A 9-year-old boy developed acute renal failure following intravenous acyclovir (30 mg/kg per day) administered for 6 days to treat herpetic encephalitis. Physical findings and urine output were normal, except for increasing blood urea nitrogen (BUN), serum creatinine and mild proteinuria. Acyclovir was discontinued. However BUN and serum creatinine continued to increase and peaked on the following day at 8.6 mmol/l of urea (24 mg/dl) and 194 mumol/l (2.2 mg/ml), respectively. Conservative treatment and hydration were carried out. The kidney function returned to normal within 1 week. The use of acyclovir when necessary in renal failure patients is discussed.

Thirty-three children received a total of 38 renal transplants (18 living related donor, and 20 cadaveric) after being on CAPD and/or CCPD (PDPD). Ten patients (12 transplants) were converted to hemodialysis pre-transplant in order to be free of the risk of peritonitis and off antibiotics, whereas 23 patients (26 transplants) were on PDPD at the time of transplant. The latter group of patients are described in greater detail. Within this group there was one episode of catheter colonization with Flavobacterium, and only three patients developed ascites post-transplant. Of the 26 transplants, catheters were removed at the time of transplant in the 13 LRD allografts but left in situ for a mean of 3.8 weeks in the 13 cadaveric transplant recipients. Peritoneal dialysis was required post-transplant in seven patients (two LRD recipients requiring a new catheter placement) without complications. Our policy of removing PD catheters at the time of transplant in LRD recipients and prior to hospital discharge in cadaveric transplant recipients has resulted in the avoidance of additional hospitalizations in 19 of the 26 transplants and avoided extra surgery in 11 of the 13 LRD transplants. We conclude that children who have been on PDPD are suitable candidates for renal transplantation and that the early removal of PD catheters, including removal at the time of transplantation in LRD recipients, is associated with a significant reduction in operative procedures for the patients.

Idiopathic hypercalciuria is known to cause many nonstone urinary tract disorders in childhood. In addition to being the most common cause of microhematuria in children, our study demonstrates that idiopathic hypercalciuria is also frequently associated with urinary incontinence of all types. Of 124 children evaluated for idiopathic hypercalciuria 28 (23%) had urinary incontinence. Of the 28 children 15 (54%) had nocturnal, 6 (21%) diurnal, and 7 (25%) nocturnal and diurnal incontinence. The random urinary calcium-creatinine ratio, which was used to screen for hypercalciuria, should be part of the initial evaluation for urinary incontinence in children. Diagnosis may be confirmed by quantitative urinary calcium excretion. Most urinary incontinence in children that is due to idiopathic hypercalciuria responds to a combination of general treatment for hypercalciuria or thiazide diuretics.

Objective: To evaluate the role of idiopathic hypercalciuria (IH) as a cause of recurrent abdominal pain (RAP) in children. Patients and methods: We retrospectively reviewed the medical records of 124 children referred for various complaints who had 24‐h urine calcium excretion greater than 2mg/kg/d or random urine calcium‐creatinine ratio greater than 0.18mg/mg. Results: Fifty‐two children with various clinical complaints had RAP or flank pain. These comprised of 22 males and 30 females, 9 mo to 15.9 y of age, mean 6.7 3.5 y. A family history of urolithiasis was present in 50% of all the children. Only 6 of the 52 children with abdominal pain had renal stones. In addition to abdominal pain, 27 children had hematuria and 10 had urinary incontinence. Mild metabolic acidosis was present in three children, parathyroid hormone activity elevated in two and serum vitamin D activity was increased in nine. All children were treated with increased fluid intake and a reduction in dietary sodium and oxalate and some required treatment with thiazide and antispasmodics. Forty‐five cases responded to treatment, 5 failed to improve from therapy, and 2, which were not followed up as patients, were not available. Conclusion: We describe 52 children with RAP or back pain due to IH and recommend that IH be considered in the differential diagnosis of RAP in childhood.

We describe 52 children with RAP or back pain due to IH and recommend that IH be considered in the differential diagnosis of RAP in childhood.