Abstract

Abstract BACKGROUND AND AIMS Lipid abnormalities are a defining feature of nephrotic syndrome. In nephrotic patients, changes such as increased total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) and decreased high-density lipoprotein cholesterol (HDL-C) as well as decreased HDL-C: TC ratio are more frequently found than in healthy subjects. The aims of this study were to evaluate the differences in the serum lipidic profile at baseline (diagnosis) among each primary glomerulopathies (PG) presenting with nephrotic syndrome (NS) and its association with several clinical parameters such as serum albumin (SAbl) and proteinuria. METHOD We conducted a retrospective cohort study with patients older than 18 years who presented with nephrotic syndrome and diagnosed with a PG by kidney biopsy in the last 10 years in a tertiary-level hospital. RESULTS The study included 60 patients: 38 were male (63.3%), with median age of 52 (IQR 27) years, 43.3% had hypertension, median serum creatinine (SCr) was 1.11 mg/dL (IQR 0.86), median protein-creatinine ratio was 7443 (IQR 5033.5) mg/g and median SAlb of 2.0 (IQR 1.03) mg/dL. At baseline, the median TC was 320.5 mg/dL (IQR 184.5), HDL-C 55 (IQR 25.5) mg/dL, LDL-C 225mg/dL (IQR 174), TG 176 (IQR 122.6) mg/dL and HDL: TC ratio 0.19 (IQR 0.13). Median follow-up time was 24 (IQR 51) months. Patients were grouped in four categories regarding the PG subtype: membranous nephropathy (MN, 38.3%), minimal change disease (MCD, 38.3%), IgA nephropathy (IgAN, 11.7%) and focal segmental glomerulosclerosis (FSGS, 11.7%). Evaluating all the patients enrolled, we found a strong negative correlation between SAlb and TC (r = –0.511, P < .001), LDL-C (r = –0.529, P < .001) and a weaker negative correlation with TG (r = –0.282, P = .030), but not with HDL-C. We did not find a statistically significant correlation between proteinuria and each cholesterol subtype or TG levels. A Kruskal–Wallis test showed that different subtypes of PG were associated with different median HDL-C (H(3) = 12.073, P = .007) and TG serum levels (H(3) = 10.128, P = .018). No statistically significant differences in the TC, LDL-C or HDL-C: TC ratio were found. Comparing all pairs of groups, we found that HDL-C levels were statistically different between MN and MCD (45.5 versus 67 mg/dL, P < .001), but not in the other pairs. The same analysis found that TG serum levels were only significantly different between IgAN and MN (114 versus 187 mg/dL, P = .008) and between IgAN and FSGS (114 versus 200 mg/dL, P = .012). MN patients that progressed to CKD stage 5D had lower median HDL-C levels at diagnosis, when compared to the patients who did not progress (41 versus 49 mg/dL, P = .037). This difference was not observed in IgA, FSGS or MCD. CONCLUSION Each GP subtype presents a different lipid profile, particularly differing on HDL and TG. Patients with MCD presented with the highest levels of HDL-C, while MN with the lowest. Regarding TG levels, FSGS presented with the highest levels while IgAN presented with the lowest. In the membranous nephropathy group, patients that progressed to ESRD had statistically significantly lower serum levels of HDL-C. As expected, SAlb is significantly associated with TC, LDL-C and TG levels, in nephrotic patients. This could be due to different levels of lecithin–cholesterol acyltransferase (an enzyme responsible for the maturation of HDL), which is increasingly lost through urine in nephrotic syndromes. The differences found in the lipidic profile between PG subtypes could have screening, therapeutic and prognosis implications in the management of cardiovascular risk in these patients. More studies are needed to understand the pathophysiology and the prognosis significance of each lipid profile.

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