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BK virus (BKV) is recognized as a significant cause of renal allograft dysfunction in adults, and there is growing awareness of its importance in the pediatric population. Eighteen pediatric renal transplant recipients and 18 age-matched controls were prospectively studied. Anti-BKV immunoglobulin G (IgG) and IgM titres were assayed in all subjects at entry to the study. Polymerase chain reaction (PCR) for BKV DNA was performed on urine and serum at entry, and prospectively tested again at 4, 8 and 12 months. Mean age +/- s.d. of transplant recipients and controls was 14.6 +/- 3.3 and 13.9 +/- 0.33 yr respectively [not significant (NS)]. Transplant patients were studied at a mean time of 5.6 +/- 4.2 yr post-transplant. 56% of transplant patients and 39% of controls were seropositive (+ve BKV IgG) (NS). Plasma BKV PCR was positive in one transplant patient (who also had positive urine PCR) and in none of the controls. The prevalence of positive urine PCR in transplant patients was greater than in controls (33% vs. 0%, p = 0.02). Positive urine BKV PCR was more commonly found in patients treated with mycophenolate than azathioprine (p = 0.04). We conclude that the prevalence of BKV seropositivity and viral activation in this Australian pediatric renal transplant population is similar to that reported in adult and pediatric populations in other countries. BK viruria was more common in children with greater immunosuppression, suggesting that this group is at higher risk of BKV induced nephropathy.

Significant differences are seen in a low-incidence urban Australian population with PSGN when compared with endemic or epidemic disease in high-risk populations. The higher rates of complications that were seen compared with previously studied populations need further clarification.

Growth hormone (GH), either directly or through insulin-like growth factor-1 (IGF-1), has a wide spectrum of physiological and renal effects. This review concentrates on the effects of GH (derived from either pituitary or recombinant technology) and IGF-1 in three main areas: (1) sodium and water homeostasis; (2) calcium and phosphate balance, bone density and interactions with mineral regulating hormones; (3) fat and lean body mass. Observations of physiological changes in states of GH deficiency and excess in humans and animal models are presented. The lack of long-term toxicological data indicates that GH treatment for short stature in non-GH deficient children, with or without renal disease, should proceed with caution.

Dimercaptosuccinic acid (DMSA) studies were performed in 113 infants less than 1 year old at risk of renal scarring. Of these patients 86 presented with urinary tract infection and 27 were asymptomatic. A voiding cystourethrogram was performed in all cases and excretory urography (IVP) was done in 99. More abnormalities were detected by DMSA study when compared to scars on IVP. When both studies were abnormal there was an excellent correlation on a site by site basis. Fever or systemic disorder was not a reliable sign to determine whether there was upper tract involvement with infection. The incidence of DMSA abnormalities in infants increased with high grade vesicoureteral reflux and decreased with low grade reflux. There was no significant difference in the incidence of abnormal kidneys between the infected and noninfected groups, suggesting that renal scarring may occur with sterile reflux.

A series of 208 patients was prospectively assessed for reflux nephropathy by intravenous urography (IVU) and 99mTc-dimercaptosuccinate (DMSA) scintigraphy. All patients were studied at least 3 months after their most recent urinary tract infection and micturating cystourethrography (MCU) was performed prior to the scintigraphic studies. DMSA scintigraphy detected significantly more cortical abnormalities than did IVU. There was also a correlation between cortical abnormalities in the DMSA studies and the degree of reflux on MCU. The validity of DMSA as a cortical imaging agent is evaluated and the histological evidence for its efficacy derived from the animal model is reviewed, lending weight to its establishment as the "gold standard" for renal cortical scarring.

Serum cystatin C more accurately reflects glomerular filtration rate (GFR) in pediatric renal transplant recipients than serum creatinine. Nineteen pediatric renal transplant recipients, 15 male and 4 female, ranging in age from 8.35 yr to 19.06 yr (median 13.52 yr), were enrolled in the study over an 18-month period. Twenty-eight measurements of 99mTc-DTPA GFR were compared with simultaneous measurements of serum cystatin C and Cr. Linear regression analysis, Pearson correlation coefficients and analysis of variance (anova) were used to determine the relationship between creatinine, cystatin C and GFR. The correlation coefficients (R2) for the relationship of 1/Cr to DTPA-GFR and for 1/cystatin C to DTPA-GFR were 0.63 and 0.58, respectively. There was no significant difference between serum cystatin C and serum creatinine as markers of GFR. Serum cystatin C, which costs more to measure than serum creatinine, offers no advantage in monitoring the renal function of pediatric renal transplant recipients.