Membranoproliferative Glomerulonephritis Type II in a 10-year-old Girl

Martha E Tibbs; Sharon P Andreoli; Carrie L Phillips

doi:10.29074/ascls.18.2.84

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Martha E Tibbs, MT(ASCP)⇑
1. is a Medical Technologist at Indiana University Hospital, Indianapolis IN
Sharon P Andreoli
1. is a pediatric nephrologist at Riley Children's Hospital, Indianapolis IN
Carrie L Phillips, MD
1. is a Nephropathologist at Indiana University, Indianapolis IN

Address for correspondence: Martha E Tibbs MT(ASCP), Indiana University Hospital, Pathology/Microbiology, UH3575, 550 N University Blvd, Indianapolis IN 46202. (317) 274-3896, (317) 278-0049 (fax). metibbs{at}iupui.edu

Extract

The clinical course of a 10-year-old female patient who presented with hematuria, proteinuria, and hypertension is described. Four months after being diagnosed with acute glomerulonephritis, the child was referred to a pediatric nephrologist due to persistent hematuria and unresolved proteinuria. A renal biopsy was performed due to the persistent urinary abnormalities and a family history of renal failure. The renal biopsy demonstrated pathological findings characteristic of membranoproliferative glomerulonephritis type II. The child was treated with an antihypertensive agent and steroids. Despite poor prognostic clinical and pathological features, she has minimal urinary abnormalities, normal renal function, and normal blood pressure on antihypertensive medication six years after the diagnosis of membranoproliferative glomerulonephritis type II.

The nephrotic and nephritic syndromes are clinical consequences of structural injury to the renal glomerulus, a vascular filter that clears the blood of waste products. Laboratory testing is required to distinguish the two syndromes. Proteinuria, the major clinical sign of nephrotic syndrome, results from altered permeability of the glomerular filtration barrier due to perturbations in visceral epithelial cells (podocytes). Nephrotic syndrome in children is the clinical manifestation of podocyte injury most commonly due to minimal change disease. Other causes include focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, or membranous glomerulopathy. Children with nephritic syndrome usually present with gross hematuria that may be accompanied by hypertension and variable degrees of proteinuria. Inflammatory processes that target glomeruli, termed acute glomerulonephritis, alter capillary wall integrity, and allow red blood cells to leak into urine. For a more comprehensive analysis of acute glomerulonephritis, the…

ABBREVIATIONS: C3 = complement component 3; GBM = glomerular basement membranes; Ig = immunoglobulin; MPGN = membranoproliferative glomerulonephritis.