Summary MATERIALS AND METHODSThe clinical course and outcome of rapidly progressive glomerulonephritis (RPGN) of variable etiology are not well defined in children. The present investigation reports on the clinical characteristics, the course and outcome, as well as the results of treatment of 13 children with apparent postinfectious RPGN. Three of 7 patients with documented streptococcal RPGN and 3 of 6 with RPGN of nonstrept&occal etiology progressed to chronic renal failure. In some patients, anticoagulant and anti--platelet therapy appear to have improved survival. The severity of crescent formation, not the presumable etiology, appears to be a reliable prognosticator. SpeculationA number of disease processes can result in renal damage of sufficient severity to cause crescent formation. The induction, resolution, or progression of crescents to sclerosis may be influenced by anticoagulant therapy.A retrospective analysis was performed on all pediatric patients seen at The University of Texas Medical Branch at Galveston since 1963 who had a rapid deterioration of renal function in association with an apparent acute onset of glomerulonephritis. Specifically, patients were included in the study population only if they met all of the following requirements: 1) documented glomerulonephritis with red blood cells casts present in the urine or the presence of red blood cells in the urine in association with proteinuria (by Labstix); 2) kidneys of normal or near-normal size, as determined by iv pyelography or tomography; 3) evidence of increasing azotemia (blood urea nitrogen, creatinine) over a maximum period of four months; 4) a renal biopsy specimen in which a substantial percentage of glomeruli were involved. This involvement included variable proliferation of cells in Bowman's space, crescents circumscribing in arc of 180' or more or glomerular obsolescence.Laboratory data, obtained by standard hospital procedures when the patient was first evaluated, were used in the tabulation of data. Oliguria was defined as a urine output of less than 200 cc/m2/day. Renal biopsies were performed 2 io 16 weeks after the progressive glomerulone~hritis (RPGN), recognized onset of symptoms by a technique which has been described Ellis (13) and further defined by Heptinstall (21), was first de-previously scribed as an unusual form of acute glomerulonephritis (AGN) Sections for light microscopy were fixed in 2% paraformaidewhich progressed to renal failure, in contrast to the typical course hyde and 2-pm sections were cut and stained with 2 or more of of rapid resolution. A clinical feature which seemed to separate the following: periodic acid-~chiff, methenamhe silver, hematox. RPGN from AGN was a period of prolonged oliguria. ylin and eosin, and Gomori's trichrome. For irnmunofluorescence, It is now known that the renal histology in RPGN is character-tissues were snap-frozen in -700 isopentane; then 4-pm sections ized by crescent formation with or without endocapillary prolif-were cut and with monospec~fic antisera to human imera...

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The plasma kallikrein-kinin system, a potent vasodilator, has been implicated in causing the protein loss of the idiopathic nephrotic syndrome. However, the kidney possesses a kallikrein-kinin system separate from the plasma system. Thus, urinary kallikrein may reflect more accurately intrarenal events. Using a radiochemical esterolytic assay we measured the urinary kallikrein excretion in a patient with a minimal lesion nephrotic syndrome during relapse. Protein excretion was initially elevated (8.1 plus or minus 2.0 gm. per 24 hours) as was urinary kallikrein excretion (96.4 plus or minus 46.6 EU per 24 hours). After initiation of steroid therapy protein and kallikrein excretion decreased significantly (p less than 0.05). During the entire study kallikrein excretion was significantly correlated with protein excretion (r equals 0.89, p less than 0.01). It is tempting to speculate that activation of the intrarenal kallikrein-kinin system participates in the protein loss characteristic of the nephrotic syndrome.