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Nephrology

  • 220 Articles
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FOXM1 drives proximal tubule proliferation during repair from acute ischemic kidney injury
Monica Chang-Panesso, … , Akio Kobayashi, Benjamin D. Humphreys
Monica Chang-Panesso, … , Akio Kobayashi, Benjamin D. Humphreys
Published November 11, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI125519.
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FOXM1 drives proximal tubule proliferation during repair from acute ischemic kidney injury

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Abstract

The proximal tubule has a remarkable capacity for repair after acute injury, but the cellular lineage and molecular mechanisms underlying this repair response are incompletely understood. Here, we developed a Kim1-GFPCreERt2 knockin mouse line (Kim1-GCE) in order to perform genetic lineage tracing of dedifferentiated cells while measuring the cellular transcriptome of proximal tubule during repair. Acutely injured genetically labeled clones coexpressed KIM1, VIMENTIN, SOX9, and KI67, indicating a dedifferentiated and proliferative state. Clonal analysis revealed clonal expansion of Kim1+ cells, indicating that acutely injured, dedifferentiated proximal tubule cells, rather than fixed tubular progenitor cells, account for repair. Translational profiling during injury and repair revealed signatures of both successful and unsuccessful maladaptive repair. The transcription factor Foxm1 was induced early in injury, was required for epithelial proliferation in vitro, and was dependent on epidermal growth factor receptor (EGFR) stimulation. In conclusion, dedifferentiated proximal tubule cells effect proximal tubule repair, and we reveal an EGFR/FOXM1-dependent signaling pathway that drives proliferative repair after injury.

Authors

Monica Chang-Panesso, Farid F. Kadyrov, Matthew Lalli, Haojia Wu, Shiyo Ikeda, Eirini Kefaloyianni, Mai M. Abdelmageed, Andreas Herrlich, Akio Kobayashi, Benjamin D. Humphreys

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Human C-terminal CUBN variants associate with chronic proteinuria and normal renal function
Mathilda Bedin, … , Corinne Antignac, Matias Simons
Mathilda Bedin, … , Corinne Antignac, Matias Simons
Published October 15, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI129937.
View: Text | PDF | Corrigendum

Human C-terminal CUBN variants associate with chronic proteinuria and normal renal function

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Abstract

Background: Proteinuria is considered as an unfavorable clinical condition that accelerates renal and cardiovascular disease. However, it is not clear if all forms of proteinuria are damaging. Mutations in CUBN cause Imerslund-Gräsbeck syndrome (IGS) featured by intestinal malabsorption of vitamin B12 and in some cases proteinuria. CUBN encodes for cubilin, an intestinal and proximal tubular uptake receptor containing 27 CUB domains for ligand binding. Methods: We used next-generation sequencing for renal disease genes to genotype cohorts of patients with suspected hereditary renal disease and chronic proteinuria. CUBN variants were analyzed using bioinformatics, structural modeling and epidemiological methods. Results: We identified 39 patients, in whom biallelic pathogenic variants in the CUBN gene are associated with chronic isolated proteinuria with childhood onset. Since the proteinuria displayed a high proportion of albuminuria, glomerular diseases such as steroid-resistant nephrotic syndrome or Alport syndrome were often the primary clinical diagnosis, motivating renal biopsies and proteinuria-lowering treatments. Yet, renal function was normal in all cases. By contrast, we did not find any biallelic pathogenic CUBN variants in patients with reduced renal function or focal segmental glomerulosclerosis. Unlike the more N-terminal IGS mutations, 37 out of the 41 proteinuria-associated CUBN variants led to modifications or truncations after the vitamin B12-binding domain. Finally, we show that four C-terminal CUBN variants are associated with albuminuria and moderately increased GFR in meta-analyses of large population-based cohorts. Conclusions: Collectively, our data suggest an important role for the C-terminal half of cubilin in renal albumin reabsorption. Albuminuria due to reduced cubilin function could be an unexpectedly common benign condition in humans that may not require any proteinuria-lowering treatment or renal biopsies.

Authors

Mathilda Bedin, Olivia Boyer, Aude Servais, Yong Li, Laure Villoing-Gaudé, Marie-Josephe Tête, Alexandra Cambier, Julien Hogan, Veronique Baudouin, Saoussen Krid, Albert Bensman, Florie Lammens, Ferielle Louillet, Bruno Ranchin, Cecile Vigneau, Iseline Bouteau, Corinne Isnard-Bagnis, Christoph J. Mache, Tobias Schäfer, Lars Pape, Markus Gödel, Tobias B. Huber, Marcus Benz, Günter Klaus, Matthias Hansen, Kay Latta, Olivier Gribouval, Vincent Morinière, Carole Tournant, Maik Grohmann, Elisa Kuhn, Timo Wagner, Christine Bole-Feysot, Fabienne Jabot-Hanin, Patrick Nitschké, Tarunveer S. Ahluwalia, Anna Köttgen, Christian Brix Folsted Andersen, Carsten Bergmann, Corinne Antignac, Matias Simons

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Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses
Seiji Kishi, … , Ryuji Morizane, Joseph V. Bonventre
Seiji Kishi, … , Ryuji Morizane, Joseph V. Bonventre
Published October 7, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI122313.
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Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses

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Maladaptive proximal tubule (PT) repair has been implicated in kidney fibrosis through induction of cell-cycle arrest at G2/M. We explored the relative importance of the PT DNA damage response (DDR) in kidney fibrosis by genetically inactivating ataxia telangiectasia and Rad3-related (ATR), which is a sensor and upstream initiator of the DDR. In human chronic kidney disease, ATR expression inversely correlates with DNA damage. ATR was upregulated in approximately 70% of Lotus tetragonolobus lectin–positive (LTL+) PT cells in cisplatin-exposed human kidney organoids. Inhibition of ATR resulted in greater PT cell injury in organoids and cultured PT cells. PT-specific Atr-knockout (ATRRPTC–/–) mice exhibited greater kidney function impairment, DNA damage, and fibrosis than did WT mice in response to kidney injury induced by either cisplatin, bilateral ischemia-reperfusion, or unilateral ureteral obstruction. ATRRPTC–/– mice had more cells in the G2/M phase after injury than did WT mice after similar treatments. In conclusion, PT ATR activation is a key component of the DDR, which confers a protective effect mitigating the maladaptive repair and consequent fibrosis that follow kidney injury.

Authors

Seiji Kishi, Craig R. Brooks, Kensei Taguchi, Takaharu Ichimura, Yutaro Mori, Akinwande Akinfolarin, Navin Gupta, Pierre Galichon, Bertha C. Elias, Tomohisa Suzuki, Qian Wang, Leslie Gewin, Ryuji Morizane, Joseph V. Bonventre

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Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule
Fei Deng, … , Ming Yang, Yashpal S. Kanwar
Fei Deng, … , Ming Yang, Yashpal S. Kanwar
Published August 22, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI129903.
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Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule

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Abstract

Overexpression of myo-inositol oxygenase (MIOX), a proximal tubular enzyme, exacerbates cellular redox injury in acute kidney injury (AKI). Ferroptosis, a newly coined term associated with lipid hydroperoxidation, plays a critical role in the pathogenesis of AKI. Whether or not MIOX exacerbates tubular damage by accelerating ferroptosis in Cisplatin-induced AKI remains elusive. Cisplatin-treated HK-2 cells exhibited notable cell death, which was reduced by ferroptosis inhibitors. Also, alterations in various ferroptosis metabolic sensors, including lipid hydroperoxidation, glutathione peroxidase 4 (GPX4) activity, NADPH and reduced glutathione (GSH) levels, and ferritinophagy, were observed. These perturbations were accentuated by MIOX overexpression, while ameliorated by MIOX knockdown. Likewise, Cisplatin-treated CD1 mice exhibited tubular damage and derangement of renal physiological parameters, which was alleviated by Ferrostatin-1 (Fer-1), a ferroptosis inhibitor. To investigate the relevance of MIOX to ferroptosis, Wild-type (WT) mice, MIOX-overexpressing transgenic (MIOX-TG) mice and MIOX knockout (MIOX-KO) mice were subjected to Cisplatin treatment. In comparison to Cisplatin-treated WT mice, Cisplatin-treated MIOX-TG mice had more severe renal pathological changes and perturbations in ferroptosis metabolic sensors, which were minimal in Cisplatin-treated MIOX-KO mice. In conclusion, these findings indicate that ferroptosis, an integral process in the pathogenesis of Cisplatin-induced AKI, is modulated by the expression profile of MIOX.

Authors

Fei Deng, Isha Sharma, Yingbo Dai, Ming Yang, Yashpal S. Kanwar

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The archaeal Dps nanocage targets kidney proximal tubules via glomerular filtration
Masaki Uchida, … , Trevor Douglas, Takashi Hato
Masaki Uchida, … , Trevor Douglas, Takashi Hato
Published August 19, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI127511.
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The archaeal Dps nanocage targets kidney proximal tubules via glomerular filtration

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Abstract

Nature exploits cage-like proteins for a variety of biological purposes, from molecular packaging and cargo delivery to catalysis. These cage-like proteins are of immense importance in nanomedicine due to their propensity to self-assemble from simple identical building blocks to highly ordered architecture and the design flexibility afforded by protein engineering. However, delivery of protein nanocages to the renal tubules remains a major challenge because of the glomerular filtration barrier, which effectively excludes conventional size nanocages. Here, we show that DNA-binding protein from starved cells (Dps) — the extremely small archaeal antioxidant nanocage — is able to cross the glomerular filtration barrier and is endocytosed by the renal proximal tubules. Using a model of endotoxemia, we present an example of the way in which proximal tubule–selective Dps nanocages can limit the degree of endotoxin-induced kidney injury. This was accomplished by amplifying the endogenous antioxidant property of Dps with addition of a dinuclear manganese cluster. Dps is the first-in-class protein cage nanoparticle that can be targeted to renal proximal tubules through glomerular filtration. In addition to its therapeutic potential, chemical and genetic engineering of Dps will offer a nanoplatform to advance our understanding of the physiology and pathophysiology of glomerular filtration and tubular endocytosis.

Authors

Masaki Uchida, Bernhard Maier, Hitesh Kumar Waghwani, Ekaterina Selivanovitch, S. Louise Pay, John Avera, EJun Yun, Ruben M. Sandoval, Bruce A. Molitoris, Amy Zollman, Trevor Douglas, Takashi Hato

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Calcium channel Orai1 promotes lymphocyte IL17 expression and progressive kidney injury
Purvi Mehrotra, … , Javier A. Neyra, David P. Basile
Purvi Mehrotra, … , Javier A. Neyra, David P. Basile
Published August 15, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI126108.
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Calcium channel Orai1 promotes lymphocyte IL17 expression and progressive kidney injury

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Abstract

We hypothesized that the store operated calcium entry (SOCE) channel, Orai1, participates in the activation of T-helper (Th17) cells and influences renal injury. In rats following renal ischemia/reperfusion (I/R), there was a rapid and sustained influx of Orai1+ CD4 T-cells and IL17 expression was restricted to Orai1-positive cells. When kidney CD4+ cells of post-AKI rats were stimulated with angiotensin II and elevated Na+ (10-7M/170 mM) in vitro, there was an enhanced response in intracellular Ca2+ and IL17 expression, which was blocked by SOCE inhibitors 2APB, YM58483/BTP2, or AnCoA4. In vivo, YM58343/BTP2 (1 mg ∙ kg-1) attenuated IL17+ cell activation, inflammation and severity of AKI following either I/R or intramuscular glycerol injection. Rats treated with high-salt diet (5-9 weeks post I/R) manifested progressive disease indicated by enhanced inflammation, fibrosis and impaired renal function. These responses were significantly attenuated by YM58343/BTP2. In peripheral blood of critically ill patients, Orai1+ cells were significantly elevated by ~10-fold and Th17 cells were elevated by ~4 fold in AKI vs non-AKI patients. Further, in vitro stimulation of CD4+ cells from AKI patients increased IL17, which was blocked by SOCE inhibitors. These data suggest that Orai1 SOCE is a potential therapeutic target in AKI and CKD progression.

Authors

Purvi Mehrotra, Michael Sturek, Javier A. Neyra, David P. Basile

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Crystal deposition triggers tubule dilation that accelerates cystogenesis in polycystic kidney disease
Jacob A. Torres, … , Michal Mrug, Thomas Weimbs
Jacob A. Torres, … , Michal Mrug, Thomas Weimbs
Published July 30, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI128503.
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Crystal deposition triggers tubule dilation that accelerates cystogenesis in polycystic kidney disease

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The rate of disease progression in autosomal-dominant (AD) polycystic kidney disease (PKD) exhibits high intra-familial variability suggesting that environmental factors may play a role. We hypothesized that a prevalent form of renal insult may accelerate cystic progression and investigated tubular crystal deposition. We report that calcium oxalate (CaOx) crystal deposition led to rapid tubule dilation, activation of PKD-associated signaling pathways, and hypertrophy in tubule segments along the affected nephrons. Blocking mTOR signaling blunted this response and inhibited efficient excretion of lodged crystals. This mechanism of “flushing out” crystals by purposefully dilating renal tubules has not previously been recognized. Challenging PKD rat models with CaOx crystal deposition, or inducing calcium phosphate deposition by increasing dietary phosphorous intake, led to increased cystogenesis and disease progression. In a cohort of ADPKD patients, lower levels of urinary excretion of citrate, an endogenous inhibitor of calcium crystal formation, correlated with increased disease severity. These results suggest that PKD progression may be accelerated by commonly occurring renal crystal deposition which could be therapeutically controlled by relatively simple measures.

Authors

Jacob A. Torres, Mina Rezaei, Caroline Broderick, Louis Lin, Xiaofang Wang, Bernd Hoppe, Benjamin D. Cowley, Jr., Vincenzo Savica, Vicente E. Torres, Saeed Khan, Ross P. Holmes, Michal Mrug, Thomas Weimbs

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ATP-binding cassette A1 deficiency causes cardiolipin-driven mitochondrial dysfunction in podocytes
G. Michelle Ducasa, … , Flavia Fontanesi, Alessia Fornoni
G. Michelle Ducasa, … , Flavia Fontanesi, Alessia Fornoni
Published July 22, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI125316.
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ATP-binding cassette A1 deficiency causes cardiolipin-driven mitochondrial dysfunction in podocytes

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Abstract

Fibroblasts from patients with Tangier disease carrying ATP-binding cassette A1 (ABCA1) loss-of-function mutations are characterized by cardiolipin accumulation, a mitochondrial-specific phospholipid. Suppression of ABCA1 expression occurs in glomeruli from patients with diabetic kidney disease (DKD) and in human podocytes exposed to DKD sera collected prior to the development of DKD. We demonstrated that siRNA ABCA1 knockdown in podocytes led to reduced oxygen consumption capabilities associated with alterations in the oxidative phosphorylation (OXPHOS) complexes and with cardiolipin accumulation. Podocyte-specific deletion of Abca1 (Abca1fl/fl) rendered mice susceptible to DKD, and pharmacological induction of ABCA1 improved established DKD. This was not mediated by free cholesterol, as genetic deletion of sterol-o-acyltransferase-1 (SOAT1) in Abca1fl/fl mice was sufficient to cause free cholesterol accumulation but did not cause glomerular injury. Instead, cardiolipin mediates ABCA1-dependent susceptibility to podocyte injury, as inhibition of cardiolipin peroxidation with elamipretide improved DKD in vivo and prevented ABCA1-dependent podocyte injury in vitro and in vivo. Collectively, we describe a pathway definitively linking ABCA1 deficiency to cardiolipin-driven mitochondrial dysfunction. We demonstrated that this pathway is relevant to DKD and that ABCA1 inducers or inhibitors of cardiolipin peroxidation may each represent therapeutic strategies for the treatment of established DKD.

Authors

G. Michelle Ducasa, Alla Mitrofanova, Shamroop K. Mallela, Xiaochen Liu, Judith Molina, Alexis Sloan, Christopher E. Pedigo, Mengyuan Ge, Javier Varona Santos, Yanio Hernandez, Jin-Ju Kim, Cyrille Maugeais, Armando J. Mendez, Viji Nair, Matthias Kretzler, George W. Burke, Robert G. Nelson, Yu Ishimoto, Reiko Inagi, Santanu Banerjee, Shaoyi Liu, Hazel H. Szeto, Sandra Merscher, Flavia Fontanesi, Alessia Fornoni

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Drp1S600 phosphorylation regulates mitochondrial fission and progression of nephropathy in diabetic mice
Daniel L. Galvan, … , Paul Overbeek, Farhad R. Danesh
Daniel L. Galvan, … , Paul Overbeek, Farhad R. Danesh
Published May 7, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI127277.
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Drp1S600 phosphorylation regulates mitochondrial fission and progression of nephropathy in diabetic mice

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Abstract

Phosphorylation of Dynamin-related protein1 (Drp1) represents an important regulatory mechanism for mitochondrial fission. Here we established the role of Drp1 Serine 600 (S600) phosphorylation on mitochondrial fission in vivo, and assessed the functional consequences of targeted elimination of the Drp1S600 phosphorylation site in progression of diabetic nephropathy (DN). We generated a knockin mouse in which S600 was mutated to alanine (Drp1S600A). We found that diabetic Drp1S600A mice exhibited improved biochemical and histological features of DN along with reduced mitochondrial fission and diminished mitochondrial ROS in vivo. Importantly, we observed that the effect of Drp1S600 phosphorylation on mitochondrial fission in the diabetic milieu was stimulus- but not cell type-dependent. Mechanistically, we showed that mitochondrial fission in high glucose conditions occurs through concomitant binding of phospho-Drp1S600 with mitochondrial fission factor (Mff) and actin-related protein 3 (Arp3), ultimately leading to accumulation of F-actin and Drp1 on the mitochondria. Taken together, these findings establish that a single phosphorylation site in Drp1 can regulate mitochondrial fission and progression of DN in vivo, and highlight the stimulus-specific consequences of Drp1S600 phosphorylation on mitochondrial dynamics.

Authors

Daniel L. Galvan, Jianyin Long, Nathanael Green, Benny H. Chang, Jamie S. Lin, Paul T. Schumacker, Luan D. Truong, Paul Overbeek, Farhad R. Danesh

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Immunoglobulin light chains generate pro-inflammatory and pro-fibrotic kidney injury
Wei-Zhong Ying, … , Lisa M. Curtis, Paul W. Sanders
Wei-Zhong Ying, … , Lisa M. Curtis, Paul W. Sanders
Published April 16, 2019
Citation Information: J Clin Invest. 2019. https://doi.org/10.1172/JCI125517.
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Immunoglobulin light chains generate pro-inflammatory and pro-fibrotic kidney injury

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Abstract

Because of the less than robust response to therapy and impact on choice of optimal chemotherapy and prognosis, chronic kidney disease has drawn attention in the treatment of multiple myeloma, a malignant hematologic disorder that can produce significant amounts of monoclonal immunoglobulin free light chains. These low molecular weight proteins are relatively freely filtered through the glomerulus and are reabsorbed by the proximal tubule. The present study demonstrated that during the process of metabolism of immunoglobulin free light chains, reactive oxygen species activated the Signal Transducer and Activator of Transcription 1 (STAT1) pathway in proximal tubule epithelium. STAT1 activation served as the seminal signaling molecule that produced the pro-inflammatory molecule, Interleukin-1β, as well as the pro-fibrotic agent, Transforming Growth Factor-β, by this portion of the nephron. These effects occurred in vivo and were produced specifically by the generation of hydrogen peroxide by the VL domain of the light chain. To the extent that the experiments reflect the human condition, these studies offered new insights into the pathogenesis of progressive kidney failure in the setting of lymphoproliferative disorders, such as multiple myeloma, that feature increased circulating levels of monoclonal immunoglobulin fragments that require metabolism by the kidney.

Authors

Wei-Zhong Ying, Xingsheng Li, Sunil Rangarajan, Wenguang Feng, Lisa M. Curtis, Paul W. Sanders

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Local TNF mediates free cholesterol–dependent podocyte injury
In this episode, Alessia Fornoni reveals that TNF promotes free cholesterol–dependent podocyte apoptosis via an NFATc1/ ABCA1-dependent mechanism.
Published August 2, 2016
Author's TakeNephrology

Anti-THSD7A is a bona fide culprit in membranous nephropathy
Nicola M. Tomas, Elion Hoxha, and colleagues provide evidence that anti-THSD7A antibodies promote the development of membranous nephropathy...
Published May 23, 2016
Scientific Show StopperNephrology

Identifying sporadic focal segmental glomerulosclerosis-associated genes
Haiyang Yu, Mykyta Artomov, Sebastian Brähler and colleagues demonstrate the genetic contribution to the development of focal segmental glomerulosclerosis...
Published February 22, 2016
Scientific Show StopperNephrology

DNA replication stress linked to ciliopathies
Gisela Slaats and colleagues reveal that ciliopathy syndrome-associated mutations in CEP290 result in replication errors and DNA damage…
Published August 24, 2015
Scientific Show StopperNephrology

Nephrotic syndrome-associated mutations
Heon Yung Gee, Fujian Zhang, and colleagues reveal that mutations in KANK family genes underlie podocyte dysfunction and are associated with nephrotic syndrome…
Published May 11, 2015
Scientific Show StopperNephrology

Podocyte macropinocytosis
Jun-Jae Chung, Tobias B. Huber, Markus Gödel, and colleagues show that albumin-bound free fatty acids increase fluid-phase uptake in podocytes…
Published April 27, 2015
Scientific Show StopperNephrology

A network of diuretic resistance
Richard Grimm and colleagues use a systems biology approach to uncover mechanisms of renal compensation that lead to diuretic resistance…
Published April 20, 2015
Scientific Show StopperNephrology

KIM-1 protects the kidney after injury
Li Yang, Craig Brooks, and colleagues at Harvard Medical School demonstrate that KIM-1-mediated phagocytosis of apoptotic cells dampens inflammatory responses after kidney injury.. .
Published March 9, 2015
Scientific Show StopperNephrology

Protection against acute kidney injury
Marina Morigi and colleagues demonstrate that sirtuin 3 expression improves survival in a murine model of acute kidney injury...
Published January 20, 2015
Scientific Show StopperNephrology

Helping polycysin-1 reach the surface
Vladimir Gainullin and colleagues reveal that polycystin-2 is required for maturation and surface localization of polycystin-1…
Published January 9, 2015
Scientific Show StopperNephrology
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