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Histologic patterns in the glomerular tufts in "Glomerulonephritis with many crescents" take three main forms: (1) compression and sclerosis of glomeruli, (2) necrotizing glomerulitis, and (3) proliferation with or without exudation. In the third group, histologic differentiation between patients with poststreptococcal glomerulonephritis with many crescents (AGN) and those with nonstreptococcal rapidly progressive glomerulonephritis (RPGN) may be impossible. In a retrospective study, quantitative morphometry of glomeruli effectively separated three patients with AGN from two patients with RPGN after the usual histologic and electron microscopic observations had failed. Parameters studied were areas of tufts and crescents and total number of cells and granulocytes in tufts and crescents. Surface areas of tufts and crescents were separately determined by photographing glomeruli, projecting and tracing outlines of tufts and crescents, and cutting out and weighing the tracings. The cell density of glomerular tufts (cell per 1000-sq. mum. area) was significantly greater in AGN than in RPGN when either total cell densities (17.64 plus or minus 0.41 versus 13.63 plus or minus 0.30) or total cells minus granulocytes (16.39 plus or minus 0.50 versus 12.99 plus or minus 0.52) were compared. The cell density in the tufts was 120 and 70 per cent greater than controls in AGN and RPGN, respectively. Exudation of inflammatory cells is contributory but not the major cause of hypercellularity in AGN. Follow-up studies with biopsies showed marked resolution in two of three patients with AGN, with normal blood urea nitrogen levels and focal scarring in the third, whereas the two patients with RPGN had either extensive scarring and reduced renal function or required chronic hemodialysis.

In those children with thoracic asphyxiant dystrophy, a genetically determined disorder, who survive infancy, the development of renal disease may be life-threatening. This report will present data obtained in six patients from three families which deals with the renal abnormalities in thoracic asphyxiant dystrophy. Both functional and anatomic abnormalities are described. Abnormalities in solute transport in the proximal tubule may be the earliest sign of renal dysfunction in this syndrome. Early glomerular changes may be more important than previously recognized. Finally, the various phenotypic expressions of this disorder are considered.

Renal blood flow has been measured in children of age 1½ to 16 years, by injecting 133Xe into the renal artery at the time of aortography or surgery. The rate of washout of radioactivity was monitored on magnetic tape and the resultant data analyzed by graphic analysis using a semi-automatic method of plotting and computing the rates and fraction of blood flow perfusing the outer and inner cortical regions of the kidney. The number, type, and results of the studies follows: 1) In 8 normal kidneys, RBF's were similar to adult values. 2) In 53 studies of RBF in children with congenital heart disease, RBF's were reduced in both cyanotic and acyanotic heart disease, were further reduced when heart failure was present (8 patients) and fell after angiography (19 patients). 3) Following renal biopsy drops in RBF may occur in intact kidneys, but not in the transplanted kidney (4 patients). 4)In chronic renal disease outer cortical blood flow is diminished. 5) 31 measurements of RBF in donor kidneys upon insertion and/or following transplantation suggest that this technique may have some value in predicting both the immediate and subsequent function of the graft. 6)In 5 patients with renal vascular hypertension, 133Xe measurements of RBF were helpful in determining secretory rates of renin in both kidneys. Supported NIH grants RR-75, RR-5624 and HE-12651.