Key result
Nephrotic syndrome remission is linked to dramatic reductions in elevated Lp(a) and apoprotein B.
Why the study?
Lipoprotein abnormalities in the nephrotic syndrome and their relation to proteinuria remission have not been extensively investigated.
Observational (n=19)
Lp(a) elevation in active nephrotic syndrome may prompt lipid surveillance; leaves open its independent role in residual cardiovascular risk.
Although lipoprotein abnormalities of the nephrotic syndrome are assumed to be related to the presence of proteinuria, this topic has not been investigated extensively. We measured lipoproteins from 19 nonuremic patients during and after remission of the nephrotic syndrome in an effort to determine the extent of their putative atherogenicity. As expected, disturbances involved primarily the apoprotein B-containing lipoproteins. No patient showed serum lipoprotein(a) [Lp(a)] < 300 mg/L during the acute phase. Lp(a) concentrations correlated significantly with those of apoprotein B, and both values decreased dramatically with the remission of the nephrotic syndrome. Surprisingly, despite the resolution of proteinuria, concentrations of intermediate-density lipoproteins and Lp(a) remained above normal in hypertriglyceridemic patients, suggesting a residual effect of nephrosis in the overall lipoprotein transport. Accumulation of atherogenic remnants should be considered a characteristic of the hyperlipidemia of the nephrotic syndrome, and aggressive treatment to reduce proteinuria is mandatory.
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Joven et al. (1995) conducted an observational in Nephrotic syndrome (n=19). Remission of proteinuria vs. Acute phase of nephrotic syndrome was evaluated on Lipoprotein(a) concentration. During the acute phase of nephrotic syndrome, all patients had serum lipoprotein(a) levels ≥300 mg/L, which decreased dramatically along with apoprotein B upon remission of proteinuria.
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