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The glomerular basement membranes (GBM) were measured in 264 patients with recurrent and persistent hematuria (152 males, 112 females), 47 patients with minimal change nephrotic syndrome (26 males, 21 females), and 91 patients with focal segmental glomerular sclerosis and nephrotic syndrome (55 males, 36 females). The average number of glomeruli measured was 2.5 per case. Analysis of the data showed GBM thickness to be significantly greater in males (n=233) than in females (n=169) (Student'st-test,P<0.01). There was no difference in GBM thickness between the two groups of nephrotics; the data were subsequently combined and the group referred to as idiopathic nephrotic syndrome. There was also no difference in GBM thickness among the immunofluorescence-defined subcategories of recurrent hematuria, and these groups were combined. GBM thickness was significantly greater in the idiopathic nephrotic syndrome than in recurrent hematuria (Kruskal-Wallis H test,PO=<0.001). Analysis of the data showed, in both conditions, a gradual increase with age throughout the span of the study (1–69 years). Regression analysis of GBM thickness and age in recurrent hematuria showedRO=0.43 andPO=<0.001, in idiopathic nephrotic syndromeRO=0.61 andPO=<0.001. The differences between nephrotic syndrome and recurrent hematuria may be based on the inclusion in the recurrent hematuria group of patients with genetically thin GBM; they may also be based on the inclusion in the idiopathic nephrotic syndrome group of patients with subendothelial thickening, a relatively frequent occurrence. These data also indicate that GBM thickness continues to increase throughout life in patients with idiopathic nephrotic syndrome and recurrent hematuria, perhaps as part of the normal aging process.

To the Editor.—We report herein a case of aseptic meningitis probably caused by administration of immune globulin, which resulted in headache, vomiting, and fever.Report of a Case.—A 2-year-old girl was admitted to the hospital on April 29, 1986, for treatment of acute idiopathic thrombocytopenic purpura. She was treated with 20 mg/d of corticosteroids for four weeks, but no rise in platelet count occurred. After three more days of this therapy, she was given 100 mg/d of hydrocortisone intravenously, followed by 0.4 g/kg/d of immune globulin prepared with polyethylene glycol for five days. Seven days after this therapy, she experienced headache and vomiting. Her temperature rose to 38.5°C and neck stiffness developed. The white blood cell count was 15.6 × 109/L (15 600/mm3), with 0.04 (4%) band forms, 0.64 (64%) segmented neutrophils, 0.27 (27%) lymphocytes, and no eosinophils. Tests for C-reactive protein were negative. The