A genetic study using a Mendelian randomization approach provides evidence that albuminuria — as well as being the result of hypertension — might also cause hypertension and cardiometabolic disease. We suggest that a mechanism behind these findings could involve sodium retention by urinary protein-induced activation of the epithelial sodium channel in the distal tubule.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Lowest nocturnal systolic blood pressure is related to heavy proteinuria and outcomes in elderly patients with chronic kidney disease
Scientific Reports Open Access 12 March 2021
-
Proteinuria—take a closer look!
Pediatric Nephrology Open Access 10 January 2020
Access options
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 / 30 days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on SpringerLink
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Remuzzi, G. & Bertani, T. Is glomerulosclerosis a consequence of altered glomerular permeability to macromolecules? Kidney Int. 38, 384–394 (1990).
Brantsma, A. H. et al. Urinary albumin excretion as a predictor of the development of hypertension in the general population. J. Am. Soc. Nephrol. 17, 331–335 (2006).
Chronic Kidney Disease Prognosis Consortium et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet 375, 2073–2081 (2010).
Haas, M. E. et al. Genetic association of albuminuria with cardiometabolic disease and blood pressure. Am. J. Hum. Genet. 103, 461–473 (2018).
Vaez, A. et al. lodGWAS: a software package for genome-wide association analysis of biomarkers with a limit of detection. Bioinformatics 32, 1552–1554 (2016).
Gansevoort, R. T. et al. Antiproteinuric effect of blood-pressure-lowering agents: a meta-analysis of comparative trials. Nephrol. Dial. Transplant. 10, 1963–1974 (1995).
Heerspink, H. J. et al. Drug-induced reduction in albuminuria is associated with subsequent renoprotection: a meta-analysis. J. Am. Soc. Nephrol. 26, 2055–2064 (2015).
Bohnert, B. N. et al. Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome. Kidney Int. 93, 159–172 (2018).
Hinrichs, G. R. et al. Albuminuria in kidney transplant recipients is associated with increased urinary serine proteases and activation of the epithelial sodium channel. Am. J. Physiol. Renal Physiol. 315, F151–F160 (2018).
Buhl, K. B. et al. Plasmin in urine from patients with type 2 diabetes and treatment-resistant hypertension activates ENaC in vitro. J. Hypertens. 32, 1672–1677 (2014).
Author information
Authors and Affiliations
Corresponding authors
Ethics declarations
Competing interests
The authors declare no competing interests.
Rights and permissions
About this article
Cite this article
Gansevoort, R.T., Snieder, H. Albuminuria as a cause of hypertension. Nat Rev Nephrol 15, 6–8 (2019). https://doi.org/10.1038/s41581-018-0073-8
Published:
Issue Date:
DOI: https://doi.org/10.1038/s41581-018-0073-8
This article is cited by
-
Lowest nocturnal systolic blood pressure is related to heavy proteinuria and outcomes in elderly patients with chronic kidney disease
Scientific Reports (2021)
-
Recent insights into sodium and potassium handling by the aldosterone-sensitive distal nephron: implications on pathophysiology and drug discovery
Journal of Nephrology (2020)
-
Proteinuria—take a closer look!
Pediatric Nephrology (2020)