American journal of physiology. Renal physiology最新文献

{"title":"PLVAP: the new villain in glomerular endothelial cell injury.","authors":"Stella Alimperti, Moshe Levi","doi":"10.1152/ajprenal.00050.2025","DOIUrl":"https://doi.org/10.1152/ajprenal.00050.2025","url":null,"abstract":"","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-04","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":"Prevention of hypertension-induced renal vascular dysfunction through a p66Shc targeted mechanism.","authors":"Bradley Miller, John D Imig, Mengjie Li, Perrin Schupbach, Sukyung Woo, Doris M Benbrook, Andrey Sorokin","doi":"10.1152/ajprenal.00331.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00331.2024","url":null,"abstract":"<p><p>Renal microvascular injury occurs in most patients with hypertension-induced nephropathy (HN). We have shown that overexpression of adaptor protein p66Shc is implicated in the loss of renal microvascular reactivity in hypertensive rats. Since sulfur heteroarotinoid A2 (SHetA2) modulates p66Shc, we tested whether SHetA2 would restore renal microvascular reactivity and mitigate kidney injury in a rat HN model. Dahl salt sensitive and p66Shc knockout (p66Shc-KO) rats were used in a well-established rat model of HN, characterized by severe renal vascular dysfunction. SHetA2 was either added acutely to isolated rat afferent arterioles or chronically administrated to rats during HN development. The ability of SHetA2 treatment to restore afferent arteriolar contraction in response to increased perfusion pressure or ATP was evaluated using the perfused juxtamedullary nephron preparation. The progression of renal damage was evaluated by measuring urinary protein excretion and conducting analysis of glomerular injury. Comparison of renal microvascular responses to perfusion pressure in p66Shc-KO rats, and parental SS rats, in the presence and absence of acute preincubation with SHetA2, revealed dose-dependent ability of SHetA2 to restore renal microvascular reactivity in SS rats with little effect upon p66Shc knockouts. Moreover, chronic treatment with SHetA2 prevented loss of renal microvascular responses and decline in renal function. SHetA2 was more potent and effective in males compared to females. Targeting p66Shc with SHetA2 diminishes renal damage and restores renal afferent arteriolar reactivity caused by hypertension. These results justify further translation of these findings to develop SHetA2 for prevention and treatment of hypertension-induced kidney damage.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766032","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 role of IGFBP-1 in the clinical prognosis and pathophysiology of acute kidney injury\".","authors":"Joseph Hunter Holthoff, Nithin Karakala, Alexei G Basnakian, Ricky D Edmondson, Todd Fite, Neriman Gokden, Yanping Harville, Christian Herzog, Kaegan G Holthoff, Luis A Juncos, Katlyn L Reynolds, Randall S Shelton, John M Arthur","doi":"10.1152/ajprenal.00173.2024","DOIUrl":"https://doi.org/10.1152/ajprenal.00173.2024","url":null,"abstract":"<p><p><b>Introduction:</b> The ability to predict progression to severe acute kidney injury (AKI) remains an unmet challenge. Contributing to the inability to predict the course of AKI is a void of understanding of the pathophysiological mechanisms of AKI. The identification of novel prognostic biomarkers could both predict patient outcomes and unravel the molecular mechanisms of AKI. <b>Methods:</b> We performed a multicenter retrospective observational study from a cohort of patients following cardiac surgery. We identified novel urinary prognostic biomarkers of severe AKI among subjects with early AKI. Of 2,065 proteins identified in the discovery cohort, insulin-like growth factor binding protein 1 (IGFBP-1) was the most promising. We validated IGFBP-1 as a prognostic biomarker of AKI in 213 patients. Additionally, we investigated its role in the pathophysiology of AKI using a murine model of cisplatin-induced AKI (CIAKI). <b>Results:</b> Urinary IGFBP-1 concentration in samples collected from patients that developed stage 1 AKI following cardiothoracic surgery were significantly higher in patients that progressed to severe AKI compared to patients that did not progress to beyond stage 1 AKI (40.28 ng/mg vs 2.8 ng/mg, p<0.0001) and predicted the progression to the composite outcome (AUC: 0.85, p< 0.0001). IGFBP-1 knockout (KO) mice showed less renal injury, cell death, and apoptosis following CIAKI, possibly through increased activation of the insulin growth factor receptor 1 (IGF-1r). <b>Conclusions:</b> IGFBP-1 is a clinical prognostic biomarker of AKI, and a direct mediator of the pathophysiology of AKI. Therapies that target the IGFBP-1 pathways may help alleviate the severity of AKI.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765926","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":"TNF inhibits NKCC2 phosphorylation by a calcineurin-dependent pathway.","authors":"Shoujin Hao, Anna Pia Lasaracina, Jarred Epps, Nicholas R Ferreri","doi":"10.1152/ajprenal.00251.2024","DOIUrl":"10.1152/ajprenal.00251.2024","url":null,"abstract":"<p><p>We previously demonstrated that tumor necrosis factor-alpha (TNF) inhibits Na⁺-K⁺-2Cl^- cotransporter (NKCC2) phosphorylation in the thick ascending limb (TAL); however, the underlying mechanism remains unclear. We tested the hypothesis that the induction of calcineurin (CN) activity and the expression of CN isoforms contribute to the mechanism by which TNF inhibits phospho-NKCC2 (pNKCC2) expression. CN activity increased by approximately twofold in primary cultures of medullary (m)TAL cells challenged with mouse recombinant TNF. In contrast, silencing TNF production in mTAL cells using lentivirus U6-TNF-ex4 reduced CN activity. pNKCC2 expression decreased in mTAL cells challenged with TNF, whereas inhibition of CN activity with cyclosporine A (CsA) increased pNKCC2 expression. Although mTAL cells express both the calcineurin A subunit (CNA) α and β isoforms, only CNA β isoform mRNA increased after mTAL cells were challenged with TNF. In vivo, both TNF and CNA β expression increased in outer medulla (OM) from mice given 1% NaCl in the drinking water for 7 days and intrarenal lentivirus silencing of TNF selectively reduced expression of CNA β. Intrarenal injection of a lentivirus that specifically silenced CNA β (U6-CNAβ-ex6) increased pNKCC2 expression and attenuated the inhibitory effects of TNF on pNKCC2 expression in freshly isolated TAL tubules. Collectively, the study is the first to demonstrate that TNF increases CN activity and specifically induces β-isoform expression in the kidney. Since NKCC2 is a known target of the CNA β isoform, these findings suggest that a CN-dependent signaling pathway involving this isoform contributes to the mechanism by which TNF inhibits pNKCC2 expression.<b>NEW & NOTEWORTHY</b> The beneficial immunosuppressive effects of CsA are tempered by renal side effects including reduction of GFR, proximal tubule damage, reduced urinary concentration, fibrosis and hypertension. As chronic administration of CN inhibitors frequently induce hypertension and renal nephropathy in humans, understanding the molecular mechanisms by which CN isoforms regulate the activity of renal transporters may provide the framework for developing new drugs that more selectively modulate the diverse functions of CN.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F489-F500"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588749","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":"Lysine acetylation of aquaporin-3 promotes water permeability but is not essential for urine concentrating ability.","authors":"Nha V Huynh, Luciano D Mendoza, Hung Nguyen, Cassidy Rehage, Elizabeth B Saurage, Parker Davis, Kelly A Hyndman","doi":"10.1152/ajprenal.00037.2025","DOIUrl":"10.1152/ajprenal.00037.2025","url":null,"abstract":"<p><p>Aquaporin-3 (AQP3) mediates basolateral water transport in the kidney principal cells contributing to urine concentration. We previously identified the acetylation of lysine 282 (K282) in the C-terminus of AQP3, which we hypothesized as a positive regulator of AQP3 water permeability. AQP3 acetylation (K282Q or Q) or deacetylation (K282R or R) mimetic mutant mice models were created using CRISPR/Cas9. Male and female wild-type (WT) and mutant mice were assigned to hydrating diets and water deprivation protocols. Urine and plasma osmolality in response to acute vasopressin receptor-2 activation with desmopressin (dDAVP) or inhibition by tolvaptan were determined. In vitro water permeability of murine principal kidney cortical collecting duct (mpkCCD) cells stably expressing AQP3 WT, Q, or R was measured. Acetylated AQP3 was prominent in the cortical to inner medullary collecting ducts of dehydrated versus hydrated mice. At baseline, the mutations did not affect the kidney transcriptome, AQP3 abundance, or subcellular localization. Urine osmolality of the mutant mice was within the normal range. With dehydration, all mice excreted concentrated urine; however, the female Q mutants exhibited significantly greater 24-h urine osmolality than WT, suggesting greater water reabsorption. In response to acute dDAVP, all mice produced concentrated urine; however, female Q mutants had a more dilute plasma than WT, further suggesting greater water retention. mpkCCD Q mutant cells exhibited greater water permeability than WT and R cells. We conclude that AQP3 K282 acetylation promotes principal cell water permeability in a sex-dependent manner; however, it is not essential for urine concentration.<b>NEW & NOTEWORTHY</b> The water channel, AQP3, is lysine 282 acetylated (acAQP3) in rodents and humans. When dehydrated, mouse cortical to inner medullary collecting ducts express acAQP3, suggesting that it promotes water reabsorption. acAQP3 expressing principal cells have high water permeability, and in vivo acute desmopressin resulted in a dilute plasma in female acAQP3 mice. However, all mice produced concentrated urine during water deprivation. Thus, acAQP3 promotes water permeability but is not essential for urine concentration during antidiuresis.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F517-F529"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588743","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":"HMGB1 drives T-cell activation in hypertensive males and females.","authors":"Elizabeth C Snyder, Riyaz Mohamed, Jennifer C Sullivan","doi":"10.1152/ajprenal.00197.2024","DOIUrl":"10.1152/ajprenal.00197.2024","url":null,"abstract":"<p><p>We previously published that hypertensive males have greater renal necrosis and a more pro-inflammatory immune profile than females. Hypertension causes the release of damage-associated molecular patterns (DAMPs), which stimulate inflammation. The goal of the current study was to determine if high-mobility group box 1 (HMGB1), a well-characterized DAMP, contributes to greater T-cell activation in hypertensive males versus females and normotensive controls of both sexes. To test this hypothesis, initial studies measured renal and plasma HMGB1 levels in 13-wk-old male and female spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats by Western blot and ELISA. Total renal CD3⁺ T-cells and IL-6⁺ cells were measured by flow cytometry. The contribution of HMGB1 to T-cell activation was measured in isolated renal T-cells via mixed lymphocyte reaction (MLR) in the presence of control IgG or anti-HMGB1 neutralizing antibody. Plasma HMGB1 levels were greater in male SHRs compared with those in female SHR and WKY rats of both sexes. Renal HMGB1 levels were higher in SHR than in WKY and tended to be greater in males versus females in both strains. Consistent with this finding, T-cell activation and renal interleukin (IL)-6 were highest in male SHR. Interestingly, anti-HMGB1 antibody treatment decreased T-cell activation to the same extent in male and female SHRs, with negligible effects on WKY. These results indicate a role for HMGB1 in T-cell activation in SHR. However, despite male SHR having greater levels of HMGB1 than females, HMGB1 does not account for sex differences in T-cell activation.<b>NEW & NOTEWORTHY</b> There is growing evidence that T-cells contribute to both the development of hypertension and sex differences in blood pressure control. Our work establishes the damage-associated molecular pattern HMGB1 as an important contributor to T-cell activation in hypertension.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F445-F451"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469930","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":"Influence of carnosine supplementation on disease progression in a rat model of focal segmental glomerulosclerosis.","authors":"Xin Xu, Diego O Pastene, Jiedong Qiu, Bero Schnell, Tim Maihöfer, Steffen Hettler, Bernhard K Krämer, Sigrid Hoffmann, Benito A Yard","doi":"10.1152/ajprenal.00017.2024","DOIUrl":"10.1152/ajprenal.00017.2024","url":null,"abstract":"<p><p>In diabetic kidney disease models, carnosine supplementation ameliorates renal pathology, but its influence in other renal pathologies is less explored. Thus, using the transgenic rat TGRNeph-hAT1 with sex-dependent focal segmental glomerulosclerosis, we first tested whether renal expression levels of carnosine system components correlate with disease. Next, we assessed whether carnosine supplementation in male rats improves pathology. In 10-wk-old phenotypically healthy male and female TGRNeph-hAT1 rats, we compared the renal expression of components of the carnosine system by qRT-PCR. Next, male TGRNeph-hAT1 rats were supplemented with carnosine in drinking water for 20 wk. Subsequently, urinary parameters, renal histology, and renal gene expression of renin-angiotensin system components were assessed. Male TGRNeph-hAT1 rats exhibited less renal expression of carnosine synthase 1, oligopeptide transporter 2, and taurine transporter and higher carnosinase 1 expression than female TGRNeph-hAT1 rats at a young age, before disease starts to develop. Male, but not female, TGRNeph-hAT1 rats developed severe albuminuria, glomerular hypertrophy, and focal and segmental glomerulosclerosis on aging. Carnosine supplementation ameliorated the glomerular hypertrophy but did not affect albuminuria, renal fibrosis, and podocyte loss. Moreover, carnosine significantly reduced renin and increased angiotensin-converting enzyme 2 expression within the kidney. Carnosine treatment alleviates glomerular hypertrophy in TGRNeph-hAT1 rats but does not improve other renal pathologies. Although amelioration of glomerular hypertrophy might be explained by changes in renal renin-angiotensin system expression, further studies are warranted to assess causality.<b>NEW & NOTEWORTHY</b> In diabetic kidney disease models, carnosine supplementation ameliorates renal pathology, but its influence in other renal pathologies is less explored. We tested whether renal expression levels of carnosine system components correlate with disease in the model of the transgenic rat TGRNeph-hAT1 with sex-dependent focal segmental glomerulosclerosis and whether carnosine supplementation in male rats improves pathology. Our results provide evidence that carnosine feeding affects the glomerular hypertrophy and renal RAS expression.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F599-F607"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143627211","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":"Nicotinamide ameliorates podocyte injury and albuminuria in adriamycin-induced nephropathy.","authors":"Kei Takahashi, Emiko Sato, Seiko Yamakoshi, Mizuki Ogane, Akiyo Sekimoto, Takamasa Ishikawa, Kiyomi Kisu, Yuji Oe, Koji Okamoto, Mariko Miyazaki, Tetsuhiro Tanaka, Nobuyuki Takahashi","doi":"10.1152/ajprenal.00297.2024","DOIUrl":"10.1152/ajprenal.00297.2024","url":null,"abstract":"<p><p>Podocytes are key components of the glomerular filtration barrier, and their injury leads to proteinuria, chronic kidney disease (CKD), and nephrotic syndrome. Effective treatments for these conditions are not well established, and prevention of podocyte injury is a crucial challenge. Nicotinamide (NAM), a form of vitamin B3, has been reported to exert beneficial effects in various renal disease models due to its antioxidant and anti-inflammatory properties and its ability to replenish nicotinamide adenine dinucleotide (NAD⁺). However, its impact on adriamycin (ADR)-induced nephropathy, a model of nephrotic syndrome caused by podocyte injury, remains unclear. We investigated the effects of NAM administration in a mouse model of ADR nephropathy. BALB/c mice were intravenously administered ADR to induce nephropathy. In the NAM-treated group, mice received 0.6% NAM in drinking water ad libitum starting 7 days before ADR administration. After 14 days, NAM treatment decreased albuminuria, glomerular sclerosis, and podocyte injury, and reduced inflammation and oxidative stress markers in the kidneys. NAM and NAD⁺ levels were decreased in ADR-treated kidneys, and the expression of the NAD⁺-consuming enzymes SIRT1 and poly(ADP-ribose) polymerase 1 (PARP-1) was decreased and increased, respectively. Nicotinamide <i>N</i>-methyltransferase expression was increased. NAM canceled these abnormalities. In cultured rat podocytes, NAD⁺ alleviated ADR-induced cytotoxicity, apoptosis, and inflammation. These findings suggest that NAM prevents ADR nephropathy and podocyte injury, likely through NAD⁺ replenishment.<b>NEW & NOTEWORTHY</b> Nephrotic syndrome can lead to end-stage kidney disease and cause severe complications. Currently, effective treatments for nephrotic syndrome have not been established, and new therapeutic approaches targeting podocyte injury are needed. Nicotinamide prevents podocyte injury in adriamycin-induced nephropathy in mice and ameliorates albuminuria, pathological changes, oxidative stress, and inflammation. Here, we provide evidence that pretreatment with nicotinamide can attenuate podocyte injury and subsequent nephropathy in mice.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F501-F516"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544901","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":"Endothelial dysfunction in the aging kidney.","authors":"Mila Borri, Marleen E Jacobs, Peter Carmeliet, Ton J Rabelink, Sébastien J Dumas","doi":"10.1152/ajprenal.00287.2024","DOIUrl":"10.1152/ajprenal.00287.2024","url":null,"abstract":"<p><p>Global population aging is an escalating challenge in modern society, especially as it impairs the function of multiple organs and increases the burden of age-related diseases. The kidneys, in particular, experience function decline, reduced regenerative capacity, and increased susceptibility to injury as they age. As a result, the prevalence of chronic kidney disease (CKD) rises with aging, further contributing to the growing health burden in older populations. One of the key factors in this process is the dysfunction of specialized renal endothelial cells (RECs), which are essential for maintaining kidney health by regulating blood flow and supporting filtration, solute and water reabsorption, and vascular integrity. As the kidneys age, REC dysfunction drives vascular and microenvironmental changes, contributing to the overall decline in kidney function. In this review, we outline the structural and functional effects of aging on the kidney's macrovascular and microvascular compartments and provide a phenotypic description of the aged endothelium. We particularly focus on the molecular and metabolic rewiring driving and sustaining growth-arrested EC senescence phenotype. We finally give an overview of senotherapies acting on ECs, especially of those modulating metabolism. Given that the pathophysiological processes underlying kidney aging largely overlap with those observed in CKD, REC rejuvenation could also benefit patients with CKD. Moreover, such interventions may hold promise in improving the outcomes of aged kidney transplants. Hence, advancing our understanding of REC and kidney aging will create opportunities for innovations that could improve outcomes for both elderly individuals and patients with CKD.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F542-F562"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401015","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":"Fueling kidney recovery: boosting BCAA metabolism to overcome nephrotoxic AKI.","authors":"Pinelopi P Kapitsinou","doi":"10.1152/ajprenal.00024.2025","DOIUrl":"10.1152/ajprenal.00024.2025","url":null,"abstract":"","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F596-F598"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569268","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}