Post-transplant Proteinuria.
- Author:
Kyu Hun CHOI
1
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea. khchoi6@yumc.yonsei.ac.kr
- Publication Type:Review
- Keywords:
Proteinuria;
Renal transplantation;
Chronic allograft nephropathy;
Graft survival;
Antiproteinuric treatment
- MeSH:
Allografts;
Angiotensin Receptor Antagonists;
Biopsy;
Blood Pressure;
Calcium Channels;
Chemokine CCL2;
Chemokines;
Creatinine;
Cyclosporine;
Cytokines;
Endothelin-1;
Epithelial Cells;
Fibrosis;
Glomerulonephritis;
Graft Survival;
Humans;
Kidney Transplantation;
Mineralocorticoid Receptor Antagonists;
Proteinuria*;
Sirolimus;
Transplantation;
Transplants;
Urinalysis
- From:The Journal of the Korean Society for Transplantation
2007;21(1):22-30
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Proteinuria is a cardinal manifestation of renal disease and has been proposed to promote progression of renal disease. Proteinuria develops in 9~41% of transplant recipients, and is diagnosed by routine urinalysis, urine protein to creatinine ratio, or 24-hour urine protein collection. Protein excretion of >200 mg/24 h is considered abnormal. The etiology of post-transplant proteinuria is diverse, including allograft rejection, recurrent or de novo glomerulonephritis, cyclosporine A nephrotoxicity, conversion to sirolimus, and chronic allograft nephropathy, which is the most common. Transplant renal biopsy is required to confirm the cause of proteinuria, and a combination of two or more of the transplant pathological categories can be present. High-grade proteinuria is believed to mediate progressive renal damage by conferring to proximal tubular epithelial cells with increased production of endothelin-1, chemokines such as monocyte chemoattractant protein-1 and cytokines, all of which promote interstitial fibrosis. It has been reported that proteinuria after renal transplantation affected not only graft survival but also patient survival. In proteinuric recipients, both the cardiovascular and noncardiovascular death risks seem to be significantly increased compared with nonproteinuric recipients. Low-grade (<1 g/24 h) proteinuria 1 year after transplantation is also associated with graft loss. The treatments for proteinuria are blood pressure control, and the use of angiotensin-converting enzyme inhibitor and/or angiotensin II receptor blockers therapy. Several options that are able to reduce proteinuia, including nondihydropyridine calcium channel blocker or aldosterone antagonists are also available. In conclusion, post-transplant proteinuria is a sensitive marker of graft dysfunction, correlated both to graft failure and to patient death. Appropriate management guided by proven cause and antiproteinuric treatments may improve the outcome.
