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Clinical Study

Unknown aspect of the old disease: does dyslipidemia in systemic AA amyloidosis differ from the dyslipidemia in primary glomerulonephritis?

, , , , , , , , & show all
Pages 1273-1279 | Received 19 Jan 2015, Accepted 20 Jun 2015, Published online: 16 Jul 2015

Figures & data

Table 1. Laboratory characteristics of the patients with systemic AA amyloidosis and primary glomerulonephritis (PG) at the time of the diagnosis.

Table 2. Distributions of serum lipid abnormalities in systemic AA amyloidosis and primary glomerulonephritis (PG).

Figure 1. Relation of serum LDL-C with serum total protein levels (A) in patients with primary glomerulonephritis etiologies and (B) in patients with systemic amyloidosis (LDL-C, mmol/L; serum total protein).

Figure 1. Relation of serum LDL-C with serum total protein levels (A) in patients with primary glomerulonephritis etiologies and (B) in patients with systemic amyloidosis (LDL-C, mmol/L; serum total protein).

Figure 2. Relation of serum LDL-C with serum hemoglobin levels (A) in patients with primary glomerulonephritis etiologies and (B) in patients with systemic amyloidosis (LDL-C, mmol/L; hemoglobin g/L).

Figure 2. Relation of serum LDL-C with serum hemoglobin levels (A) in patients with primary glomerulonephritis etiologies and (B) in patients with systemic amyloidosis (LDL-C, mmol/L; hemoglobin g/L).

Table 3. Relationship of the serum lipid parameters with serum albumin, proteinuria and C-reactive protein in patients with systemic AA amyloidosis and primary glomerulonephritis (PG).

Table 4. A multivariate analysis of the overall patients with nephrotic proteinuria [both caused by systemic AA amyloidosis and primary glomerulonephritis (PG)].

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