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Clinical Chemistry, Vol 35, 2121-2123, Copyright © 1989 by American Association for Clinical Chemistry
I Karadi, L Romics, G Palos, J Doman, I Kaszas, A Hesz and GM Kostner
3rd Department of Medicine, Semmelweis Medical University, Budapest, Hungary.
We measured serum cholesterol, triglyceride, and lipoprotein Lp(a) concentrations in serum of 37 patients with massive proteinuria of different origin, comparing values with those for age- and sex-matched controls and finding significantly increased Lp(a) concentration in the total group of patients compared with controls. Lp(a) concentration was not correlated with serum cholesterol, triglyceride, serum creatinine, daily urinary protein loss, or selectivity index. Selecting the patients according to their histological diagnosis obtained by renal needle biopsy, we found divergent results in seven patients with minimal change disease (MCD) compared with 11 patients with membranoproliferative glomerulonephritis. Lp(a) in MCD patients did not differ from that controls (101 +/- 102 and 90 +/- 115 mg/L) and correlated positively with total daily urinary protein loss (r = 0.7962, P less than 0.05). In contrast, the patients with membranoproliferative glomerulonephritis had significantly higher Lp(a) values than the controls (219 +/- 222 mg/L), and Lp(a) concentrations correlated negatively with the daily protein loss in urine (r = - 0.6545, P less than 0.05). The most surprising results were the marked Lp(a) concentrations in serum of three patients with primary amyloidosis and nephrosis syndrome. Our results indicate a regulatory role of the kidney in the metabolism of Lp(a) and different effects on the serum Lp(a) concentration, depending on the type of damage to renal tissue.
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