OBJECTIVES: To determine whether patients with acute myocardial infarction undergoing thrombolysis with streptokinase develop changes in renal function. DESIGN: Prospective assessment of renal function in 60 consecutive patients admitted with acute myocardial infarction. SETTING: Tertiary referral centre and city general hospital. PATIENTS: 60 consecutive patients with acute myocardial infarction. Thirty eight were given streptokinase and 17 tissue plasminogen activator (alteplase) and five no thrombolytic agent (non-streptokinase group). MAIN OUTCOME MEASURES: Proteinuria and creatinine clearance on admission (day 1) and on days 3 and 6; serum urea and creatinine concentrations on days 1 and 7; streptokinase IgG on days 1, 2, and 7. RESULTS: Significant proteinuria (> 0.15 g/24 h) was found in 31 (82%) of the 38 patients in the streptokinase group (mean 0.47 g/24 h (95% confidence interval 0.35 to 0.6 g/24 h)) in the 24 hours after admission compared with six (27%) out of 22 in the non-streptokinase group (mean 0.17 g/24 h (0.12 to 0.2 g/24 h); P = 0.008). In the streptokinase group this decreased to the normal range by day 3 (mean 0.15 g/24 h (0.1 to 0.22 g/24 h); P = 0.0001 v baseline). Electrophoresis of urine showed the proteinuria to be glomerular in origin. Creatinine clearance and serum creatinine and urea concentrations were similar in both groups. In the streptokinase group detectable streptokinase IgG titres were found in 28 out of 32 (87%) patients. The median titre on admission was 16 (range 0-110); it fell to 3 (range 0-80; P = 0.001) by day 2 and increased to 61 (range 0-7700; P = 0.0002 v baseline) by day 7. CONCLUSIONS: Streptokinase was associated with significant early onset proteinuria of glomerular origin. This started to resolve by day 3 and resulted in no deterioration in overall renal function. The temporal relation to the initial fall in antibody titre suggests that it could be the result of immune complex deposition in the glomeruli.
OBJECTIVES: To determine whether patients with acute myocardial infarction undergoing thrombolysis with streptokinase develop changes in renal function. DESIGN: Prospective assessment of renal function in 60 consecutive patients admitted with acute myocardial infarction. SETTING: Tertiary referral centre and city general hospital. PATIENTS: 60 consecutive patients with acute myocardial infarction. Thirty eight were given streptokinase and 17 tissue plasminogen activator (alteplase) and five no thrombolytic agent (non-streptokinase group). MAIN OUTCOME MEASURES: Proteinuria and creatinine clearance on admission (day 1) and on days 3 and 6; serum urea and creatinine concentrations on days 1 and 7; streptokinase IgG on days 1, 2, and 7. RESULTS: Significant proteinuria (> 0.15 g/24 h) was found in 31 (82%) of the 38 patients in the streptokinase group (mean 0.47 g/24 h (95% confidence interval 0.35 to 0.6 g/24 h)) in the 24 hours after admission compared with six (27%) out of 22 in the non-streptokinase group (mean 0.17 g/24 h (0.12 to 0.2 g/24 h); P = 0.008). In the streptokinase group this decreased to the normal range by day 3 (mean 0.15 g/24 h (0.1 to 0.22 g/24 h); P = 0.0001 v baseline). Electrophoresis of urine showed the proteinuria to be glomerular in origin. Creatinine clearance and serum creatinine and urea concentrations were similar in both groups. In the streptokinase group detectable streptokinase IgG titres were found in 28 out of 32 (87%) patients. The median titre on admission was 16 (range 0-110); it fell to 3 (range 0-80; P = 0.001) by day 2 and increased to 61 (range 0-7700; P = 0.0002 v baseline) by day 7. CONCLUSIONS: Streptokinase was associated with significant early onset proteinuria of glomerular origin. This started to resolve by day 3 and resulted in no deterioration in overall renal function. The temporal relation to the initial fall in antibody titre suggests that it could be the result of immune complex deposition in the glomeruli.