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Cyclosporine-induced changes in glomerular filtration rate and urea excretion

D A Laskow1, J J Curtis, R G Luke

  • 1Department of Surgery, University of Alabama Medical Center, Birmingham 35294.

Abstract

Insights

Cyclosporine impairs renal function in transplant patients during volume depletion, causing reversible nephrotoxicity. This effect is linked to compromised kidney compensatory mechanisms, not proximal tubular damage.

Area of Science:

  • Nephrology
  • Transplantation Immunology
  • Pharmacology

Background:

  • Cyclosporine is a critical immunosuppressant but carries a risk of nephrotoxicity.
  • Understanding cyclosporine's renal effects is vital for managing transplant recipients.

Purpose of the Study:

  • To investigate the impact of cyclosporine on renal function during induced intravascular volume depletion in renal transplant recipients.
  • To assess the reversibility of cyclosporine-induced renal changes.

Main Methods:

  • Two groups of renal transplant patients (cyclosporine vs. no cyclosporine) underwent a 10-day protocol.
  • Mild intravascular volume depletion was induced via sodium restriction and furosemide.
  • Renal function (GFR, clearances, sodium excretion) was measured before and after volume depletion and a sodium load.

Main Results:

  • Cyclosporine-treated patients showed significant decreases in GFR and clearances, with increased BUN post-depletion.
  • These renal function impairments in cyclosporine users resolved after intravenous sodium chloride infusion.
  • Azathioprine-treated patients exhibited stable renal function throughout the protocol.

Conclusions:

  • Cyclosporine predisposes renal transplant recipients to acute, reversible nephrotoxicity.
  • This nephrotoxicity arises from impaired renal compensatory mechanisms during volume depletion.
  • Proximal tubular function, indicated by urea and sodium reabsorption, remains unaffected.

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