Above-normal urinary excretion of albumin and retinol-binding protein in patients with acute myocardial infarction.

Concentrations of albumin and retinol-bindung protein (REP) in urine are more sensitive indicators of renal dysfunction in hypertensive patients than the serum creatinmne concentration and the Albustix#{174}reaction (Ames, Tarrytown, NY) (1). Many patients with heart failure had abovenormal urinary albumin and REP concentrations (2), and these values decreased as the patients were treated with captopril (3). Patients with diabetes mellitus often have above-normal urinary albumin and REP (4, 5), and this might dispose them to cardiovascular events (6). We have now studied the urinary excretion of albumin, REP, and creatinine in 22 patients admitted for acute myocardial infarction (AM!) (17 men and 4 women). One of these patients had noninsulin-dependent diabetes mellitus, two had hypertension, and two had had AM! earlier. Diagnosis of AM! was based on patients’ history, determination of serum creatine kinase subunit MB, serum lactate dehydrogenase isoenzyme 1, and electrocardiograms (7) according to the World Health Organization criteria (8). The study was in accordance with the ethical standards of the Helsinki Declaration of 1975 as revised in 1983. Of the 22 patients studied, 15 were admitted within 24 h after onset of symptoms and were grouped as early admissions; the other 7 were admitted later in the clinical course and were grouped as late admissions. Twelve were given streptokinase and two were entered into a double-blind study comparing actilyse and placebo. None of the late admissions underwent thrombolysis. All patients were given acetylsalicylic acid regularly (150-300 mg/day). The patients were mobilized gradually according to a seven-step protocol during the first week of admission (7). Creatinune concentrations in serum and urine were measured with a photometric method (Jaffe). All patients had a serum creatinine concentration <120 mol/L. We determined the concentrations of albumin and REP in the first voided sample of urine by immunochemical assays on the day of admission (day 0) and in the first voided urine on days 1, 2, and 5 (5, 9) afterwards. The upper limits of the reference ranges for urinary albumin and REP concentrations were 0.45 pmol/L and 0.21 mgfL, respectively (5, 9). On the day of admission, 13 of the 22 patients had an above-normal urinary albumin concentration; 8 of the 22 had an above-normal urinary REP concentration. The urinary albumin and REP values correlated (Spearman p = 0.65, P = 0.001, Spearman rank correlation coefficient test). The urinary REP concentrations were higher in the early admission group (median 1.43, range 0.18-80.30) than the late admission group (median 0.06, range 0.04-43.0) (P = 0.04, Mann-Whitney U-test, two-tailed). The urinary albumin concentrations were slightly higher in the early admissions (median 0.82, range 0.074.3 1) than in the late admissions (median 0.20, range 0.02-62.10). The urinary creatinine concentrations were similar (median 8.70 vs 6.06 mmol/L). The urinary albumin and REP of the early admissions decreased significantly from day 0 to day 1 and from day 2 to day 5 (P <0.05, WicoxonPratt test, two-tailed). Urinary creatinine concentrations increased slightly during the first 3 days (Table 1). Half of the patients with AM! may have had above-normal urinary albumiii and REP concentrations in the initial phase of the cardiac event. We found a lower proportion of above-normal values in patients with hypertension and a higher proportion in patients with heart failure (1, 2). The above-normal albumin and RBP concentrations are due to dysfunction of the glomeruli and the proximal tubuli, respectively (1-3). Most of the above-normal urinary albumin and REP excretion in our present study was a temporary phenomenon, reflecting the initial phase of the AM!. The time course for urinary albumin and REP concentrations after the onset of symptoms did not differ between the groups of patients given streptokinase and those not (10). Thus the above-normal urinary excretion of albumin and REP in the acute phase of the AM! may mainly reflect transitory hemodynamic and neurohormonal changes. This phase is characterized by above-normal concentrations of norepinephrine, renun, angiotensun-converting enzyme, and aldosterone; the neurohormonal activation begins to subside within the first 72 h (11). Although mobilization of the patients during the first week of hospitalization might have increased their urinary protein excretion, other effects following the AM! seemed to more greatly decrease their concentrations of urinary albumin and RBP. Gosling et al. suggested that the microalbuminuria of the acute phase of AMI was due to an inflammatory reaction in the renal vascular system (12). However, this explanation does not fit with the rapid reversibility of the renal dysfunctions. Above-normal urinary albumin excretion was viewed as a cardiovascular risk factor in other studies (6). But the interrelation may be more complex. Our study shows that the acute events of an AM! may cause similar, albeit transitory, renal dysfunctions.