Management of proteinuria in clinical practice after kidney transplantation

Proteinuria is a marker of poor prognosis in kidney transplant recipients as well as in nontransplant patients with chronic kidney disease. It negatively influences the rate of deterioration of graft renal function, graft survival, and more importantly, patient survival. This review analyzes the current knowledge on the management of this crucial aspect in kidney transplantation. The reduction of proteinuria has demonstrated a beneficial effect on kidney function and also on patient survival in nontransplant patients with chronic kidney disease, but unfortunately, to date, it has not been possible to demonstrate the same benefit in the kidney transplant population (although it probably exists). Nevertheless, the appearance of proteinuria in a renal transplant patient must always be followed by an investigation on its etiology, and many times, it should include a graft biopsy to adequately categorize the underlying process responsible for the proteinuria and to establish a correct therapy. Furthermore, in spite of the cause of proteinuria, it should be treated to reduce to normal or near-normal levels with the objective to eliminate or reduce its negative effects on the graft and the cardiovascular system of the patient. The drugs that interfere with the renin-angiotensin-aldosterone system, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, are the cornerstone of the management of this complication, and recently, direct renin inhibitors have added to the armamentarium. Mono-, dual-, and triple-therapy modalities are discussed, as well as other therapies and nonpharmacologic measures.