JSM Renal Medicine

Malignant Hypertension in Lupus Nephritis

Research Article | Open Access Volume 2 | Issue 1 |

  • 1. Department of Internal Medicine and Nephrology, Cairo University, Egypt
+ Show More - Show Less
Corresponding Authors
Ahmed Abdalla Hassan, Department of Internal Medicine and Nephrology, Cairo University, Cairo, Egypt, Tel: 20-100-2958010;

Hypertension with rapid worsening of renal function is a rare presentation of lupus nephritis. The aim of this work is to ascertain the prevalence and prognostic importance of malignant hypertension at the onset of LN. We also searched for a correlation between malignant hypertension and LN histological class. We have retrospectively assessed 15 cases of malignant hypertension and SLE with LN. Eleven were males (73.3%). Mean age was 36 years. Mean interval between diagnosis of SLE and the appearance of renal complications was 110 months. Clinical presentation consisted of malignant hypertension (DBP> 115 mm Hg with hypertensive retinopathy grades III-IV). At presentation, 12/15 (80%) showed renal insufficiency (mean creatinine was 3.8 mg/dl). Mean proteinuria level was 4.2 g/24h and microhematuria was observed in 73.3% of cases. Immunologic studies showed decreased C3 (66.6%) and circulating cryoglobulins in 13.3%. Renal biopsies showed class IV (10/15, 66.7%), III (1/15, 6.6%) and V GN (4/15, 26.7%). Of the 15 patients, crescentic transformation occurred in 7 (46.6 %) and TMA occurred in one patient (6.6 %) on top of class IV-S. After a mean follow up of 24 months, 5 patients (33%) had recovered normal renal function, and 6 (40%) had started chronic dialysis.

Conclusion: Malignant hypertension associated with LN was a high risk clinical presentation with rapid worsening of renal function.


Soliman AR, Hassan AA, Soliman MA, Eldeeb MM, Roshd DA, et al. (2017) Malignant Hypertension in Lupus Nephritis. JSM Renal Med 2(1): 1009.


•    Malignant hypertension
•    SLE
•    Lupus nephritis


LN: Lupus Nephritis; SLE: Systemic Lupus Erythematosus; C3: Complement 3; C4: Complement 4; TMA: Thrombotic Microangiopathy


SLE is characterized by a wide spectrum of clinical manifestations, including renal, pulmonary, cardiovascular, and neuropsychiatric abnormalities [1]. Numerous studies report a high prevalence of hypertension in women with SLE, reaching as high as 74% in some cohorts [2-6]. Development of hypertension, in patients with SLE, is more common in patients with advanced lupus-related renal pathology or impairment of renal function. In addition to advanced renal disease as a cause of hypertension, anti-rheumatic drugs including corticosteroids and cyclosporin might be associated with either the onset or aggravation of hypertension [7].

Malignant hypertension has been reported in association with autoimmune rheumatic diseases and in patients with the antiphospholipid antibody syndrome (APS) alone or with SLE and is relatively well described in the medical literature [8]. However, there are few reports on the clinical presentation of malignant hypertension in patients with SLE in the medical literature.

Here, our objective is to ascertain the prevalence and prognostic importance of malignant hypertension at the onset of clinical LN. We also searched for a correlation between malignant hypertension and histological class of LN.


In the period 1999-2010, all patients with SLE who presented to Nephrology and/or Rheumatology departments of Kasr alAini School of Medicine and had undergone renal biopsies were retrospectively assessed. Patients who had no evidence of LN according to the WHO classification were excluded, as were patients who were on corticosteroid therapy just prior to the renal biopsy.

A total of 63 patients (42 females) satisfied these criteria and were selected for the study. Patients were regarded as being hypertensive’s if they had a sitting blood pressure equal to or greater than 140/95 mmHg on at least two different occasions. The recorded blood pressure was the mean diastolic pressure of the two determinations. None of the patients was receiving antihypertensive medication before being admitted. Hypertension was classified as being mild (diastolic 95-99 mmHg), moderate (100- 114 mmHg) or severe (> 115 mmHg). Clinical presentation of malignant hypertension was the presence of diastolic BP> 115 mmHg with hypertensive retinopathy grades III-IV.

The histological classification was obtained from the pathologist’s reports which utilize the standard WHO classification of glomerular involvement in SLE. All histology was subsequently re-evaluated by a single senior pathologist who searched specifically for hypertensive renal vascular lesions. Informed consent was obtained from each patient for blood sampling and renal biopsy. The research was in compliance with the Declaration of Helsinki.


Table 1 shows characteristics of all LN patients. Of the 15 patients with LN and malignant hypertension, eleven were males (73.3%). Their mean age was 36 years (26-51). Nine out of 15 (60%) had associated lower limb skin rash and the number of positive antineutrophil cytoplasm antibodies (p-ANCA) at presentation was seen in 5 out of 15 (33.3%). Two out of 15 (13.3%) were co infected by hepatitis C virus and 1/15 (6.6%) by hepatitis B. Mean interval between diagnosis of SLE and the appearance of renal complications was 110 months (4-206). Clinical presentation consisted of malignant hypertension (diastolic BP> 115 mmHg with hypertensive retinopathy grades III-IV). At presentation, 12/15 (80%) showed renal insufficiency (mean serum creatinine was 3.8mg/dl). Mean level of proteinuria was 4.2g/24h and micro hematuria was observed in 73.3% of cases. Immunologic studies showed decreased C3 (66.6%) and circulating cryoglobulins in 13.3%

Table 2 shows the WHO histological classification of renal biopsies for malignant and non-malignant hypertensives compared to normotensives. For the 15 patients with LN and malignant hypertension, renal biopsies showed diffuse (IV) proliferative glomerulonephritis (10/15, 66.7%), focal (III) proliferative glomerulonephritis (1/15, 6.6%) and membranous (V) GN (4/15, 26.7%). In addition, crescentic transformation occurred in 7 of them (46.6 %) and TMA occurred in one patient (6.6 %) on top of class IV-S.


In our study, we found that patients with malignant hypertension were predominantly males (73%). This is consistent with what was reported by Kaplan [9] that men are affected 2 times more often than women by malignant hypertension. However, Tao et al. [10], who retrospectively studied 19 patients with LN complicated by malignant hypertension, found that 3 only were men (16%).

In addition, of the 15 patients with malignant hypertension, 12 (80%) presented with renal insufficiency with a mean serum creatinine of 3.8 mg % compared to 1.9 mg % in the non-malignant hypertensive and normotensive groups (P- value = 0.001). Similar results were found by Tao et al. [10], who reported that impaired renal function was noticed in 17 of the 19 patients (89%) with an average serum creatinine of 2.08 mg%. This could be explained by 2 factors; first, most of our patients with malignant hypertension had proliferative LN which is known to be associated with renal insufficiency and hypertension. Second, with severe elevations of BP, endothelial injury and fibrinoid necrosis of the arterioles ensue [11]. This process results in ischemia and the release of additional vasoactive mediators generating a vicious cycle of on-going injury. The renin–angiotensin system is often activated leading to further vasoconstriction and the production of proinflammatory cytokines such as interleukin-6 (IL-6) [12,13]. Furthermore, NADPH oxidase activity increases and generates reactive oxygen species [14]. The volume depletion that results from pressure natriuresis further simulates the release of vasoconstrictor substances from the kidney. These collective mechanisms can culminate in end-organ hypoperfusion, ischemia and dysfunction that manifests as a hypertensive emergency [15].

Moreover, of the 15 patients with malignant hypertension, 9 (60%) were found to have skin rash on the lower limbs compared to 7 patients only (14.6 %) in the non-malignant hypertensive and normotensive groups (P- value = 0.0001). However, we did not find a more detailed description of this rash in the medical records.

It is known that skin and/or mucous membranes are involved at some point in over 80 % of patients with SLE [16]. Skin lesions from vascular involvement in lupus include periungual erythema, live do reticularis, telangiectasia, Raynaud phenomenon, and various forms of vasculitis; they occur in approximately 50 % of patients [17].

In our study and in relation to ANCA prevalence in SLE patients, of the 15 patients with malignant hypertension, 5 (33.3%) were found to have positive p-ANCA compared to 3 patients only (6.3 %) in the non-malignant hypertensive and normotensive groups (P- value = 0.001).

Approximately 20% of patients with SLE have ANCA positivity by indirect IF (IIF), mainly with a perinuclear pattern (p-ANCA). ANCA seropositivity by ELISA is less frequent and the target antigens are most commonly lactoferrin, cathepsin G, and MPO [18].

There are conflicting reports on the significance of ANCA positivity in patients with SLE [18]. Pauzner et al. [19], reported that Antineutrophil cytoplasmic antibodies may be seen in some patients with SLE but do not correlate with disease activity or the presence or severity of vasculitis and are rarely if ever directed against either the proteinase-3 or myeloperoxidase antigen. Others reported that SLE and LN may promote neutrophil degranulation and facilitate ANCA autoantibody formation [20].

Nasr et al. [20], reported 10 cases of LN with ANCA-associated glomerulonephritis, the evolution of these patients after the treatment by corticosteroids and cyclophosphamide was marked by lethal infectious complications in three patients, complete remission in six patients with a relapse in one case and resistance to treatment in one patient.

Nasr et al. [20], evoked the probability of an overlap between lupus nephropathy and ANCA extracapillary glomerulonephritis and suggested to search systematically the positivity of ANCA by ELISA test in a lupus patient whenever renal histology shows extensive necrotizing lesions with a non-significant endocapillary proliferation and rare sub-endothelial deposits.

Regarding the renal pathology of our patients, class IV LN was found to be the most predominent class among patients with malignant hypertension (66.7 %), while classes II and V were the most frequently encountered ones among the normotensives and those having non-malignant hypertension respecively. In addition, of the 15 patients with malignant hypertension, crescentic transformation occurred in 7 of them (46.6 %) and TMA occurred in one patient (6.6 %) on top of class IV-S.

It is known that SLE involves the kidney in up to 60% of patients [21]. The important prognostic factors associated with poor renal outcome include: diffuse proliferative glomerulonephritis; high activity and chronicity scores in renal biopsies; presence of cellular crescents, hypertension and impaired renal function at presentation; acute nephritic syndrome with rapidly deteriorating renal function; nephrotic range of proteinuria; lack of initial response to immunosuppressive treatment; renal relapses; African race and the male sex [22].

LN classes I and II have a similar indolent course. By contrast, without early treatment, classes III and IV LN are progressive. They share similar clinical patterns, natural histories and responses to therapy and differ only in the quantitative involvement of glomeruli being less than 50% in class III but more than 50% in class IV [23].

Even with aggressive therapy, some patients with proliferative LN will have a progressive decline in renal function leading to end-stage renal disease (ESRD) [24,25]. The severity of chronic tubulointerstitial disease and extensive crescent formation also correlate with long-term prognosis in LN, as they do in many other chronic progressive glomerular diseases [26].

Class IV LN is known to be the most common and most severe form of LN. With active disease, proliferative and necrotizing lesions and crescent formation all may be present, affecting more than 50 % of glomeruli on light microscopy [27].

Vascular disease is also common in LN and may assume several morphologically distinct forms [28]. Although vascular lesions contribute to disease severity and may influence prognosis, they are not factored into the WHO classification or the activity and chronicity indices [29]. As a result, vascular lesions may not be well-recognized and may be overlooked.

The four well-recognized vascular lesions in LN include: uncomplicated vascular immune deposits, non inflammatory necrotizing vasculopathy (lupus vasculopathy), thrombotic microangiopathy and necrotizing vasculitis [30].

Among various lupus renal vascular changes, thrombotic microangiopathy (TMA) presented with the most severe clinical manifestations and high mortality [31].

Since the pathogenesis of TMA in LN is complex and unclear, detailed descriptions about it were lacking in the literature. In fact, TMA in LN consisted of a group of diseases, including antiphospholipid syndrome (APS), thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS), scleroderma, malignant hypertension and calcineur in inhibitor-associated thrombotic micro angiopathy and so on. The pathogenesis of TMA in SLE was complicated [32].

Recently, Danielle et al. demonstrated that activation of the complement classical pathway might be a crucial factor in the development of TMA in LN [33].

The prevalence of renal TMA in our cohort with LN was 1.6% (1/ 63), which is similar to that in previous studies (0.5% to 10%) [34,24].

Although with more intensive immunosuppressive therapy, patients with TMA had a poorer renal outcome than those without renal TMA. Renal TMA was found as an independent risk factor for renal outcome in LN [32].

In this study, we showed that ESRD remains highly prevalent among lupus patients who were previously admitted with malignant hypertension, with 40% started regular hemodialysis, 27% had CKD and 33% recovered normal renal function after a mean follow-up of 24 months. In comparison, most of the patients with non-malignant hypertension recovered normal renal function (47%), while 16% only started regular hemodialysis after a mean follow-up of 21 months.

Although the prognosis of malignant hypertension has improved considerably over the past decades, renal dysfunction remains an important cause of morbidity and mortality [35]. Yet some patients have a remarkable recovery of kidney function after adequate control of blood pressure is achieved [36].

There are few data regarding the outcomes of a hypertensive crisis. In a study of 315 patients with malignant hypertension, 40% were alive after 33 months. The most common causes of death were renal failure (39.7%), stroke (23.8%), MI (11.1%), and heart failure (10.3%) [25].

Furthermore, studies of patients presenting to the emergency room with a hypertensive crisis have demonstrated that most do not receive the appropriate evaluation, medical regimen, and discharge instructions proposed by the current guidelines. Two studies of patients presenting to the emergency room with a hypertensive crisis found that serum chemistry was only obtained in 70% to 73% of patients, electrocardiogram in 53% to 70% of patients, chest x-ray in 24% to 46% of patients, and urinalysis in 43% to 44% of patients. Two-thirds of the total number of patients evaluated did not have a funduscopic examination in the emergency room, and only 19% discharged had modification of their antihypertensive regimen. Overall, only 6% obtained the tests recommended by the guidelines, and 10% had no tests performed [37,38].

The known duration of hypertension and procuring the serum urea level at presentation has been found to be the main predictors of survival in hypertensive crisis, with poorer outcomes for black patients [39].

The 1-year mortality rate is 79% for patients with untreated hypertensive emergencies [40], and 5-year survival rate among all patients who present with hypertensive crisis is 74% [25].

This study has both strengths and limitations. Strengths include the contribution of clinically relevant and previously unavailable data on long-term renal outcome of an unselected and well described cohort of patients with LN and malignant hypertension. Limitations include its retrospective nature and consequently the possibility of coding errors. In addition, unavailability of antiphospholipid antibodies for many patients was another limitation.

Table 1: Clinical and laboratory parameters of patients with SLE.

Parameter Malignant hypertension N=15 No malignant hypertension N=48 P value
Sex, males (%) 11 (73.3) 10 (20.1) 0.0001
Mean age (range) 36 (26-51) 32 (19-47) NS
Mean interval to renal complications in months (range) 110 (4-206) 102 (1-197) NS
Renal insufficiency at presentation (serum creatinine >1.35 mg/dl), number (%) 12 (80) 28 (58.3) 0.001
Skin rash on lower limbs, number, % 9 (60) 7 (14.6) 0.0001
Serum creatinine at presentation, mean ±SD 3.8 ±3.4 1.9 ± 1.6 0.001
Proteinuria in gm/24 hour at presentation, mean ± SD 4.2±3.1 3.0 ± 2.5 NS
Microhematuria at presentation, number (%) 11 (73.3) 29 (60.4) NS
ANCA at presentation, number (%) 5 (33.3) 3 (6.3) 0.001
HCV co-infection, number (%)
HBV co-infection, number (%)
2 (15.3)
1 (6.6)
7 (14.6)
1 (2)
Decreased serum C3, number (%) 10 (66.6) 25 (52.1) NS
Circulating cryoglobulins, number (%) 2 (13.3) 9 (18.8) NS
ANCA: Anti-Neutrophil Cytoplasmic Antibody; HCV: Hepatitis C Virus p HBV: Hepatitis B Virus p C3: Complement 3

Table 2: WHO histological classification of malignant and non-malignant hypertensive’s compared to normotensives. Percentages are given in parentheses.

WHO class Malignant hypertensives N= 15 Mild and moderate hypertensives N= 19 Normotensives N= 29
I - - -
II - 3 (15.8) 17 (58.7)
III 1 (6.6) 1 (5.2) 4 (13.8)
IV 10 (66.7) 5 (26.3) 1 (3.5)
V 4 (26.7) 8 (42.2) 7 (24.0)
VI - 2 (10.5) -
N.B: Among the 15 patients with LN and malignant hypertension, crescentic transformation occurred in 7 of them (3 with class IV, 3 with class V and the one with class III) and thrombotic micro angiopathy occurred in one patient on top of class IV-S



In conclusion, malignant hypertension associated with LN was a high risk clinical presentation with rapid worsening of renal function. Inhibition of renin-angiotensin system in addition to immunosuppressive drugs might induce a recovery of normal renal function.


We acknowledge Dr. Sawsan Fadda, professor of Pathology, Cairo University, Egypt and Dr. Wesam Ismail, assistant professor of Pathology, Beni Suef University, Egypt for revising renal histopathology of our patients.


1. Ruiz-Irastorza G, Khamashta MA, Castellino G, Hughes GR. Systemic lupus erythematosus. Lancet. 2001; 357: 1027-1032.

2. Al-Herz A, Ensworth S, Shojania K, Esdaile JM. Cardiovascular risk factor screening in systemic lupus erythematosus. J Rheumatol. 2003; 30: 493-496.

3. Budman DR, Steinberg AD. Hypertension and renal disease in systemic lupus erythematosus. Arch Intern Med. 1976; 136: 1003-1007.

4. Mandell BF. Cardiovascular involvement in systemic lupus erythematosus. Semin Arthritis Rheum. 1987; 17: 126-141.

5. Petri M. Detection of coronary artery disease and the role of traditional risk factors in the Hopkins Lupus Cohort. Lupus. 2000; 9: 170-175.

6. Selzer F, Sutton-Tyrrell K, Fitzgerald S, Tracy R, Kuller L, Manzi S. Vascular stiffness in women with systemic lupus erythematosus. Hypertension. 2001; 37: 1075-1082.

7. Choe Jung-Yoon, Park Sung-Hoon, Kim Ji-Young, Jung Hyun-Young, Kim Seong-Kyu. A Case of Systemic Lupus Erythematosus Presenting as Malignant Hypertension with Hypertensive Retinopathy. Korean J Intern Med. 2010; 25: 341-344.

8. Jouquan J, Pennec Y, Mottier D, Youinou P, Cledes J, Leroy JP, et al. Accelerated hypertension associated with lupus anticoagulant and false-positive VDRL in systemic lupus erythematosus. Arthritis Rheum. 1986; 29: 147.

9. Kaplan NM. Treatment of hypertensive emergencies and urgencies. Heart Dis Stroke. 1992; 1: 373-378.

10. Tao JL, Li H, Tang Y, Wen YB, Li XW. Lupus nephritis complicated with malignant hypertension: from renal vascular pathology to clinical relevance. Chin Med Sci J. 2008; 23: 81-87.

11. Ault MJ, Ellrodt AG. Pathophysiological events leading to the endorgan effects of acute hypertension. Am J Emerg Med. 1985; 3: 10-15.

12. Funakoshi Y, Ichiki T, Ito K, Takeshita A. Induction of interleukin-6 expression by angiotensin II in rat vascular smooth muscle cells. Hypertension. 1999; 34: 118-125.

13. Han Y, Runge MS, Brasier AR. Angiotensin II induces interleukin-6 transcription in vascular smooth muscle cells through pleiotropic activation of nuclear factor-kappa B transcription factors. Circ Res. 1999; 84: 695-703.

14. Lassegue B, Griendling KK. Reactive oxygen species in hypertension: an update. Am J Hypertens. 2004; 17: 852-860.

15. Marik Paul E, Rivera Racquel. Hypertensive emergencies: an update. Curr Opin Crit Care. 2011; 17: 569-580.

16. Walling HW, Sontheimer RD. Cutaneous lupus erythematosus: issues in diagnosis and treatment. Am J Clin Dermatol. 2009; 10: 365-381.

17. Sontheimer RD, Gilliam JN. Systemic lupus erythematosus and the skin. In: Systemic Lupus Erythematosus, Lahita RG (Ed), Churchill Livingstone, New York. 1992.

18. Sen D, Isenberg DA. Antineutrophil cytoplasmic autoantibodies in systemic lupus erythematous. Lupus. 2003; 12: 651-658.

19. Pauzner R, Urowitz M, Gladman D, Gough J. Antineutrophil cytoplasmic antibodies in systemic lupus erythematosus. J Rheumatol. 1994; 21: 1670.

20. Nasr SH, D’Agati VD, Park HR, Sterman PL, Goyzueta JD, Dressler RM, et al. Necrotizing and crescentic lupus nephritis with antineutrophil cytoplasmic antibody seropositivity. Clin J Am SocNephrol. 2008; 3: 682-690.

21. Mok CC, Tang SSK. Incidence and predictive factors of renal disease in Chinese patients with systemic lupus erythmatosus. Am J Med. 2004; 117: 791-795.

22. Mok CC. Prognostic factors in lupus nephritis. Lupus. 2005; 14: 39-44.

23. Weening JJ, D’Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, et al. Classification of glomerulonephritis in systemic lupus erythematosus revisited. Kidney Int. 2004; 65: 521-530.

24. Tsumagari T, Fukumoto S, Kinjo M, Tanaka K. Incidence and significance of intrarenal vasculopathies in patients with systemic lupus erythematosus. Hum Pathol. 1985; 16: 43-49.

25. Lip GY, Beevers M, Beevers DG. Complications and survival of 315 patients with malignant-phase hypertension. J Hypertens. 1995; 13: 915-924.

26. Contreras G, Pardo V, Cely C, Borja E, Hurtado A, De La Cuesta C, et al. Factors associated with poor outcomes in patients with lupus nephritis. Lupus. 2005; 14: 890-895.

27. Schwartz MM, Lan SP, Bonsib SM, Gephardt GN, Sharma HM. Clinical outcome of three discrete histologic patterns of injury in severe lupus glomerulonephritis. Am J Kidney Dis. 1989; 13: 273.

28. Appel GB, Pirani CL, D’Agati V. Renal vascular complications of systemic lupus erythematosus. J Am Soc Nephrol. 1994; 4: 1499-1515.

29. D’Agati VD, Appel GB. Mechanisms of acute inflammation and vascular injury in systemic lupus erythematosus. In: Dubois’ Lupus Erythematosus, 7th Edition. Editors: Wallace, Daniel J, Hahn, Bevra Hannahs. Lippincott Williams & Wilkins. 2007; 55: 1095-1111.

30. Cooka HT, Lightstone L. Systemic Lupus Erythematosus: Renal Involvement. Handbook of Systemic Autoimmune Diseases, Volume 7. The Kidney in Systemic Autoimmune Diseases. Justin C. Mason and Charles D. Pusey, editors. 2008.

31. Lansigan F, Isufi I, Tagoe CE. Microangiopathic haemolytic anaemia resembling thrombotic thrombocytopenic purpura in systemic lupus erythematosus: the role of ADAMTS13. Rheumatology. 2011; 50: 824- 829.

32. Song D, Wu LH, Wang FM, Yang XW, Zhu D, Chen M, et al. The spectrum of renal thrombotic microangiopathy in lupus nephritis. Arthritis Res Ther. 2013; 15: R12.

33. Cohen D, Koopmans M, Kremer Hovinga IC, Berger SP, Roos van Groningen M, Steup-Beekman GM, et al. Potential for glomerular C4d as an indicator of thrombotic microangiopathy in lupus nephritis. Arthritis Rheum. 2008; 58: 2460-2469.

34. Banfi G, Bertani T, Boeri V, Faraggiana T, Mazzucco G, Monga G, et al. Renal vascular lesions as a marker of poor prognosis in patients with lupus nephritis. GruppoItaliano per lo Studio dellaNefrite Lupica (GISNEL). Am J Kidney Dis. 199; 18: 240-248.

35. Milne FJ, James SH, Veriava Y. Malignant hypertension and its renal complications in black South Africans. S Afr Med J. 1989; 76: 164-167.

36. Isles CG, McLay A, Jones JM. Recovery in malignant hypertension presenting as acute renal failure. Q J Med. 1984; 53: 439-452.

37. Bender SR, Fong MW, Heitz S, Bisognano JD. Characteristics and management of patients presenting to the emergency department with hypertensive urgency. J Clin Hypertens. 2006; 8: 12-18.

38. Karras DJ, Kruus LK, Clenki JJ, Wald MM, Chiang WK, Shayne P, et al. Evaluation and treatment of patients with severely elevated blood pressure in academic emergency departments: a multicenter study. Ann Emerg Med. 2006; 47: 230-236.

39. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies: prevalence and clinical presentation. Hypertension. 1996; 27: 144-147.

40. Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003; 7: 374-384.

Received : 10 Apr 2017
Accepted : 12 May 2017
Published : 15 May 2017
Annals of Otolaryngology and Rhinology
ISSN : 2379-948X
Launched : 2014
JSM Schizophrenia
Launched : 2016
Journal of Nausea
Launched : 2020
JSM Internal Medicine
Launched : 2016
JSM Hepatitis
Launched : 2016
JSM Oro Facial Surgeries
ISSN : 2578-3211
Launched : 2016
Journal of Human Nutrition and Food Science
ISSN : 2333-6706
Launched : 2013
JSM Regenerative Medicine and Bioengineering
ISSN : 2379-0490
Launched : 2013
JSM Spine
ISSN : 2578-3181
Launched : 2016
Archives of Palliative Care
ISSN : 2573-1165
Launched : 2016
JSM Nutritional Disorders
ISSN : 2578-3203
Launched : 2017
Annals of Neurodegenerative Disorders
ISSN : 2476-2032
Launched : 2016
Journal of Fever
ISSN : 2641-7782
Launched : 2017
JSM Bone Marrow Research
ISSN : 2578-3351
Launched : 2016
JSM Mathematics and Statistics
ISSN : 2578-3173
Launched : 2014
Journal of Autoimmunity and Research
ISSN : 2573-1173
Launched : 2014
JSM Arthritis
ISSN : 2475-9155
Launched : 2016
JSM Head and Neck Cancer-Cases and Reviews
ISSN : 2573-1610
Launched : 2016
JSM General Surgery Cases and Images
ISSN : 2573-1564
Launched : 2016
JSM Anatomy and Physiology
ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Tropical Medicine and Research
ISSN : 2578-3165
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Annals of Clinical and Experimental Metabolism
ISSN : 2572-2492
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
Annals of Clinical Cytology and Pathology
ISSN : 2475-9430
Launched : 2014
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
TEST Journal of Dentistry
ISSN : 1234-5678
Launched : 2014
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
Author Information X