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Morphine induces albuminuria by compromising podocyte integrity

Xiqian Lan1, Partab Rai, Nirupama Chandel

  • 1Renal Molecular Research Laboratoy, Feinstein Institute for Medical Research, Hofstra North Shore LIJ Medical School, Great Neck, New York, USA.

Plos One
|April 5, 2013
PubMed

Insights

Morphine harms kidney filtration by damaging podocytes and reducing slit diaphragm molecules. This study reveals morphine

Area of Science:

  • Nephrology
  • Pharmacology
  • Cell Biology

Background:

  • Chronic kidney disease (CKD) progression is linked to morphine use.
  • The effect of morphine on the glomerular filtration barrier, particularly the slit diaphragm (SD), remains largely unknown.
  • Podocyte integrity is crucial for maintaining kidney filtration function.

Purpose of the Study:

  • To investigate the impact of morphine on the glomerular filtration barrier.
  • To specifically examine morphine's effects on podocyte integrity and slit diaphragm molecules (SDCM).

Main Methods:

  • In vivo studies: Mice treated with morphine or saline, followed by urine collection and kidney analysis (immunohistochemistry, Western blot).
  • In vitro studies: Human podocytes treated with morphine, followed by analysis of SD markers.
  • Exploration of receptor pathways (opiate mu and kappa) and signaling pathways (AKT, p38, JNK) involved.

Main Results:

  • Morphine administration led to increased albuminuria and podocyte foot process effacement in mice.
  • Expression of synaptopodin and SDCM (nephrin, podocin, CD2AP) was significantly decreased in podocytes exposed to morphine, both in vivo and in vitro.
  • Morphine-induced reduction in SDCM was mediated by opiate receptors (MOR, KOR), oxidative stress, and signaling pathways (AKT, p38, JNK).

Conclusions:

  • Morphine compromises the integrity of the glomerular filtration barrier.
  • Morphine alters podocyte structure and function by downregulating key slit diaphragm molecules.
  • These effects are mediated through opiate receptors, oxidative stress, and specific intracellular signaling pathways, contributing to kidney damage.

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