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Background Chronic kidney disease (CKD) manifested as reduced GFR and/or albuminuria, has been known to accelerate arterial stiffness and early vascular aging (EVA). Diabetes, hypertension, and glomerular disorders are the leading causes of CKD and renal failure. The question which etiology contributes more to this vascular phenomenon‑hypertensive and diabetic CKD or CKD secondary to immune‑mediated glomerulonephritis—remained unclear. Objective To compare pulse wave velocity (PWV ), a marker of arterial stiffness, between CKD patients of different etiologies: hypertensive and diabetic nephrosclerosis. vs. CKD secondary to glomerular disorders. Methods Clinical data were collected on 56 patients followed at the Nephrology and Hypertension Institute in Sam‑ son Assuta Ashdod University Hospital. All patients had at least one visit at our Nephrology clinics prior to recruitment. All patients with a glomerular disorder had a clinical‑pathological diagnosis based on a recent kidney biopsy. Pulse wave velocity (PWV ) was measured using a validated Sphygmocor XCEL device. Univariate and multivariate analyses were performed to compare PWV between hypertensive/diabetic CKD and CKD secondary to glomerular disorders. Results PWV was significantly higher in the hypertensive/diabetic CKD group, compared to the CKD ‑ GN group, with an average of. 12.2 m/s vs 8.3 m/s, respectively (p < 0.001). In a multivariate linear regression model, having CKD secondary to glomerulonephritis was associated with a signifi‑ cantly lower PWV (B = − 3.262, p < 0.001), compared with CKD secondary to hypertension and diabetes, with adjust‑ ment of age, creatinine, and comorbidities. Conclusion CKD Patients secondary to glomerulonephritis, have lower PWV when compared to CKD patients with diabetes and/or hypertension, even after adjusting for age, renal function, and the presence of comorbidities. It is intriguing to further study the possible protective role of immunosuppression on the arterial properties of CKD patients. Keywords CKD, Glomerulonephritis, Pulse wave velocity, Aortic stiffness, Inflammation *Correspondence: Adi Leiba email@example.com Full list of author information is available at the end of the article © The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. Lencovsky et al. Artery Research We compared CKD due to hypertension and/or dia- 1 Introduction betes (CKD-HTN/DM) with CKD secondary to glo- Arterial stiffness refers to a pathological process in which merulopathies (CKD-GN). All patients had at least one continuous and intermittent distention of the aorta with visit at our Nephrology clinics prior to recruitment. each heartbeat and during lifespan causes fatigue and CKD (GN) patients had a clinico-pathological diagno- fracture of the elastin fibers, and accumulation of colla - sis based on a kidney biopsy done at our institute within gen, leading to increased stiffening and decreased elastic - 3 years prior to study recruitment. Patients in this group ity of the aorta’s wall . The stiffer the artery, the higher had multiple glomerular disorders as the etiology for the pressure wave speed, which results in increased pulse their CKD. Patients with HTN or DM-related CKD had wave velocity (PWV) . been formally diagnosed by a nephrologist with a clinical Aging (normal or accelerated) as well as high blood diagnosis of essential hypertension, hypertensive nephro- pressure (BP)  are the main determinants of the sclerosis, benign nephrosclerosis, diabetic nephropathy, decline in arterial wall elasticity. Additional associated or diabetic kidney disease. They were excluded if they contributors are hyperlipidemia, diabetes mellitus (DM) were found to have an accompanying glomerular disease. and chronic kidney disease (CKD) [4–6]. Biopsy was not mandatory in the CKD-HTN/DM group. During the development and progression of CKD, The CKD-GN could have hypertension or diabetes, as the aortic compliance decreases, reducing systolic vol- long as their nephropathy was clearly due to the immune ume (SV) buffering capacity, resulting in an exaggerated mediated glomerulonephritis. increase of the systolic blood pressure (SBP) and a drop Patients with end-stage renal disease (ESRD) who were in diastolic blood pressure (DBP) . either on renal replacement therapy or had a renal trans- The most common causes of CKD leading to renal fail - plant were excluded, as well as patients under the age of ure are poorly controlled diabetes, uncontrolled hyper- 18, and pregnant women. Patients with immune disor- tension, and a variety of glomerular disorders . While ders, whose primary disease was extra-renal (skin, joints, the effect of hypertension and diabetes on arterial stiff - intestine, nerves) were also excluded. ness is quite established, autoimmune dysregulation, Data was collected from patients’ EMRs (electronic underlying most glomerulopathies, was not considered, medical records). Data included demographic details, until recently, as an accelerator of early vascular aging comorbidities, year of diagnosis, chronic medications, (EVA). However, a recent association was found between updated blood and urine test results etc. Each patient increased arterial stiffness and chronic inflammatory underwent a full physical examination, brachial blood states such as systemic lupus erythematosus (SLE), rheu- pressure measurement by an automated oscillometric matoid arthritis (RA), psoriatic arthritis, Crohn’s disease device, and a non-invasive central (aortic) blood pres- etc. [8, 9]. sure measurement (PWA—Pulse Wave Analysis) using CKD secondary to glomerular disorders (CKD-GN), applanation tonometry based S phygmocor XCEL device due to the known natural course of the diseases, is char- (Atcor Medical, Sydney, Australia). acterized by immune dysregulation, treatment with dif- Patients were supine at rest. Three brachial blood pres - ferent immunosuppressive drugs, and a relapsing and sure measurements were automatically recorded, and the remitting course . It is quite different from the low average brachial value was reported as well as the central grade, persistent inflammatory milieu of diabetic and blood pressure. To determine the carotid–femoral PWV, hypertensive CKD. The effects of these unique character - the pulse wave was recorded simultaneously at the femo- istics on arterial wall remodeling were not fully studied. ral artery (using a unique BP cuff over the thigh) and at In this study, we measured pulse wave velocity (PWV, the carotid artery by a tonometer probe. The distance m/sec), a validated marker of arterial stiffness, in CKD between the neck (at the palpated carotid pulse) and the secondary to glomerular disorders (CKD-GN) compared upper edge of the thigh cuff was measured and 80% of with that of CKD secondary to hypertension or diabetes this distance was automatically reported (direct measure- (CKD- HTN/DM). ment) . The study was approved by Samson Assuta Ash - dod Hospital’s IRB, and all patients signed an informed 2 Methods consent. Fifty-six patients were enrolled in our study. According to the definition of CKD, all patients recruited had either estimated glomerular filtration rate (eGFR) < 60 ml/ 2.1 Statistical Analysis min/1.73 m or urinary albumin to creatinine ratio The dependent variable was PWV measured by meter/ (uACR) ≥ 30 mg/gram, persistent over more than sec. Univariate analysis was performed to compare 3 months . the groups’ background characteristics and laboratory L encovsky et al. Artery Research findings (patients with CKD-GN vs. patients with 3 Results CKD- HTN/DM). All categorical variables are pre- The study included fifty-six patients, thirty-one of whom sented as numbers and frequencies (%). Most con- were in the CKD-GN group and 25 in the CKD-HTN/ tinuous variables were not normally distributed and DM group (Table 1). therefore presented as median (IQR). The distribu- Figure 1 presents the different etiologies in the CKD- tion of PWV in both groups was normal. We used the GN group, the most common being IgA nephropathy Mann–Whitney U test to examine the relationship 52%) and membranous nephropathy (19%). between quantitative independent variables and glo- Twenty-one of the 56 subjects (37.5%) were females. merular disease. We used the chi-square test to exam- The median age was 52.5 (IQR 37–67). The CKD-GN ine the relationship between nominal independent group patients were younger than the CKD-HTN/DM variables and glomerular disease (no corrections were patients (41 vs. 67 years old, p < 0.001) and had fewer needed). A univariate linear regression model was used comorbidities (Table 1). to determine the effect of independent parameters Both groups had similar diastolic BP values, both associated with glomerular disease on PWV. Param- brachial and central (p value = 0.95). Patients in the eters were then selected for the multivariate analysis CKD-HTN/DM group had an elevated brachial systolic based on their level of significance (p-value < 0.2), their BP compared to CKD-GN-147 mmHg vs. 123 mmHg clinical significance, and the confounding potential of (p = 0.0011) (Table 2). Interestingly, central (aortic) BP the main comparison in the study. as measured by Pulse Wave Analysis (PWA) was not significantly different between groups (132 mmHg vs 119 mmHg, p = 0.23). Table 1 Epidemiological characteristics in the study group and the control group All subjects (n = 56, 100%) CKD-GN (n = 31, 55.4%) CKD-HTN/DM (n = 25, 44.6%) p value Age (years) median (IQR) 52.5 (37–67) 41 (28–52) 67 (58.5–75) < 0.001 Gender (female) n (%) 35 (62.5%) 20 (64.5%) 15 (60%) 0.729 BMI (KG/M2) median (IQR) 27.8 (25.3–30.6) 26.9 (22.3–28.4) 30.5 (28.1–32.5) < 0.001 Glucose (MG/DL) median (IQR) 102 (94–123) 96 (89–103) 118.5 (102–146.9) < 0.001 HBA1C (%) median (IQR) 5.6 (5.3–6.4) 5.4 (5.2–5.6) 6.2 (5.6–7.2) 0.003 LDL (MG/DL) median (IQR) 94.5 (75.5–135.5) 128.4 (94.5–150.3) 82.6 (71–106.5) 0.003 Triglycerides (MG/DL) median (IQR) 126 (90.5–190) 105 (78.8–136.5) 155 (109–234) 0.002 Albumin (MG/DL) median (IQR) 3.9 (3.7–4.3) 3.9 (3.6–4.3) 4 (3.8–4.4) 0.367 Hemoglobin level (MG/DL) median (IQR) 12.7 (11.1–13.7) 12.9 (11.4–13.7) 12.6 (10.5–14.2) 0.936 Creatinine (MG/DL) median (IQR) 1.26 (0.9–1.6) 1.1 (0.9–1.4) 1.4 (1.2–1.7) 0.056 GFR median (IQR) 50 (38.2–90) 86 (45.8–106.8) 42 (37–53) 0.002 Urine protein‑ creatinine ratio (PCR) MEDIAN (IQR) 653.1 (193.5–1104) 733.7 (416–1227.8) 345.1 (131.2–759.5) 0.119 Urine albumin‑ creatinine ratio (ACR) median (IQR) 94.1 (26.4–300) 137.1 (34.9–316.8) 94.1 (22.8–225.8) 0.314 Urine protein median (IQR) 300.7 (177.3–852.9) 277.5 (176.8–870.3) 337.7 (155.6–856) 0.975 Smoking n (%) 12 (22.6%) 4 (13.3%) 8 (34.8%) 0.064 Diabetes mellitus n (%) 17 (30.4%) 2 (6.5%) 15 (60%) < 0.001 Hypertension n (%) 30 (60%) 10 (38.5%) 20 (83.3%) 0.001 Raas inhibitors n (%) 34 (69.4%) 18 (72%) 16 (66.7%) 0.686 Calcium channel blockers n (%) 15 (30.6%) 4 (16%) 11 (45.8%) 0.024 Beta blockers n (%) 17 (34.7%) 3 (12%) 14 (58.3%) 0.001 Diuretics n (%) 14 (28.6%) 2 (8%) 12 (50%) 0.001 Alpha blockers n (%) 8 (16.3%) 2 (8%) 6 (25%) 0.108 Statins n (%) 27 (55.1%) 8 (32%) 19 (79.2%) 0.001 Drug treatment for diabetes n (%) 16 (32.7%) 2 (8%) 14 (58.3%) < 0.001 Treatment for dyslipidemia n (%) 24 (51.1%) 11 (47.8%) 13 (54.2%) 0.664 IQR interquartile range, BMI body mass index, HbA1C hemoglobin A1C, LDL low-density lipoprotein cholesterol, GFR glomerular filtration rate, RAAS renin– angiotensin–aldosterone system Mann–Whitney test U b 2 χ test Lencovsky et al. Artery Research Eology of GN 3% 3% 3% 6% 7% 7% 52% 19% IgA nephropathy Membranous nephropathy Vasculis FSGS SLE Alport synndrome IgM nephropathy Mesnagial proliferaon Fig. 1 Etiologies of Glomerulonephritis. This pie chart describes the frequency (by percentages) of the different etiologies of glomerulonephritis in the CKD‑ GN group. FSGS focal segmental glomerulosclerosis, SLE systemic lupus erythematosus Table 2 Brachial blood pressure, Central (Aortic) blood pressure and Pulse Wave Velocity (PWV) in both CKD‑ GN and CKD‑HTN/DM groups All subjects (n = 56, 100%) CKD-GN (n = 31, 55.4%) CKD- HTN/DM p value (n = 25, 44.6%) Arterial stiffness (PWV ), (ms) Median (IQR) 10 (7.9–12.1) 8.3 (7.2–10) 12.2 (10.5–13.6) < 0.0011 Systolic brachial BP, (mmHg) Median (IQR) 134 (121–152) 123 (118–131) 147.5 (134.3–163) 0.0011 Diastolic brachial BP, (mmHg) Median (IQR) 76 (67–85) 76 (67–83) 75.5 (66.8–87.3) 0.9581 Central systolic BP, (mmHg) Median (IQR) 127.5 (107–148.5) 119 (103–146) 132 (116.5–151) 0.2281 Central diastolic BP, (mmHg) Median (IQR) 76 (70–87) 76 (71–84) 76 (68.5–88.5) 0.9491 PWV pulse wave velocity, IQR interquartile range, BP blood pressure Mann-Whitney U test P < 0.05 in bold Patients with CKD- GN were found to have a signifi - 95%CI = 0.069–0.152, p < 0.001), presence of diabetes cantly lower PWV as compared with CKD-HTN/DM mellitus (B = 3.058, 95%CI = 1.201–4.915, p = 0.002) and patients—8.3 m/s vs. 12.2 m/s, respectively (p < 0.0001, eGFR (B = − 0.048, 95%CI = − 0.077–0.018, p = 0.002). Table 2). In a multivariate model adjusted for age, comorbidi- The univariate linear regression models are sum - ties (diabetes, hypertension), and creatinine levels—only marized in Table S1. Variables that had the most the presence of CKD-GN and age were found to be sig- noticeable effects on PWV were age (B = 0.111, nificant variables (p = 0.006 and p = 0.039 accordingly; L encovsky et al. Artery Research Table 3 A multivariate linear regression analysis—factors accompanying hormones such as PTH, fetuin-A, klotho associated with PWV (P < 0.05 in bold) and FGF23), angiotensin II, aldosterone, asymmetric dimethylarginine (ADMA), endothelin-1, increased sym- Variable B Beta P value 95%CI pathetic activity and baroreflex dysfunction- all cause an Glomerular disease − 3.262 − 0.489 0.006 − 5.531 − 0.993 interplay of events leading to oxidative stress, endothelial Age (years) 0.063 0.351 0.039 0.003 0.123 dysfunction, increased vascular tone, inflammation and Diabetes − 0.379 − 0.054 0.689 − 2.331 1.574 vascular calcification . Hypertension − 1.435 − 0.211 0.131 − 3.313 0.443 One might speculate, looking at our results, that among Creatinine (mg/dl) 0.775 0.210 0.083 − 0.106 1.656 CKD patients with rheumatological and immunological disorders, this interplay of events is somewhat different. Our group had previously published a study on col- chicine-treated Familial Mediterranean Fever (FMF) Table 3). No collinearity was found between the inde- patients. We have demonstrated that they had PWV pendent variables (using Spearman correlation with a values similar to healthy controls, suggesting a favorable cutoff of r < 0.6). No interactions between the independ- outcome of intermittent, waxing and waning inflamma - ent variables were detected. According to this model, tion, as opposed to chronic, low-grade, inflammation. CKD-GN was associated with lower PWV compared We also suggested that colchicine could have a protective with CKD- HTN/DM (B = − 3.262, 95% CI − 5.531 to role on arterial structure and function . − 0.993, p < 0.001). Similar findings were demonstrated in a study that compared patients with IgA nephropathy, the most com- 4 Discussion mon type of glomerulonephritis (GN), to polycystic kid- In this study, we found that patients with CKD second- ney disease (PKD) and controls. In this study, arterial ary to glomerular disorders have a PWV which is far less stiffness in both groups was higher than in the control than that of CKD of diabetic/hypertensive origin (8.3 m/s group. However, a pre-specified subgroup analysis dem - vs. 12.2 m/s). onstrated IgA nephropathy patients to have lower PWV Laurent et al. and The Reference Values for Arte - than the PKD group . rial Stiffness’ Collaboration published reference values IgA nephropathy, just like FMF, is a disease with inter- of PWV stratified by age and blood pressure categories mittent inflammation rather than the classical chronic [12, 13]. People at an age range of 60–69 years and stage low-grade inflammatory state of diabetic or hypertensive I hypertension (thus comparable to our CKD-HTN/DM CKD. And it is therefore safe to assume that PWV should group) had a median PWV of 10.7 m/sec. A median value act in a similar way . of 12.2 m/sec, as in our hypertensive and diabetic CKD In a study by Karras et al. on 161 consecutive renal group is significantly higher. transplant patients, mean PWV decreased from 10.8 m/ In the CKD-GN group (median age 41, median bra- sec in the third month post-transplant to 10.1 m/sec after chial systolic BP 123 mmHg) we have measured a median 12 months (p < 0.001), interestingly there was no relation PWV of 8.3 m/sec, somewhat higher than that of age and between vascular function improvement and GFR . BP matched reference values of 7.4 m/sec , but still It is possible that immunosuppressive treatment (pred- significantly lower than the arterial stiffness observed in nisone, colchicine, post-transplant immunosuppression) our CKD-HTN/DM group. interferes with the inflammatory milieu in CKD, which Being a marker of arterial stiffness, our study confirms is the cornerstone of arterial stiffening. Since patients in the well-known connection between CKD and early our GN group had previously been on different immu - vascular aging . Moreover, our study demonstrates, nomodulatory drugs, it can possibly explain the low val- regarding the effects on large arteries, that not all CKD ues of PWV seen in our CKD-GN group. is the same; When assessing CKD of different etiologies Our study’s main limitations are a small sample size and their impact on vascular structure and function, as well as baseline differences between groups. For that CKD secondary to diabetes and hypertension is a very reason, we used a multivariate regression model, that low-grade, chronic inflammatory state leading to the took into account the main possible confounders (age, aforementioned changes in the vascular structure of the presence of diabetes, presence of hypertension and CKD great arteries and slow gradient increase in the arterial severity). Still, residual confounders are always a possi- stiffness . bility. Another limitation is the lack of accurate data on Accumulation of advanced glycation end products multiple immunomodulatory and immunosuppressive (AGEs), due to increased production and decreased elim- treatments given to our CKD-GN patients during the ination occurs even in non-diabetic CKD. AGEs, together course of their disease. Pulse was not documented during with high sodium load, uric acid, phosphate (and Lencovsky et al. Artery Research 3. Sun Z. Aging, arterial stiffness, and hypertension. Hypertension. measurements and therefore we could not address the 2015;65(2):252–6. https:// doi. org/ 10. 1161/ HYPER TENSI ONAHA. 114. 03617. possible SBP amplification. 4. Aminuddin A, Lazim MRMLM, Hamid AA, Hui CK, MohdYunus MH, The strengths of our study are the accurate histological Kumar J, et al. The association between inflammation and pulse wave velocity in dyslipidemia: an evidence‑based review. Mediators Inflamm. diagnosis of our GN patients, which had recent kidney 2020;2020:1–11. biopsies done at our institute, as well as comprehensive 5. Doyon A, Schaefer F. Taking the pulse of a sick kidney: arterial stiffness in clinical and laboratory data on all patients. glomerulonephritis. Pediatr Nephrol. 2011;26:161–3. 6. Zanoli L, Lentini P, Briet M, Castellino P, House AA, London GM, et al. In conclusion, our study suggests that CKD secondary Arterial stiffness in the heart disease of CKD. J Am Soc Nephrol. to immune-mediated GN carries a lower risk of early vas- 2019;30(6):918–28. cular aging and stiffening, as compared to CKD related to 7. Official Journal of the International Society of Nephrology KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic hypertension and diabetes. Since cardiovascular morbid- Kidney Disease. 2012. Available from: www. publi catio nethi cs. org ity and mortality are the main burden of disease in CKD 8. Zanoli L, Ozturk K, Cappello M, Inserra G, Geraci G, Tuttolomondo A, et al. patients, further study is needed to delineate the exact Inflammation and aortic pulse wave velocity: a multicenter longitudinal study in patients with inflammatory bowel disease. J Am Heart Assoc. mechanisms underlying such vascular protection. 2019. https:// doi. org/ 10. 1161/ JAHA. 118. 010942. 9. Booth AD, Wallace S, McEniery CM, Yasmin BJ, Jayne DRW, et al. Inflam‑ Supplementary Information mation and arterial stiffness in systemic vasculitis: a model of vascular inflammation. Arthritis Rheum. 2004;50(2):581–8. The online version contains supplementary material available at https:// doi. 10 Couser WG, Johnson RJ. The etiology of glomerulonephritis: roles of org/ 10. 1007/ s44200‑ 023‑ 00034‑4. infection and autoimmunity. Kidney Int. 2014;86:905–14. 11. Weber T, Ammer M, Rammer M, Adji A, O’Rourke MF, Wassertheurer S, Below is the link to the electronic supplementary material.Supplementary et al. Noninvasive determination of carotid‑femoral pulse wave velocity file1 (DOCX 21 KB) depends critically on assessment of travel distance: a comparison with invasive measurement. J Hypertens. 2009;27(8):1624–30. 12. Laurent S, Cockcroft J, Van Bortel L, Boutouyrie P, Giannattasio C, Hayoz Author Contributions D, et al. Expert consensus document on arterial stiffness: methodological OL: author of the article, AAA: Scientific editing, EG: Data collection. RTBI: issues and clinical applications. Eur Heart J. 2006;27(21):2588–605. Statistical analysis, MA: patients’ enrollment and data collection, OK: patients 13. Blacher J, Asmar R, Djane S, London GM, Safar ME. Aortic pulse wave enrollment and data collection, AL: Head of the nephrology department in velocity as a marker of cardiovascular risk in hypertensive patients. Hyper‑ Assuta Ashdod, scientific editing, statistical analysis. tension. 1999;33:1111–7. 14 Inserra F, Forcada P, Castellaro A, Castellaro C. Chronic kidney disease and Funding arterial stiffness: a two ‑ way path. Front Med. 2021. https:// doi. org/ 10. No funding was provided. 3389/ fmed. 2021. 765924. 15 Krata N, Zagożdżon R, Foroncewicz B, Mucha K. Oxidative Stress in Kidney Availability of Data and Materials Diseases: The Cause or the Consequence? Arch Immunol Ther Exp The datasets used and/or analyzed during the current study are available from ( Warsz). 2018;66(3):211–20. the corresponding author upon reasonable request. 16. Kukuy O, Livneh A, Mendel L, Benor A, Giat E, Perski O, et al. Normal arterial stiffness in familial Mediterranean fever. Evidence for a pos‑ sible cardiovascular protective role of colchicine. Clin Exp Rheumatol. Declarations 2017;35:S32–7. 17. Késoi I, Sági B, Tóth OI, Vas T, Fazekas A, Kovács T, et al. Different effect Conflicts of Interest of IgA nephropathy and polycystic kidney disease on arterial stiffness. The authors have no conflicts of interest to declare. Kidney Blood Press Res. 2011;34(3):158–66. 18. Abdi‑Ali A, Mann MC, Hemmelgarn BR, MacRae JM, Turin TC, Benedikts‑ Ethical Approval and Consent to Participate son H, et al. IgA nephropathy with early kidney disease is associated with The study was approved by Samson Assuta Ashdod Hospital’s IRB, and all increased arterial stiffness and renin‑angiotensin system activity. J Renin patients signed an informed consent. Angiotensin Aldosterone Syst. 2015;16(3):521–8. 19. Karras A, Boutouyrie P, Briet M, Bozec E, Haymann JP, Legendre C, et al. Consent for Publication Reversal of arterial stiffness and maladaptative arterial remodeling after Not applicable. kidney transplantation. J Am Heart Assoc. 2017. https:// doi. org/ 10. 1161/ JAHA. 117. 006078. Author details Faculty of Health Sciences, Joyce and Irving Goldman Medical School at Ben Gurion, University of the Negev, Beersheba, Israel. Department of Nephrology and Hypertension Institute, Samson Assuta Ashdod Hospital, Ashdod, Israel. Sheba Medical Center, Tel Hashomer, Ramat Gan, Israel. Received: 17 April 2023 Accepted: 23 May 2023 References 1. Boutouyrie P, Chowienczyk P, Humphrey JD, Mitchell GF. Arterial stiffness and cardiovascular risk in hypertension. Circ Res. 2021;128:864–86. 2. Fiori G, Fuiano F, Scorza A, Conforto S, Sciuto SA. Non‑invasive methods for PWV measurement in blood vessel stiffness assessment. IEEE Rev Biomed Eng. 2022;15:169–83.
Artery Research – Springer Journals
Published: Sep 1, 2023
Keywords: CKD; Glomerulonephritis; Pulse wave velocity; Aortic stiffness; Inflammation
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