American journal of physiology. Renal physiology最新文献

{"title":"Effects of propofol and sevoflurane anesthesia on renal blood flow and oxygenation during major hemorrhage in pigs.","authors":"Robert Frithiof, Micael Taavo, Arash Emami, Stephanie Franzén","doi":"10.1152/ajprenal.00146.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00146.2025","url":null,"abstract":"<p><p>Hemorrhage and hypotension leading to renal hypoperfusion are common causes of acute kidney injury (AKI). Anesthetic agents may affect renal hemodynamics, potentially altering renal outcomes during hypovolemia. This study evaluated the effects of two commonly used anesthetics, propofol and sevoflurane, on renal blood flow (RBF) and oxygenation during hemorrhage. Fourteen pigs (30 ± 2 kg) were anesthetized with either propofol or sevoflurane, with fentanyl as an opioid supplement in both groups. Following baseline measurements, hemorrhage was induced to maintain a mean arterial pressure (MAP) below 50 mmHg for 30 minutes, after which resuscitation was performed using a 1:1 replacement of whole blood and Ringer's acetate. Acute renal function recovery was evaluated one hour post-resuscitation. At baseline, sevoflurane anesthetized animals had lower RBF and renal oxygen delivery, and higher renal vascular resistance compared with the propofol group. During hemorrhage the change in these variables were comparable. After resuscitation, cardiovascular and RBF recovery was similar between the groups. However, oxygen delivery remained significantly lower in the sevoflurane group compared with the propofol group. Additionally, renal vascular resistance was significantly higher during sevoflurane anesthesia compared with propofol after recovery. In conclusion, compared with propofol anesthesia, sevoflurane anesthesia reduced RBF and renal oxygen delivery already at baseline. The difference in oxygen delivery persisted after hemorrhage even though RBF was comparable between groups.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145056607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electron Paramagnetic Resonance Imaging to Detect Acute Kidney Injury.","authors":"Shun Kishimoto, Kazumasa Horie, Nallathamby Devasahayam, Kota Yamashita, Gadisetti V R Chandramouli, Kazutoshi Yamamoto, Jeffrey R Brender, James B Mitchell, Murali C Krishna, W Marston Linehan, Daniel Crooks","doi":"10.1152/ajprenal.00215.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00215.2025","url":null,"abstract":"<p><p>Renal oxygenation is essential for maintaining kidney function. Disruptions in oxygen delivery can lead to renal hypoxia, which can exacerbate kidney injury through multiple pathways, including inflammation, oxidative stress, and ischemia-reperfusion injury. Despite the recognized importance of oxygenation in renal pathology, non-invasive and reliable methods for assessing kidney oxygen levels are limited. Current techniques either lack sensitivity or involve invasive procedures, restricting their use in routine monitoring. Therefore, there is a pressing need for innovative approaches to map renal oxygenation, particularly in kidney injury. This study evaluated Electron Paramagnetic Resonance (EPR)-based oxygen imaging using the paramagnetic tracer Ox071 to map kidney oxygen levels in mice with cyclophosphamide-induced kidney injury. Urine pO₂ was also assessed as a potential surrogate marker. EPR oximetry accurately measured kidney oxygen distribution, revealing a temporary increase in pO₂ post-injury. Urine oximetry, however, did not reliably reflect changes in kidney oxygenation. Furthermore, EPR oximetry provided high-resolution spatial mapping of oxygen levels within the kidney, allowing for a detailed understanding of the impact of hypoxia on renal tissue. EPR oximetry is a promising, non-invasive tool for monitoring renal oxygenation, offering high-resolution mapping and longitudinal assessment. Its ability to provide detailed information about oxygen distribution within the kidney makes it a valuable tool for studying the pathophysiology of renal diseases and for developing novel therapeutic strategies.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145055428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary K⁺ supplementation restores normal aldosterone level in Na⁺-deprived renal tubule-specific CAP1/Prss8-deficient mice.","authors":"Elodie Ehret, Muriel Auberson, Dongmei Wang, Olivier Staub, Edith Hummler","doi":"10.1152/ajprenal.00224.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00224.2025","url":null,"abstract":"<p><p>We previously reported that Na⁺-deprived mice lacking CAP1/Prss8 in kidney tubules maintained ENaC-mediated sodium balance albeit persistent hypoaldosteronism, hence indicating an uncoupling from aldosterone production. This further suggested an implication of the serine protease CAP1/Prss8 (prostasin) in the crosstalk of the kidney with the adrenal gland that does not express prostasin. When these knockout (Ko) mice were additionally exposed to a high K⁺ diet, plasma K⁺ levels and plasma aldosterone concentrations were normalized and no longer different from the control mice. The mRNA transcript expression of the adrenal aldosterone synthase <i>Cyp11b2</i> that was lower in Na⁺-deprived <i>CAP1/Prss8</i> Ko animals was in the normal range. Plasma aldosterone levels were similar to control animals indicating that K⁺ rescued the hypoaldosteronism in Na⁺-deprived <i>CAP1/Prss8</i> Ko animals. These data suggest that <i>CAP1/Prss8</i> (prostasin) is implicated in the regulation of aldosterone synthesis or production and that the consequences of <i>CAP1/Prss8</i> deficiency can be compensated by high dietary K⁺ supplementation. Prostasin may therefore present a promising regulator of aldosterone production by affecting the adrenal steroidogenic pathway.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145056609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The nuclear export inhibitor selinexor improves kidney function in a rat model of focal segmental glomerulosclerosis.","authors":"Yingying Gao, Mohamed Hamed, Ina Verena Martin, Ute Raffetseder, Xiyang Liu, Anna Leitz, Marcus J Moeller, Eleni Stamellou, Ramona Jühlen, Angela Schulz, Reinhold Kreutz, Jürgen Floege, Rafael Kramann, Wolfram Antonin, Tammo Ostendorf","doi":"10.1152/ajprenal.00143.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00143.2025","url":null,"abstract":"<p><p>Focal segmental glomerulosclerosis (FSGS) is a common glomerular pathology characterized by podocyte injury, which can lead to kidney failure. Among the factors contributing to podocyte damage are mutations in nuclear pore complexes (NPCs), which regulate nuclear-cytoplasmic transport of proteins and RNAs. Defective NPCs can accumulate in highly differentiated, non-dividing cells such as podocytes. However, their role in podocyte dysfunction is largely unexplored, particularly as a potential therapeutic target. To address this, we investigated the effects of selinexor (KPT-330), a drug that inhibits XPO1-mediated nuclear-cytoplasmic protein export. In HeLa cells, KPT-330 restored compromised NPC function. Munich Wistar Froemter (MWF) rats, a model for spontaneous FSGS development, aged 10 weeks, were treated with KPT-330 for 10 weeks and then observed for another 20 weeks. Improvements in kidney function were observed at the end of the 10-week treatment period, with serum creatinine significantly lower in the KPT-330 group (34.11±1.77 μmol/L) versus the vehicle group (39.25±3.54 μmol/L, P<0.01). Serum cystatin C levels remained lower in the KPT-330 group (3.62±0.39 μg/ml) versus vehicle (4.19±0.44 μg/ml, P<0.05) after additional 20 weeks without treatment. Hyperlipidemia was significantly reduced immediately after the end of the 10-week KPT-330 treatment compared to vehicle (triglyceride, 1.23±0.34 mmol/L vs. 1.92±0.4 mmol/L, P<0.01; total cholesterol, 1.47±0.08 mmol/L vs. 2.96±0.44 mmol/L, P<0.0001). However, histopathological parameters, including glomerulosclerosis, podocyte numbers, and activation of parietal epithelial cells, showed that kidney damage continued to progress. Thus, KPT-330 has beneficial effects on kidney function, but was not sufficient to halt histological progression of glomerular damage.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SerpinE2 deficiency exacerbates glomerular Injury in diabetic nephropathy through dysregulated angiogenesis and inflammatory responses.","authors":"Leila Idir, Junjie Yu, Philippe Bonnin, Benjamin Richard, Stéphane Loyau, Yacine Boulaftali, Marie-Christine Bouton, Véronique Arocas","doi":"10.1152/ajprenal.00193.2025","DOIUrl":"10.1152/ajprenal.00193.2025","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is a multifactorial disease in which inflammation and angiogenesis play a crucial role. SerpinE2, or protease nexin-1 (PN-1), is a protease inhibitor of the serpin family, expressed by vascular and inflammatory cells. In this study, we addressed the role of SerpinE2 in DN, using the models of streptozotocin-induced type-1 and db/db type-2 diabetes. Our results indicated that SerpinE2^-/- diabetic mice presented histological features of an aggravated nephropathy compared to wild-type (WT) mice, with higher hypertrophy of glomeruli, greater collagen IV accumulation and reduced nephrin expression. Moreover, renal function was worsened in SerpinE2^-/- diabetic mice with urine albumin to creatinine ratio much higher compared to WT. Consistent with the previously demonstrated anti-angiogenic properties of SerpinE2, we observed that glomerular vascularization was higher in SerpinE2^-/- than in WT- diabetic mice in early type-1 diabetes, associated with increased proliferation of glomerular cells. Accordingly, renal blood flow reduction in response to diabetes was lower in SerpinE2^-/- than in WT mice. In addition, we measured higher mRNA levels of inflammatory cytokines and of midkine in diabetic SerpinE2^-/- kidneys compared to WT. Altogether, our results indicate that SerpinE2 may play a protective role in the development of DN by limiting glomerular damage throughout regulation of early process in angiogenesis and inflammation.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The organelle tethering protein PDZD8 regulates endolysosomal maturation and TLR9-NF-κB signaling in cisplatin-induced acute kidney injury.","authors":"Yuto Takenaka, Hiroshi Maekawa, Yu Ah Hong, Midori Sakashita, Qi Li, Chigusa Kitayama, Koki Nakamura, Madina Saipidin, Jin Shang, Yusuke Hirabayashi, Masaomi Nangaku, Reiko Inagi","doi":"10.1152/ajprenal.00020.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00020.2025","url":null,"abstract":"<p><p>Acute kidney injury (AKI) is a life-threatening condition with high morbidity and mortality, characterized by inflammation linked to organelle stress. Despite its clinical significance, effective therapies remain limited. While organelle dysfunction is recognized as a driver of inflammation in AKI, the role of inter-organelle communication in this process remains poorly understood. PDZD8, a tethering protein on the endoplasmic reticulum (ER), facilitates ER-endolysosome contact that is essential for endolysosomal maturation. The mature endolysosome is a prerequisite for activating the DNA-sensing innate immune receptor, Toll-like receptor 9 (TLR9). Here, we investigated the role of PDZD8 in the TLR9-NF-κB pathway during AKI using <i>Pdzd8</i> knockout (KO) mice and <i>in vitro</i> knockdown in human proximal tubular cells (PTCs). <i>Pdzd8</i> KO mice showed reduced severity of cisplatin-induced AKI and reduced activation of the NF-κB pathway. Mechanistically, PDZD8 knockdown in PTCs impaired endolysosomal maturation and acidification. This functional disruption impeded the proper translocation of TLR9 to endolysosomes, thereby inhibiting the signaling cascade leading to NF-κB activation. Notably, PDZD8 knockdown did not alter mitochondrial morphology or the cytosolic leakage of mitochondrial DNA, an endogenous ligand for TLR9. These findings indicate that PDZD8 is crucial for maintaining endolysosomal homeostasis and regulating the TLR9-NF-κB pathway in cisplatin-induced tubular injury.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous Uromodulin and Tubular Responses in a Model of Oxalate-Induced Kidney Injury.","authors":"Larissa de Araújo, Neydiana Pina-Lopes, Beatriz Costa Silvestre Pereira, Juliana Martins da Costa-Pessoa, Maria Oliveira-Souza","doi":"10.1152/ajprenal.00164.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00164.2025","url":null,"abstract":"<p><p>Crystalline nephropathies are associated with kidney injury. Uromodulin (Umod), a glycoprotein produced in the kidneys, regulates salt transport, protecting against urinary tract infections, kidney stones, and kidney injury, contributing to innate immunity. After cleavage by the protease hepsin, Umod is secreted into the tubular lumen. We hypothesize that exogenous Umod may reduce injury associated with crystalline nephropathy. Both <i>in vivo</i> and <i>in vitro</i> models were used. Eight-week-old C57BL/6J male mice were treated with sodium oxalate (NaOx, 9 mg/100 g body weight) and/or Umod (5 μg/animal) and compared to controls. The ST-1cell line (mouse thick ascending limb of loop of Henle) was treated with CaOx (200 μg/mL) for 6 or 24 hours and compared with controls. NaOx treatment caused tubular injury and upregulated pro-inflammatory and pro-fibrotic factors. Exogenous Umod attenuated NaOx-induced kidney injury. <i>In vitro</i>, CaOx treatment decreased Umod expression and induced apoptosis in ST-1 cells, confirmed by elevated caspase-8 immunostaining, while Umod reduced the apoptotic response. This study demonstrates that Umod co-treatment attenuated several aspects of NaOx-induced kidney injury. These findings suggest that the multifunctional nature of Umod may have clinical relevance and support the potential utility of urinary Umod as a biomarker of kidney health.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLVAP: the new villain in glomerular endothelial cell injury.","authors":"Stella Alimperti, Moshe Levi","doi":"10.1152/ajprenal.00050.2025","DOIUrl":"10.1152/ajprenal.00050.2025","url":null,"abstract":"","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F323-F324"},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143784652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the endocannabinoid system to suppress mTORC1 hyperactivation in TSC-associated kidney disease.","authors":"Eden Abergel, Hadass Pri-Chen, Shulamit Wallach-Dayan, Liad Hinden, Joseph Tam, Oded Volovelsky, Morris Nechama","doi":"10.1152/ajprenal.00097.2025","DOIUrl":"10.1152/ajprenal.00097.2025","url":null,"abstract":"<p><p>Tuberous sclerosis complex (TSC) promotes renal cyst formation and chronic kidney disease through mechanistic target of rapamycin complex 1 (mTORC1) dysregulation, yet effective treatments remain limited. Using mouse models with <i>Tsc1</i> deletion in nephron progenitor cells and CRISPR-edited human kidney cells, we assessed the role of the endocannabinoid system in TSC-associated kidney disease. <i>Tsc1</i> deletion led to significant alterations in endocannabinoid levels and the expression of metabolizing enzymes. These molecular changes were accompanied by receptor dysregulation, characterized by CB1R upregulation and CB2R downregulation in cyst-lining epithelial cells. A similar receptor imbalance was observed in <i>TSC1</i>-deficient human kidney cells, suggesting a conserved pathogenic mechanism. Treatment with the peripheral CB1R antagonist JD5037 significantly reduced mTORC1 activity and c-Myc expression in cultured cells and ex vivo kidney organ cultures. These findings identified CB1R as a potential therapeutic target, linking endocannabinoid dysregulation to TSC kidney pathology.<b>NEW & NOTEWORTHY</b> This study reveals for the first time that TSC-associated kidney disease involves significant dysregulation of the endocannabinoid system in both murine models and human kidneys, characterized by altered endocannabinoid levels, enzyme expression changes, CB1R upregulation, and CB2R downregulation in cyst-lining epithelial cells. Treatment with the peripheral CB1R antagonist effectively suppressed mTORC1 hyperactivation and c-Myc expression, identifying CB1R as a novel therapeutic target for TSC-associated renal pathology.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F325-F334"},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The nephronophthisis protein <i>GLIS2</i>/<i>NPHP7</i> is required for the DNA damage response in kidney tubular epithelial cells.","authors":"Lena K Ebert, Lukas Schloesser, Laura E Frech, Manaswita Jain, Claudia Dafinger, Max C Liebau, Thomas Benzing, Bernhard Schermer, Gisela G Slaats","doi":"10.1152/ajprenal.00076.2025","DOIUrl":"10.1152/ajprenal.00076.2025","url":null,"abstract":"<p><p>Nephronophthisis (NPH) is an autosomal-recessive cystic kidney disease representing the most frequent genetic cause of end-stage kidney failure in children and adolescents. NPH is caused by genetic variants in >20 NPHP genes. Although nearly all NPHP genes encode ciliary proteins, classifying NPH as a renal ciliopathy, there is evidence for a pathogenic role of a compromised DNA damage response (DDR). Here, we present a novel <i>Nphp7/Glis2</i>-deficient mouse model with an early stop codon using CRISPR/Cas9-mediated genome editing (<i>Glis2</i>^Y122X). Homozygous mice displayed dilated kidney tubules progressing to cystic kidney disease with significant fibrosis at a higher age. Interestingly, the kidneys of these animals exhibited an accumulation of DNA damage (DD) early on, even before any functional impairment of the kidneys became apparent. Interactome analysis for GLIS2 revealed an array of DDR-related proteins within the GLIS2 protein complex. Consistent with the in vivo data, the knockdown of <i>Glis2</i> in kidney epithelial cells led to increased DNA damage. Moreover, supporting the role of GLIS2 in the DDR, we demonstrate that a substantial proportion of GLIS2 is present within the chromatin fraction of cells, which is further increased upon UV-induced DD. Live-cell imaging revealed the rapid recruitment of green fluorescent protein (GFP)-tagged GLIS2 to sites of laser-induced DD, a response diminished in Glis2^Y122X and a variant of Glis2 resembling a known patient mutation. Overall, our data provide compelling evidence for the direct involvement of GLIS2 in the DDR, highlighting the loss of genome stability as an important factor contributing to the pathogenesis of renal ciliopathies.<b>NEW & NOTEWORTHY</b> Nephronophthisis (NPH) is a pediatric cystic kidney disease and ciliopathy. We present a novel <i>Glis2/Nphp7</i>-deficient mouse model that shows early accumulation of DNA damage before detectable kidney dysfunction. The GLIS2 protein complex includes DNA damage response factors. GLIS2 localizes to chromatin and rapidly relocates to sites of DNA damage. These findings position GLIS2 as a direct player in genome stability, highlighting impaired DDR as a key contributor to NPH pathogenesis.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F335-F346"},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}