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

Angiotensin-converting enzyme (ACE) inhibitor therapy has recently been shown to be effective in the treatment of post-renal transplant erythrocytosis (PTE). In an attempt to assess the effect of drug treatment on serum erythropoietin level, glomerular filtration rate, and urinary protein excretion, we prospectively evaluated 8 consecutive cadaveric renal transplant recipients with PTE treated with ACE inhibitor therapy 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 failed to respond to ACE inhibition (HCT > 50%), and 2 patients with PTE developed anemia (HCT < 35%) while maintained on drug treatment. Although 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 change in individual erythropoietin levels was not identified. At the conclusion of the study, the serum erythropoietin levels were undetectable in 4 patients, decreased in 1, unchanged in 2, and increased in the only patient with PTE who failed to respond to drug treatment. All patients 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 throughout the study. Microalbuminuria (spot urinary albumin/creatinine ratio 1: between 30 and 200 mg/g) developed in 5 patients with PTE and coincided with the onset of erythrocytosis (25.2 +/- 7 mg/g before PTE and 76.3 +/- 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 patients (17.3 +/- 12 mg/g). Improvement in microalbuminuria occurred in the absence of significant changes in mean arterial blood pressure or glomerular filtration rate. In addition, neither microalbuminuria nor PTE recurred in the 2 anemic patients who required discontinuation of ACE inhibitor therapy. We conclude that (1) ACE inhibitor therapy is an effective treatment for PTE and is not associated with a significant alteration in I-125-iothalamate clearances over a 3-month period; (2) changes in erythropoietin levels are not solely responsible for the improvement in HCT seen in our patients during treatment with an ACE inhibitor; (3) PTE is associated with the development of microalbuminuria, and (4) ACE inhibitor therapy significantly reduces PTE-associated microalbuminuria.