MO310LIPID DISORDERS IN NEPHROTIC SYNDROME

Abstract

\n \n \n Lipid disorders are a characteristic manifestation that accompanies the presentation of nephrotic syndrome (NS). The pathophysiology underlying its origin is debated in the literature. It is important to collect large series of patients to accurately characterize these manifestations.\n The aim of this study was to carry out an analysis of the lipid alterations detected in the presentation of NS, as well as its evolution, in a large cohort of patients treated in the Nephrology Service of a tertiary referral hospital.\n \n \n \n 111 NS outbreaks corresponding to 71 patients seen in the last 12 years were analyzed.\n \n \n \n 53 patients had a single outbreak. 18 patients (25.35%) had 2 or more outbreaks. 63.1% of the outbreaks affected males. Mean age 54.76 ± 18.46 years (17-85). Charlson comorbidity index 2.62 ± 2.43 points (0-8). The mean of drugs ingested daily prior to NS was 4 ± 3.88 (0-13) There were no significant differences between men and women regarding these three parameters. A renal biopsy was performed in the first outbreak in 67 patients with the result of: 21 membranous nephropathy, 11 minimal change nephropathy, 17 mesangial glomerulonephritis, 8 focal segmental glomerulosclerosis, 2 IgA nephropathy, 5 AA amyloidosis, 3 AL amyloidosis.\n 90.1% of the patients had high cholesterol levels (> 200 mg/dL). 73% of the patients had high LDL cholesterol (> 160 mg/dL). 72.1% of the patients had triglycerides (TG) above normal levels (> 150 mg/dL). 47.75% of the patients had a high atherogenic index (> 5).\n The mean levels at the presentation of NS were: total cholesterol 338.07 ± 111.61 mg/dL; HDL cholesterol 67.92 ± 25.46 mg/dL; LDL cholesterol 227.76 ± 99.28 mg/dL; TG 215.48 ± 97.27; atherogenic index 5.12 ± 2.47. There were no significant differences regarding these variables and the various glomerular diseases. Patients with prior dyslipidemia history, showed significantly lower cholesterol levels, 309.69 ± 98.08 mg/dL vs 363.53 ± 115.55 mg/dL, perhaps because they were already taking statins (we do not have this data).\n There is a significant correlation between total cholesterol and LDL cholesterol with serum albumin, but not between total cholesterol or LDL with proteinuria. There is a correlation between TG with both albumin and proteinuria. There is a significant inverse correlation between the neutrophil/lymphocyte ratio (NLR) and total cholesterol and LDL cholesterol. The higher the NLR, the lower the cholesterol. It gives the impression that the sicker/inflamed the patient is, the lower the ability to synthesize cholesterol. In our series, patients with acute kidney injury (AKI) or previous chronic kidney disease (CKD) had significantly lower cholesterol levels. AKI 306.84 ± 105.24 mg/dL vs no AKI 354.04 ± 110.50 mg/dL. CKD 293 ± 124.15 mg/dL vs no CKD 347.07 ± 106.27 mg/dL.\n In multivariate analysis, the variables associated with the level of total cholesterol and LDL cholesterol were serum albumin and the Charlson comorbidity index. Regarding the triglyceride level, the associated variables were serum albumin and proteinuria.\n In the evolution of the patients, both total cholesterol and triglycerides improved significantly after reaching NS remission: final cholesterol 190 mg/dL; Final triglycerides 141 mg/dL.\n \n \n \n As in other series, we detected a high prevalence of lipid alterations in our population of adult patients with NS. Hypoalbuminemia appears as the factor that is independently associated with cholesterol and triglyceride levels. The lipid alterations improve in a parallel way as the NS picture does.\n