IgA nephropathy

Stamellou, Eleni; Seikrit, Claudia; Tang, Sydney C. W.; Boor, Peter; Tesař, Vladimir; Floege, Jürgen; Barratt, Jonathan; Kramann, Rafael

doi:10.1038/s41572-023-00476-9

Cited by 21 publications

(8 citation statements)

References 274 publications

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“…Similar to the relationship between hypothyroidism and CKD, lower FT4 may contribute to the progression of renal function in IgA nephropathy through the following aspects ( 1 ). Hemodynamic changes: Lower FT4 cause decreased cardiac contractility, decreased circulating blood volume, and renal hypoperfusion ( 13 ).…”

Section: Discussionmentioning

confidence: 99%

The predictive value of free thyroxine combined with tubular atrophy/interstitial fibrosis for poor prognosis in patients with IgA nephropathy

Yang,

Zhou,

Cui

et al. 2024

Front. Endocrinol.

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BackgroundIgA nephropathy (IgAN), the most common type of glomerulonephritis, has great individual differences in prognosis. Many studies showed the relationship between thyroid hormones and chronic kidney disease. However, the relationship between free thyroxine (FT4), as a thyroid hormone, and IgAN is still unclear. This study aimed to evaluate the impact of FT4 on IgAN prognosis.MethodsThis retrospective study involved 223 patients with biopsy-proven IgAN. The renal composite outcomes were defined as: (1) ESRD, defined as eGFR < 15 ml/(min·1.73 m2) or initiation of renal replacement therapy (hemodialysis, peritoneal dialysis, renal transplantation); (2) serum creatinine doubled from baseline; (3) eGFR decreased by more than 50% from baseline. The predictive value was determined by the area under the curve (AUC). Kaplan-Meier and Cox proportional hazards analyses assessed renal progression and prognosis.ResultsAfter 38 (26–54) months of follow-up, 23 patients (10.3%) experienced renal composite outcomes. Kaplan-Meier survival curve analysis showed that the renal survival rate of the IgAN patients with FT4<15.18pmol/L was lower than that with FT4≥15.18pmol/L (P < 0. 001). Multivariate Cox regression model analysis showed that FT4 was a protective factor for poor prognosis of IgAN patients, whether as a continuous variable or a categorical variable (HR 0.68, 95%CI 0.51–0.90, P =0.007; HR 0.04, 95%CI 0.01–0.20, P <0.001). ROC curve analysis showed that FT4 combined with t score had a high predictive value for poor prognosis of IgAN patients (AUC=0.881, P<0.001).ConclusionFT4 was a protective factor for IgAN. In addition, FT4 combined with tubular atrophy/interstitial fibrosis had a high predictive value for poor prognosis of IgAN.

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Section: Discussionmentioning

confidence: 99%

The predictive value of free thyroxine combined with tubular atrophy/interstitial fibrosis for poor prognosis in patients with IgA nephropathy

Yang,

Zhou,

Cui

et al. 2024

Front. Endocrinol.

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“…4 ). IgAN is the most common cause of glomerulonephritis and is due to deposition of complexes of abnormally glycosylated immunoglobulin A in the renal glomerulus 30 . We applied a standard panel of 377 genes not specifically developed for kidney 31 .…”

Section: Extending Topact To Imaging Platformsmentioning

confidence: 99%

Multiscale topology classifies cells in subcellular spatial transcriptomics

Benjamin,

Bhandari,

Kepple

et al. 2024

Nature

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Spatial transcriptomics measures in situ gene expression at millions of locations within a tissue1, hitherto with some trade-off between transcriptome depth, spatial resolution and sample size2. Although integration of image-based segmentation has enabled impactful work in this context, it is limited by imaging quality and tissue heterogeneity. By contrast, recent array-based technologies offer the ability to measure the entire transcriptome at subcellular resolution across large samples3–6. Presently, there exist no approaches for cell type identification that directly leverage this information to annotate individual cells. Here we propose a multiscale approach to automatically classify cell types at this subcellular level, using both transcriptomic information and spatial context. We showcase this on both targeted and whole-transcriptome spatial platforms, improving cell classification and morphology for human kidney tissue and pinpointing individual sparsely distributed renal mouse immune cells without reliance on image data. By integrating these predictions into a topological pipeline based on multiparameter persistent homology7–9, we identify cell spatial relationships characteristic of a mouse model of lupus nephritis, which we validate experimentally by immunofluorescence. The proposed framework readily generalizes to new platforms, providing a comprehensive pipeline bridging different levels of biological organization from genes through to tissues.

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“…IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide. [1] It is characterized by the deposition of IgA in the mesangium, a condition that can result in end-stage renal disease (ESRD or end-stage kidney disease, ESKD) within 20 years for 40% of patients. Nonetheless, accurately predicting which IgAN patients will advance to ESRD remains challenging.…”

Section: Introductionmentioning

confidence: 99%

Refractory IgA Nephropathy: A Challenge for Future Nephrologists

Di Leo,

Annese,

Papadia

et al. 2024

Medicina

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IgA nephropathy (IgAN) represents the most prevalent form of primary glomerulonephritis, and, on a global scale, it ranks among the leading culprits behind end-stage kidney disease (ESKD). Presently, the primary strategy for managing IgAN revolves around optimizing blood pressure and mitigating proteinuria. This is achieved through the utilization of renin–angiotensin system (RAS) inhibitors, namely, angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs). As outlined by the KDIGO guidelines, individuals who continue to show a persistent high risk of progressive ESKD, even with comprehensive supportive care, are candidates for glucocorticoid therapy. Despite these therapies, some patients have a disease refractory to treatment, defined as individuals that present a 24 h urinary protein persistently >1 g after at least two rounds of regular steroids (methylprednisolone or prednisone) and/or immunosuppressant therapy (e.g., mycophenolate mofetil), or who do not tolerate regular steroids and/or immunosuppressant therapy. The aim of this Systematic Review is to revise the current literature, using the biomedical database PubMed, to investigate possible therapeutic strategies, including SGLT2 inhibitors, endothelin receptor blockers, targeted-release budesonide, B cell proliferation and differentiation inhibitors, fecal microbiota transplantation, as well as blockade of complement components.

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IgA nephropathy

Cited by 21 publications

References 274 publications

The predictive value of free thyroxine combined with tubular atrophy/interstitial fibrosis for poor prognosis in patients with IgA nephropathy

The predictive value of free thyroxine combined with tubular atrophy/interstitial fibrosis for poor prognosis in patients with IgA nephropathy

Multiscale topology classifies cells in subcellular spatial transcriptomics

Refractory IgA Nephropathy: A Challenge for Future Nephrologists

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