Background: Children with relapsing minimal change nephrotic syndrome (MCNS) receive repeated courses of high dose oral prednisolone to control their proteinuria. A number of small studies using different radiological techniques have shown bone mineral density (BMD) to be reduced during ongoing therapy in childhood, though no previous studies have comprehensively investigated the impact of this therapy on final adult BMD.

Aims: To evaluate BMD in adults with previous childhood MCNS.

Methods: Adults previously reported in a large follow up study of children with biopsy proven MCNS (

) were contacted and asked to participate. Following the collection of basic anthropometric data, areal BMD (aBMD) was measured using DXA of the spine (L1-4), and volumetric BMD (vBMD) of the distal radius was measured using pQCT.

Results: Twenty seven of the original 62 adults agreed to participate. Their mean (SD) age at investigation was 37.9 (4.7) years. During childhood, they suffered 8.9 (9.3) disease relapses, each of which was treated with prednisolone using the standard ISKDC relapse regimen. Final adult height of the cohort was −0.4 (0.95) (p 0.054). There was a significant reduction in radial trabecular vBMD: the mean (SD) z score was −0.96 (1.05) and t score −1.05 (1.09), p<0.0001. However, the total radial (cortical and trabecular) vBMD was not reduced (mean (SD) z score 0.12 (1.0) and t score 0.05 (1.1), p 0.53 and 0.81). Spinal aBMD was similarly normal (mean (SD) z score −0.21 (1.23) and t score −0.29 (1.21), p 0.39 and 0.23).

Conclusions: Adult survivors of childhood MCNS have a significant reduction in forearm trabecular vBMD, consistent with the known effects of corticosteroids on trabecular bone. As combined cortical and trabecular forearm and lumbar spine BMD are not reduced, they may not be at increased risk of forearm or vertebral fracture.


R. C. L. Holt1, S. A. Ralph2, J. Davies2, N. J. A. Webb1, P. E. C. Brenchley2. 1Department of Nephrology, Royal Manchester Children’s Hospital; 2Manchester Institute of Nephrology and Transplantation

Introduction: We have tested the hypothesis that disordered heparanase activity has a role in the pathogenesis of childhood onset SSNS.

Methods: Twenty eight SSNS patients were studied in remission and 14 in the proteinuric phase. Twenty four healthy subjects served as age and sex matched controls. Heparanase activity (HA) was quantified in urine and plasma using a heparan sulphate degradation assay. Peripheral blood mononuclear cell (PBMC) heparanase mRNA was quantified by real time RT-PCR.

Results: Urine HA was significantly higher in proteinuric patients (median values with interquartile range, IR; 14.26 μ/mg creatinine, 8.37–17.60 μ/mg) than remission patients (7.43 μ/mg, 5.06–11.48 μ/mg; p 0.016, Mann-Whitney); remission urine HA was also significantly higher than control values (2.29 μ/mg, 1.67–3.32 μ/mg; p 0.000, MW). Proteinuric patients exhibited significantly lower plasma HA (811 μ/ml, 479–1092 μ/ml) than remission patients (1148 μ/ml, 1059–1215 μ/ml; p 0.003, MW); remission plasma HA was also significantly lower than control values (1391 μ/ml, 1071–1628 μ/ml; p 0.012, MW). There was no correlation between urine and plasma HA levels in proteinuric patients (r 0.000, p 1.000, Spearman, 2 tailed). No significant differences were observed between the study groups in heparanase mRNA expression by PBMC (proteinuric phase: 2.49 arbitrary units, IR 1.41–3.45 au; remission: 2.04 au, IR 1.60–2.36 au; control: 2.40 au, IR 1.81–3.93 au; p 0.156, Kruskal-Wallis).

Conclusions: Urine and plasma HA were abnormal in the remission group and markedly abnormal in the proteinuric group. Elevated urine HA, persisting in confirmed proteinuria free remission, may suggest an intra-renal source of dysregulated heparanase, which may be relevant to the pathogenesis of SSNS.


A. M. Durkan1, J. H. McColl2, P. Gray1, M. M. Fitzpatrick3, I. J. Ramage1. 1Yorkhill NHS Trust, Glasgow, G3 8SJ, 2Department of Statistics, University of Glasgow; 3Leeds Teaching Hospitals NHS Trust, Beckett Sreett, Leeds

PD is the predominant method of renal replacement therapy in paediatric nephrology centres. PD access failure is recognised to occur less frequently than with vascular access for hemodialysis but remains a significant cause of morbidity within the paediatric end stage population. A two centre retrospective observational study was undertaken of 159 patients (84 male) initiating PD for end stage renal failure to determine factors associated with initial peritoneal dialysis catheter survival. Catheter survival was assessed as right censored survival data with univariate analysis undertaken using a log rank test and for continuous variables Cox regression, with multivariate analysis undertaken using a stepwise Cox regression. Variables assessed included grade of operator (staff surgeon v trainee), height, weight, body mass index (BMI), sex, serum albumin, age at catheter insertion, time between presentation and initiation of peritoneal dialysis, and number of episodes of peritonitis. Grade of operator was significantly associated with catheter survival (p<0.00005) staff better than trainee, as were weight (p<0.00005), BMI (p<0.00005), height (p<0.001), and serum albumin (p<0.039), with other variables not reaching statistical significance. The median catheter survival was 1119 days (95% CI 683 to 1555) for catheters inserted by staff surgeons and 229 days (84 to 374) for catheters inserted by trainees. Cox proportional hazards model, forward stepwise fitting demonstrated both operator grade (p<0.00005) and height (p<0.0005) to be significantly associated with catheter survival (χ2 goodness of fit test, p 0.434) with the final model demonstrating hazard ratios for grade of operator of 0.274 (0.0150 to 0.501) and for height 0.981 (0.972 to 0.991) per 1 cm difference in height. There was no significant effect of serum albumin on multivariate analysis although a correlation was observed with height 0.301 (0.14 to 045). Dialysis access is a life long requirement for children with end stage renal disease and although catheter survival is less in smaller children the grade of operator significantly affects catheter survival, which should be undertaken whenever possible by an experienced operator.


R. Slack, K. C. Hawkins, L. Gilhooley, G. M. Addison, M. A. Lewis, N. J. A. Webb. Departments of Nephrology and ICU, Royal Manchester Children’s Hospital

Background: ARF is a well recognised complication of severe meningococcal septicaemia. Although the large majority of survivors appear to recover renal function, allowing renal replacement therapy (RRT) to stop, little is known about long term renal outcome.

Aims: To evaluate the long term renal outcome of children admitted to the intensive care unit (ICU) with meningococcal septicaemia associated ARF requiring RRT.

Methods: Casenote review of all children with meningococcal septicaemia admitted to ICU from Jan 1996 to Dec 2000 and identification of those requiring RRT. Prospective evaluation of renal function (51Cr-EDTA, plasma cystatin C, and creatinine), proteinuria (24 h urine collection), blood pressure, and DMSA scan.

Results: 209 patients were admitted during the study period, of whom 21 required RRT. This was commenced because of oliguric acute renal failure and never as a therapy to clear cytokines. Mortality was higher in the RRT group (28.6% compared with 9.6% in those not requiring RRT, p 0.03), although there was no difference in disease severity score. The median (range) duration of RRT was 14.5 (1–39) days. Of the 15 RRT survivors, 12 agreed to participate at a median (range) time post-diagnosis of 4.2 (2.7–7.1) years. Two children had evidence of reduced GFR (36 and 37 ml/min/1.73 m2), one of whom also had significant proteinuria, hypertension, and focal DMSA changes. One child had significant proteinuria alone (0.74 g/24 h) and one had a focal defect on DMSA; there was no prior history of UTI. Eight children had no abnormality detected. Non-renal morbidity was high, with 4/12 having lost limbs (fingers, forearm, arm, and both legs) and 4 with significant central (2) or peripheral (2) neurological injury.

Conclusions: As paediatric ICU care improves, a higher proportion of patients with severe meningococcal septicaemia and ARF are surviving. The high prevalence of renal dysfunction detected in this study mandates that these children undergo periodic renal assessment and remain under long term follow up.


M. Aslam, A. R. Watson on behalf of the Trent and Anglia Nephrourology GroupChildren and Young People’s Kidney Unit, Nottingham City Hospital, Nottingham NG5 1PB

Aims: MCDK is one of the commonest antenatally detected urinary tract abnormalities. Because vesicoureteric reflux (VUR) is common in the contralateral kidney (11–37% of series), an MCUG has been part of a prospective postnatal investigation protocol. We reviewed the outcomes for MCDK patients to ascertain whether an initial MCUG is necessary.

Methods: Children with MCDK were followed prospectively with ultrasound scan (USS), MCUG, and DMSA scan at the time of diagnosis with clinic review and USS at 2, 5, and 10 years. Prophylactic antibiotics were given to children with VUR grade 2 or greater. Urinary tract infections (UTIs) were recorded for all patients at the time of clinic visits along with blood pressure and growth measurements. The involution rate was calculated using Kaplan Meier statistics.

Results: 189 patients have been recorded on our database between 1987 and 2002, with 149 patients being followed to 2 years, 85 to 5, and 30 to 10 years, respectively. 16% of those who had an initial MCUG had reflux into the atretic ureter and 18% into the contralateral kidney. VUR was mild (grade 1/5) in 15%, moderate (grade 2–3) 81%, and gross (4%) in 1 child who had ureteric dilatation and renal dysplasia of the contralateral kidney. 16 children had reported UTIs but none was hospitalised. There was no significant difference in the incidence of UTIs between those with or without reflux and no patients developed hypertension. No scarring was identified in the contralateral kidney on further USS imaging at 2 and 5 years in either group. 73% of MCDKs had undergone complete involution by 10 years.

Conclusions: Although 18% of infants with MCDK had VUR in the contralateral kidney it was mild to moderate in the majority with no increase in UTIs or detectable renal scarring. We suggest abandoning the use of the MCUG as part of the routine postnatal investigations and targeting those with USS features suggestive of VUR or those presenting with a proven UTI under 1 year of age. The natural history of MCDK is still being defined with 27% of patients having an identifiable renal remnant at 10 years of age.


S. Russell1, E. Neill1, S. Dhiya2, T. J. Beattie1, A. V. Murphy1, I. J. Ramage1, S. F. Ahmed2, H. Maxwell1. 1Renal Unit, Royal Hospital for Sick Children, Glasgow; 2Bone & Endocrine Research Group, Royal Hospital for Sick Children, Glasgow

Aims: To compare body mass index (BMI) to fat mass (FM) and lean body mass (LM) using dual x ray absorpiometry (DXA) in children with chronic renal insufficiency (CRI) and post-transplant patients (Tx).

Patients and Method: Twenty seven children with CRI (median age 11 years, 10th, 90th percentiles: 4.3, 14) and 19 Tx children (median age 15 years: 10.7,17.6) had anthropometry, DXA, and assessment of nutritional intake. The calorie and protein intake was calculated from dietary histories and expressed as a percentage of the recommended allowance.

Results: In the CRI group, the median GFR was 27.4 ml/min/1.73 m2 (7.1, 69) and the median duration of illness was 9.3 years (2, 12). Median Ht SDS and BMI SDS were −1.6 (−2.7, 1.3) and −0.1 (−1.4, 1.7), respectively. Median calorie intake was 95% (81, 118) and the protein intake was 100% (93, 129). Median percentage FM SDS was 0.8 (−0.5, 1.2) and LM SDS was −1.8 (−3.5, −0.5). In the Tx group the median illness duration was 9.7 years (3.6, 16.5) and the median duration post-transplant was 3.3 years (3.8, 8.8). Median Ht and BMI were −1.4 (SD −3, 0.2) and 0.5 (−1.8, 2.5), respectively. Median calorie intake was 107% (90, 122) and protein intake was 113% (101, 152). Median percentage FM SDS was 1.4 (0.3, 2.4) and LM SDS was −2.3 (−4.7, −0.8). The median BMI SDS for the whole group at 0.5 (−1.7, 1.7) was significantly lower than the percentage FMSDS 1.1 (−0.1, 2.5) and significantly higher than the LM SDS −1.89 (−4.2, −0.5) (p<0.005). There was a significant relationship between energy and protein intake and BMI SDS and percentage FM SDS but not with LM SDS in the Tx group (r 0.6, p<0.05). This was not evident in the CRI group. In the Tx group, there was an inverse association between BMI and time since Tx (r 0.5, p<0.05). LM was low in the CRI group and remained so post-transplant.

Conclusion: BMI is not an accurate representation of body composition in children with chronic renal disease who seem to have a relatively high FM and a low LM. Nutritional supplementation of these children should not exclusively rely on BMI. The pattern of disordered body composition in these children may pose a long term risk of cardiovascular disease and osteoporosis.

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