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Related Experiment Videos

Glomerular size-selective barrier dysfunction in nephrotoxic serum nephritis.

P A Alfino1, J Neugarten, R G Schacht

  • 1Department of Medicine, New York University School of Medicine, New York.

Kidney International
|August 1, 1988
PubMed
Summary

Antihypertensive therapy in nephrotoxic serum nephritis (NSN) prevents glomerular permselectivity defects. This treatment preserves glomerular filtration rate and reduces protein and gamma-globulin excretion in hypertensive rats.

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Area of Science:

  • Nephrology
  • Hypertension Research
  • Glomerular Physiology

Background:

  • Nephrotoxic serum nephritis (NSN) is a model of hypertensive kidney injury.
  • Previous studies showed antihypertensive therapy ameliorates proteinuria and glomerular damage in NSN.
  • The effect of hypertension treatment on glomerular permselectivity in NSN remains to be fully elucidated.

Purpose of the Study:

  • To investigate glomerular permselectivity in hypertensive NSN.
  • To determine the impact of antihypertensive treatment on the size-selective barrier function in NSN.

Main Methods:

  • Hypertensive NSN rats were treated with a combination of antihypertensive drugs to maintain normotensive levels.
  • Control rats remained hypertensive.
  • Glomerular filtration rate, 24-hour urinary protein excretion, and 24-hour urinary gamma-globulin excretion were measured.

Related Experiment Videos

  • Fractional clearances of polydisperse neutral dextrans were assessed to evaluate glomerular size permselectivity.

    • Main Results:

    • Untreated hypertensive NSN rats showed reduced glomerular filtration rate and increased urinary protein and gamma-globulin excretion.
    • Hypertensive rats exhibited enhanced fractional clearances of dextrans with radii exceeding 50 angstroms, indicating loss of permselectivity.
    • Antihypertensive therapy preserved glomerular filtration rate and significantly reduced urinary protein and gamma-globulin excretion.
    • Normotensive NSN rats did not develop the defect in glomerular size permselectivity.

    Conclusions:

    • Hypertensive NSN leads to "gaps" in the glomerular basement membrane, impairing size-selective barrier function and allowing excretion of large molecules.
    • Antihypertensive therapy effectively averts this defect in glomerular permselectivity.
    • Maintaining normotension is crucial for preserving glomerular barrier integrity in NSN.