ASSOCIATION OF POSTRENAL TRANSPLANT ERYTHROCYTOSIS AND MICROALBUMINURIA - RESPONSE TO ANGIOTENSIN-CONVERTING ENZYME-INHIBITION

Angiotensin-converting enzyme (ACE) inhibitor therapy has recently bee n shown to be effective in the treatment of post-renal transplant eryt hrocytosis (PTE). In an attempt to assess the effect of drug treatment on serum erythropoietin level, glomerular filtration rate, and urinar y protein excretion, we prospectively evaluated 8 consecutive cadaveri c renal transplant recipients with PTE treated with ACE inhibitor ther apy for 3 months. In response to ACE inhibition, the mean hematocrit ( HCT) value decreased from 53.7 +/- 0.6% before treatment to 42.7 +/- 2 .2% at the conclusion of the study (p = 0.03). However, I patient fail ed to respond to ACE inhibition (HCT > 50%), and 2 patients with PTE d eveloped anemia (HCT < 35%) while maintained on drug treatment. Althou gh the mean serum erythropoietin level decreased during ACE inhibition (from 22.8 +/- 8.4 to 9.4 +/- 5.3 mU/ml; p = 0.06), a consistent chan ge in individual erythropoietin levels was not identified. At the conc lusion of the study, the serum erythropoietin levels were undetectable in 4 patients, decreased in 1, unchanged in 2, and increased in the o nly patient with PTE who failed to respond to drug treatment. All pati ents tolerated the ACE inhibitor therapy without developing cough. or hyperkalemia. In addition, serum creatinine levels, I-125-iothalamate clearances, and mean arterial blood pressures were unchanged throughou t the study. Microalbuminuria (spot urinary albumin/creatinine ratio 1 : between 30 and 200 mg/g) developed in 5 patients with PTE and coinci ded with the onset of erythrocytosis (25.2 +/- 7 mg/g before PTE and 7 6.3 +/- 36.7 mg/g at the time of PTE detection). At the conclusion of the study, the urinary albumin excretion had normalized in all 5 patie nts (17.3 +/- 12 mg/g). Improvement in microalbuminuria occurred in th e absence of significant changes in mean arterial blood pressure or gl omerular filtration rate. In addition, neither microalbuminuria nor PT E recurred in the 2 anemic patients who required discontinuation of AC E inhibitor therapy. We conclude that (1) ACE inhibitor therapy is an effective treatment for PTE and is not associated with a significant a lteration in I-125-iothalamate clearances over a 3-month period; (2) c hanges in erythropoietin levels are not solely responsible for the imp rovement in HCT seen in our patients during treatment with an ACE inhi bitor; (3) PTE is associated with the development of microalbuminuria, and (4) ACE inhibitor therapy significantly reduces PTE-associated mi croalbuminuria.