Corrigendum: c-Jun amino terminal kinase signaling promotes aristolochic acid-induced acute kidney injury.

[This corrects the article DOI: 10.3389/fphys.2021.

Cyclophilin D Promotes Acute, but Not Chronic, Kidney Injury in a Mouse Model of Aristolochic Acid Toxicity.

The plant-derived toxin, aristolochic acid (AA), is the cause of Chinese Herb Nephropathy and Balkan Nephropathy. Ingestion of high dose AA induces acute kidney injury, while chronic low dose ingestion leads to progressive kidney disease. Ingested AA is taken up by tubular epithelial cells of the kidney, leading to DNA damage and cell death.

c-Jun Amino Terminal Kinase Signaling Promotes Aristolochic Acid-Induced Acute Kidney Injury.

Aristolochic acid (AA) is a toxin that induces DNA damage in tubular epithelial cells of the kidney and is the cause of Balkan Nephropathy and Chinese Herb Nephropathy. In cultured tubular epithelial cells, AA induces a pro-fibrotic response the c-Jun amino terminal kinase (JNK) signaling pathway. This study investigated the role of JNK signaling with a JNK inhibitor (CC-930) in mouse models of acute high dose AA-induced kidney injury (day 3) and renal fibrosis induced by chronic low dose AA exposure (day 22).

Cyclophilin Inhibition Protects Against Experimental Acute Kidney Injury and Renal Interstitial Fibrosis.

Cyclophilins have important homeostatic roles, but following tissue injury, cyclophilin A (CypA) can promote leukocyte recruitment and inflammation, while CypD can facilitate mitochondrial-dependent cell death. This study investigated the therapeutic potential of a selective cyclophilin inhibitor (GS-642362), which does not block calcineurin function, in mouse models of tubular cell necrosis and renal fibrosis. Mice underwent bilateral renal ischemia/reperfusion injury (IRI) and were killed 24 h later: treatment with 10 or 30 mg/kg/BID GS-642362 (or vehicle) began 1 h before surgery.

Initial mycophenolate dose in tacrolimus treated renal transplant recipients, a cohort study comparing leukopaenia, rejection and long-term graft function.

The evidence supporting an initial mycophenolate mofetil (MMF) dose of 2 g daily in tacrolimus-treated renal transplant recipients is limited. In a non-contemporaneous single-centre cohort study we compared the incidence of leukopaenia, rejection and graft dysfunction in patients initiated on MMF 1.5 g and 2 g daily.

Cyclophilin A Promotes Inflammation in Acute Kidney Injury but Not in Renal Fibrosis.

Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease is largely unknown.

Accuracy and Utility of Estimating Lean Body Mass and Nutritional Status in Patients with Chronic Kidney Disease on Long-Term Hemodialysis Using Anthropometric Skinfold Thickness Measurements.

Malnutrition is common in patients on hemodialysis (prevalence of 30% to 50%) and is associated with higher mortality. Lean body mass (LBM) assessment is an accurate way of assessing nutritional status. The dual-energy X-ray absorptiometry (DEXA) scan is a reliable method in assessing body compositions and LBM; however, it is expensive and largely inaccessible.

Cyclophilin D promotes tubular cell damage and the development of interstitial fibrosis in the obstructed kidney.

Cyclophilin D (CypD) is an important component in mitochondrial-dependent tubular cell death in acute kidney injury. However, it is not known whether CypD contributes to tubular cell damage in chronic interstitial fibrosis. We investigated this question in the unilateral ureter obstruction (UUO) model of renal interstitial fibrosis.

Renal transplant ultrasound: The nephrologist's perspective.

One of the principal roles of a nephrologist is to closely monitor renal transplant allograft function and promptly evaluate any dysfunction. Renal transplant sonography has a major role in this assessment process given its ability to easily define renal transplant anatomy and surrounding structures. Abnormalities can be extrarenal or involve vascular, parenchymal and urological components of the graft and these can acutely or chronically influence graft function and survival.