LIPOPROTEIN(A) IN NEPHROTIC SYNDROME AND END-STAGE RENAL-DISEASE

Lipoprotein(a) [Lp(a)] may be elevated in patients with the nephrotic syndrome and patients on hemodialysis or continuous ambulatory periton eal dialysis. High levels of Lp(a) are due to proteinuria or an activa ted acute-phase response. Serum concentrations greater than 30 mg/dl a re independently associated with coronary heart disease. Data from cel l culture studies suggest that it is not uptake of Lp(a) by mesangial cells but trapping by matrix proteins that contributes to the generati on of glomerular apo(a) deposits. Lp(a) alters mesangial cell DNA synt hesis and stimulates the generation of reactive oxygen species. Prolon ged exposure to T-p(a) causes mesangial cell death in vitro culture ex periments. Lp(a) does not alter autocrine transforming growth factor-p transcription in human mesangial cells and has unlike low-density lip oprotein, no effect on the production of the extracellular matrix prot ein fibronectin. Future cell culture studies on the role of Lp(a) in r enal disease have to address whether Lp(a) induces cell death via apop tosis and to what extent the generation of oxygen radicals is involved in this process.