Primary focal segmental glomerulosclerosis: mi<scp>RNA</scp>s and targeted therapies

Leierer, Johannes; Mayer, Gert; Kronbichler, Andreas

doi:10.1111/eci.12676

Cited by 5 publications

(4 citation statements)

References 54 publications

(98 reference statements)

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“…Therefore, urinary levels of miR-196a, miR-30a-5p, and miR-490 could be an efficient biomarker for FSGS disease progression. 133 3.8 | IgA nephropathy (Figure 7). 150 F I G U R E 7 MicroRNA in Renal Cell Carcinoma (RCC).…”

Section: Focal Segmental Glomerulosclerosismentioning

confidence: 99%

“…Therefore, urinary levels of miR-196a, miR-30a-5p, and miR-490 could be an efficient biomarker for FSGS disease progression. 133…”

Section: Focal Segmental Glomerulosclerosismentioning

confidence: 99%

“…Also, the combination of miR‐196a, miR‐30a‐5p, and miR‐490 were the greatest promising miRNAs that could even improve the diagnosis of FSGS. Therefore, urinary levels of miR‐196a, miR‐30a‐5p, and miR‐490 could be an efficient biomarker for FSGS disease progression 133 …”

Section: Micrornas As Diagnostic Markersmentioning

confidence: 99%

See 2 more Smart Citations

MiRNAs as potential biomarker of kidney diseases: A review

Ramanathan

Padmanabhan²

2020

Cell Biochemistry & Function

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Section: Focal Segmental Glomerulosclerosismentioning

confidence: 99%

“…Therefore, urinary levels of miR-196a, miR-30a-5p, and miR-490 could be an efficient biomarker for FSGS disease progression. 133…”

Section: Focal Segmental Glomerulosclerosismentioning

confidence: 99%

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MiRNAs as potential biomarker of kidney diseases: A review

Ramanathan

Padmanabhan²

2020

Cell Biochemistry & Function

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“…However, a mouse model for NPHS2 has recently been reported ( 50 ) and may have important consequences also for the development of specific molecular treatment approaches. Other investigations have indicated a role of specific miRNAs in the etiology of FSGS, which may be amenable to specific treatment ( 51 ). Taken together, studies into the molecular biology of SRNS have a yet undiscovered potential to develop new treatment modalities and potentially a cure for certain genetic forms of SRNS.…”

Section: Experiences In Specific Genetic Disordersmentioning

confidence: 99%

Treatment of Genetic Forms of Nephrotic Syndrome

Kemper

Lemke

2018

Front. Pediatr.

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Idiopathic steroid-resistant nephrotic syndrome (SRNS) is most frequently characterized by focal segmental glomerulosclerosis (FSGS) but also other histological lesions, such as diffuse mesangial sclerosis. In the past two decades, a multitude of genetic causes of SRNS have been discovered raising the question of effective treatment in this cohort. Although no controlled studies are available, this review will discuss treatment options including pharmacologic interventions aiming at the attenuation of proteinuria in genetic causes of SRNS, such as inhibitors of the renin–angiotensin–aldosterone system and indomethacin. Also, the potential impact of other interventions to improve podocyte stability will be addressed. In this respect, the treatment with cyclosporine A (CsA) is of interest, since a podocyte stabilizing effect has been demonstrated in various experimental models. Although clinical response to CsA in children with genetic forms of SRNS is inferior to sporadic SRNS, some recent studies show that partial and even complete response can be achieved even in individual patients inherited forms of nephrotic syndrome. Ideally, improved pharmacologic and molecular approaches to induce partial or even complete remission will be available in the future, thus slowing or even preventing the progression toward end-stage renal disease.

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