LONG TERM MEMODIALYSIS (HD) IN CHILDREN AND 1510ADOLESCENTS. Valerie Johnson, Robert A. Weiss and Ira Greifer, Albert Einstein College of Medicine, Dept. of Pediatrics, Bronx, N.Y. Despite agreement among pediatric nephrologists that renal transplantation is the therapy of choice, succe- ssful transplantation is often impossible due to cyto- toxic antibodies. Ten pts (mean age at onset HD 10.8 yrs) have been on maintenance HD for more than 4 yrs (mean duration 5.3 yrs). 8 pts. have undergone success- ful transplantation with grafts functioning less than six months. Vascular access, even in children OK 8 kg, has been by fistula exclusively. Mean fistula survival in 9 pts has been 59.7 months although a tenth patient has required 19 access procedures over 6 yrs. Manifes- tations of osteodystrophy such as epiphyseal slipping, genu valgum and brown tumors have been observed in 8/ 10, often due to poor compliance with the medication regimen. Linear growth has been poor even when corr- ected for skeletal age, despite biochemical control of uremia and nutritional counseling. An additional com- plication has been hemochromatosis (serum ferritin 11,000) in one adolescent and elevated serum ferritins in seven other pts. Promoting psychosocial maturation and rehabilitation through the use of "group therapy" sessions have been successful in achieving full school attendance and realistic career planning in all pat- ients. IDIOPATHIC HYPERCALCURIA (IHC) AND GROSS HEMA- el511 TURlA (GH) IN CHILDREN. Alok Kalia and Luther B. Travis, Univ. of Texas Med. Br., Dept. of Pediatrics,Galveston,Tx. Although onset of GH prior to calculus formation has been reported, the association of GH and IHC without clinical or radiological evidence of nephrolithiasis has not been described. Six children have been identified who presented with asymptomatic and recurrent GH in whom no calculus could be demonstrated radiographically. Investigations did not reveal any renal or urinary tract pathology which could account for the hema- turia. ICH was documented in five; the sixth later passed a calcium oxalate calculus. Five had a family history of renal calculi. Three con- tinued to have recurrentgross and micmscopic hematuria with the initial renal calculusdeveloping after 6 months, 5 years and 10 years. Two of the others were started on a thiazide diuretic and the sixth on chlor- thalidone soon after onset of hematuria and confirmation of IHC. There was prompt cessation of hematuria without recurrence after 9, 9 and 24 months. W e suggest that measurement of urinary calcium excretion as part of the initial evaluation of a child with GH may, in some cases, obviate invasive investigations and allow for effective therapy. MONONUCLEAR CELL CHEMOTAXIS IN EXPERIMENTAL INTERSTI- TIAL NEPHRITIS. Thomas L. Kenned and Martha Merrow, university of Connecticut Health bnter, Department of Pediatrics, Farmington, Connecticut and Michael E. Norman, The Children's Hospital of Philadelphia, Philidelphia. Because the inflammatory infiltrate in antitubular basement membrane nephritis in guinea pigs (Steblay nephritis) is pre- dominantly mononuclear, the stimulus for monocyte and macrophage recruitment was studied. The tubulointerstitial inflammation begins 10-14 days following injection with heterologous tubular basement membrane antigen. Sera were obtained from the renal vein in order to avoid the difficulties of systemic inactivation or dilution encountered when trying to identify chemotactic activity (CA) from peripheral blood. These samples, as well as renal homogenates, were compared to renal arterial sera for CA using peritoneal mononuclear cells. Sera and homogenates were obtained from nephritic and control animals at several times in the course of the disease. CA is detected in samples obtained from day 7-15 and is maximal at day 10. The CA is heat stable and is most prominent in the renal venous serum suggesting an origin from the kidney. Use of the sera as a chemoattractant for guinea pig polymorphonuclear leukocytes produces no cell recruitment and suggests the CA is specific for mononuclear celk The alternative pathway of complement has been implicated in the pathogenesis of Steblay nephritis and complement derived chemo- tactic factors may prove to be responsible for CA. However, measurable complement activation reflected in decreased hemolyt- &a,a$&gfgt(g~~~?.or in depleti" of complement proteins (C3, PERITONITIS IN CHILDHOOD NEPHROTIC SYNDROME. Alan M. Krensky, Warren E. Grupe, Julie R. In elfin er. Har- 1513 a d i c a l school. Department of Peziatrib. Child- ren's Hospital Medical Center. Boston, Massachusetts. A retrospective review (1970-1980) of 310 children with idio- pathic nephrotic syndrome revealed 24 episodes of peritonitis in 19 patients (6.9 2 3.7 years old). None were on cytotoxic drugs and only 64% were on steroids at the onset of peritonitis. All had proteinuria; 23 occurred during a relapse and one was at pre- sentation of nephrosis. No morphologic subtype was at significant -1y greater risk for peritonitis. Abdominal pain, tejnderness, edema, ascites, leukocytosis (22,300 f 7,700 wbc/mm ) were uni- versal. Other signs and symptoms included: fever (96%), anorexia (65%), vomiting (65%), diarrhea (52%J,and abdominal. wall cellu- litis (22%); 17/19 had > 1000 wbc/mm of peritoneal fluid. Gram stain was positive in only 7/18. Organisms isolated included pneumococcus (13), E. coli (5), E. coli and B. fragilis (1-with appendicitis), and a-streptococcus (1); 4 were culture negative. Only 1/8 pneumococci typed is not included in the commercial vac- cine (type 33). All pneumococci and E. coli were sensitive to all antibiotics routinely tested. Serum IgG levels in 13 episodes measured were dramatically reduced (116277 mg%) compared to 43 control nephrotics (579+293;p < 0.001). Thus, peritonitis is stil.1 common in patients with nephrosis (6%); second episodes are frequent (26%); pneumococcus is the most frequent agent (54%) with 7/8 types represented in available vaccine. Patients in relapse, with ascites, edema, and severe hypogammaglobulinemia appear at greatest risk. ELEVATION OF NEPHROGENOUS CYCLIC ADENOSINE MONOPHOS- PHATE (Neph CAMP) AS EVIDENCE OF EARLY RENAL OSTEODYS- Harmon, Julie R. Ingelfinger, John A. Kirkpatrick. Harvard Medi- cal School, Children's Hospital Medical Center, Departments of Pediatrics and Radiology, Boston, Massachusetts. To determine at which point in chronic renal insufficiency (CRI) the physiologic conditions for altered bone metabolism ap- pear, radiographs, serum chemistries, parathyroid hormone (PTH), and neph cAMP were evaluated in 25 children with CRI compared to 7 children with benign renal disease and normal renal function: PATIENT 1 2 g Phos Alk P PTH Ne h cAMP GROUP mg/dl mg/dl 3 1 !.IlE9/ml nmo$lOOmlGF Normal 7 0.6 9.7 3.9 9 50 1.4 CRI 10 5.7 8.6 5.3 160 370 5.4 Hemodialysis 5 9.0 9.5 3.4 94 181 4.6 Transplant 10 2.4 9.7 4.6 76 155 3.3 Normal range .3-.95 9-11 3.5-4.5 50-125 20-60 0-4 Neph cAMP increases linearly with creatinine (Cr) (r=0.81) and PTH (r=0.89) except for patients on chronic hemodialysis, in whom a metabolic steady state did not exist, or for patients with ser- um Cr > 8.0mg/dl. Serum Cr appropriate for age and height was un- iversally associated with neph CAMP< 4.0nmo1/100mlGF, while neph cAMP was elevated in 9/15 patients with Cr > l.Omg/dl and all patients with Cr > 3.5mg/dl. Both PTH and neph CAMP were elevated in-asymptomatic patients with Cr as low as 1.45mg/dl. Neph cAMP > 4.0nmo1/100mlGF is a reliable, non-invasive measure of early changes consistent with the development of renal osteodystrophy even before routine changes are evldent. Depts. of Ped. Neph. & Med. Linear growth failure is a major complication of CRF unique to children and is related to renal osteodystrophy (ROD). 19 chil- dren, ages 2.8-16.4 yrs with CRF and BH of osteomalacia (OM), os- teitis fibrosa (OF) or bdth (OFM) were given 1-2 mcg/kg/d of 25D to evaluate effects on ROD & GV. GV was defined by standard de- viation scores on Tanner growth charts, the preferred method of expressing growth in pts with CRF. Group GV (meanfSEM) was -1.75f.45 in the pre-Rx year, increasing to +.2f.31 after the 1st Rx yr, and correlated with an increase in serum 250 of 42f8 nglml to 244'20 nglml (r=.37, p<.002). Pre-Rx BH showed 7 pts with OM, 9 with OFM, & 3 with OF. Pre-Rx GV was similar in the 3 groups, but increased in OM (p<.002) while remaining unchanged in OFM (p=NS) after the 1st Rx year. Data were insufficient to analyze OF pts. BH after the 1st Rx year normalized in 4/7 OM, 2/9 OFM, and 213 OF. GV remained unchanged (p=NS) after 1st Rx year over the subsequent 3 Rx yrs in all BH groups despite 7 pts progress- ing to ESRF. Changes in GV & BH did not correlate with C02, P04, Ca, iPTH or GFR when pre-Rx levels were compared to 1st or later Rx years. In conclusion: 250 often heals abnormal BH, especially OM; is associated with an increase in GV after 1st Rx year and its preservation in ensuing Rx years. Supported in part by The Upjohn Company.