testicular axis o f 31 males, aged 11.7-20.0 years , piandrosterone (DHEA), DHEA sulfate (DS), and urinary 7 keto steroids were normal when related to pubertal tage in Groups I and 11. In Group I 1 1 adrenal androens ( A 4 , DHEA,DS) were decreased while T was normal. uteinizing hormone levels were normal in all. F S H normal range 1 - 6 ng/ml) was significantly increased i I (11.9 1.5) and GI1 (30.3 + 11.5). In GI11 F S H as normal i n patients with serum creatinines < 2 mg%. S H levels were uniformly elevated in Tanner I - V atients with Cr '5 mg% and also correlated positive1 ' THE EFFECTS OF BODY BURDENS OF LEAD ON RAT KIDNEY. Fine, B.P., Jortner, B.,& T and Gause, D. (Spon. by F. Behrle), New Jersey Medical School, Dept. of Pediatrics, Newark, New Jersey. Lead induced chronic nephropathy is seen after prolonged occupational exposure to lead and has been produced in experimental animals. There is also suggestive clinical and experimental evidence that development of chronic lead nephropathy may be related to renal growth. Lead acetate was administered by three i.p. injections for a total dose of 125 mg/kg of body weight to 30 Sprague-Dawley rats during the fifth week of life. A control group received i.p. sodium acetate during the same period. One half of each group was studied.after eight weeks and the remainder after 32 weeks. At 32 weeks there was a persistent elevation of blood lead concentrations (control 0.138k.04, exp. 0.367t.04 ug/gm; p < .05) and renal tissue lead concentrations (control 1.882 .19, exp. 8.22.93 ug/gm; p.< .05) ; however, body weight, kidney weight, and renal tissue FNA and DNA concentrations were not significantly different from the controls. Numerous renal tubular giant cells and intranuclear inclusions were found in the experimental group at 8 weeks but were reduced in number markedly by 32 weeks. There was no evidence of a generalized progressive nephropathy. These results indicate that after an acute exposure to lead in the growing rat progressive morphologic changes of the kidnc are not seen despite persistent elevations of renal lead concentrations. CHRONIC HYPONATREMIA AND MlOFA L Aaron L Friedman, Russell W. EA:sn::~OLi?t:lk':'"r Segar. University of Wisconsin School of Medicine, Hospitals, Department of Pediatrics, Madison, Wisconson. Persistent hyponatremia (Na 126 mEq/L) was found in a 30 month old girl with typical features of MFH. Hyponatremia, serum hypoosmolality (250 mOsm/~), urine hyperosmolality (u/P osm 3: 1) and continued urinary sodium excretion suggested the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Renal, adrenal, pulmonary and drug etiologies for SIADt were excluded. 5 mEq/kg hypertonic Na CI resulted in less than ) marked increasc expected rise in serum Na (1 1 5 to 120 ~ E ~ / Land in urine Na excretion (26 to 95 mEq/~). Water loading (25 mllkg D5W) leading to serum osmolality fall from 250 to 227 mOsm/L or volume expansion (25 ml/kg 0.9% Na C1 iv) did not lead to forma. tion of dilute urine (lowest U osm 686 mOsm/L). Also plasma AD1 measured by radioimmunoassay did not fall to 0 (lowest value 1.4 uIU/ml). These findings suggested resistance of hypothalami( center to afferent stimuli from volume and osmoreceptors which normally inhibit ADH release. Only fluid restriction (40 ml/kg/ 24h) successfully raised serum Na to normal. Serum Na returned to hyponatremic levels on 3 days ad lib diet. MFH has been asso. ciated with deficiencies of anterior and posterior pituitary hormones. This report documents persistent ADH excess and further suggests hypothalamic abnormalities in MFH. PATHOPHYSIOLOGY O F CHRONIC HEREDITARY HYDROEPHROSIS IN T H E RAT. Jeffrey Friedman and ohn E. Lewy, Dept. o f Peds., Cornell University Medical College, New York, New York. W e have developed and reported o n a colony o f rats with congenital, unilateral (right sided) hydronephrosis (Ped. Res., 11:550, 1977). The hydronephrotic kidneys (HNK) o f these animals have decreased clearances o f inulin and para-aminohippurate, renal blood flow and filtration fraction (ff), and increased fractional sodium and water excretion. Radiolabelled microspheres (S) were utilized to determine intrarenal blood flow distribution (ID). T e n animals with unilateral HNK and 5 controls were given intraaortic S injections. Clearance studies were similar to our previous report. ID are expressed as % o f total renal blood flow f o r t h c outer (OC) and inner (IC) halves o f the renal cortex adjusted for tissue weight. Control animals had a n O C o f 69.8 + 2.1% for left kidneys and a n O C o f 70.4 + 3 . . % for right kidneys (p >.2). HNK animals had a right HNK 3C o f 76.9 + 2.3% and a left non-HNK O C o f 70.7 + 2.7% (p <.025). This redistribution o f renal cortical blood flow toward the O C may be responsible for the decrease in f f previously observed. T h e resulting diminution 0:' ?eritubular oncotic pressure might contribute to the increased salt and water excretion from the obstructed tidney relative to its non-hydronephrotic mate. l2 CRYOPROTEINS IN PRIMARY GLOMERULOPATHIES. Eduardo Garin, . Sandra G. Austin and George A. Richard. (Spon. by Elia M. Ayoub), Univ. of Fla., College of Med., Dept. of Pediatrics, Gainesville. serial serum samples from 85 children with glomerulopathies and 14 healthy controls were examined for the presence of cryoproteins. The patients were divided in six groups according to their clinical and glomerular pathologic findings. The incidence and the protein concentration of the cryoprecipitates were determine Group # of patients Incidence Mean cryoprotein concentration (rng.2 Control 14 10114 1.75 Minimal lesion a) Hematuria 22 21/22 1.46 b) Nephrotic syndrome 25 25/25 2.62 Focal glomerulosclerosis I$ 10111 1.81 Membranous nephropathy 818 3.58 Acute glomerulonephritis 11 9/11 0.77 9 719 2.46 Hembranoproliferative The incidence and concentration of serum cryoprotein in patients with glomerulopathies were not different f r w the control group, regardless of the immunopathologic findings. No correlation was found between the clinical course and the presence of cryoproteins. Cryoproteins in patients with glomerulopathies are not indicators of an immunologic mediated disease and do not have a prognostic value. ,1066 H PATTERN OF RESPONSE TO PREDNISONE AND INHUNOPATHOLOGIC FINDINGS IN PATIENTS WITH IDIOPATHIC, MINIMAL LESION, NEPHROTIC SYNDROME. Eduardo H. Garin, William H. Donnelly, and George A. Richard. (~pon. by Elia M. Univ. of Fla. College of Med., Dept. of Pediatrics, Gainesville. Sixty-seven patients with idiopathic, nephrotic syndrome underwent renal biopsy. All had minimal lesion by light microscopy. Immunopathologic studies for complement (C3) and immunoglobulins (IgG, IgM and IgA) were carried out in all the specimens. The patients were divided according to their response to prednisone into steroid resistant (11). frequent relapser (39) and infrequent relapser (17). Immunofluorescent findings on renal biopsy were the following: w), Category # of specimens Resistant 11 Frequent relapser 39 Infrequent relapser 17 C3 only 1 3 - C3 + Ig 3 4 - Ig only 2 6 6 There was no correlation between the deposition of immunolobulins and the pattern of response to prednisone. However, omplement (C3) was found only in patients with a steroid esistant or frequent relapsing nephrotic syndrome (p < 0.05).