Lipoprotein(a) Levels and Fibrinolytic Activity in Patients with Nephrotic Syndrome
Author(s) -
A. Segarra,
Pilar Chacón,
L Piera
Publication year - 1996
Publication title -
nephron
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 1423-0186
pISSN - 0028-2766
DOI - 10.1159/000189012
Subject(s) - medicine , nephrotic syndrome , lipoprotein(a) , lipoprotein , cholesterol
Servicios de Nefrología y Bioquímica, Hospital Universitario Valle Hebrón, Barcelona, Espãna A. Segarra Medrano, Servicio de Nefrología, Anexo planta 7, Hospital , Universitario Valle Hebrón, Paseo Valle Hebrón s/n, E-08035 Barcelona (Spain) Dear Sir, We have read with interest the original paper by Hong et al. [1] about the relationship between lipoprotein(a) levels and fibrinolytic activity in patients with nephrotic syndrome and we would like to add our experience on this subject. We prospectively measured serum concentrations of lipids, apoproteins Al, B, CII, CIII, lipoprotein(a), fibrinogen, renal function, proteinuria fibrinopeptide A (FPA), betathromboglobulin (BTG) and platelet factor 4 (PF4) in a sample of 30 patients with biopsyproven active nephrotic syndrome. There were 20 males and 10 females, age 45 ± 16, BMI23.6 ± 1.7, serum creatinine 2.1 ± 1.4 mg/dl, fibrinogen 6.8 ± 2.4 g/l, proteinuria 6.5 ± 2 g/day, total cholesterol: 410 ± 250 mg/dl, HDL C 45 ± 11 mg/dl, LDL C 296 ± 112 mg/dl, triglycerides 295 ± 110 mg/dl, serum albumin 2.5 ± 1 g/l, apo Al 125 ± 15 mg/dl, apo B 180 ± 10 mg/dl, apo CII 14 ± 6 mg/dl, apo CIII 24 ± 7 mg/ dl, Lp(a) median 35 mg/dl, interquartile range [10-80]. The etiology of nephrotic syndrome was as follows: minimal change disease (n = 5), focal glomerulosclerosis (n=10), membranous nephropathy (n = 6), IgA glo-merulonephritis (n = 9). The reference values were obtained from a matched group of 30 healthy volunteers. Patients were prospectively followed for a period of 48 months in order to analyze the evolution of serum lipoprotein levels and Lp(a) levels and to investigate the occurrence of thrombotic episodes. Every 6 months, we determined serum lipid and Lp(a) levels, 24-hour proteinuria and we also performed a Doppler study of the femoral veins, renal veins, cava and suprahepatic veins. All patients with minimal change disease and 5 patients with focal glomerulosclerosis were treated with steroids. Four patients with membranous nephropathy were treated with steroids plus cyclophosphamide. All nonresponding patients were treated with enalapril (5-20 mg/ day). During the nephrotic phase, patients showed levels of cholesterol (410 ± 250 vs. 198 ± 42, p < 0.001), LDL C (296 ± 112 vs. 128 ± 16, p < O.001), apo CII (14 ± 6 vs. 4.5 ± 2, p < 0.001), apo CIII (24 ± 7 vs. 6 ± 2.5, p < 0.001), and Lp(a) (35 [10-80] vs. 14 [1-56], p < 0.001), significantly higher than those of the healthy controls. Likewise, the levels of FPA (2.5 ± 1 ng/ml vs. 1 ± 0.65, p < 0.001) and BTG (45 ± 18 vs. 23 ± 10 ng/ml, p < 0.001) were higher in nephrotic patients than those of the healthy controls. The serum level of PF4 was not different from that of controls (6 ± 4 ng/ml vs. 5 ± 2.5
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