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Five patients, all children, are described who excreted urine consistently hypotonic to plasma. The primary conditions affecting the kidney were cystinosis, medullary cystic disease, cystic disease of the kidney and obstructive uropathy. In all instances the infusions of Pitressin ® during water diuresis had little or no effect on urine concentration, hence the term Pitressin-resistant hyposthenuria. The data seemed best explained by positing that both the distal convolution in the cortex and the collecting system were not normally permeable to water in the presence of antidiuretic hormone (ADH) or Pitressin. A similar state in less obvious form probably exists when an imposed osmotic diuresis leads to hyposthenuria. This condition normally does not appear to be present in the uremia of chronic glomerulonephritis or pyelonephritis, but does appear to be rather frequent in the conditions causing uremia in children.

THE occurrence of shock has been reported as a rare complication of the nephrotic syndrome. A number of reports have demonstrated the association of hypovolemia with shock in the nephrotic state.1-5Farr described recurrent "nephrotic crises" usually associated with infection and hypoaminoacidemia. Although plasma volumes were not estimated and hypotension was not reported, four out of five children reported had high venous hematocrit determinations during the crisis.6 The present report describes the occurrence of shock in four children during the course of treatment for the nephrotic syndrome. Report of Cases Case1.—The patient was a 9½-year-old Negro boy who presented with the nephrotic syndrome in October 1961. He was treated with prednisone initially in a dose of 15 mg every eight hours (q.8h.) with remission of proteinuria and edema within three weeks. During the ensuing nine months, he had four relapses while being maintained on 20 mg of

The prevalence and significance of proteinuria in children has not been well documented. Approximately 4,000 students from 6 to 18 years of age have been tested for proteinuria during the past two years, utilizing a "test stix" (Hema Combistix) for initial screening. One hundred and seventy-five students with urine protein concentration of 30 mg. per cent or greater on the first screening test were subjected to complete history-taking and physical examinations, as well as 12 hour day and 12 hour night urine collections for quantitative protein determinations. Similar studies were carried out with 100 students of various ages who had no detectable protein on the first screening test. Initial screening revealed that approximately 250 children had 1+ or greater proteinuria, an incidence of 7 per ceut. In the 100 students who tested negative for urinary protein, the mean daytime urine protein was 55 mg. per 12 hours and the mean of the nighttime was 42 mg. per 12 hours. In children testing 1+ or greater for protein, the day 12 hour urine protein was 90 mg. and the night was 48 mg. Clinical evaluation and family histories of the two groups did not reveal any significant differences. Six children with proteinuria in excess of 250 mg. for any 12 hour period have undergone complete evaluation. The renal biopsies revealed minimal alterations by light microscopy, ranging from slight focal hypercellularity to focal thickening of the basement membranes of the glomerular capillaries. These studies quantitate urine protein excretion in children at various ages and demonstrate that there is a significant incidence of proteinuria as measured by qualitative screening, as well as by quantitative methods.