Renal transplantation for pediatric end stage renal disease (ESRD) is a preferred option in dealing with these chronically ill patients. The pediatric renal transplant program at University of Missouri-Kansas City School of Medicine was begun in 1986 at St. Luke's Hospital and subsequently shifted to the Children's Mercy Hospital as experience was accumulated. To date 35 transplants have been performed in 31 recipients. Fifty-one per cent of the patients transplanted were adolescents (older than 13 years) and 91% of the patients were older than 4 years. Sixteen of the 35 transplants were from living related donors and 19 patients received their kidneys from cadaveric donors. Immunosuppression consisted of corticosteroids, azathioprine, cyclosporine and antilymphoblast globulin. No patients died following transplantation with a functioning kidney. Allograft survival with living related transplants at one year and three years was 91% and 86% respectively. Cadaveric allograft survival at one year and three years was 78% and 46% respectively. Most kidneys were lost due to either acute or chronic rejection although there were three patients who lost their kidney due to primary nonfunction, including one child age 23 months. The growth pattern of all but the youngest children (< or = 2 years) following transplantation showed no evidence of accelerated growth. Results in this early series of pediatric renal transplant patients is encouraging from the standpoint of patient and allograft survival and even though accelerated growth is not seen in the older children, it seems to offer a better quality of life for children with end stage renal disease.

Objective To evaluate the ability of tidal peritoneal dialysis to decrease the pain and frequency of hemoperitoneum associated with peritoneal calcification. Design Prospective case evaluation. Setting The Home Peritoneal Dialysis Unit, Children's Mercy Hospital. Patient Seven-year-old male with diffuse peritoneal calcifications, daily abdominal pain, and recurrent hemoperitoneum. Intervention Tidal peritoneal dialysis was conducted with an initial fill volume of 45 mL/kg and a tidal inflow volume of 23 mL/kg. The patient also maintained a daytime pass volume of 45 mL/kg. Duration of treatment was 7 months. Results The patient's abdominal pain resolved 2 days after initiating tidal peritoneal dialysis. No episodes of hemoperitoneum or abdominal pain have occurred for 7 months. Conclusion Tidal peritoneal dialysis is a unique approach to the achievement of symptomatic relief in the patient with peritoneal calcification.

Studies in the last decade demonstrated that in children tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/GFR) is identical to TP/GFR; TP indicating tubular phosphate reabsorption under basal conditions, without phosphate load. TP/GFR is calculated from the formula TP/GFR = SP-UP x SCr:UCr, based on simultaneous urine and blood creatinine and phosphate concentrations, and is applicable in both the fasting and non-fasting child. These studies also demonstrated that the use of Walton and Bijvoet nomogram in children may result in overestimation of TmP/GFR compared with TP/GFR calculated from the above formula. When using the formula, one should bear in mind that creatinine is used to express GFR and as a result a significant deviation from true GFR may occur in patients with renal failure. Therefore when employing TP/GFR for the investigation of the renal handling of phosphate in children, three factors should be taken into consideration: (1) the formula in reality expresses TP/CCr; (2) only data obtained by exactly the same methodology can be used as reference values; data obtained from studies in which the nomogram was utilized or in which methods other than CCr were used to measure GFR should not be used for reference; (3) in patients with renal failure, TP/CCr will significantly overestimate TP/Cinulin.

Scant information exists on the prognosis of infants with renal failure who receive peritoneal dialysis in the first month of life. We reviewed the outcome of 23 such patients 1 year after the onset of renal failure. Diagnoses included acute tubular necrosis (11 infants), renal dysplasia (5), obstructive uropathy (4), polycystic kidney disease (1), renal vein thrombosis (1), and renal artery thrombosis (1). Seven of the eleven patients with acute tubular necrosis had had cardiac surgery. At 1 year, eight (35%) of the patients had died, six (26%) had a full recovery, seven (30%) were receiving long-term dialysis awaiting a transplant, and two (9%) had chronic renal failure. Effective dialysis, characterized by the reversal of metabolic disturbances or attainment of fluid balance, was accomplished in all patients. The mean duration of dialysis was 4.5 months (range, 0.1 to 12 months). The most common complications of dialysis were peritonitis and catheter exit site infection. Despite the provision of supplemental calories via nasogastric tube, the majority of patients receiving long-term dialysis showed impaired growth and mild developmental abnormalities. Peritoneal dialysis is an effective means of renal replacement therapy in the neonatal period; however, the morbidity and mortality rate for this population remains high.

The patient was a 17-year-old black female who was maintained on CCPD for more than seven years. Her course on dialysis was complicated by numerous episodes of bacterial peritonitis. During the most recent 12-month period, there were five episodes of peritonitis due to gram-positive and gram-negative bacteria. No fungi were isolated from any of the peritoneal fluid cultures. Antibiotic therapy included numerous intraperitoneal courses of broad spectrum antibiotics. The patient had been on intraperitoneal cefotaxime and vancomycin for two weeks for treatment of peritonitis when she developed intermittent abdominal pain and transient cloudy dialysate efflu ent. Three separate samples of peritoneal fluid were obtained over the next 11 days. Each of the samples grew the syncephalastrum species but no bacteria. The cell count and differential of the first dialysate fluid sample demonstrated a predominance of polymorphonuclear leukocytes (PMN) (Table 1). The peritoneal catheter was removed, and the patient's dialysis therapy was converted to hemodialysis at the patient's request. The patient received 10 days of amphotericin B and her symptoms resolved.

To investigate the biochemical nature of nephrocalcinosis in children with hypophosphatemic rickets treated with orally administered phosphate and vitamin D, we studied five such patients, aged 3.7 to 12.3 years, during treatment and again 3 days after it had been discontinued. Treatment was associated with significant increases in mean serum phosphate concentration and urine phosphate/creatinine ratio, from 0.71 to 1.03 mmol/L and from 3.61 to 9.42 mmol/mmol, respectively. Significant correlation was found between urine phosphate/creatinine and oxalate/creatinine ratios (r = 0.670; p less than 0.01); however, the mean urine oxalate/creatinine ratio of 65.0 mumol/mmol while patients were taking phosphate orally was not significantly different from the ratio of 59.0 mumol/mmol when treatment was discontinued. Kidney biopsy specimens from three of the patients showed that the renal calcifications were located mainly intratubularly and were composed exclusively of calcium phosphate. In a further investigation of the nature of phosphate-induced nephrocalcinosis, six 6-week-old male Hyp mice, the murine analog of the human disease, received oral phosphate therapy with drinking water for 48 days; six others served as control animals. Mice in the experimental group excreted more phosphate (p less than 0.001) and less calcium (p less than 0.01) than control mice did, and medullary nephrocalcinosis, with a high kidney calcium content, developed (p less than 0.001). Histologic sections showed that the renal calcifications were located intratubularly and were composed of calcium phosphate. We conclude that, both in children with hypophosphatemic rickets and in the Hyp mouse, the development of nephrocalcinosis is associated with high oral phosphate intake and subsequent deposition of calcium phosphate precipitates in the kidney.

In summary, all children and families who present with nocturnal enuresis should be offered education, reassurance, and ongoing support as a premier component of any treatment regimen. At the same time, the family should be informed about all the treatment options that exist with a goal of tailoring the specific treatment to the individual patient. In most cases, this approach will lead to child, family, and physician satisfaction.