The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Mechanisms and Treatment of CKD
Open accessAbstract
As CKD continues to increase worldwide, along with the demand for related life-saving therapies, the financial burden of CKD will place an increasing drain on health care systems. Experimental studies showed that glomerular capillary hypertension and impaired sieving function with consequent protein overload play a pathogenic role in the progression of CKD. Consistently, human studies show that proteinuria is an independent predictor of progression and that its reduction is renoprotective. At comparable BP control, inhibitors of the renin-angiotensin system (RAS), including angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), more effectively than non-RAS inhibitor therapy reduce proteinuria, slow progression to ESRD, and even improve the kidney function achieving disease regression in some cases. In participants with diabetes, RAS inhibitors delay the onset of microalbuminuria and its progression to macroalbuminuria, and ACE inhibitors may reduce the excess cardiovascular mortality associated with diabetic renal disease. In addition to RAS inhibitors, however, multimodal approaches including lifestyle modifications and multidrug therapy will be required in most cases to optimize control of the several risk factors for CKD and related cardiovascular morbidity. Whether novel medications may help further improve the cost-effectiveness of renoprotective interventions is a matter of investigation.
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Cites
Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization
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Self-citationThe effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy
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A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease
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Self-citationAngiotensin-receptor blockade versus converting-enzyme inhibition in type 2 diabetes and nephropathy
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Bardoxolone Methyl and Kidney Function in CKD with Type 2 Diabetes
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Cited by
MicroRNAs in kidney physiology and disease
Trionfini, P., Benigni, A., & Remuzzi, G. (2015) · Nature Reviews Nephrology · doi:10.1038/nrneph.2014.202 · Cited by 353
Self-citationRediscovering Beta-2 Microglobulin As a Biomarker across the Spectrum of Kidney Diseases
Argyropoulos, C. P., Chen, S. S., Ng, Y.-H., Roumelioti, M.-E., Shaffi, K., Singh, P. P., & Tzamaloukas, A. H. (2017) · Frontiers in Medicine · doi:10.3389/fmed.2017.00073 · Cited by 308
Rovin, B. H., Barratt, J., Cook, H. T., Noronha, I. L., Reich, H. N., Suzuki, Y., Tang, S. C. W., Trimarch, H., & Floege, J. (2025) · Kidney International · doi:10.1016/j.kint.2025.04.004 · Cited by 206
Metadata
- Authors
- Ruggenenti, P., Cravedi, P., & Remuzzi, G.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2012-12
- Volume
- 23
- Issue
- 12
- Pages
- 1917-1928
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2124602789
- Cited by
- 286
- References
- 15
- FWCI
- 16.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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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.
