Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Oct;70(4):687-694.
doi: 10.1161/HYPERTENSIONAHA.117.08314. Epub 2017 Jul 31.

Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease

Karen A Griffin  1
Affiliations
Review

Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease

Karen A Griffin. Hypertension. 2017 Oct.
No abstract available

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Schematic illustration of differences in susceptibility to hypertension-induced renal damage (HIRD) between patients with essential hypertension (benign and malignant nephrosclerosis) and those with diabetic and non-diabetic CKD with respect to BP thresholds and slopes of the relationship between BP and HIRD (Reproduced from Ref. with permission).
Fig. 2
Fig. 2
Quantitative relationships between radiotelemetrically measured systolic BP and renal injury in rats with intact autoregulation (normotensive Sprague-Dawley controls [SD, circles]; spontaneously hypertensive rat [SHR, triangles]; stroke-prone SHR [SHRsp; diamonds]; SHR [gray triangles] and SHRsp [gray diamonds] placed on a high salt diet) and in the 5/6 renal ablation model of CKD [squares], with impaired autoregulation. The renal damage score represents a composite of vascular and glomerular damage scores in the SHRsp and % GS in the 5/6 ablation model (reproduced with permission from Ref. , based on data from Ref. 14,18). Minimal injury is seen in SHR with intact autoregulation despite severe hypertension. Injury in the salt-sensitive SHRsp administered a high NaCl diet occurs at blood pressures that exceed the autoregulatory capacity while the 5/6 renal ablation model, with impaired autoregulation, exhibits a much lower BP threshold for hypertensive injury than normal or SHR kidneys.
Fig 3
Fig 3
a) Summary of renal autoregulatory patterns obtained in rats with 1) intact kidneys and normal autoregulation (——), 2) vasodilated vascular bed and normal autoregulation as after uninephrectomy) ( – – – ) and 3) vasodilated vascular bed and impaired autoregulation (i.e., 5/6 renal ablation model of CKD) (– · – · –). (Reprinted with permission from reference 6).
Fig. 4
Fig. 4
A comparison of the qualitative relationship between BP and renal damage in the continuous exogenous Ang II infusion model of HTN (300–500 ng/kg/min for 4 weeks) with the salt-supplemented stroke prone spontaneously hypertensive rat (SHRsp) model of malignant HTN and the hypertensive 5/6 renal ablation model of CKD in Sprague-Dawley rats. The average systolic BP (final 4 wks) and renal damage scores for each of the three models are shown. As can be seen, the rats with Ang II-induced HTN develop very limited HIRD despite an average systolic BP that is as high as the SHRsp. Moreover, in contrast to the strong correlations between BP and HIRD in both the SHRsp and 5/6 ablation models shown in Fig. 2, the Ang II-infused rats exhibit a much weaker correlation and a flatter slope (increase in HIRD/mmHg increase in average systolic BP) (r2 = 0.27, slope 0.28±0.11; p < 0.025). By comparison, the slope value for SHRsp were 1.13±0.24 and 1.3±0.15 for the 5/6 ablation model, p< 0.01 for both model vs. the Ang II model). (Adapted with permission from the cited references).
Fig. 5
Fig. 5
Compilation of data obtained in our laboratory which illustrates the quantitative relationships between BP and glomerulosclerosis (GS) in rats with 5/6 renal ablation who were left untreated or received either dehydropyridine (DHP) calcium channel blockers or RAS blockade. The deleterious effects of calcium channel blockers on GS as compared to untreated or RAS blockade treated rats are evident. (Reproduced from Ref. with permission).
Fig. 6
Fig. 6
A schematic illustration of the potential differences in individual susceptibility to hypertensive renal damage. These differences are indicated by the differences in the BP threshold for renal (glomerular) damage and the slope of the relationships between BP and glomerular injury. (Reproduced from Ref. with permission).
See this image and copyright information in PMC

References

    1. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risk of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296–1305. - PubMed
    1. Hsu CY, McCulloch CE, Darbinian J, Go AS, Iribarron C. Elevated blood pressure and risk of end-stage renal disease in subjects without baseline kidney disease. Arch Intern Med. 2005;165:923–928. - PubMed
    1. Kopp JB. Rethinking hypertensive kidney disease: arterionephrosclerosis as a genetic, metabolic, and inflammatory disorder. Curr Opin Nephrol Hypertens. 2013;22:266–272. - PMC - PubMed
    1. Olson JL. Renal Disease caused by hypertension. In: Jennette JC, Olson JL, Schwartz MM, Silva FG, editors. Heptinstall’s Pathology of the Kidney. Lippincott Williams & Wilkins; Philadelphia, PA: 2006. pp. 937–990. Sixth. II.
    1. Bidani AK, Griffin KA. Pathophysiology of hypertensive renal damage: implications for therapy. Hypertension. 2004;44:595–601. - PubMed

Publication types

MeSH terms