Hypertensive nephropathy as an outcome of unilateral nephrectomy in kidney cancer

Aim. To study the adaptive mechanisms of structural and functional changes in a single kidney after nephrectomy for kidney cancer. Materials and Methods. A total of 179 operations of two types were performed: nephrectomy and kidney resection in patients with cancerous lesions. Postoperative ultrasound was performed size control and dopplerography of the vessels of the contralateral single kidney, monitoring-control of blood pressure. Results. In case of kidney resection, the adaptive mechanisms controlling the volume of functioning tissue are preserved. The load on the organ remains minimal and physiological, and is not redistributed, blood pressure remains close to baseline. Nephrectomy does not lead to functional changes in a single kidney, but to adaptive and pathophysiological structural damage as a result of increased plasma pressure, organ reboot, its vicarious hypertrophy, which is accompanied by venous edema of interstitium as a pressure factor on the tissue, increased tone of arterioles, the development of secondary organ ischemia, circulatory hypoxia and increased blood pressure. All this fits into the clinical picture of hypertensive nephropathy. Conclusions. The potential risk of hypertension and hypertensive nephropathy in patients undergoing nephrectomy, compared with patients after organ-saving surgery, is significantly higher. One of the most important manifestations of hypertension in the elderly is a violation of the structure and function of target organs, which include: the brain, heart, blood vessels, kidney. Nephrectomy forms a pathological vicious circle, contributing to the development and further progression of renal and cardiovascular failure.

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First experience of superselective embolization of renal arteries supplying the tumor with subsequent laparoscopic kidney resection

Cancer Urology ◽

10.17650/1726-9776-2021-17-3-30-36. ◽

2021 ◽

Vol 17 (3) ◽

pp. 30-36

Author(s):

V. L. Astashov ◽

V. V. Shapovalov ◽

V. V. Balanyuk ◽

A. I. Zagorul’ho ◽

D. V. Kozlov ◽

...

Keyword(s):

Blood Loss ◽

Renal Artery ◽

Kidney Cancer ◽

Renal Tumors ◽

Two Stage ◽

Second Stage ◽

Superselective Embolization ◽

Single Kidney ◽

Functioning Kidney ◽

Kidney Resection

Background. Patients with signs of tumor lesions in a single kidney or in the only one functioning kidney, with bilateral renal tumors are at high risk of functional failure or insufficiency of the kidney after surgery. Joint discussions with specialists in X-ray endovascular surgeries resulted in the development of a treatment algorithm for patients with localized kidney cancer who require organ-sparing surgery without ischemic kidney resection.Objective: to evaluation of the immediate results of two-stage surgical treatment of localized kidney cancer in patients with signs of tumor lesions in a single kidney or in the only one functioning kidney, with bilateral renal tumors, including superselective embolization of the artery supplying the tumor at the first stage, and laparoscopic kidney resection without renal ischemia parenchyma at the second stage.Materials and methods. This study included 5 patients with localized kidney cancer, who underwent two-stage treatment at Moscow Regional Oncology Dispensary between 24.03.2021 and 19.04.2021. The first stage included superselective embolization of the artery supplying the tumor; the second stage implied laparoscopic kidney resection 6-7 days following the first stage.Results. The median age of the patients was 62 years (range: 42-73 years). Four patients (80%) had unilateral kidney lesions, while 1 patient (20 %) had bilateral (synchronous) kidney cancer. The mean RENAL score was 8 (range: 6-10); patients were distributed as follows: score 4-6 in 40 %, score 7-9 in 40 %, and score >10 in 20 % of patients. At the first stage, patients underwent endovascular embolization of the branches of the renal artery. Patients had superselective embolization of either middle (n = 3; 60 %), upper (n = 1; 20 %), or lower (n = 1; 20 %) segmental arteries supplying the tumor. In one of them (20 %), we identified 3 large arterial branches; in another one (20 %), we identified 2 large arterial branches.At the second stage, we performed laparoscopic kidney resection. None of the patients required renal artery clamping, because there was an excellent visualization of the demarcation zone and no significant blood loss. The resection area was sutured in 1 case (20 %). In 2 individuals (40 %), a hemostatic sponge was installed in the removed tumor bed. In the remaining 2 cases (40 %), hemostasis was ensured by coagulation. The median blood loss was 100 mL (range: 50-200 mL). The postoperative period was uneventful in all patients. None of the patients developed symptoms of acute renal failure.Conclusion. Thus, superselective embolization of arteries supplying a kidney tumor has undeniable advantages in organ-sparing surgeries for patients with localized kidney cancer and some additional kidney problems, when organ preservation is crucial for patient's life.

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The Capabilities of Amlodipine/Lisinopril Single-Pill Combination in the Treatment of Newly Diagnosed Arterial Hypertension in a Middle-Aged Patient (Case Report)

Rational Pharmacotherapy in Cardiology ◽

10.20996/1819-6446-2020-03-03 ◽

2020 ◽

Vol 16 (2) ◽

pp. 221-230

Author(s):

A. I. Kochetkov ◽

M. V. Lopukhina ◽

E. A. Kotaeva ◽

A. A. Kirichenko ◽

O. D. Ostroumova

Keyword(s):

Blood Pressure ◽

Arterial Hypertension ◽

Left Ventricular ◽

Favorable Effect ◽

Newly Diagnosed ◽

Functional Changes ◽

Collagen Formation ◽

Cardiovascular Morbidity And Mortality ◽

Single Pill ◽

Left Atrial Stiffness

Arterial hypertension (AH) is one of the most significant modifiable risk factors that increase cardiovascular morbidity and mortality worldwide, including Russia. The complex of structural and functional changes in the heart that occurs during AH consists not only in the formation of left ventricular (LV) myocardial hypertrophy, but also in the myocardial stiffness increasing due to collagen formation and cardiomyocytes apoptosis. These abnormalities are substrate for diastolic function disturbances, electrical myocardial instability and ischemia. The article provides a clinical case of amlodipine/lisinopril single-pill combination (A/L SPC) use in real clinical practice in a patient with stage II grade 2 newly diagnosed AH and its effect on blood pressure and echocardiographic myocardial fibrosis markers, including speckle tracking parameters The high antihypertensive efficacy of A/L SPC, a favorable effect on blood pressure circadian rhythm, as well as pronounced target-organ protective properties, in particular the ability to reduce LV and left atrial stiffness, were demonstrated. So, we conclude that A/L SPC improve the elastic properties of the left heart.

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Spontaneous one-kidney rats are more susceptible to develop hypertension by DOCA-NaCl and subsequent kidney injury compared with uninephrectomized rats

AJP Renal Physiology ◽

10.1152/ajprenal.00555.2015 ◽

2016 ◽

Vol 310 (10) ◽

pp. F1054-F1064 ◽

Cited By ~ 9

Author(s):

Xuexiang Wang ◽

Ashley C. Johnson ◽

Jennifer M. Sasser ◽

Jan M. Williams ◽

Leah C. Solberg Woods ◽

...

Keyword(s):

Blood Pressure ◽

Kidney Function ◽

Time Course ◽

Kidney Injury ◽

Solitary Kidney ◽

Course Evaluation ◽

Significant Rise ◽

Kidney Weight ◽

Unilateral Renal Agenesis ◽

Single Kidney

There is little clinical data of how hypertension may influence individuals with nephron deficiency in the context of being born with a single kidney. We recently developed a new rat model (the heterogeneous stock-derived model of unilateral renal agenesis rat) that is born with a single kidney and exhibits progressive kidney injury and decline in kidney function with age. We hypothesized that DOCA-salt would induce a greater increase in blood pressure and therefore accelerate the progression of kidney injury in rats born with a solitary kidney compared with rats that have undergone unilateral nephrectomy. Time course evaluation of blood pressure, kidney injury, and renal hemodynamics was performed in the following six groups of animals from weeks 13 to 18: 1) DOCA-treated rats with a solitary kidney (DOCA+S group), 2) placebo-treated rats with a solitary kidney, 3) DOCA-treated control rats with two kidneys (DOCA+C group), 4) placebo-treated control rats with two kidneys, 5) DOCA-treated rats with two kidneys that underwent uninephrectomy (DOCA+UNX8 group), and 6) placebo-treated rats with two kidneys that underwent uninephrectomy. DOCA+S rats demonstrated a significant rise ( P < 0.05) in blood pressure (192 ± 4 mmHg), proteinuria (205 ± 31 mg/24 h), and a decline in glomerular filtration rate (600 ± 42 μl·min−1·g kidney weight−1) relative to the DOCA+UNX8 (173 ± 3 mmHg, 76 ± 26 mg/24 h, and 963 ± 36 μl·min−1·g kidney weight−1) and DOCA+C (154 ± 2 mmHg, 7 ± 1 mg/24 h, and 1,484 ± 121 μl·min−1·g kidney weight−1) groups. Placebo-treated groups showed no significant change among the three groups. An assessment of renal injury markers via real-time PCR/Western blot analysis and histological analysis was concordant with the measured physiological parameters. In summary, congenital solitary kidney rats are highly susceptible to the induction of hypertension compared with uninephrectomized rats, suggesting that low nephron endowment is an important driver of elevated blood pressure, hastening nephron injury through the transmission of elevated systemic blood pressure and thereby accelerating decline in kidney function.

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Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

AJP Renal Physiology ◽

10.1152/ajprenal.00252.2006 ◽

2007 ◽

Vol 292 (2) ◽

pp. F861-F867 ◽

Cited By ~ 17

Author(s):

Melvin R. Hayden ◽

Nazif A. Chowdhury ◽

Shawna A. Cooper ◽

Adam Whaley-Connell ◽

Javad Habibi ◽

...

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Systolic Blood Pressure ◽

Proximal Tubule ◽

Structural Damage ◽

Kidney Tissue ◽

Proximal Tubule Cell ◽

Ang Ii ◽

Sprague Dawley ◽

Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

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Transcriptomic analysis reveals inflammatory and metabolic pathways that are regulated by renal perfusion pressure in the outer medulla of Dahl-S rats

Physiological Genomics ◽

10.1152/physiolgenomics.00034.2018 ◽

2018 ◽

Vol 50 (6) ◽

pp. 440-447 ◽

Cited By ~ 2

Author(s):

Louise C. Evans ◽

Alex Dayton ◽

Chun Yang ◽

Pengyuan Liu ◽

Theresa Kurth ◽

...

Keyword(s):

Blood Pressure ◽

Perfusion Pressure ◽

Left Kidney ◽

Respiratory Control ◽

Renal Perfusion ◽

Renal Physiology ◽

Sequencing Analysis ◽

Functional Changes ◽

Renal Perfusion Pressure ◽

Novel Approach

Studies exploring the development of hypertension have traditionally been unable to distinguish which of the observed changes are underlying causes from those that are a consequence of elevated blood pressure. In this study, a custom-designed servo-control system was utilized to precisely control renal perfusion pressure to the left kidney continuously during the development of hypertension in Dahl salt-sensitive rats. In this way, we maintained the left kidney at control blood pressure while the right kidney was exposed to hypertensive pressures. As each kidney was exposed to the same circulating factors, differences between them represent changes induced by pressure alone. RNA sequencing analysis identified 1,613 differently expressed genes affected by renal perfusion pressure. Three pathway analysis methods were applied, one a novel approach incorporating arterial pressure as an input variable allowing a more direct connection between the expression of genes and pressure. The statistical analysis proposed several novel pathways by which pressure affects renal physiology. We confirmed the effects of pressure on p-Jnk regulation, in which the hypertensive medullas show increased p-Jnk/Jnk ratios relative to the left (0.79 ± 0.11 vs. 0.53 ± 0.10, P < 0.01, n = 8). We also confirmed pathway predictions of mitochondrial function, in which the respiratory control ratio of hypertensive vs. control mitochondria are significantly reduced (7.9 ± 1.2 vs. 10.4 ± 1.8, P < 0.01, n = 6) and metabolomic profile, in which 14 metabolites differed significantly between hypertensive and control medullas ( P < 0.05, n = 5). These findings demonstrate that subtle differences in the transcriptome can be used to predict functional changes of the kidney as a consequence of pressure elevation.

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Abstract P266: Thromboxane-prostanoid Receptors (tp-rs) Mediate Hypertension, H2o2 Generation and Impaired Renal Afferent Arteriolar Myogenic Responses Leading to Nephropathy in Doca/salt Mice

Hypertension ◽

10.1161/hyp.68.suppl_1.p266 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Christopher S Wilcox ◽

Lingli Li ◽

En Yin Lai ◽

Adam Hosszu ◽

William J Welch

Keyword(s):

Blood Pressure ◽

Perfusion Pressure ◽

High Salt ◽

Myogenic Tone ◽

Prostanoid Receptors ◽

Hypertensive Nephropathy ◽

Sham Treatment ◽

H2o2 Generation ◽

Afferent Arterioles ◽

Myogenic Responses

Background: DOCA/uninephrectomy/high salt (DOCA) is a model of hypertensive nephropathy. Afferent arteriolar myogenic responses prevent hypertensive renal barotrauma but myogenic tone is blocked by vascular generation of H 2 O 2 . Since thromboxane-prostanoid receptors (TP-Rs) generate H 2 O 2 , we tested the hypothesis that they mediate hypertensive nephropathy. Methods: DOCA and Sham TP-R +/+ and -/- mice (n=6/group) were studied at 2 weeks and myogenic responses recorded from the diameter of perfused single afferent arterioles studied in a bath preparation during increased perfusion pressure (40 to 80 mmHg). Results: DOCA treatment in TP-R +/+ mice increased (p<0.001) 24-hour excretion of H 2 O 2 (45 ± 3 vs 220 + 15 nmol) , TxB 2 (4 ± 2 vs 29 ± 4 pmol) and albumin (20 ± 5 vs 270 ± 20 mg) and increased MAP by 35 ± 5 mmHg. However, all effects of DOCA were prevented in TP-R -/- mice. Sham treatment had no effect in TPR +/+ or -/- mice. Myogenic responses were severely impaired in DOCA vs sham WT mice (Δ diameter: -4 ± 1 vs -8 ± 1%; p< 0.005). Myogenic responses also were reduced by incubation of arterioles with 10 -10 mol·l -1 of the TP-R mimetic, U-46,619 vs vehicle added to the bath for 10 minutes (Δ diameter: -7 ± 1 vs -10 ± 1%; p<0.01) and in WT mice infused for 3 days with U-46,619 (500 ng·kg -1 ·d -1 x 3) vs vehicle (Δ diameter: -3 ± 1 vs -10 ± 1%; p<0.005). Conclusion: Hypertensive nephropathy is dependent on TP-Rs that mediate the increase in H 2 O 2 and blood pressure and likely the impaired myogenic responses that expose the kidney to barotrauma

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Abstract 099: Functional Remodeling of the Renal Vasculature Precedes the Establishment of Salt-sensitive Hypertension in Eln-deficient Mice

Hypertension ◽

10.1161/hyp.68.suppl_1.099 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Elizabeth A Owens ◽

Li Jie ◽

Beverly Reyes ◽

Elisabeth J Van Bockstaele ◽

Patrick Osei-Owusu

Keyword(s):

Blood Pressure ◽

Structural Damage ◽

Vascular Dysfunction ◽

Renal Perfusion ◽

Dietary Sodium ◽

Intraluminal Pressure ◽

Renal Vasculature ◽

Salt Loading ◽

Vascular Stiffening ◽

Renal Vascular

Vascular stiffening due to elastin deficiency is a leading risk for hypertension and chronic kidney disease (CKD). However, the mechanisms by which elastin deficiency is involved in the pathogenesis of hypertension and/or CKD are poorly understood. Here, we used elastin heterozygous mice ( Eln+/- ), an animal model of elastin insufficiency, to test the hypothesis that renal dysfunction due to elastin deficiency occurs independently of and precedes the development of hypertension in this mouse model. We assessed blood pressure (BP) and renal hemodynamics in 30-day (P30) and 12-week old anesthetized male and female mice. At P30, mean blood pressure of Eln+/- was similar to wild type (WT) controls ( Eln+/- , 79 ± 5 vs. WT, 69±3 mmHg, P = 0.06); however, renal blood flow was lower ( Eln+/- 2.9 ± 0.2 vs. WT 4.0 ± 0.5 mL/min/g KW, P = 0.03) whereas renal vascular resistance (RVR; Eln+/- 29 ± 3 vs. WT 18 ± 3 mmHg/mL/min/g KW, P = 0.03) was augmented at baseline in Eln+/- mice. At 12 wks old, RVR remained elevated while filtration fraction was higher in male Eln+/- relative to WT mice ( Eln+/- 44 ± 3 vs. WT 38±5 % P = 0.07). Eln+/- mice showed isolated systolic hypertension that was evident only at nighttime ( Eln+/- 136 ± 2 vs. WT 112 ± 6 mmHg, P <0.01). Acute salt loading with 6% dietary sodium increased daytime systolic blood pressure only in male Eln+/- mice ( Eln+/- 118 ± 5 vs. WT 102 ± 6 mmHg, P = 0.03), causing a rightward shift and blunted slope of the pressure-natriuresis curve. Renal interlobar artery basal tone and myogenic response to increasing intraluminal pressure at P10 were similar ( Eln+/- 78 ± 3 vs. WT 67 ± 6 % P = 0.06) whereas they were augmented at P30 ( Eln+/- 63 ± 4 vs. WT 49 ± 6 % P = 0.05) and at 12 wks old in Eln+/- mice ( Eln+/- 50 ± 2 vs. WT 33 ± 3 % P < 0.01), and normalized by the AT1R blocker, candesartan ( Eln+/- 22 ± 9 vs. WT 8 ± 5 % P = 0.10). We conclude that AT1R mediates augmented mechanotransduction and renal vascular dysfunction due to Eln insufficiency that in turn contribute to altered renal sodium handling and increased BP. Such prolonged systemic BP elevation leads to glomerular structural damage due to high renal perfusion pressure. Therefore, therapies that target the AT1R to control BP in patients with elastin deficiency may be beneficial in preventing hypertension-evoked kidney damage.

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Cardiovascular functions in the dog rewarmed rapidly and slowly from deep hypothermia

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.198.2.333 ◽

1960 ◽

Vol 198 (2) ◽

pp. 333-335 ◽

Cited By ~ 3

Author(s):

H. E. D'Amato ◽

Suzanne Kronheim ◽

B. G. Covino

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Superior Vena ◽

Vena Cava ◽

Deep Hypothermia ◽

Cardiovascular Collapse ◽

Cardiovascular Failure ◽

Myocardial Failure ◽

Cardiovascular Functions

Heart rate, blood pressure, cardiac output and cardiac minute work were measured in pentobarbitalized dogs prior to induction of hypothermia, at rectal temperatures of 25°C or 20°C and following rapid rewarming in warm water or slow rewarming by wrapping in heated sheeting. During rapid rewarming from either 25°C or 20°C no consistent failure in recovery of normal cardiovascular function was observed, although 1 out of 10 dogs did suffer cardiovascular collapse during rapid rewarming. Slow rewarming from 25° and 20°C resulted in consistent failure of some or all of these functions to recover to prehypothermic levels. Moreover, 5 out of 15 slowly rewarmed dogs suffered cardiovascular collapse during the rewarming process. In five dogs slowly rewarmed from 20°C saline was infused into the superior vena cava. This procedure resulted in moderate increases in blood pressure but dramatic increases in cardiac output and minute work (200% and 270%, respectively), thereby negating myocardial failure as the primary cause of the occasionally observed cardiovascular failure.

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White Matter Lesions and Cognitive Impairment as Silent Cerebral Disease in Hypertension

The Scientific World JOURNAL ◽

10.1100/tsw.2006.99 ◽

2006 ◽

Vol 6 ◽

pp. 494-501 ◽

Cited By ~ 13

Author(s):

Cristina Sierra ◽

Antonio Coca

Keyword(s):

Blood Pressure ◽

Cognitive Impairment ◽

White Matter ◽

Indirect Evidence ◽

White Matter Lesions ◽

Cerebral White Matter ◽

Cognitive Changes ◽

Cerebral Disease ◽

Functional Changes ◽

Cerebral White Matter Lesions

Although the pathogenesis and clinical significance of cerebral white matter lesions remain controversial, it is well established that age and hypertension are the most important factors related to the presence of these lesions. Hypertension is known to be the most important factor for developing stroke and vascular dementia. In addition, the presence of cerebral white matter lesions is an important prognostic factor for the development of stroke, and also for cognitive impairment and dementia. The mechanisms underlying hypertension-related cognitive changes are complex and are not yet fully understood. Correlations between cerebral white matter lesions and elevated blood pressure provide indirect evidence that structural and functional changes in the brain over time may lead to lowered cognitive functioning when blood pressure control is poor or lacking.Some authors have suggested that the presence of white matter lesions in hypertensive patients could be considered an early marker of brain damage.

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Association between antenatal blood pressure and 5-year postpartum retinal arteriolar structural and functional changes

BMJ Open Ophthalmology ◽

10.1136/bmjophth-2019-000355 ◽

2019 ◽

Vol 4 (1) ◽

pp. e000355 ◽

Cited By ~ 1

Author(s):

Ralene Sim ◽

Izzuddin Aris ◽

Yap-Seng Chong ◽

Tien Yin Wong ◽

Ling-jun Li

Keyword(s):

Blood Pressure ◽

Mediation Analysis ◽

Degrees Of Freedom ◽

Underlying Mechanism ◽

Structure And Function ◽

Functional Changes ◽

Microvascular Changes ◽

And Function ◽

Retinal Arteriolar

ObjectiveStudies have shown that hypertensive disorders of pregnancy (HDP) are associated with both postpartum retinal microvascular changes and cardiovascular (CV) risks. However, the underlying mechanism of HDP transitioning to microvascular and macrovascular changes remains unknown, due to the interaction between microvasculature and CV risks. In this study, we examined whether associations between antenatal systolic blood pressure (SBP) and postpartum retinal arteriolar changes are independent of postpartum CV risks.MethodsWe included 276 Singaporean mothers attending both baseline index pregnancy (2009–2010) and 5-year postpartum follow-up visits (2014–2015). We measured SBP at baseline. At follow-up, we assessed retinal microvascular structure and function with retinal photography and dynamic vessel analyser, together with CV risks using a validated 2008 Framingham Risk Score (FRS). We performed a traditional four-step mediation analysis using linear regression by adjusting for a series of baseline characteristics: age, ethnicity, college degree, prepregnancy body mass index and gestational diabetes mellitus diagnosis at baseline.ResultsWe found that each 10 mm Hg increase in baseline SBP was associated with reduced arteriolar calibre (−1.3 µm; 95% CI −3.0 to 0.2) and fractal dimension (−0.4 degrees of freedom (df); −1.0 to 0.2), and significantly with increased arteriolar constriction (0.5%; 0.001 to 1.0) at 5-year postpartum. Even though baseline SBP was associated with postpartum FRS, the latter was not associated with any retinal arteriolar measures. Therefore, no further mediation analysis was required.ConclusionOur study suggested that elevated SBP during pregnancy was associated with suboptimal retinal arteriolar structure and function independent of postpartum CV risks.

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