Oncotic pressure and edema formation in hypoalbuminemic HIV-infected patients with proteinuria

Human immunodeficiency virus nephropathy (HIVN) continues to challenge nephrologic consultative services at major urban institutions. Although noted in the literature, the decreased incidence of peripheral edema in HIVN has been unexplained to date. In HIV patients, total proteins frequently are found to be elevated due to an elevated globulin fraction. The impact that plasma proteins, specifically globulins, have on the total oncotic pressure has not been reported in HIVN, but may play a role in the paucity of edema noted in this proteinuric population. To evaluate the contributions of serum globulin to the total oncotic pressure and the presence or absence of edema in HIVN, we randomly selected 27 patients with proteinuria greater than 2.5 g/24 hr and serum albumin less than 3.1 g/dL from patients presenting to the nephrology outpatient clinic at the University of Miami/Jackson Memorial Hospital. Seventeen of the patients (63%) had a known diagnosis of HIV infection (group 1). These patients were subdivided into two subgroups: those presenting with clinically evident edema on physical examination (n = 7 [41%; group 1A) and those who had an absence of edema (n = 10 [59%]; group 1B). Conversely, group 2 comprised 10 patients without known HIV infection, of whom six (60%) had edema (group 2A) and four (40%) did not (group 2B). Blood pressures were noted, and mean arterial pressure was calculated using standard formulas. Serum albumin, serum total proteins, and urine total proteins were measured using standard laboratory methods. Oncotic pressures for albumin (α), globulin (β), and total protein (c) were calculated using the following formula: COPpl = α(2.8c + 0.18c 2 + 0.012c 3) + β(0.9c − 0.12c 2 + 0.004c 3). We used Student's t-test to analyze the data. There is no significant difference between the albumin concentrations of HIV patients without edema (group 1B) and non-HIV patients with edema (group 2A), with mean concentrations of 2.3 ± 0.1 g/dL versus 2.3 ± 0.15 g/dL, respectively ( P = NS). Group 1B, however, has a total oncotic pressure of 17.1 ± 1.5 mm Hg, wheres both groups with edema (groups 1A and 2A) have statistically significant lower total oncotic pressures (12.1 ± 2.3 mm Hg and 12.9 ± 1.1 mm Hg, respectively; P < 0.05). The globulin oncotic pressure may account for some of the differences in total oncotic pressures, being significantly higher for those patients without edema in group 1B compared with group 2A (7.1 ± 0.9 mm Hg v 3.9 ± 0.4 mm