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Microalbuminuria is the earliest clinical abnormality in diabetic kidney disease. High glucose (HG) concentrations are associated with the induction of oxidative stress in podocytes, leading to disruption of the glomerular filtration barrier. Our recent study revealed a significant decrease in the membrane-bound fraction of Klotho in podocytes that were cultured under HG conditions.

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Background: Uremia (UR) is caused by increased UR-related toxins in the bloodstream. We explored the mechanism of enterogenous toxin methylmalonic acid (MMA) in calcium-phosphorus metabolic disorder in UR rats via the Wnt/β-catenin pathway.

Methods: The UR rat model was established by 5/6 nephrectomy.

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The endoplasmic reticulum (ER) is a vital organelle responsible for protein quality control, including the folding, modification, and transport of proteins. When misfolded or unfolded proteins accumulate in the ER, it triggers endoplasmic reticulum stress (ERS) and activates the unfolded protein response (UPR) to restore ER homeostasis. However, prolonged or excessive ERS can lead to apoptosis.

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Steroid-resistant nephrotic syndrome as paraneoplastic syndrome of Waldenström macroglobulinemia: a case report.

CEN Case Rep

January 2025

Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Yokohama City Seibu Hospital, Yokohama, Japan.

Reports of glomerulonephritis associated with lymphoproliferative disorders are common, but reports of minimal change disease (MCD) accompanying non-Hodgkin's lymphoma are rare. Here, we present a case of a 45-year-old woman diagnosed with primary Waldenström's macroglobulinemia (WM) during MCD treatment. Her kidney biopsy revealed endothelial cell injury in parts of the MCD.

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Glomerular endothelial cell (GEnC) injury is a common feature across the wide spectrum of glomerular diseases. We recently reported that the endothelial-specific knockout of increases the susceptibility to GEnC injury and subsequent development of subacute thrombotic microangiopathy (TMA). However, the mechanism(s) mediating GEnCs response to injury in TMA are poorly understood.

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