Sindhu Kaza

Impact of body mass index on progression of primary immunoglobulin a nephropathy

The role of obesity in the progression of primary glomerular diseases is controversial. A few studies report overweight/obesity as a risk factor for disease progression in immunoglobulin A nephropathy (IgAN), and the real impact of it still remains unclear. The aim of this study was to elucidate the effect of body mass index (BMI) on disease progression and proteinuria in patients with IgAN in Indian population. A cohort of biopsy-proven primary IgAN patients diagnosed between March 2010 and February 2015 who had a follow-up for a minimum of 12 months were included in the study. We defined two groups of patients according to the BMI value at diagnosis: non-obese group (Group N) with BMI <23 Kg/m2 and the overweight/obese group (Group O) with BMI >23 Kg/m2 as per Asia-Pacific task force criteria. Baseline characteristics were compared between the groups. The estimated glomerular filtration rate (eGFR) and urine protein-creatinine ratio (UPCR) were followed up at entry time, 6 months, 12 months, and at the end of follow-up. Outcomes studied were change in eGFR, proteinuria, and progression to end-stage renal disease. Statistical analysis was done using the Statistical Package for the Social Sciences version 15.0. Of 51 patients, 25 (49%) had BMI <23 kg/m2 (Group N) and 26 (51%) had BMI >23 kg/m2 (Group O) (P = 0.01). The baseline clinical, histopathological, and treatment characteristics of both the groups were comparable. The BMI at the time of diagnosis did not have any significant effect on eGFR (P = 0.41) or proteinuria (P = 0.99) at presentation. At the end of follow-up, both the groups had a similar reduction of proteinuria (UPCR) (P = 0.46) and eGFR (P = 0.20). Two patients in each group have reached chronic kidney disease Stage 5. In the present study, BMI at presentation did not have any impact on eGFR or proteinuria, either at diagnosis or at follow-up. It needs further large multicenter randomized control studies to see the effect of BMI on progression of IgAN.

374 Ana negative renal limited lupus nephritis –a rare entity

Background and aims Antinuclear antibodies (ANA) in serum is considered a decisive diagnostic test for SLE. ANA negative SLE is a subgroup of SLE that is infrequently recognised. We report an unusual case of seronegative SLE which presented as rapidly progressive renal failure with no other systemic manifestations. Methods 34 year old female presented with fever, nephrotic range proteinuria and rapidly progressive renal failure. She did not have any other systemic features of SLE. Her clinical, biochemical and serological findings are as shown in table 1. She had low complementemia, but her ANA, ANA profile including anti double stranded DNA (anti- dsDNA) antibodies and anti cardiolipin antibody was negative.Renal biopsy on light microscopy showed diffuse proliferative glomerulonephritis with a full house on immunofluorescence including C1q consistent with class 4 lupus nephritis (Figure 1). A diagnosis of ANA negative renal limited lupus nephritis was made. Abstract 374 Table 1 Abstract 374 Figure 1 Results She was treated with pulse methyl prednisolone followed by oral steroids1mg/kg/day and pulse cyclophosphamide 500–750 mg/m2 body surface area as per NIH protocol. She recovered completely and is on follow-up for two years. She has remained persistently negative for all ANA antibodies including anti-dsDNA antibodies. Conclusions Ours is an unusual case of ANA negative renal limited lupus nephritis. The low complement levels, full house nephropathy in immunofluorescence and response to therapy were important clues in diagnosing the case. We report this patient to highlight the possibility of SLE in seronegative patients as well in order to avoid delay in the management.