“Trust my morphology”, the key message from a kidney stone

International audienceThe Consensus Conference Group recently published an article in Urolithiasis highlighting the importance of urine and stone analysis in the metabolic evaluation of kidney stone formers (KSF) [1]. Indeed, each kidney stone contains the imprints of the conditions which created them during their 'lifetime in the kidney'. The morpho-constitutional classification method (MCC) established by Prof Michel Daudon correlates the morphological characteristics of stones with specific metabolic disorders [2]. Briefly, it distinguishes 7 types and 21 subtypes according to the crystalline composition and shape, color and structure of stones identified using an optical stereomicroscope (Table 1). This very specific method is easy to learn and provides the opportunity to quickly identify highly recurrent diseases, sometimes serious in their clinical consequences. Indeed, subtypes Ic, Ie, IIId, IVa2 and

Blocking TGF-β signaling pathway preserves mitochondrial proteostasis and reduces early activation of PDGFRβ+ pericytes in aristolochic acid induced acute kidney injury in wistar male rats

The platelet-derived growth factor receptor β (PDGFRβ)+ perivascular cell activation becomes increasingly recognized as a main source of scar-associated kidney myofibroblasts and recently emerged as a new cellular therapeutic target.In this regard, we first confirmed the presence of PDGFRβ+ perivascular cells in a human case of end-stage aristolochic acid nephropathy (AAN) and thereafter we focused on the early fibrosis events of transforming growth factor β (TGFβ) inhibition in a rat model of AAN.Neutralizing anti-TGFβ antibody (1D11) and its control isotype (13C4) were administered (5 mg/kg, i.p.) at Days -1, 0, 2 and 4; AA (15 mg/kg, sc) was injected daily.At Day 5, 1D11 significantly suppressed p-Smad2/3 signaling pathway improving renal function impairment, reduced the score of acute tubular necrosis, peritubular capillaritis, interstitial inflammation and neoangiogenesis. 1D11 markedly decreased interstitial edema, disruption of tubular basement membrane loss of brush border, cytoplasmic edema and organelle ultrastructure alterations (mitochondrial disruption and endoplasmic reticulum edema) in proximal tubular epithelial cells. Moreover, 1D11 significantly inhibited p-PERK activation and attenuated dysregulation of unfolded protein response (UPR) pathways, endoplasmic reticulum and mitochondrial proteostasis in vivo and in vitro.The early inhibition of p-Smad2/3 signaling pathway improved acute renal function impairment, partially prevented epithelial-endothelial axis activation by maintaining PTEC proteostasis and reduced early PDGFRβ+ pericytes-derived myofibroblasts accumulation

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Membranous Nephropathy and Anti-Podocytes Antibodies: New Implications for the Diagnostic Workup and Disease Management in 2018

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