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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2000  |  Volume : 11  |  Issue : 3  |  Page : 370-380
Lupus Nephritis among Arabs - Differences with other Races; Emphasis on Clinicopathological and Serological Perspectives

Department of Internal Medicine, Mafraq Hospital, Abu Dhabi, United Arab Emirates

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Data on ethnic differences of lupus nephritis (LN) are extremely scattered in the literature. Furthermore, most of the publications on LN in Arabs have in fact discussed the condition within the general frame of systemic lupus erythematosus (SLE) disease in mixed, but Arab-dominated groups of patients, and fewer, in exclusively Arab individuals. Lupus nephritis however, seems to be common, occurring in 37-69% of SLE patients in the Arab dominated groups and in 50% of the exclusively Arab group. In two out of three groups who reported their renal biopsy results, WHO class III was the most common histopathological type (36% and 54% respectively). Interestingly, the relatively high prevalence of nephropathy in the two groups was associated with a low prevalence of discoid lupus. Arabs with LN who have been studied for serological correlation, did not exhibit any specific or distinctive entity of autoantibody profile. Nonetheless, contradictory data have been noticed in relation to dsDNA antibodies, as they significantly correlated with LN in some of the Arab dominated groups, but not in the uniformly Arab group. Anti­RNP antibodies significantly correlated with non-nephritic SLE patients in the latter group, suggesting a possible protective role of these antibodies. The previously reported correlation between anti-Sm antibodies was not confirmed in the Arab groups. Like the other features of SLE, the differences related to LN in various populations are very likely to be multifactorial rather entirely being ethnical. Lupus nephritis in Arabs however, requires further demarcation by evaluating larger number of patients preferably through multicenter studies.

Keywords: Lupus nephritis, Arabs, Ethnicity.

How to cite this article:
Al Attia HM. Lupus Nephritis among Arabs - Differences with other Races; Emphasis on Clinicopathological and Serological Perspectives. Saudi J Kidney Dis Transpl 2000;11:370-80

How to cite this URL:
Al Attia HM. Lupus Nephritis among Arabs - Differences with other Races; Emphasis on Clinicopathological and Serological Perspectives. Saudi J Kidney Dis Transpl [serial online] 2000 [cited 2021 Apr 10];11:370-80. Available from: https://www.sjkdt.org/text.asp?2000/11/3/370/36659

   Introduction Top

Systemic lupus erythematosus (SLE) is a heterogeneous disease of disordered immunity, marked clinically by multi systemic inflammatory involvement. The course and prognosis are highly variable. The clinical features of SLE have been extensively described from different geographical parts in the world, with some variations among different racial groups.[1],[2],[3] In the English literature, most publications from the Middle East on SLE have described disease characteristics among groups that largely consisted of Arabs.[4],[5],[6],[7],[8],[9],[10] Nevertheless, information on renal manifes­tations were either scarce or not specifically referred to with detail. Yet, there have been reports describing disease entities in exclusively Arab patients. [11],[12],[13] One report referred to lupus nephritis (LN) with specific exposure to serological profile.[12] More data on this condition, however, need to be extrapolated, and this review is an attempt to present some of the currently available relevant information on LN in Arabs and non-Arabs. It may encourage workers to conduct more comprehensive studies in this line.

General considerations

Renal involvement is a frequent feature of SLE, occurring in 40-75% in various populations of patients, most often within five years of the disease onset. [14] It is one of the most significant causes of morbidity, health expenditure and mortality in patients with SLE. [15] The disease has higher risk and mortality rates in Blacks compared to Whites. [16],[17],[18],[19],[20],[21] Lupus nephritis in Orientals has also been reported to be more aggressive than that in Westerners. [22] It appeared from a race-controlled human leukocyte antigen frequency analysis among African American patients that non-HLA mediated genetic factors and/or environmental factors contribute to the increased risk of nephritis in black patients with SLE. [19] In a recent study from South Africa, the majority of patients with advanced disease were in fact socio-economically deprived Blacks in whom renal replacement therapy was not feasible. [23] On the other hand, Indo-Asians in South Africa had worse prognosis compared to Black patients, indicating a possible ethnical influence on the prognosis. [20] Recent hospital-based data from India have shown that Indo-Asians have the highest rate of renal involvement (73%) compared to other races. [24] With respect to gender, LN is more prevalent in males than females but there have been contradicting views regarding its severity and prognosis. A disease with poor prognosis was reported among Caucasians, Brazilians, and US residents of Asian descent,[25],[26],[27],[28] versus another one with more benign course among Israeli, Taiwani and Thai males. [29],[30],[31] No similar study looked at this issue in Arab males.

Histopathological perspectives

Renal manifestations are also highly variable in clinical presentation and in histo­pathology-related prognosis. The spectrum ranges from mild asymptomatic proteinuria to a rapidly progressive glomerulonephritis leading to end-stage renal disease (ESRD). The clinical heterogeneity is accompanied by diverse histological abnormalities in renal biopsy. [32] The World Health Organization (WHO) classification of lupus nephritis provides a practical and widely accepted system for categorizing the bulk of renal lesions observed on biopsy of patients with lupus nephritis.[33],[34],[35] The scheme uses information obtained from light, immuno­fluorescent, and electron microscopic evaluation. [36] A recent modification of the scheme is shown in [Table - 1].

In several studies of lupus kidney disease, approximately 25% of renal biopsy specimens showed focal proliferative (WHO class III), 37% showed diffuse proliferative (WHO class IV) and 13% showed membranous (WHO class V) glomerulonephritis. Patients with (WHO classes III-V) have more serious forms of lupus nephritis.[35] The frequency of various classes in Arab groups and non­Arabs are shown in [Table - 2]. In contrast to these widely held finding, the WHO class III appeared more common than class IV in the series from Kuwait and the UAE.[10],[12]

These results however, may have been biased by the relatively small number of biopsies studied in these two series. LN occurred in 54% of Omani Arabs with SLE. In those who had renal biopsy, 42% had class VI (personal communication). In the male gender, class IV was also found to be the commonest in the morphology of renal biopsy. Data in males from Taiwan indicated that, 47% were of class IV, 24% of class II, 18% of class III and 12% of class V. [30] Nonetheless, the prognostic value of the classification was questionable in studies among Chinese [37] and South Africans [20] as it either showed little correlation with clinical and renal information or, did not offer accurate prognosis regarding mortality. Renal biopsy therefore, provides important information for proper diagnosis and management of patients suspected of having lupus nephritis and also determines whether aggressive therapy is likely to be efficacious.

Immunopathogenesis and newer perspectives

Renal injury in lupus nephritis appears to be driven by the inflammatory response to immune complex deposition within the kidney. It is well recognized that dsDNA antibody complexes participate in the pathogenesis of LN through the activation of complement and clotting systems. [38],[39],[40]

However, since not all patients with dsDNA antibodies develop nephritis, other auto­antibodies against non-nuclear antigens such as histone, RNA polymerase, laminin and C1q have been postulated to be patho­genic in LN. [41],[42] Some authors have suggested that increased anti-C1q antibodies may predict renal flares. [43] Current information indicate that besides DNA/anti nDNA complexes, molecules such as trombo-modulin, intracellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1,[44],[45],[46] and inflammatory cytokines; IL-1α, IL-1β, TNF and IL-6 may have certain roles in the pathogenesis of LN.[47],[48],[49] It has also been found that serum level of the soluble vascular cell adhesion molecule (sVCAM­1) is significantly elevated in patients with active LN (WHO classes III-IV). It increased with disease activity and decreased during treatment. The level of this molecule therefore can be used as a useful marker for LN activity.[50] Prolactin (PRL) is an important immunoregulator and may have a role in the pathogenesis of SLE. [51] The high levels of serum and urinary PRL in patients with severe renal disease support a relationship between the immune and neuroendocrine systems in this disease. [52]

Clinical and laboratory aspects

Different prevalence rates of LN have been reported in various studied populations [Table - 3]. LN is fairly common in Arab studied groups with SLE (37-69%), particu­larly among those from Saudi Arabia. It has previously been indicated that the presence of discoid lupus (DL) in patients with SLE would appear to signify an improved prognosis with a low frequency of renal disease. [53] Nonetheless, contradictory results have been noticed in various populations in relation to this conclusion. Blacks for instance, are known to have high prevalence of DL (25-28%) and high prevalence (nearly 50%) of LN with poor prognosis too.[54],[55] Some populations have a reciprocal relationship between frequency of DL and prevalence of LN such as Orientals, [56],[57],[58] Indo-Asians, [24] Latin Americans, [54] Iraqis [4] and Arabs in UAE. [13] It was more apparent in the former three groups where a large number of patients has been studied. Such a finding however, was not confirmed in the data of the groups from Saudi Arabia [8] and Kuwait. [10] Nonetheless, the relationship is of a clinicoepidemiological significance and worthy further substantiation in future studies [Table - 3].

The significance of hypertension in LN has been investigated in various populations and there is a general agreement that its development, whether or not related to LN, carries an unfavorable prognosis. Even at an early stage, hypertension and hypertensive renal vascular lesions appear to correlate well with the impairment of renal function. [22],[59],[60] Hypertension, thrombocyto-penia and leucopenia were found to be predictors of nephritis in Orientals with SLE. [61] Furthermore, severe thrombocytopenia predicted ESRD in African Americans patients with LN.[62] The presence of cellular casts and/or proteinuria typically provides concurrent evidence for significant LN.[63] Renal relapse is associated with an increase of proteinuria and/or serum creatinine and the appearance of red and/or white blood cells casts is a reliable predictor of relapse particularly among patients with base line protein excretion of 1gm/day or more. [64] Regarding the correlation with histopatho­logy, persistent or worsening proteinuria is a poor predictor of adverse outcome of renal function in proliferative LN. On the other hand, nephrotic-range proteinuria is a marker of disease severity and is used as an indicator for therapy.[65]

Serological variables have been evaluated as indicators or predictors of acute LN. The condition is often associated with dsDNA antibodies and such correlation has been widely recognized in several populations including Caucasians,[66],[67],[68],[69] Mestizo, [70] Africans,[55],[71],[72] and Asians. [72] Among the Arabs in UAE, such a correlation was not confirmed, perhaps due to fact that the markedly high prevalence of these antibodies in nephritic and non-nephritic patients (100% versus 81%, P = NS) had led to the loss of their potential marker value in determining any correlation with LN. [12] However, this finding was not exceptional as similar results were also observed in Oriental patients from Singapore [57] and in a group of black American women. [73] Such correlation, however, was marginally significant in the Arab-dominated group from Kuwait (P = 0.042). [9] High titers of antibodies are seen more frequently in proliferative (WHO class II-IV) than in membranous LN. Nonetheless, some incon­sistent observations have been reported [74] and reflect, in part, the inability to distinguish and quantify pathogenic antibodies in the circulation. Furthermore, antibody avidity seems to have a role in the disease expression. High avidity anti dsDNA antibodies have been associated with LN. [69],[72],[75] The avidity of these antibodies has not been studied in any of the Arab groups. It was also shown that not all anti DNA antibodies are pathogenic and only some with the conserved 16/6 idiotype are associated with nephritis. [1],[70],

Some studies in Whites have demonstrated that only the presence of anti Ro/SS-A in SLE patients was associated with a high prevalence of nephritis (53%) [76] , whereas, there was a relative paucity of LN when both anti Ro/ SS-A and anti La/ SS-B antibodies are present. [66],[76],[77] Furthermore, a low frequency of nephritis has been reported in SLE patients who have anti RNP antibodies but LN may occur when these antibodies are associated with anti Sm or Ro and, notably, with anti dsDNA antibodies. [78] Anti RNP antibodies have some control on an unknown but potent "anti nephritic" factor, perhaps though suppression of anti dsDNA or anti Sm production. [79],[80] Our data from the Arabs in UAE [12] were in agreement with the finding of a negative relationship between LN and anti RNP antibodies (anti RNP of 0/13 (0%) in nephritis versus 6/18 (33%) in non - nephritic, P = 0.028). Similar finding was observed in Turkish patients where only two out of 44 patients (4.5%) with LN were positive for anti-RNP. [69] No significant correlation was reported in the Arab­dominated group from Kuwait, [9] European, [67] and Black patients. [54],[71],[73] Paradoxically, the prevalence of anti-RNP has been found to be high (60-70%) in Black populations with LN including Americans [54],[71] and South Africans. [55] Some workers have reported correlation of anti­Sm in Whites with milder LN or with low proportion of patients who progress to ESRD. [81],[82],[83],[84] This correlation was also seen in Brazilian males, [27] but could not be confirmed by others in Arab groups, [8],[9],[12] European [67],[68] or Turkish [69] patients. Workers from Oklahoma have demonstrated a distinctive serological profile in black women with LN. It is characterized by the presence of three precipitin antibody profile of anti­Sm, anti-RNP and anti-Ro/SS-A, but without anti-La/ SS-B. [18] Other workers from New Orleans were unable to confirm such finding in their own Afro-American patients. [71],[73] We too were unable to demonstrate this profile when we studied the Arab patients with LN. [12] In Whites, low prevalence of nephropathy has been reported in patients with SLE who are rheumatoid factor (RF) positive. [67],[85] Such correlation was not seen in the Arab, [12] African [55],[71] or Turkish [69] patients with nephritis. So far, Arabs with LN who have been studied for autoantibody correlation did not appear to be have a specific or distinctive entity of autoantibody profile [Table - 4]; a finding that appears compatible with most series in other populations.

The discrepancies obtained from various studies on LN can easily be attributed to (a) whether there has been a bias in the selection of patients (b) the methods used for the detection of autoantibodies, and (c) the racial and environmental differences between the groups of patients studied. It is becoming increasingly acknowledged that ethnical differences in the clinical expression of SLE (for which other factors, such as socioeconomic conditions do not account), imply that genetic factors may play important roles in these differences. This is most likely the case for anti-RNP and anti-Sm antibody response, [86] which appear to have the strongest clinical associations with ethnicity. [3],[54] Finally, the task of defining various aspects of LN in Arabs is far from being accomplished. In order to demarcate the condition, studying larger number of patients in a multicenter research work is highly required.

   Acknowledgment Top

My thanks to Mrs. N. Abdulmajeed for her assistance in preparing the tables of the review.

   References Top

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Correspondence Address:
Haider M Al Attia
Department of Internal Medicine, Mafraq Hospital, P.O. Box 2951, Abu Dhabi
United Arab Emirates
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PMID: 18209329

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