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Ultrasonic evaluation of renal cortex arterial area enables differentiation between hypertensive and glomerulonephritis-related chronic kidney disease.

ABSTRACT: Identifying the primary etiology of cardio-renal syndrome in a timely manner remains an ongoing challenge in nephrology. We hypothesized that hypertensive kidney damage can be distinguished from chronic glomerulonephritis at an early stage of chronic kidney disease (CKD) using ultrasound (US) Doppler sonography.Fifty-six males (age 54 ± 15, BMI 28.3 ± 3.5 kg/m(2)) with hypertension and stable CKD at stages 2-4 [38 with essential hypertension (HT-CKD); 18 with glomerulonephritis (GN-CKD)] were studied. Blood tests, UACR, echocardiography, ABPM, carotid IMT, and an ultrasound dynamic tissue perfusion measurement (DTPM) of the renal cortex were performed.HT-CKD patients had reduced proximal renal cortex perfusion as well as reduced total and proximal renal cortex arterial area. Proximal renal cortex arterial area ≤0.149 cm(2) identified hypertension-related CKD with a sensitivity of 71% and a specificity of 78% (AUC 0.753, p < 0.001).Evidence of diminished arterial vascularity or perfusion of renal proximal cortex, both derived from US Doppler, could be helpful in differentiating hypertensive nephropathy from glomerulonephritis-related CKD.

SUBMITTER: Lubas A

PROVIDER: S-EPMC5556137 | biostudies-other | 2017 Jun

REPOSITORIES: biostudies-other

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Project description:BACKGROUND:Increased nerve activity causes hypertension and kidney disease. Recent studies suggest that renal denervation reduces BP in patients with hypertension. Renal NE release is regulated by prejunctional α2A-adrenoceptors on sympathetic nerves, and α2A-adrenoceptors act as autoreceptors by binding endogenous NE to inhibit its own release. However, the role of α2A-adrenoceptors in the pathogenesis of hypertensive kidney disease is unknown. METHODS:We investigated effects of α2A-adrenoceptor-regulated renal NE release on the development of angiotensin II-dependent hypertension and kidney disease. In uninephrectomized wild-type and α2A-adrenoceptor-knockout mice, we induced hypertensive kidney disease by infusing AngII for 28 days. RESULTS:Urinary NE excretion and BP did not differ between normotensive α2A-adrenoceptor-knockout mice and wild-type mice at baseline. However, NE excretion increased during AngII treatment, with the knockout mice displaying NE levels that were significantly higher than those of wild-type mice. Accordingly, the α2A-adrenoceptor-knockout mice exhibited a systolic BP increase, which was about 40 mm Hg higher than that found in wild-type mice, and more extensive kidney damage. In isolated kidneys, AngII-enhanced renal nerve stimulation induced NE release and pressor responses to a greater extent in kidneys from α2A-adrenoceptor-knockout mice. Activation of specific sodium transporters accompanied the exaggerated hypertensive BP response in α2A-adrenoceptor-deficient kidneys. These effects depend on renal nerves, as demonstrated by reduced severity of AngII-mediated hypertension and improved kidney function observed in α2A-adrenoceptor-knockout mice after renal denervation. CONCLUSIONS:Our findings reveal a protective role of prejunctional inhibitory α2A-adrenoceptors in pathophysiologic conditions with an activated renin-angiotensin system, such as hypertensive kidney disease, and support the concept of sympatholytic therapy as a treatment.

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Ultrasonic evaluation of renal cortex arterial area enables differentiation between hypertensive and glomerulonephritis-related chronic kidney disease.

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