Renal Consequences of Therapeutic Interventions in Premature Neonates

Fryer, Hayley J; Welsh, Gavin I.

doi:10.1159/000497162

Cited by 12 publications

(11 citation statements)

References 47 publications

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“…The data (Figure S1A-C) showed that there was no difference in body weight and kidney weight between the experiment and control group. Studies in rodents, sheep, and non-human primates suggested that corticosteroids might harm the kidneys by significantly reducing the number of nephrons [28] . To investigate the effects of excessive GCs treatment on the kidneys, we performed kidney histological studies to detect the potential alterations in kidney morphology.…”

Section: Dex Treatment Affected the Expression Of Genes Involved In Metabolism Inflammation And Immune Responsementioning

confidence: 99%

High-dose dexamethasone injection disordered metabolism and multiple protein kinases expression in the mouse kidney

Zhang

Ran

et al. 2021

Bioscience Reports

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Glucocorticoids (GCs) have been widely used in clinical treatment as anti-inflammatory, anti-shock and immunosuppressive medicines. However, the effect of excessive GCs on immune response and metabolism of kidney remains unclear. Here, we profiled the gene expression of kidney from mice with high-dose dexamethasone (DEX) treatment. A total of 1193 differentially expressed genes (DEGs) were screened in DEX treatment group compared with the saline group, including 715 down- regulated and 478 up-regulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of these DEGs showed extracellular matrix (ECM)–receptor interaction, cell adhesion molecules signaling pathway were significantly enriched, and that the vast majority of DEGs were involved in monocarboxylic acid metabolism, leukocyte cell–cell adhesion and fatty acid metabolism. Gene set enrichment analysis (GSEA) revealed that DEGs were strongly associated with immune-response and cell adhesion gene sets, such as Fc γ R-mediated phagocytosis, leukocyte transendothelial migration, T-cell receptor signaling pathway, cell adhesion, ECM–receptor interaction and focal adhesion-associated pathways. KEGG pathway analysis of differentially expressed kinases (DEKs) showed T-cell receptor and forkhead box class O signaling pathway were enriched. Furthermore, we found multiple protein kinases expression were dysregulated greatly after dexamethasone treatment, including classical effector of GCs stimulation-serum and GC-regulated kinase. These protein kinases are involved in multiple signaling pathways in mice kidney, such as mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We profiled the gene expression of the kidney from high-dose dexamethasone-treated mice and provided important information for further study the mechanism of side effects of GCs in clinical therapy.

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Section: Dex Treatment Affected the Expression Of Genes Involved In Metabolism Inflammation And Immune Responsementioning

confidence: 99%

High-dose dexamethasone injection disordered metabolism and multiple protein kinases expression in the mouse kidney

Zhang

Ran

et al. 2021

Bioscience Reports

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“…An ambiguous role is played by drugs administered to preterm and low birth weight babies. The therapeutic benefit of drugs is balanced against the frequently unknown nephrotoxic potential [12][13][14][15].…”

Section: Clinical Aspectsmentioning

confidence: 99%

Shaping of the nephron – a complex, vulnerable, and poorly explored backdrop for noxae impairing nephrogenesis in the fetal human kidney

Minuth

2020

Mol Cell Pediatr

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Background: The impairment of nephrogenesis is caused by noxae, all of which are significantly different in molecular composition. These can cause an early termination of nephron development in preterm and low birth weight babies resulting in oligonephropathy. For the fetal human kidney, there was no negative effect reported on the early stages of nephron anlage such as the niche, pretubular aggregate, renal vesicle, or comma-shaped body. In contrast, pathological alterations were identified on subsequently developing S-shaped bodies and glomeruli. While the atypical glomeruli were closely analyzed, the S-shaped bodies and the pre-stages received little attention even though passing the process of nephron shaping. Since micrographs and an explanation about this substantial developmental period were missing, the shaping of the nephron in the fetal human kidney during the phase of late gestation was recorded from a microanatomical point of view. Results: The nephron shaping starts with the primitive renal vesicle, which is still part of the pretubular aggregate at this point. Then, during extension of the renal vesicle, a complex separation is observed. The medial part of its distal pole is fixed on the collecting duct ampulla, while the lateral part remains connected with the pretubular aggregate via a progenitor cell strand. A final separation occurs, when the extended renal vesicle develops into the comma-shaped body. Henceforth, internal epithelial folding generates the tubule and glomerulus anlagen. Arising clefts at the medial and lateral aspect indicate an asymmetrical expansion of the S-shaped body. This leads to development of the glomerulus at the proximal pole, whereas in the center and at the distal pole, it results in elongation of the tubule segments. Conclusions: The present investigation deals with the shaping of the nephron in the fetal human kidney. In this important developmental phase, the positioning, orientation, and folding of the nephron occur. The demonstration of previously unknown morphological details supports the search for traces left by the impairment of nephrogenesis, enables to refine the assessment in molecular pathology, and provides input for the design of therapeutic concepts prolonging nephrogenesis.

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“…Indeed, Gjerde et al found a relation between preterm birth and ESRD in males but not in females; this gender difference was not revealed in the LBW or SGA group [ 8 ]. Potentially, preterm infants might have enough renal reserve, but postnatal (nephrotoxic) medication during their admission at the neonatal intensive care unit is what might put them at risk [ 10 ].…”

Section: Different Underlying Mechanismsmentioning

confidence: 99%

Long-term renal disease after prematurity or fetal growth restriction: who is at risk?

Terstappen

Lely

2020

Nephrology Dialysis Transplantation

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Renal Consequences of Therapeutic Interventions in Premature Neonates

Cited by 12 publications

References 47 publications

High-dose dexamethasone injection disordered metabolism and multiple protein kinases expression in the mouse kidney

High-dose dexamethasone injection disordered metabolism and multiple protein kinases expression in the mouse kidney

Shaping of the nephron – a complex, vulnerable, and poorly explored backdrop for noxae impairing nephrogenesis in the fetal human kidney

Long-term renal disease after prematurity or fetal growth restriction: who is at risk?

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