Clinical Journal of the American Society of Nephrology · 2007 · 112 citations · 27 references
MedicineNephrologyPathologyPediatric NephrologyRenal PathologyRenal PathophysiologyGlomerular DiseasesGlomerular PathophysiologyPediatric Renal PathologyPodocyte InjuryRenal DiseaseRenal ImmunopathologyCumulative Urinary ExcretionDisease Progression PredictionHenoch-schönlein PurpuraHistologic ExaminationKidney Biopsy FindingsKidney DiseasesRenal Biopsy DiagnosisRenal Biopsy Findings
Recent studies have revealed that podocytopenia leads to glomerular scarring and that the loss of podocytes into the urine may be a cause of podocytopenia. The purpose of this study was to examine whether serial examinations of urinary podocytes (u-podo) could be a useful predictor of disease progression in children with glomerulonephritis. Urine samples and renal biopsy specimens from 20 patients (10 males and 10 females; mean age 11.8 yr; range 4 to 24 yr) with IgA nephropathy (n = 17) and Henoch-Schönlein purpura nephritis (n = 3) were analyzed. Forty-four renal biopsies were performed on 20 patients. Proteinuria (g/d per 1.73 m2), hematuria (score), and u-podo (cells/ml) were examined twice a month in 24 intervals between two biopsies (mean 16.7 mo; range 4 to 58 mo) and average and cumulative values were determined for the intervals. Renal histologic changes were scored on the basis of acute intracapillary, acute extracapillary, acute tubulointerstitial, chronic intracapillary, chronic extracapillary, and chronic tubulointerstitial lesions, as well as glomerulosclerosis. It was found that hematuria, proteinuria, u-podo, and acute lesion scores decreased during the intervals examined, whereas chronic lesion scores increased. Changes in acute histology scores correlated well with hematuria, proteinuria, and u-podo excretion, whereas chronic histology scores and glomerulosclerosis both correlated well with cumulative u-podo excretion. Patients with severe histologic progression of disease also had persistent u-podo excretion. These findings provide additional data to support a potential causative role for prolonged urinary loss of podocytes in disease progression in children with IgA nephropathy and Henoch-Schönlein purpura nephritis.
27
Podocyte loss and progressive glomerular injury in type II diabetes.
Maria Enrica Pagtalunan, Paul L. Miller, S Jumping-Eagle et al. · Journal of Clinical Investigation · 1997 · 1.1K citations · Full text
Medicine, Nephrology, Pathology +17
Podocyte Depletion Causes Glomerulosclerosis
Bryan L. Wharram, Meera Goyal, Jocelyn Wiggins et al. · Journal of the American Society of Nephrology · 2005 · 732 citations
Medicine, Nephrology, Pathology +17
Apoptosis in podocytes induced by TGF-β and Smad7
Mario Schiffer, Markus Bitzer, Ian S. Roberts et al. · Journal of Clinical Investigation · 2001 · 585 citations · Full text
Medicine, Cell Biology, Nephrology +17
Predicting renal outcome in IgA nephropathy.
M. Gene Radford, James V. Donadío, Eric J. Bergstralh et al. · Journal of the American Society of Nephrology · 1997 · 443 citations
Medicine, Nephrology, Pathology +17