The long-term course of cyclosporine-associated chronic nephropathy

The long-term course of cyclosporine-associated chronic nephropathy. We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as cont...

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Bibliographic Details
Published in:Kidney international 1988-02, Vol.33 (2), p.590-600
Main Authors: Myers, Bryan D., Sibley, Richard, Newton, Lynne, Tomlanovich, Stephen J., Boshkos, Christopher, Stinson, Edward, Luetscher, John A., Whitney, Darlene J., Krasny, David, Coplon, Norman S., Perlroth, Mark G.
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cyclosporins - adverse effects
Drug toxicity and drugs side effects treatment
Heart Transplantation
Humans
Kidney Diseases - chemically induced
Kidney Diseases - pathology
Kidney Diseases - physiopathology
Kidney Failure, Chronic - chemically induced
Kidney Glomerulus - pathology
Kidney Glomerulus - ultrastructure
Longitudinal Studies
Medical sciences
Microscopy, Electron
Pharmacology. Drug treatments
Postoperative Care
Toxicity: urogenital system
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Summary:The long-term course of cyclosporine-associated chronic nephropathy. We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as controls. Despite equivalent cardiac performance, GFR in those treated with CsA was depressed, 47 ± 3 versus 94 ± 4 ml/min/1.73m2 (P < 0.001). CsA therapy was also associated with significant elevation of renal vascular resistance (RVR), proteinuria, arterial hypertension, and impaired intrarenal conversion of inactive prorenin to active renin. Histopathological changes associated with CsA included an obliterative arteriolopathy with deposition of protein-aceous material in necrotic arteriolar walls, and associated tubulointer-stitial damage. A minority of glomerbuli exhibited either ischemic collapse or sclerosis. Area perimeter analysis revealed enlargement of the remaining glomeruli with significant expansion of the mesangium. Longitudinal examination over a 48 month period (N = 15) during which CsA was reduced in dosage or withdrawn revealed persistent hypofiltration, increasingly elevated RVR and heavier proteinuria. Further histopathological deterioration was observed when renal tissue was sampled a second time in six patients, and three members of the experimental group developed end-stage renal disease. We conclude that continuous CsA therapy for more than 12 months causes a chronic injury to renal microvessels that is rarely reversible and potentially progressive.
ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1988.38