Further description of early clinically silent lupus nephritis.

Thirty silent lupus nephritis (SLN) patients were compared to 16 individuals bearing overt lupus nephritis (OLN). Results included: years of systemic lupus erythematosus (SLE) diagnosis were significantly earlier (4.6 +/- 2.8 years) in SLN than in OLN (7.18 +/- 3.61) (P < 0.05). Neurological compromise, hypertension, normocitic anemia and lymphopenia were significantly prevalent in OLN than in SLN (P < 0.05). Beside normal urinary sediment and renal function tests, the SLN group showed a moderate increase of both activity (AI) and chronicity (CI) renal pathology index when compared to highly increased AI and CI in OLN (P < 0.05). Seventy percent of SLN patients were ISN/RPS Classes I (6.6%) and II (63.3%) while 81% of OLN cases were Classes III, IV (37.5%) and V. IgG, IgA, IgM, lambda chain, C3 and fibrinogen immune deposits were found in 90% or over in both SLN and OLN individuals while in 60% or over, both groups also showed kappa chain, Clq and C4 deposits. While prevalence of ANA, anti-dsDNA and anti-C1q antibodies were similar in both groups, anti-histone, anti-RNP, CIC and CH50 serum levels were significantly different in OLN versus SLN (P < 0.05). We strongly suggest that indeed SLN is the earliest stage in the natural history of lupus nephritis.

Cluster analysis of antinuclear autoantibodies in the prognosis of SLE nephropathy: are anti-extractable nuclear antibodies protective?

To investigate the possible role of anti-ENA autoantibodies in the pathogenesis of SLE nephropathy, we performed a cross sectional clustering study of 91 SLE patients using 75 clinical and laboratory variables examining the presence of anti-dsDNA and ENA autoantibodies by ELISA and Western blot. We applied principal component, hierarchical cluster, multiple correspondence and logistical regression analysis. Two polar forms of SLE nephropathy and five clinical groups were identified: group 1 without overt nephropathy (n = 37), group 2 with nephropathy and only proteinuria (n = 19), group 3 nephropathy and only hematuria (n = 11), group 4 with hematuria and proteinuria (n = 14) and group 5 on renal failure (n = 10). When analyzed individually, levels of anti-dsDNA and single anti-ENA antibodies did not allow us to differentiate between renal and non-renal groups. However, when the anti-ENA autoantibodies were analyzed as a cluster, a high predictive value for clinical nephropathy was obtained. Thus, the absence of ENA antibodies (ENA ve or Venezuelan cluster) increased eleven-fold the odds ratio to develop SLE nephropathy. We suggested that the ENA ve cluster may predict development of the most severe forms of renal lupus while the ENA Sm/RNP and the ENA Ro/La/Sm/RNP clusters could be associated with the absence and the most benign form of SLE nephropathy. It must be interesting to apply similar cluster methodology in an SLE population with different ethnic background.

Auricular chondritis and diffuse proliferative glomerulonephritis in primary Sjögren's syndrome.

Bilateral auricular inflammation with histological changes of relapsing polychondritis was observed in a female patient with primary Sjögren's syndrome. This was accompanied by rapidly progressive renal insufficiency due to diffuse proliferative glomerulonephritis. To our knowledge this is the first well documented case of primary Sjögren's syndrome associated with chondritis and glomerulonephritis, further emphasising the wide spectrum of extraglandular manifestations in this autoimmune disorder.