Oxidative stress, macrophage infiltration and CD163 expression are determinants of long-term renal outcome in macrohematuria-induced acute kidney injury of IgA nephropathy

Nephron Clin Pract. 2012;121(1-2):c42-53. doi: 10.1159/000342385. Epub 2012 Oct 19.

Abstract

Background: Macroscopic hematuria (MH) may cause acute kidney injury (AKI) in IgA nephropathy. Up to 25% of patients with MH-associated AKI do not recover baseline renal function. Our objective was to identify subjects at high risk for an adverse renal function.

Methods: We examined macrophages, oxidative stress markers (NADPH-p22 and HO-1) and the hemoglobin scavenger receptor (CD163) in renal biopsy specimens from 33 MH-AKI patients with complete recovery (CR, n = 17) or incomplete recovery (IR, n = 16) of renal function after 6.72 (range 0.5-21.5) years of follow-up.

Results: CD163-expressing macrophages, HO-1 and NADPH-p22 expression were located in areas surrounding tubules with iron deposits and filled with erythrocyte casts. CD163-positive macrophages score and HO-1- and p22-positive staining correlated positively with percentage of tubules with erythrocyte casts and tubular necrosis. Macrophage infiltration, CD163-positive macrophage score, NADPH-p22- and HO-1-positive staining areas were significantly greater in IR patients when compared with CR patients. The CD163-positive macrophage score and oxidative stress markers (p22 and HO-1) were negatively correlated with renal function outcome, as determined by estimated glomerular filtration rate (eGFR) and proteinuria, at the end of the follow-up period. In multivariate analysis, the CD163-positive macrophage score remained significantly associated with final eGFR and proteinuria after adjustment by age, gender, duration of MH, initial eGFR and proteinuria.

Conclusions: Increased macrophage infiltration, CD163 expression and oxidative stress are significant prognostic factors for an IR of renal function in patients with MH-associated AKI. These molecular pathways may be involved in the renal response to injury and could be useful to improve diagnosis and therapeutics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / physiopathology*
  • Analysis of Variance
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • CD163 Antigen
  • Cell Movement
  • Chi-Square Distribution
  • Female
  • Follow-Up Studies
  • Glomerular Filtration Rate
  • Glomerulonephritis, IGA / complications*
  • Glomerulonephritis, IGA / pathology
  • Hematuria / complications*
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Kidney / pathology
  • Kidney / physiopathology
  • Macrophages / metabolism*
  • Macrophages / physiology
  • Male
  • Middle Aged
  • Multivariate Analysis
  • NADPH Oxidases / metabolism
  • Oxidative Stress
  • Receptors, Cell Surface / metabolism
  • Recovery of Function*
  • Statistics, Nonparametric
  • Time Factors

Substances

  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD163 Antigen
  • Receptors, Cell Surface
  • Heme Oxygenase-1
  • NADPH Oxidases
  • CYBA protein, human