Abstract
IntroductionBone loss in Lupus Nephritis (LN) patients is common and multifactorial. The aim of this study was to evaluate the bone status of newly diagnosed LN patients and their correlation with inflammatory factors involved in LN physiopathology.MethodsWe studied 15 pre-menopausal patients with ≤2 months of diagnosed SLE and LN. Patients with prior kidney or bone disease were excluded. In addition to biochemical evaluation (including 25-hydroxyvitamin D3 [25(OH)D] and Monocyte Chemotactic Protein (MCP1) dosage), we performed bone biopsies followed by osteoblast culture, histomorphometric and immunohistochemistry analysis.ResultsLN patients presented a mean age of 29.5±10 years, a proteinuria of 4.7±2.9 g/day and an estimated glomerular filtration rate (GFR) of 37(31–87) ml/min/1,73 m2. They were on glucocorticoid therapy for 34±12 days. All patients presented vitamin D insufficiency (9.9±4.4 ng/ml, range 4–20). Urinary MCP1 correlated negatively with 25(OH)D (r = −0.53, p = 0.003) and positively with serum deoxypyridinoline (r = 0.53, p = 0.004). Osteoblasts isolated from LN bone biopsies presented a significantly higher expression of MCP-1 when compared to controls (32.0.±9.1 vs. 22.9±5.3 mean fluorescence intensities, p = 0.01). LN patients presented a significantly reduced osteoid volume, osteoid thickness, osteoid surface, mineralization surface and bone formation rate, associated with an increased eroded surface and osteoclast surface. Patient’s bone specimens demonstrated a reduced immunostaining for osteoprotegerin (0.61±0.82 vs. 1.08±0.50%, p = 0.003), and an increased expression of Receptor Activator of NF-κB ligand (RANKL) (1.76±0.92 vs. 0.41±0.28%, p<0.001) when compared to controls.DiscussionNewly diagnosed LN patients presented a significant disturbance in bone metabolism, characterized by an impaired bone formation and mineralization, associated with an increase in resorption parameters. Glucocorticoid use, vitamin D insufficiency and inflammation might be involved in the physiopathology of bone metabolism disturbance.
Highlights
Bone loss in Lupus Nephritis (LN) patients is common and multifactorial
The results of the clinical, biochemical and histological classification of LN are described in the table 1
Our study show that newly diagnosed lupus nephritis patients presented a reduced bone formation and mineralization, associated with an increased bone resorption
Summary
Bone loss in Lupus Nephritis (LN) patients is common and multifactorial. The aim of this study was to evaluate the bone status of newly diagnosed LN patients and their correlation with inflammatory factors involved in LN physiopathology. Bone loss is a common (with osteopenia and osteoporosis been reported in 25– 74% and 1.4–68% of patients, respectively), and a potentially preventable condition associated with SLE [2,3]. The etiology of bone loss in SLE is probably multifactorial, involving both traditional and disease-related risk factors [3]. The risk of fractures seems to increase 75% within the first 3 months of therapy, before a substantial decline in BMD [9], and possibly due to the loss of bone strength [10]. It is not clear the minimum dose and duration of glucocorticoid therapy that could increase the risk of fracture. Some investigators have reported a relationship between SLE and lower BMD in patients never receiving corticosteroids [19,21,22], suggesting that SLE activity per se may be a risk factor for bone loss
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