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The long-term course of cyclosporine-associated chronic nephropathy

B D Myers1, R Sibley, L Newton

  • 1Department of Medicine, Stanford University Medical Center, California.

Kidney International
|February 1, 1988
PubMed

Insights

Cyclosporine (CsA) therapy in heart transplant patients causes chronic kidney injury, leading to reduced kidney function and progressive renal damage. This injury to renal microvessels is often irreversible.

Area of Science:

  • Nephrology
  • Transplantation Immunology
  • Cardiovascular Medicine

Background:

  • Cyclosporine (CsA) is a key immunosuppressant in organ transplantation.
  • Chronic kidney injury is a significant concern in long-term transplant recipients.
  • The specific renal effects of CsA in cardiac transplant recipients require detailed evaluation.

Purpose of the Study:

  • To assess the incidence and nature of chronic renal injury in cardiac transplant recipients treated with CsA.
  • To compare renal function and pathology in CsA-treated patients versus azathioprine-treated controls.
  • To investigate the reversibility and progression of CsA-induced nephropathy.

Main Methods:

  • Evaluation of 37 cardiac transplant recipients on CsA (12-24 months) and 24 controls on azathioprine (>24 months).
  • Assessment of glomerular filtration rate (GFR), renal vascular resistance (RVR), proteinuria, and blood pressure.
  • Histopathological examination of renal biopsies, including arteriolopathy, tubulointerstitial damage, and glomerular changes.
  • Longitudinal follow-up over 48 months with dosage adjustments and repeat biopsies in a subset of patients.

Main Results:

  • CsA-treated patients showed significantly depressed GFR (47 vs 94 ml/min/1.73 m2) compared to controls.
  • CsA therapy was associated with elevated RVR, proteinuria, hypertension, and impaired renin activity.
  • Histopathology revealed obliterative arteriolopathy, tubulointerstitial damage, glomerular changes, and mesangial expansion.
  • Longitudinal data indicated persistent hypofiltration, increased RVR, and worsening proteinuria even after CsA reduction or withdrawal.
  • Three patients developed end-stage renal disease, and further histopathological deterioration was observed.

Conclusions:

  • Continuous CsA therapy for over 12 months induces chronic, rarely reversible, and potentially progressive injury to renal microvessels.
  • CsA-associated nephropathy involves vascular, interstitial, and glomerular damage.
  • Early identification and management strategies are crucial to mitigate long-term renal consequences in CsA-treated patients.

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