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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2020  |  Volume : 31  |  Issue : 4  |  Page : 814-820
Arterial Hypertension in Systemic Lupus Erythematosus: About 40 Cases

Department of Internal Medicine, Habib Thameur Hospital; Faculty of Medicine of Tunis, University of Tunis, El Manar, Tunis, Tunisia

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Date of Submission22-Jun-2019
Date of Decision06-Sep-2019
Date of Acceptance24-Sep-2019
Date of Web Publication15-Aug-2020


The aim of this study was to determine the prevalence and the etiologic profile of hypertension (HTN) in systemic lupus erythematosus (SLE). A retrospective analysis was performed on 153 patients with SLE who attended our center for 16 years from January 2000 to December 2016. The diagnosis of SLE was established according to the classification criteria of the American College of Rheumatology in 1990. The prevalence of HTN in patients with SLE was 26.1% (40/153)' with an average delay of appearance of 21 months. There were 37 women and three men with a mean age of 46’ eight years (20–70). HTN was associated with lupus nephritis (n = 8)' other renal impairments (n = 6)' and corticosteroid treatment (n = 20). Essential HTN was found in six cases. Cardiovascular factors associated with HTN were: diabetes (n = 14)' sedentary life (n = 15)' obesity (n = 12)' and dyslipidemia (n = 8). Main clinical manifestations associated with HTN were: arthralgia/arthritis (24 cases)' cutaneous involvement (22 cases)' and hematological manifestations (16 cases). Anti-phospholipid syndrome was found in 12 cases. Coronary artery disease’ arteritis of lower limb’ and transient ischemic attacks complicated the course of HTN in six patients. Angiotensin-converting-enzyme inhibitors were the most commonly used drug for treatment in this group. HTN was frequently associated with corticosteroid treatment in this study. We feel that the use of corticosteroids should be avoided as far as possible in all patients with SLE.

How to cite this article:
Rachdi I, Daoud F, Zoubeidi H, Somai M, Fekih Y, Dhaou BB, Aydi Z, Boussema F. Arterial Hypertension in Systemic Lupus Erythematosus: About 40 Cases. Saudi J Kidney Dis Transpl 2020;31:814-20

How to cite this URL:
Rachdi I, Daoud F, Zoubeidi H, Somai M, Fekih Y, Dhaou BB, Aydi Z, Boussema F. Arterial Hypertension in Systemic Lupus Erythematosus: About 40 Cases. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2023 Feb 8];31:814-20. Available from: https://www.sjkdt.org/text.asp?2020/31/4/814/292315

   Introduction Top

Systemic lupus erythematosus (SLE) is an auto-immune inflammatory disease that predominantly affects women during their reproductive years.[1] The most commonly involved systems are the skin’ mucous membranes’ joints’ kidney’ central nervous system’ and lungs. The higher risk of cardiovascular disease (CVD) in SLE has been recognized since the 70s when Urowitz et al displayed a bimodal mortality peak for lupus patients; the first was attributed to disease activity and infections in the early course and the second to CVD during the follow-up period.[2] Arterial hypertension (HTN) represents one of the CV risk factors and a determinant of the progression of atherosclerosis.[3],[4] The prevalence of HTN in SLE is estimated to be 20%–75%.[5],[6],[7] However, pathophysiological mechanisms promoting HTN in SLE remain elusive.[1] The aim of this study is to determine the prevalence and the etiologic profile of HTN in Tunisian patients with SLE.

   Patients and Methods Top

A retrospective monocentric analysis was performed on 153 patients with SLE who attended our center for 16 years from January 2000 to December 2016. The diagnosis of SLE was established according to the classification criteria of the American College of Rheumatology in 1990. The diagnosis of HTN was confirmed when the systolic blood pressure was above or equal to 140 mm Hg and/or the diastolic blood pressure was above or equal to 90 mm Hg. The HTN was classified as severe if the systolic pressure above or equal to 180 mm Hg or diastolic pressure was above or equal to 120 mm Hg. Renal biopsy was performed in 18 cases with signs of renal impairment or lupus nephritis (LN). The histological classification was obtained from the pathologist’s reports using the standard WHO classification of the glomerular involvement in SLE. Only patients aged > 18 years were included.

The results were expressed in the number of cases and/or percentages for the qualitative variables and on average for the quantitative ones. Data collection and descriptive analysis were carried out with the Statistical Package for the Social Sciences (SPSS) version 11.0 (SPSS Inc., Chicago, IL, USA).

   Results Top

The prevalence of HTN in patients with SLE was 26.1% (40/153), with an average delay of onset of 21 months. There were 37 women and three men. The mean age was at 46.8 years (20–70).

The diagnosis of HTN preceded the diagnosis of SLE in four patients. It was concomitant in seven patients and diagnosed during the progression of SLE in 29 patients. HTN was severe in 14 patients. HTN was systolic (n = 23), diastolic (n = 12), and both (n =5).

The main clinical and biological characteristics associated with those SLE patients with HTN, were age, articular and skin involvement, and the presence of antinuclear antibodies and anti-DNA antibodies.

These characteristics are reported in [Table 1]. Renal biopsy was performed in 14 cases.
Table 1: Main clinical and biological characteristics of patients with SLE and HTN.

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Arterial HTN in SLE patients was associated with LN (n = 8), renal impairment (n = 6), and corticosteroid treatment (n = 20). HTN was essential in six cases. These results are illustrated in [Figure 1]. LN corresponded to a class III (n =3), IV (n =3), V (n =1), and II (n =1).
Figure 1:

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Antiphospholipid syndrome was noted in 12 cases.

CV factors associated with HTN were: sedentary life (n = 15), diabetes (n = 14), age above 50 years (n = 13), obesity (n = 12), dyslipi- demia (n = 8), family history of CVD (n = 8), and smoking (n = 4). HTN was complicated by coronary artery disease (n = 2), arteritis of lower limbs (n = 2), and transient ischemic attack (TIA) (n = 2) [Table 2].
Table 2: Cardiovascular risk factors associated to hypertension in patients with systemic lupus erythematosus.

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Twenty patients were treated by cortico- steroids: 14 at a dose of 1 mg/kg/day and six at a dose of 0.5 mg/kg/day. All patients were treated by anti-malarial drugs: Hydroxychlo- roquine (n = 35) and chloroquine (n = 5). Immunosuppressive therapies were prescribed to 20 patients: cyclophosphamide (n = 10), azathioprine (n = 9), mycophenolate mofétil (n = 3) and methotrexate (n = 3).

HTN was treated with angiotensin-converting- enzyme inhibitors alone in 27 patients or in combination with diuretics in 10 and calcium channel blockers in three.

Twenty-eight patients were treated by mono- therapy and 13 by more than one antihyper- tensive drug. The HTN was well controlled in 32 patients with a mean follow up duration of 38 months. Fifteen patients were under statins.

   Discussion Top

In this study, we have evaluated the prevalence and the etiologic profile of HTN in 153 Tunisian patients with SLE.

Several studies revealed an increased prevalence of HTN in patients with SLE, ranging from 20% to 75%.[5],[6],[7],[8],[9],[10],[11],[12] In our Tunisian cohort, about a quarter of SLE patients developed HTN. This variability can be explained by genetic contributors conferring increased susceptibility for HTN in some ethnicities.

HTN is a major risk factor for CVD and is highly prevalent in women with SLE, as noted in our study as well as in other reported studies.[3’4] In normal healthy young women (ages 15–44 years)' the prevalence of HTN is low (3%–14%).[13] In contrast’ the prevalence of HTN in women with SLE can be considerably higher’ ranging from 35% to 74%' depending on the cohort studied.[5],[14],[15],[16] This female predominance can be explained by the fact that SLE is a chronic auto-immune inflammatory disorder that predominantly affects women during their reproductive years.[1] The second mechanism by which women are more susceptible to HTN through SLE is through estrogen-mediated increases in autoantibody production.[17]

The mean age was at 35 years in most of the studies.[5],[6],[7],[8],[9],[10],[11],[12] In our cohort’ the mean age was at 46.5 years. This difference could be explained by the predominance of corticosteroid-induced HTN in our cohort more than by SLE itself (LN or renal impairment).

The pathogenesis of HTN and the development of CVDs in SLE are not fully under- stood.[1] Many factors may contribute to HTN in SLE patients involving age’ sex’ metabolic changes’ ethnicity.[8’18] In a cohort of 112 lupus patients’ Sabio et al’ identified renal disease’ insulin levels’ and SLE disease activity index (SLEDAI) as independent predictors of HTN in patients with SLE. Non-obesity related insulin levels was the main predictor of HTN in the younger age subset (<40 years)' while age and obesity in the older group (>40 years).[8] An adverse night-time blood pressure pattern (steady’ nondipping HTN or nocturnal HTN/reverse dipping) was more frequent in SLE.[19]

On the other hand’ disease-related factors (immune system dysfunction’ inflammation’ renal involvement’ drug side effects) also may contribute to HTN in SLE patients.[17]

Growing evidence suggests a link between chronic inflammation and HTN. Therefore’ elucidation of mechanisms that promote HTN in SLE may be of significant value in these patients. In approximately 50% of patients with SLE’ the kidneys are affected in the form of immune complex glomerulonephritis and nearly all patients show evidence of kidney injury on biopsy.[20]

Renal involvement is responsible of HTN either by renal failure or LN. The incidence of HTN in patients with LN increased with both histological activity and loss of renal func- tion.[21] It was shown that hyperplasic forms of LN such as class III’ IV and V are the most related forms related to HTN. The endothelial dysfunction of renal cells plays a major role in lupus-related HTN.[21]

However’ there are reports suggesting that LN and HTN can occur independently of each other. Despite the absence of LN’ Shaharir et al’ noted that 53% of SLE patients were hypertensive.[9] Impaired renal function contributes certainly to the prevalent HTN in SLE patients high-lighting the importance of the kidney in the long-term control of blood pressure.

Several other mechanisms’ including the renin-angiotensin system’ endothelin’ oxida- tive stress’ steroids’ peroxisome proliferato- activated receptor-γ, and perhaps most importantly’ chronic inflammation and cytokines’ tumor necrosis factor-α as well as B-cell hyperactivity and autoantibody production.[22] In our cohort’ corticosteroids were associated with 50% of patients with HTN. One of the most common treatments for SLE is the use of corticosteroids’ and chronically elevated levels of corticosteroids can promote endothelial dysfunction and HTN.[23] Corticosteroids can be responsible of diabetes which also is a CV risk factor.[23] The effect of corticosteroids was found to be independent of disease activity and traditional CV risk factors in a cohort of patients with SLE.[7] Therefore’ an awareness should be kept on the importance of an appropriate dose and duration of steroids in SLE.

Naiker et al studied retrospectively 44 patients with LN. Among them’ 17 patients developed HTN. It was moderate in the majority of cases.[21] In the same cohort’ the incidence of impaired renal function was significantly higher in the hypertensives compared to the normotensives (P = 0.04).[21]

HTN has well-known harmful effects on the heart’ the kidneys’ the brain’ the eyes’ and the arteries. In fact’ it increases the risk for coronary artery disease’ heart failure’ chronic kidney disease, stroke, intracerebral hemorrhage, TIA, and peripheral arterial disease.[1],[7] These effects can also lead to a major functional damage leading to stroke, blindness, and kidney damage needing hemodialysis. Several studies have shown that HTN is an important determinant of atherosclerosis contributing to both plaque formation and arterial stiffening.[24],[25] Another study estimated the risk of CV events among patients with SLE to be 2.6 times higher compared with the general population.[7] Kiani et al identified HTN as independently associated factor with the progression of carotid IMT and plaque in a longitudinal study of 187 SLE patients.[26] It is also an independently associated factor to deterioration of renal function in LN. In the other hand, lupus is now regarded as an independent risk factor for the development of CV comorbidity,[27] implying that other factors inherent to the disease itself contribute to the CV events seen in these patients. In addition to accelerated atherosclerosis in SLE patients, the organs are also weakened by the disease itself with prolonged length of hospitalization and increased in-hospital mortality comparing to patients without SLE.[28] In our cohort, fifteen percent of the patients had CV events.

Guidelines for monitoring CV risk in rheumatoid arthritis exist, but in SLE patients, they are not yet available.[27],[29] CV risk should be considered, and comorbidities should be managed promptly. The first goal is to have an adequate control standard Framingham risk factors (age, smoking, systolic blood pressure, total cholesterol, high-density lipoprotein). Patients with SLE have to stop smoking, maintain an ideal weight and avoid sedentary lifestyle. Normal fasting plasma glucose levels should be maintained.[27] and keep blood pressure under control according to the European guidelines on CV diseases prevention which has stated, the optimal BP level should be <130/80 mm Hg.[30]

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers seem to be an efficacious and safe first-choice antihypertensive treatment in SLE patients. especially in patients with renal involvement.[31]

It seems also that ACEIs decrease the risk of disease activity and can delay renal disease.[31] A study of the effect of ACEIs in patients with LN and severe HTN, showed that they improve renal function in 64% of patients although also improving blood pressure control.[32]

In our cohort, most of our patients were treated by angiotensin blockers with good blood pressure control. If the blood pressure is not well controlled by monotherapy, a calcium blocker or thiazidic diuretic must be added.

The β-blockers should be used as second-line agents. In fact, they may precipitate or aggravate Raynaud’s phenomenon and can cause drug-induced lupus in some cases.[33]

Thiazide diuretics should be used with caution in SLE patients because of their potential metabolic side effects, including hypercholesterolemia, hypertriglyceridemia, and hyperglycemia.[34] It is recommended to use aspirin, in the absence of contraindications, in patients with SLE who have a history of CV disease, HTN or smoking and those who have positive antiphospholipid antibodies, or lupus anticoagulant or hypercholesterolemia.[35] Antimalarial medication is recommended for all SLE patients in the absence of contraindications. Hydroxychloroquine seems to be cardioprotective. It has direct and indirect benefits on cardiovascular risk by reducing the activity of SLE. Besides, hydroxychloroquine seems to reduce the fasting blood glucose concentration and lowering total cholesterol in patients receiving steroids.[36]

   Conclusion Top

HTN is frequent in SLE with variable causes. It was frequently caused by corticosteroid treatment in our study. The prevention of HTN in SLE is based on the monitoring of adverse effects of corticosteroids and correct management of LN. Recommendations in randomized clinical trials are expected to confirm the value of good management of HTN in patientswith SLE in reducing CV risk.

Conflict of interest: None declared.

   References Top

Ryan MJ. The pathophysiology of hypertension in systemic lupus erythematosus. Am J Physiol Regul Integr Comp Physiol 2009;296: R1258-67.  Back to cited text no. 1
Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J Med 1976;60:221-5.  Back to cited text no. 2
Petri M, Perez-Gutthann S, Spence D, Hochberg MC. Risk factors for coronary artery disease in patients with systemic lupus erythematosus. Am J Med 1992;93:513-9.  Back to cited text no. 3
Sella EM, Sato EI, Barbieri A. Coronary artery angiography in systemic lupus erythematosus patients with abnormal myocardial perfusion scintigraphy. Arthritis Rheum 2003;48:3168- 75.  Back to cited text no. 4
Budman DR, Steinberg AD. Hypertension and renal disease in systemic lupus erythematosus. Arch Intern Med 1976;136:1003-7.  Back to cited text no. 5
Mandell BF. Cardiovascular involvement in systemic lupus erythematosus. Semin Arthritis Rheum 1987;17:126-41.  Back to cited text no. 6
Magder LS, Petri M. Incidence of and risk factors for adverse cardiovascular events among patients with systemic lupus erythe- matosus. Am J Epidemiol 2012;176:708-19.  Back to cited text no. 7
Sabio JM, Vargas-Hitos JA, Navarrete- Navarrete N, et al. Prevalence of and factors associated with hypertension in young and old women with systemic lupus erythematosus. J Rheumatol 2011;38:1026-32.  Back to cited text no. 8
Shaharir SS, Mustafar R, Mohd R, Mohd Said MS, Gafor HA. Persistent hypertension in lupus nephritis and the associated risk factors. Clin Rheumatol 2015;34:93-7.  Back to cited text no. 9
Fernández-Nebro A, Rúa-Figueroa É López- Longo FJ, et al. Cardiovascular events in systemic lupus erythematosus: A nationwide study in spain from the RELESSER registry. Medicine (Baltimore) 2015;94:e1183.  Back to cited text no. 10
McMahon M, Skaggs BJ, Sahakian L, et al. High plasma leptin levels confer increased risk of atherosclerosis in women with systemic lupus erythematosus, and are associated with inflammatory oxidised lipids. Ann Rheum Dis 2011;70:1619-24.  Back to cited text no. 11
Tselios K, Koumaras C, Urowitz MB, Gladman DD. Do current arterial hypertension treatment guidelines apply to systemic lupus erythematosus patients? a critical appraisal. Semin Arthritis Rheum 2014;43:521-5.  Back to cited text no. 12
Health, United States. With chartbook on trends in health of Americans. Hyattsville, MD: National Center for Health Statistics; 2007.  Back to cited text no. 13
Doria A, Shoenfeld Y, Wu R, et al. Risk factors for subclinical atherosclerosis in a prospective cohort of patients with systemic lupus erythematosus. Ann Rheum Dis 2003; 62:1071-7.  Back to cited text no. 14
Petri M. Detection of coronary artery disease and the role of traditional risk factors in the Hopkins Lupus Cohort. Lupus 2000;9:170-5.  Back to cited text no. 15
Al-Herz A, Ensworth S, Shojania K, Esdaile JM. Cardiovascular risk factor screening in systemic lupus erythematosus. J Rheumatol 2003;30:493-6.  Back to cited text no. 16
Venegas-Pont M, Ryan MJ. Can estrogens promote hypertension during systemic lupus erythematosus? Steroids 2010;75:766-71.  Back to cited text no. 17
Chaiamnuay S, Bertoli AM, Roseman JM, et al. African-American and hispanic ethnicities, renal involvement and obesity predispose to hypertension in systemic lupus erythematosus: Results from LUMINA, a multiethnic cohort (LUMINAXLV). Ann Rheum Dis 2007;66: 618-22.  Back to cited text no. 18
Sabio JM, Martinez-Bordonado J, Sánchez- Berná I, et al. Nighttime blood pressure patterns and subclinical atherosclerosis in women with systemic lupus erythematosus. J Rheumatol 2015;42:2310-7.  Back to cited text no. 19
Guo Q, Lu X, Miao L, Wu M, Lu S, Luo P. Analysis of clinical manifestations and pathology of lupus nephritis: A retrospective review of 82 cases. Clin Rheumatol 2010;29:1175-80.  Back to cited text no. 20
Naiker IP, Chrystal V, Randeree IG, Seedat YK. The significance of arterial hypertension at the onset of clinical lupus nephritis. Postgrad Med J 1997;73:230-3.  Back to cited text no. 21
Taylor EB, Ryan MJ. Understanding mechanisms of hypertension in systemic lupus erythematosus. Ther Adv Cardiovasc Dis 2017;11:20-32.  Back to cited text no. 22
Kasturi S, Sammaritano LR. Corticosteroids in lupus. Rheum Dis Clin North Am 2016;42:47- 62, viii.  Back to cited text no. 23
McMahon M, Skaggs BJ, Sahakian L, et al. High plasma leptin levels confer increased risk of atherosclerosis in women with systemic lupus erythematosus, and are associated with inflammatory oxidised lipids. Ann Rheum Dis 2011;70:1619-24.  Back to cited text no. 24
Tektonidou MG, Kravvariti E, Konstantonis G, Tentolouris N, Sfikakis PP, Protogerou A. Subclinical atherosclerosis in Systemic Lupus Erythematosus: Comparable risk with Diabetes Mellitus and Rheumatoid Arthritis. Autoimmun Rev 2017;16:308-12.  Back to cited text no. 25
Kiani AN, Post WS, Magder LS, Petri M. Predictors of progression in atherosclerosis over 2 years in systemic lupus erythematosus. Rheumatol Oxf Engl 2011;50:2071-9.  Back to cited text no. 26
Giannelou M, Mavragani CP. Cardiovascular disease in systemic lupus erythematosus: A comprehensive update. J Autoimmun 2017;82: 1-2.  Back to cited text no. 27
Shah MA, Shah AM, Krishnan E. Poor outcomes after acute myocardial infarction in systemic lupus erythematosus. J Rheumatol 2009;36:570-5.  Back to cited text no. 28
Mosca M, Tani C, Aringer M, et al. European League Against Rheumatism recommendations for monitoring patients with systemic lupus erythematosus in clinical practice and in observational studies. Ann Rheum Dis 2010; 69:1269-74.  Back to cited text no. 29
Graham I, Atar D, Borch-Johnsen K, et al. European guidelines on cardiovascular disease prevention in clinical practice: Executive summary. Fourth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts). Eur Heart J 2007;14:1-40.  Back to cited text no. 30
Duran-Barragan S, McGwin G Jr., Vila LM, Reveille JD, Alarcon GS, Cohort Lam U. Angiotensin-converting enzyme inhibitors delay the occurrence of renal involvement and are associated with a decreased risk of disease activity in patients with systemic lupus erythematosus results from LUMINA (LIX): A multiethnic US cohort, Rheumatol Oxf Engl 2008;47:1093-6.  Back to cited text no. 31
Stojan G, Petri M. Atherosclerosis in systemic lupus erythematosus. J Cardiovasc Pharmacol 2013;62:255-62.  Back to cited text no. 32
Herlitz H, Edenö C, Mulec H, Westberg G, Aurell M. Captopril treatment of hypertension and renal failure in systemic lupus erythematosus. Nephron 1984;38:253-6.  Back to cited text no. 33
Mohokum M, Hartmann P, Schlattmann P. The association of Raynaud syndrome with β- blockers: A meta-analysis. Angiology 2012;63: 535-40.  Back to cited text no. 34
Wajed J, Ahmad Y, Durrington PN, et al. Prevention of cardiovascular disease in systemic lupus erythematosus—proposed guidelines for risk factor management. Rheumatology 2004;43:7-12.  Back to cited text no. 35
Petri M. Hydroxychloroquine use in the baltimore lupus cohort: Effects on lipids, glucose and thrombosis. Lupus 1996;5 Suppl 1:S16-22.  Back to cited text no. 36

Correspondence Address:
Imene Rachdi
Department of Internal Medicine, Habib Thameur Hospital, Tunis
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.292315

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