TABLE 2.
Distribution of APOE mutations in lipoprotein glomerulopathy patients
| Mutation location | ||||
|---|---|---|---|---|
| LDLR‐HSPG | LDLR‐non‐HSPG | Other regions | Control | |
| n | 31 | 5 | 59 | 60 |
| Male, n (%) | 15 (48.4) | 1 (20.0) | 31 (52.5) | 31 (51.7) |
| Positive family history, n (%) | 14 (45.2) | 3 (60.0) | 12 (32.4) | — |
| Age (year) | 31.3 ± 17.7 | 40.0 ± 18.7 | 37.0 ± 12.9 | 35.0 ± 12.8 |
| MAP (mmHg) | 105.4 ± 14.0 a | 107.2 ± 25.1 | 111.0 ± 20.8 a | 94.4 ± 11.1 |
| ln(Upro) (g/24 hr) | 1.0 ± 0.9 a , b | 0.3 ± 0.6 a | 1.5 ± 0.9 a | 1.9 ± 0.5 |
| eGFR (ml/min per 1.73 m2) | 95.4 ± 35.3 | 104.4 ± 28.6 | 83.9 ± 31.7 a | 95.3 ± 27.5 |
| ln(TG) (mmol/L) | 1.1 ± 0.5 | 0.6 ± 0.5 | 1.1 ± 0.5 | 1.1 ± 0.6 |
| ln(TC) (mmol/L) | 1.8 ± 0.4 a | 1.9 ± 0.3 a | 1.8 ± 0.5 a | 2.3 ± 0.4 |
| ln(apoE) (mg/dL) c | 2.7 ± 0.4 a , b | 1.9 ± 0.3 | 2.0 ± 0.5 a | 1.8 ± 0.3 |
Abbreviations: apoE, apolipoprotein E; EPI‐eGFR, estimated glomerular filtration rate using EPI; LDLR‐HSPG, mutations in HSPG binding region within low‐density lipoprotein receptor binding region; LDLR‐nonHSPG, mutations in low‐density lipoprotein receptor binding region outsides HSPG binding region; MAP, mean arterial pressure; n, number; TC, total cholesterol; TG, triglyceride; Upro, urine protein.
Compared with control group (MATERIALS AND METHODS 2.4), p < .05.
Compared with other regions group, p < .05.
ln(apoE): 83 of the 95 LPG patients and 19 (two focal segmental glomerulosclerosis and 17 minimal change disease) of the control group had apoE data. Among the 83 LPG patients, 27 had mutations in LDLR‐HSPG, two in LDLR‐nonHSPG, and 54 in other regions.