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Articles by Krishnaji Kulkarni
Total Records ( 2 ) for Krishnaji Kulkarni
  Matthew Konerman , Krishnaji Kulkarni , Peter P. Toth and Steven R. Jones
  Lipoprotein(a) [Lp(a)] is a complex lipoprotein consisting of a low-density lipoprotein (LDL)-like ApoB100-containing core particle covalently bound to apo(a), a large functionally complex glycoprotein. The mechanisms of Lp(a) metabolism and its interactions with cell-surface lipoprotein receptors are incompletely understood. In this study, we investigated the relationship of Lp(a) to other lipoproteins at high and normal levels of serum triglycerides (TGs). We measured serum lipid and Lp(a) particle concentrations in 148 unselected primary- and secondary-prevention patients. Subjects with TG > 200 mg/dL were classified as having high TG in accordance with National Cholesterol Education Program Adult Treatment Panel III guidelines. Our analysis revealed mean TG levels of 100 and 270 mg/dL in the normal and high TG groups, respectively. Lp(a)-C, Lp(a)-P, and Lp(a) cholesterol content per particle [Lp(a)-C/Lp(a)-P] did not differ between groups. At normal TG levels, stepwise multiple linear regression revealed that Lp(a)-P correlated with Lp(a)-C (P < 10−6), ApoAI (P = .0001), the high-density lipoprotein cholesterol subfraction ratio (HDL2-C/HDL3-C; P = .002), and dense very-low-density lipoprotein cholesterol (VLDL3-C; P = .04), overall model R = 0.74. At high TG levels, Lp(a)-P very strongly correlated primarily with HDL2-C/HDL3-C and TG-related variables with minimal dependence on Lp(a)-C (P = .09), overall model R = 0.96. These findings provide evidence of shared metabolic mechanisms for Lp(a), HDL, TG, and very low-density lipoprotein at high serum TG. Future studies are needed to elucidate common mechanisms, enzymes, and receptors involved in Lp(a) and HDL/TG metabolism with a focus on how these mechanisms are modified in the setting of hypertriglyceridemia.
  Matthew Konerman , Krishnaji Kulkarni , Peter P. Toth and Steven R. Jones
  There is little known about the relative predictive value of different lipoprotein(a) [Lp(a)] assays in clinical use, although each has been shown to predict similar incremental risk over conventional clinical and lipid risk factors. Thus, we examined the classification behavior of two commonly used Lp(a) assays and their associations with other lipid parameters. Serum lipid and Lp(a) concentrations were measured in 144 primary and secondary prevention patients. Lp(a) cholesterol [Lp(a)-C] was measured with the Vertical Auto Profile (upper limit of normal, 10 mg/dL). Lp(a) particle concentrations [Lp(a)-P] were measured with an isoform-independent molar assay (upper limit of normal, 70 nmol/L). The subjects were divided into the following four groups on the basis of their Lp(a)-C and Lp(a)-P levels: normal Lp(a)-P and Lp(a)-C; high Lp(a)-P and normal Lp(a)-C; normal Lp(a)-P and high Lp(a)-C; and high Lp(a)-P and Lp(a)-C. The proportion of subjects with values above the upper limit of normal was similar with both assays (P = .15). However, the Lp(a)-C and Lp(a)-P assays discordantly classified 23% of the study's subjects. In addition, the four Lp(a)-defined groups displayed differences in their relationships with other lipoproteins. The two groups with elevated Lp(a)-C showed significant associations with higher high-density lipoprotein cholesterol, apolipoprotein AI, and high-density lipoprotein cholesterol/apolipoprotein AI ratios. Triglycerides were also noted to be above normal in discordant and normal within concordant Lp(a) groups. Finally, the amount of cholesterol per Lp(a) particle [Lp(a)-C/Lp(a)-P] varied widely across the four groups. These findings suggest that the four Lp(a)-defined groups are physiologically discrete. Further investigation is warranted to assess which parameters among Lp(a)-P, Lp(a)-C, and Lp(a)-C/Lp(a)-P can be used to more accurately characterize Lp(a)-associated cardiovascular risk.
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