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Cited by 263

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Mechanisms of progression of chronic kidney disease

Open access
Fogo, Agnes B.·2007·Pediatric Nephrology
DOI 10.1007/s00467-007-0524-0
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Abstract

Chronic kidney disease (CKD) occurs in all age groups, including children. Regardless of the underlying cause, CKD is characterized by progressive scarring that ultimately affects all structures of the kidney. The relentless progression of CKD is postulated to result from a self-perpetuating vicious cycle of fibrosis activated after initial injury. We will review possible mechanisms of progressive renal damage, including systemic and glomerular hypertension, various cytokines and growth factors, with special emphasis on the renin–angiotensin–aldosterone system (RAAS), podocyte loss, dyslipidemia and proteinuria. We will also discuss possible specific mechanisms of tubulointerstitial fibrosis that are not dependent on glomerulosclerosis, and possible underlying predispositions for CKD, such as genetic factors and low nephron number.

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Metadata

Authors
Fogo, A. B.
Venue
Pediatric Nephrology
Publisher
Springer Science and Business Media LLC
Published
2007-07-24
Volume
22
Issue
12
Pages
2011-2022
ISSN
  • 0931-041X (ISSN-L)
  • 1432-198X
DOI
10.1007/s00467-007-0524-0
OpenAlex
W2162024627
Cited by
263
References
3
FWCI
10.15
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Mechanisms of progression of chronic kidney disease. https://app.cochat.ai/papers/10.1007/s00467-007-0524-0
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Fogo, A. B. (2007). Mechanisms of progression of chronic kidney disease. Pediatric Nephrology. https://doi.org/10.1007/s00467-007-0524-0

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.