Clinical Acute Kidney Injury and Histologic Acute Tubular-Interstitial Injury and Their Prognosis in Diabetic Nephropathy.

Introduction: Histologic acute tubular-interstitial injury (hATI) is often observed in patients with diabetic nephropathy (DN). This study aimed to determine the relationship between hATI and clinical acute kidney injury (cAKI) and evaluate significance of hATI in patients with DN.

Methods: Patients with biopsy-proven DN through 2003-2018 in our center were selected.

Modeling of the transport, hygroscopic growth, and deposition of multi-component droplets in a simplified airway with realistic thermal boundary conditions.

Accurate predictions of the droplet transport, evolution, and deposition in human airways are critical for the quantitative analysis of the health risks due to the exposure to the airborne pollutant or virus transmission. The droplet/particle-vapor interaction, i.e.

Angiotensin II induces calcium/calcineurin signaling and podocyte injury by downregulating microRNA-30 family members.

Unlabelled: Angiotensin II (AngII) is capable of inducing calcium/calcineurin signaling and podocyte injury; however, the precise underlying mechanism is not well understood. Because we have previously demonstrated that microRNA-30s (miR-30s) inhibit calcium/calcineurin signaling in podocytes, we hypothesize that AngII may induce podocyte injury by downregulating miR-30s and thereby activating calcium/calcineurin signaling. To test this hypothesis, we used an AngII-induced podocyte injury mouse model.

Increased miR-374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy.

The number of B cells is increased and the O-glycans of IgA1 are incompletely galactosylated in IgA nephropathy (IgAN). Here we report that expression of phosphatase and tensin homolog (PTEN) and Cosmc is decreased in B cells, and correlates with B cell number and the aberrant glycosylation of IgA1 in IgAN. Patients with IgAN exhibit higher miR-374b in B cells compared to controls.