The DOI matches its Crossref record; 150 of the 150 references it cites were found in a registry or an index.
Adverse renal consequences of obesity
Abstract
Emerging evidence indicates that obesity, even in the absence of diabetes, contributes significantly to the development and progression of chronic kidney disease (CKD). Glomerular hyperfiltration/hypertrophy in response to the increased metabolic needs of obesity are postulated to lead to the development of glomerulosclerosis (GS) in a manner analogous to that in reduced renal mass states. Nevertheless, the individual risk for developing GS with obesity is very low. It is proposed that glomerular hyperfiltration/hypertrophy are per se not pathogenic in the absence of an enhanced glomerular blood pressure (BP) transmission, and the modest preglomerular vasodilation that is likely present in the large majority of obese individuals is not sufficient to result in such increased BP transmission. However, in the small subset of obese individuals who are also born with a substantially reduced nephron number, there is a greater risk of enhanced glomerular BP transmission due to the substantially greater preglomerular vasodilation. Of perhaps greater clinical importance, similar additive deleterious effects of obesity on BP transmission would be expected in individuals with reduced renal mass, either congenital or acquired, or with concurrent renal disease, leading to accelerated progression. Of note, a low birth weight may be a risk factor for not only reduced nephron numbers at birth, but also for obesity and hypertension, resulting in a clustering of risk factors for progressive GS. Therefore, even though the individual risk for developing obesity GS is low, the cumulative impact of obesity on the public health burden of CKD is likely to be large because of its huge prevalence.
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Cited by
Glomerular hyperfiltration in diabetes: mechanisms, clinical significance, and treatment
Tonneijck, L., Muskiet, M. H. A., Smits, M. M., van Bommel, E. J., Heerspink, H. J. L., van Raalte, D. H., & Joles, J. A. (2017) · Journal of the American Society of Nephrology · doi:10.1681/asn.2016060666 · Cited by 887
Madamanchi, C., Alhosaini, H., Sumida, A., & Runge, M. S. (2014) · International Journal of Cardiology · doi:10.1016/j.ijcard.2014.08.007 · Cited by 357
Obesity and chronic kidney disease
Jiang, Z., Wang, Y., Zhao, X., Cui, H., Han, M., Ren, X., Gang, X., & Wang, G. (2023) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00179.2022 · Cited by 267
Impaired fasting glucose is associated with renal hyperfiltration in the general population
Melsom, T., Mathisen, U. D., Ingebretsen, O. C., Jenssen, T. G., Njølstad, I., Solbu, M. D., Toft, I., & Eriksen, B. O. (2011) · Diabetes Care · doi:10.2337/dc11-0235 · Cited by 134
Schwingshackl, L., & Hoffmann, G. (2014) · PLoS ONE · doi:10.1371/journal.pone.0097656 · Cited by 125
Metadata
- Authors
- Griffin, K. A., Kramer, H., & Bidani, A. K.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2008-04
- Volume
- 294
- Issue
- 4
- Pages
- F685-F696
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2096040474
- Cited by
- 256
- References
- 150
- FWCI
- 13.44
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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