Kidney and hypertension
Open accessAbstract
There is a unique relationship between the kidney and blood pressure (BP): on the one hand, renal dysfunction and particularly renal disease cause an increase in BP, while on the other hand, high BP accelerates loss of function of the diseased kidney. Transplantation studies, both in experimental animals and humans, documented that "blood pressure goes with the kidney," a normotensive recipient of a kidney genetically programmed for hypertension (HT) will develop HT, while conversely hypertensive patients with renal failure receiving the kidney of a normotensive donor may develop normotension. Family studies showed higher BP values and more frequent HT in first degree relatives of patients with primary glomerulonephritis or diabetic nephropathy, both type 1 and type 2. The notion that HT accelerates the loss of renal function has been proposed at the turn of the century, but definite evidence by observational and interventional studies has only been provided in the last two decades. The issue has been much confounded by the mistaken believe that damaged kidneys require higher BP values in order to function properly. The mechanisms of BP increase in renal disease comprise: salt retention, inappropriate activity of the renin-angiotensin system (RAS) and of the sympathetic nerve system as well as impaired endothelial cell-mediated vasodilatation. There is ample evidence both in primary renal disease (AIPRI and REIN trials) and in nephropathy of type 1 and type 2 diabetes (IDNT, RENAAL) that pharmacological blockade of the RAS by angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor blockers has BP-independent renoprotective effects. More recently, it has also been shown that blockade of the sympathetic nerve system has BP-independent effects on albuminuria and on glomerulosclerosis.
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Sympathetic activation aggravates existing hypertension, proteinuria, interstitial fibrosis and glomerulosclerosis.
“Sympathetic activation aggravates existing hypertension, proteinuria, interstitial fibrosis and glomerulosclerosis104.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [104]
Sympathetic activation is present in the early phases of renal disease, in the absence of uremia, being seen in patients with nephrotic syndrome and with autosomal dominant polycystic kidney disease despite normal renal function, and increases with disease progression.
“Sympathetic activation is present in the early phases of renal disease, in the absence of uremia, being seen in patients with nephrotic syndrome and with autosomal dominant polycystic kidney disease despite normal renal function, and increases with disease progression103.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [103]
In rats with 5/6 nephrectomy, the hypertension and sympathetic activation are abolished by dorsal rhizotomy, which abolishes renal afferent nerve input to the central nervous system.
“These clinical observations have a parallel in experimental studies in rats with 5/6 nephrectomy103, where the hypertension and sympathetic activation in this renal failure model is abolished by dorsal rhizotomy, which abolishes renal afferent nerve input to the central nervous system.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [103]
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The Sympathetic Nervous System Alterations in Human Hypertension
Grassi, G., Mark, A., & Esler, M. (2015) · Circulation Research · doi:10.1161/circresaha.116.303604 · Cited by 616 · see citing works
Sympathetic Activation in Chronic Renal Failure
Schlaich, M. P., Socratous, F., Hennebry, S., Eikelis, N., Lambert, E. A., Straznicky, N., Esler, M. D., & Lambert, G. W. (2009) · Journal of the American Society of Nephrology · doi:10.1681/asn.2008040402 · Cited by 408 · see citing works
- Authors
- Adamczak, M., Zeier, M., Dikow, R., & Ritz, E.
- Affiliations
- Heidelberg University (DE)
- Medical University of Silesia (PL)
- Corresponding author
- Ritz, Eberhard
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2002-05
- Volume
- 61
- Issue
- 80
- Pages
- S62-S67
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2045494721
- Cited by
- 95
- References
- 60
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 6 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 4 · 2014: 3 · 2013: 3 · 2012: 3
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Kidney International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- renal dysfunction, blood pressure, kidney transplantation, genetic hypertension, renal failure, salt retention, renin-angiotensin system, sympathetic nervous system, endothelial dysfunction, ACE inhibitors, angiotensin receptor blockers, renal protection, albuminuria, glomerulosclerosis, diabetic nephropathy, glomerulonephritis
- MeSH terms
- Humans, Hypertension, Renal
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