The prognostic impact of the combination of a geriatric nutritional risk index (GRNI) and modified creatinine index, both of which assess nutritious status in hemodialysis patients, has not yet been well investigated thus far. Patients receiving maintenance hemodialysis in our institutes between February 2011 and January 2017 were retrospectively included. The baseline GRNI and modified Creatinine index were calculated and the impact of their combination on 5-year all-cause mortality following the index hemodialysis was investigated. A total of 183 patients (68.3 ± 12.4 years, 98 men, hemodialysis duration 97 ± 89 months) were followed from the index hemodialysis for 5.5 years. Mean GNRI was 91.2 and mean modified Creatinine index was 22.2 in men and 19.6 in women. The 5-year survival was significantly stratified by the median values of GNRI and modified Creatinine index (p < 0.05 for both). Patients with low GNRI and a low modified Creatinine index had lower 5-year survival than those with the other three combination patterns (p < 0.05). A combination of GNRI and modified Creatinine index may be a promising tool to risk stratify mortality in dialysis patients.

These results suggest that a ≥30% decline in eGFR over 1 or 2 years adds prognostic information about risk for ESRD in patients with type 2 diabetes and macroalbuminuria, supporting the consideration of percentage decline in eGFR as a surrogate endpoint among macroalbuminuric cases in type 2 diabetes. On the other hand, our study suggests that additional analyses on the relationship between remission of macroalbuminuria and risk of ESRD are needed in type 2 diabetes.

No abstract

An overlap of systemic lupus erythematosus (SLE) and antineutrophil cytoplasmic antibodies- (ANCA-) associated vasculitis (AAV) is extremely rare: approximately 40 cases have been reported to date. A literature review indicates that they are more common in women in their forties, and simultaneous onset has been reported in 69% of cases. In addition, both lupus nephritis and ANCA-associated glomerulonephritis were observed on renal biopsy. This report presents the case of a 35-year-old woman with an 8-month history of polyarthralgia who was admitted to our hospital. She was diagnosed with SLE due to typical clinical presentation of the disease: polyarthritis, lymphocytopenia, hypocomplementemia, presence of antinuclear and anti-dsDNA antibodies, and proteinuria. However, purpura were scattered, and the titer of antimyeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA) was high. A skin biopsy revealed leukocytoclastic vasculitis that involved poor immune complex deposition. A renal biopsy showed necrotizing glomerulonephritis with cellular and fibrocellular crescent formation that involved deposition of IgM and C3c only in the mesangial area and the peripheral capillaries. Additionally, no electron-dense deposits were observed under electron microscopy. These pathological findings were consistent with AAV rather than with SLE. Therefore, we finally diagnosed the patient with both SLE and microscopic polyangiitis. After treatment with methylprednisolone and intravenous cyclophosphamide pulse therapies, renal function improved and MPO-ANCA levels decreased. In cases of suspected overlap between SLE and AAV, appropriate diagnosis and treatment are important.

An 83-year-old woman with a 1-year history of scheduled intravitreal injection of vascular endothelial growth factor (VEGF) inhibitor (aflibercept) was diagnosed with nephrotic syndrome due to focal segmental glomerulosclerosis with histopathological findings of segmental infiltration of foam cells in the glomerular capillaries. Her nephrotic syndrome improved immediately following the termination of aflibercept intravitreal injection without steroid therapy. Although widely used to treat ophthalmic diseases, we should keep in mind that even intravitreal injection of VEGF inhibitor, as opposed to systemic administration, can cause kidney injury.

Renal production of 5-HT is enhanced compared with that of DA in essential hypertensives with microalbuminuria. This imbalance may contribute to the genesis of hypertensive glomerular damage.

No abstract

No abstract