{"id":52439,"date":"2026-03-05T08:24:16","date_gmt":"2026-03-05T08:24:16","guid":{"rendered":"https:\/\/www.theisn.org\/?page_id=52439"},"modified":"2026-04-28T11:35:59","modified_gmt":"2026-04-28T11:35:59","slug":"edigest-isn-journals-march-2026","status":"publish","type":"page","link":"https:\/\/www.theisn.org\/edigest-isn-journals-march-2026\/","title":{"rendered":"eDIGEST: ISN Journals"},"content":{"rendered":"

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March 2026 Edition<\/h4>\n

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Impact Factor 2024<\/strong><\/p>\n

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12.6<\/h3>

Kidney International<\/i>\u00ae<\/sup><\/p><\/div> <\/div>[\/vc_column_inner][vc_column_inner width=”1\/3″]

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5.7<\/h3>

Kidney International Reports<\/i>\u00ae<\/sup><\/p><\/div> <\/div>[\/vc_column_inner][vc_column_inner width=”1\/3″]

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89.6<\/h3>

Kidney International Supplements<\/i><\/p><\/div> <\/div>[\/vc_column_inner][\/vc_row_inner][\/vc_column][\/vc_row][vc_row el_class=”drop-shadow-“][vc_column][vc_column_text]<\/p>\n

Advancing pediatric kidney care: New insights in ISN Journals<\/h3>\n

From cystic kidney disease genetics to cardiovascular risk in pediatric dialysis and measuring life participation, pediatric kidney care research is rapidly evolving. This selection of recent papers from Kidney International<\/em><\/a>\u00ae<\/sup> and Kidney International Reports<\/em><\/a>\u00ae<\/sup> highlights the science and strategies driving more precise, preventive, and equitable kidney care for children.[\/vc_column_text][vc_single_image image=”52585″ img_size=”full” alignment=”center”][\/vc_column][\/vc_row][vc_row][vc_column css=”.vc_custom_1605872418428{margin-top: 30px !important;}”][vc_column_text]<\/p>\n\n\n\n
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KIDNEY INTERNATIONAL<\/em> ARTICLES<\/h3>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

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\nDisruption of the human cystin-1 myristoyl-electrostatic switch causes polycystic kidney disease that phenocopies autosomal recessive polycystic kidney disease
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Yang and colleagues describe two unrelated families with enlarged, cystic kidneys consistent with autosomal recessive polycystic kidney disease (ARPKD).<\/p>\n

Genetic analyses identified homozygous pathogenic variants in CYS1, expanding evidence that cystin-1 deficiency contributes to fibrocystic kidney disease and underscoring the importance of cystin for appropriate ciliary localization.<\/p>\n

Using CRISPR\/Cas9 models and 3D culture systems, the authors show that loss of cystin or disruption of its N-myristoylation promotes cystogenesis. Mechanistically, cystin trafficking appears to be governed by a myristoyl\u2013electrostatic switch, with serine-17 phosphorylation downstream of ciliary cAMP\u2013PKA signaling reducing membrane association and favoring cyst growth.<\/p>\n

Collectively, these findings position CYS1 as an important ARPKD gene and provide a mechanistic link between cAMP signaling, ciliary protein trafficking, and cyst formation.<\/p>\n

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Optimizing cardiovascular outcomes in pediatric dialysis<\/a><\/h3>\n

Cardiovascular disease is the major determinant of long-term outcomes in children receiving dialysis. This review emphasizes that the injury trajectory begins well before dialysis and then accelerates during kidney replacement therapy. The burden reflects a mix of traditional risks (hypertension, dyslipidemia, insulin resistance) and kidney-specific drivers (volume overload, chronic inflammation, anemia, CKD\u2013mineral bone disorder, endothelial dysfunction, and uremic toxin exposure). In practice, cardiovascular risk in pediatric dialysis is cumulative and multifactorial, not a late complication that appears only after years of treatment.<\/p>\n

A key contribution of the review is its focus on treatment-related factors. Conventional dialysis schedules may leave children exposed to persistent fluid, pressure, and toxin stress, while peritoneal dialysis and standard hemodialysis carry different cardiovascular trade-offs. More intensive strategies are biologically plausible, but pediatric outcomes evidence remains limited. The clinical takeaway is prevention-first and pathway-based: earlier surveillance, tighter blood pressure and volume control, individualized dialysis prescriptions, and proactive management of metabolic and inflammatory drivers starting in early CKD and continuing through dialysis.<\/p>\n

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Primary hyperoxaluria(s): From trials to real-life data and pipeline therapies <\/a><\/h3>\n

Primary hyperoxaluria (PH) comprises a group of autosomal recessive disorders that can lead to recurrent kidney stone disease, early kidney failure, systemic oxalosis, and the need for combined liver\u2013kidney transplantation.<\/p>\n

In this mini-review, Bacchetta et al. summarize recent advances in PH pathophysiology, diagnostics, and therapeutics, highlighting the transformative role of RNA interference (RNAi), which enables precise, sequence-specific silencing of target mRNA.<\/p>\n

Small interfering RNA therapies (lumasiran, nedosiran) offer a targeted, liver-directed strategy to reduce hepatic oxalate production and have shown significant, sustained reductions in urinary oxalate in patients with PH1.<\/p>\n

Despite these advances, key challenges remain, including timely diagnosis, longitudinal assessment of systemic oxalate burden, limited long-term outcome data, and equitable global access to high-cost therapies. Emerging approaches such as gene editing, mRNA-based therapies, and oral alternatives may further broaden the treatment landscape and improve accessibility.<\/p>\n

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SGLT-2 inhibition in pediatric CKD: Advances, challenges, and opportunities <\/a><\/h3>\n

Adult trials demonstrating cardiovascular and renal benefits with SGLT-2 inhibitors have typically relied on traditional chronic kidney disease (CKD) endpoints such as proteinuria\/albuminuria and estimated glomerular filtration rate (eGFR). However, pediatric CKD differs from adult disease, with less proteinuria and a higher proportion of congenital and non-glomerular etiologies.<\/p>\n

Participants in a 2023 stakeholder workshop highlighted the pressing need for pediatric evidence and noted increasing off-label use of SGLT-2 inhibitors in pediatric care. Child-specific safety concerns include dehydration or volume depletion, infections, and potential impacts on growth, bone health, and neurodevelopment.<\/p>\n

Pediatric clinical trials should prioritize age-appropriate, disease-relevant endpoints and consider integrating biomarkers of tubular injury and early cardiovascular morbidity alongside safety indicators such as growth velocity and neurocognitive outcomes. Ongoing studies (e.g., EMPAKIDNEY-Kids, DOUBLE-PROTECT) and observational cohorts of children already receiving SGLT-2 inhibitors will be critical to inform safety and effectiveness. Coordinated international collaboration is needed to close the evidence gap and ensure equitable access to renoprotective therapies for children with CKD.<\/p>\n

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Establishing a core outcome measure for life participation in children with chronic kidney disease: A Standardized Outcomes in Nephrology \u2014 children and adolescents with chronic kidney disease (SONG-Kids) consensus workshops report <\/a><\/h3>\n

The SONG-Kids initiative advances a needed shift in pediatric CKD research: measuring what matters most to children, not only what is easiest to quantify clinically.<\/p>\n

In consensus workshops involving 171 participants across 16 countries, a consistent priority emerged \u2014 children and families value \u201clife participation,\u201d including the ability to attend school, maintain friendships, and take part in everyday activities, alongside symptom control and survival.<\/p>\n

The proposed core outcome measure is notable for its developmental sensitivity and real-world feasibility, using age-appropriate language and flexible interpretation to reflect different contexts and stages of childhood. By centering outcomes defined by children themselves, SONG-Kids provides a roadmap for trials and care models that better capture lived experience and ultimately support children with CKD to thrive, not just survive.<\/p>\n

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KIDNEY INTERNATIONAL<\/em> REPORTS ARTICLES<\/h3>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

[\/vc_column_text][vc_single_image image=”11509″ img_size=”140×30″ css=”.vc_custom_1631694694168{margin-bottom: 10px !important;background-color: #007f91 !important;}”][vc_tta_accordion spacing=”5″ c_position=”right” active_section=”1″ el_class=”accordion-isn”][vc_tta_section title=”Optimization of kidney disease: Improving global outcomes criteria for AKI for the pediatric population” tab_id=”kir1″][vc_column_text css=”.vc_custom_1772535405633{padding-top: 6px !important;padding-right: 6px !important;padding-bottom: 6px !important;padding-left: 6px !important;}”]\"\"<\/p>\n

Pediatric acute kidney injury (AKI) definitions still rely largely on adult-derived criteria, applying fixed serum creatinine thresholds despite strong age- and sex-related variation in creatinine biology during childhood. This can cause diagnostic misclassification and reduce prognostic precision in routine pediatric care.<\/p>\n

To address this gap, the authors developed a pediatric-adapted Kidney Disease: Improving Global Outcomes framework (pKDIGO) designed to better align diagnostic thresholds with pediatric physiology. They validated pKDIGO in two large retrospective cohorts from China, Beijing Children\u2019s Hospital (n=57,229) and an external Zhejiang PICU cohort (n=8,276), and compared performance against KDIGO, modified KDIGO, pROCK, and pRIFLE, using in-hospital mortality as the primary endpoint.<\/p>\n

pKDIGO showed stronger discrimination (AUROC ~0.75 in the Beijing Children\u2019s Hospital cohort), and AKI stage escalation demonstrated a clear dose\u2013response relationship with mortality risk. These findings were directionally replicated in the external PICU cohort.<\/p>\n

Overall, pKDIGO appears to be a clinically relevant advance in pediatric AKI phenotyping and risk stratification, with potential to support earlier recognition, improved triage, and more targeted intervention pathways for children at highest risk.<\/p>\n

Read more<\/a> View visual abstract<\/a>[\/vc_column_text][\/vc_tta_section][vc_tta_section title=”Implementing patient navigation for children with chronic kidney disease” tab_id=”kir2″][vc_column_text css=”.vc_custom_1772536071357{padding-top: 6px !important;padding-right: 6px !important;padding-bottom: 6px !important;padding-left: 6px !important;}”]\"\"<\/p>\n

This article on implementing patient navigation for children with chronic kidney disease (CKD) highlights how structured navigation programs can reduce long-standing disparities by improving access to services, strengthening care coordination, and deepening family engagement.<\/p>\n

The authors outline seven practical implementation strategies, such as securing sustainable funding, embedding navigators within multidisciplinary teams, supporting navigator well-being, and tailoring support to the needs of the most vulnerable families.<\/p>\n

The take-home message is clear: Navigation should not be an \u201cadd-on,\u201d but an integrated component of CKD care pathways to reduce fragmentation, strengthen shared decision-making, and promote more equitable outcomes for socioeconomically disadvantaged children.<\/p>\n

Read more<\/a> View visual abstract<\/a>[\/vc_column_text][\/vc_tta_section][vc_tta_section title=”Reference change value acute kidney injury criteria in critically ill children” tab_id=”kir3″][vc_column_text css=”.vc_custom_1772536314957{padding-top: 6px !important;padding-right: 6px !important;padding-bottom: 6px !important;padding-left: 6px !important;}”]\"\"<\/p>\n

Serum creatinine shows substantial biological and analytical variability in children, making acute kidney injury (AKI) definitions based on small creatinine changes vulnerable to fluctuations.<\/p>\n

The pediatric reference change value optimized for AKI (pROCK) is a newer creatinine-based criterion for defining AKI with limited evidence of accuracy. A new study demonstrates its specificity. The authors prospectively enrolled consecutive children aged 1 month to 18 years admitted to a tertiary care pediatric intensive care unit (PICU) between February 2023 and December 2024. AKI within 7 days of PICU admission was assessed using pROCK and compared with conventional AKI criteria.<\/p>\n

Of 907 screened patients, 478 were eligible and followed until discharge. Agreement between pROCK and KDIGO was good for stage 3 AKI (kappa = 0.76) and very strong for diagnosing any AKI and no AKI (kappa = 0.91 for both). pROCK had the highest specificity (96.2%), whereas KDIGO had the highest sensitivity (100%). pROCK was an independent predictor of mortality.<\/p>\n

Overall, pROCK may improve specificity, particularly in infants and young children with low baseline creatinine; however, further refinement should incorporate urine output requirements.<\/p>\n

Read more<\/a> View visual abstract<\/a>[\/vc_column_text][\/vc_tta_section][vc_tta_section title=”Markers of mineral metabolism in children with CKD stages 2 to 5D” tab_id=”kir5″][vc_column_text css=”.vc_custom_1772698334339{padding-top: 6px !important;padding-right: 6px !important;padding-bottom: 6px !important;padding-left: 6px !important;}”]\"\"<\/p>\n

This cross-sectional study of 170 children with chronic kidney disease (CKD) stages 2\u20135D used age- and sex-adjusted z-scores to characterize early CKD\u2013mineral and bone disorder (CKD-MBD).<\/p>\n

Compared with healthy peers, stage 2 already showed higher sclerostin, total FGF23, and alkaline phosphatase, with lower phosphate and vitamin D metabolites, while iPTH, iFGF23, and soluble Klotho were largely unchanged.<\/p>\n

With progression, abnormalities intensified: total fibroblast growth factor (23FGF23), alkaline phosphatase, and phosphate rose from stage 3a onward, whereas calcium, 1,25-dihydroxy vitamin D3, and soluble Klotho declined; hyperphosphatemia and hypocalcemia appeared mainly in stages 4\u20135D.<\/p>\n

The pattern suggests FGF23\/sclerostin changes precede \u201cclassic\u201d derangements, supporting earlier CKD-MBD surveillance during growth and attention to modifiable factors such as vitamin D and iron status.<\/p>\n

Read more<\/a> View visual abstract<\/a>[\/vc_column_text][\/vc_tta_section][vc_tta_section title=”Urinary microbiome dysbiosis in children with congenital uropathies at varying risk for urinary tract infections” tab_id=”kir4″][vc_column_text css=”.vc_custom_1772536544896{padding-top: 6px !important;padding-right: 6px !important;padding-bottom: 6px !important;padding-left: 6px !important;}”]
\nUsing 16S rRNA sequencing, this prospective cohort study compared urinary microbiomes in 36 children with CAKUT (low- vs. high-risk of urinary tract infection [UTI]) and 44 controls. Diversity decreased stepwise from controls to low-risk to high-risk CAKUT, with distinct community clustering and greater inter-individual variability in those at the highest risk, consistent with dysbiosis even before symptomatic infection.<\/p>\n

During follow-up, UTI-free survival was lower in the high-risk group, and baseline microbiome profiles tended to be more \u201ccontrol-distant\u201d among children who later developed a UTI. Depletion of health-associated consortia correlated with poorer UTI-free survival, and specific taxa tracked with higher or lower future risk.<\/p>\n

These findings support urinary microbiome profiling as a non-invasive tool to refine risk stratification and better target prophylaxis while promoting antimicrobial stewardship.<\/p>\n

Read more<\/a> [\/vc_column_text][\/vc_tta_section][\/vc_tta_accordion][\/vc_column][\/vc_row]<\/p>\n","protected":false},"excerpt":{"rendered":"

[vc_row][vc_column][vc_column_text css=”.vc_custom_1773150823260{margin-bottom: 3px !important;border-bottom-width: 1px !important;padding-bottom: 10px !important;border-bottom-color: #6fc8bb !important;border-bottom-style: solid !important;}”] March 2026 Edition [\/vc_column_text][vc_single_image image=”26675″ img_size=”full”][\/vc_column][\/vc_row][vc_row el_class=”impact” css=”.vc_custom_1718977543002{margin-top: 0px !important;margin-right: 5px !important;margin-bottom: 20px !important;margin-left: 5px !important;border-top-width: 1px !important;border-right-width: 1px !important;border-bottom-width: 1px !important;border-left-width: 1px !important;padding-top: 20px !important;background-color: #f4f4f4 !important;border-left-color: #077ba4 !important;border-left-style: dotted !important;border-right-color: #077ba4 !important;border-right-style: dotted !important;border-top-color: #077ba4 !important;border-top-style: dotted !important;border-bottom-color: #077ba4 !important;border-bottom-style: dotted […]<\/p>\n","protected":false},"author":5,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-52439","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/pages\/52439"}],"collection":[{"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/users\/5"}],"replies":[{"embeddable":true,"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/comments?post=52439"}],"version-history":[{"count":5,"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/pages\/52439\/revisions"}],"predecessor-version":[{"id":53624,"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/pages\/52439\/revisions\/53624"}],"wp:attachment":[{"href":"https:\/\/www.theisn.org\/wp-json\/wp\/v2\/media?parent=52439"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}