We ± 21.3 years; P = 0.05). We know

believe that under reporting of lupus in Pakistan has given basis to the false
belief that SLE is not a common disease in Pakistan. SLE is very common in our
community and the true frequency of SLE, however, can only be obtained by
conducting a community-based study and creation of registry protocols. It is
pretty straightforward that the more SLE patients screened more chances to find
patients with renal involvement. One study that is worth mentioning here in
which basically population based frequency of systemic lupus erythematosus and
lupus nephritis has been calculated 144 in south east Michigan from
2002-2004. They used American College of Rheumatism criteria to pick patients
of Systemic Lupus erythematosus. Data were collected by various abstractors who
had completed standardized, rigorous training, which included completion of
pilot abstractions which were reviewed in detail by the
rheumatologist-investigators against the source documentation. Continual assurance
of quality of data abstraction included re abstraction of 5% of the records, as
well as physician review of all abstractions and provision of feedback. For each
potential case, researchers manually reviewed all available records. They found
overall age-adjusted prevalence and incidence (ACR definition) per 100,000
persons were 5.5 (95% confidence interval 95% CI 5.0–6.1) and 72.8 (95% CI
70.8–74.8) and among females, the incidence was 9.3 per 100,000 persons and the
prevalence was 128.7 per 100,000 persons. Only 7 cases were estimated to have
been missed, adjustment for which did not affect the rates. Systemic lupus
erythematosus was 2.3-fold higher in black persons than in white persons, and
10-fold higher in females than in males. Among incident cases, the mean ± SD
age at diagnosis was 39.3 ± 16.6 years. Black SLE patients had a higher
proportion of renal disease and end-stage renal disease (ESRD) (40.5% and
15.3%, respectively) as compared to white SLE patients (18.8% and 4.5%,
respectively). Black patients with renal disease were diagnosed as having
systemic lupus erythematosus at younger age than white patients with renal
disease (mean ± SD 34.4 ± 14.9 years versus 41.9 ± 21.3 years; P = 0.05). We know estimating the frequency
prevalence of systemic lupus erythematosus (SLE) in the general population is
challenging and resource-intensive to perform. In part, this is due to a
protean and systemic nature of the disease and the attendant diagnostic
complexity that requires the synthesis of a multitude of clinical observations
and laboratory findings, often obtained from a variety of health care settings.
In the United States, the fragmented health care system and lack of existing
infrastructure suitable for the surveillance of autoimmune diseases such as
systemic lupus erythematosus further complicates the implementation of
population-based measures to ascertain and validate cases. Epidemiologic data is
importants to our understanding of the risk and burden of disease in the
population. However, such data are challenging and resource intensive to derive
in a fragmented health care system and for diseases such as systemic lupus
erythematosus, in which a heterogeneous constellation of clinical and
laboratory features is essential to establish a diagnosis. Surveillance outside
of the tertiary care setting is imperative for recording the full spectrum of
systemic lupus erythematosus, in order to identify cases receiving health care
in other settings. In the socio-demographically diverse MILES source population
of 2.4 million, there were, on average, 133 new cases and 1,708 prevalent cases
of systemic lupus erythematosus annually during 2002–2004, yielding
age-standardized incidence and prevalence estimates per 100,000 persons of 5.5
and 72.8, respectively. Using more complete case-finding sources, they were
able to quantify at a new level of statistical precision the higher risk and
burden of SLE among women and minorities in the general population of the US.

majority of previously available data on the epidemiology of systemic lupus
erythematosus were derived from predominantly homogeneous populations of European
descent. Though caution was exercised when comparing results between studies
that was heterogeneous in terms of methodologies and population structures, in
relation to the weighted data, their rates in Michigan appear to be similar for
SLE incidence, though 3-fold higher for SLE prevalence. The larger
prevalence-to-incidence ratio in their population, coupled with the higher
prevalence range in the more recent review, suggests that prevalence may be
increasing, in part due to improved survival, over the last 2 decades. The net
migration in Michigan (i.e., the balance of in- and out-migration) from 1985
through the end of the surveillance period was relatively stable, including
that among young adults (a reasonable proxy for a “healthy” population subset).
However, the possibility that persons with preexisting lupus migrated into the
source population in order to be more proximate to medical care cannot be

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found a female-to-male incidence ratio of 6.2:1 and a female-to-male prevalence
ratio of 10.1:1; hence, males accounted for a higher proportion of newly
diagnosed cases as compared to existing cases in the overall population, a
pattern that pertained to both black patients and white patients. Studies
examining race have documented higher rates in persons of African descent: a
study from Allegheny County, PA (for the years 1985–1990) found an ~3-fold
incidence of SLE among black females versus white females (9.2 versus 3.5 per
100,000 persons) In their population, black persons had the highest risk and
burden of SLE, with a 2.1-fold higher incidence and a 2.3-fold higher
prevalence (1 in 537 black females) than white persons, ratios somewhat smaller
than those reported elsewhere. The ability to compare disease patterns in other
racial and ethnic groups is limited by the small numbers of these minorities in
our geographic region, though data suggest that black persons have a higher
prevalence of SLE than Asian/Pacific Islander or Hispanic persons.

shown by the age-specific incidence rates, systemic lupus erythematosus began
earlier in the reproductive years in black females. In late childhood, there
was already a trend for black girls to have an increased incidence compared to
white girls, and in the 20–50-year range, there was an early incidence peak in
black women, as compared to statistically lower levels that plateaued among
white women. The incidence rates in black versus white women did not differ
significantly. Higher genetic load (number of SLE-susceptibility risk alleles)
has been associated with earlier disease onset among African American, but not
European American, SLE patients and gene–environment interactions may further
underlie observed racial differences in the natural history of this disease.

study had several limitations. First, it was based on review of medical
records, rather than direct patient examination, as most population-based
epidemiologic studies must. Second, race and ethnicity were ascertained from
records, not self-reports, which would be the gold standard. Misclassification
may be a particular concern for persons of Hispanic/Latino ethnicity, since
many medical records systems do not assess Hispanic ethnicity as a separate
variable from race, which in theory, could lead to underestimation. Third,
although we tried to reach all targeted health care sources, a few (see the
case ascertainment section above) did not permit access, and the slow
cooperation of others necessitated active record reviews through 2011,
requiring increased allocation of resources in order to complete the planned
surveillance activities. The nonparticipating sites did not appear to differ
systematically from the participating sites in terms of the demographics of the
populations served or other discernible features. Fourth, they have likely
underestimated incident and prevalent cases, as there may be undiagnosed cases
in the community that have not reached the health care system for screening and
diagnosis, and other cases may have received care outside the catchment area.
However, the capture–recapture analyses estimated that surveillance program
missed only 7 cases in the source population, pointing to highly effective
methods of defining catchment areas (based on a pilot analysis of health care
utilization patterns) and case ascertainment. Fifth, they were unable to enlist
the systematic cooperation of primary care providers for even more
comprehensive findings, but the interactions we did have suggested that primary
care practices are likely to refer SLE patients and are therefore unlikely to
represent a large source of additional cases.

study also has several strengths. First, it included multiple case-finding
sources, including health care facilities in a county contiguous to the source
population, which helped to ensure complete ascertainment in a mobile
population. Second, for each patient, there was comprehensive abstraction and
synthesis of detailed clinical and laboratory data from multiple sources. With
the public health authority from the MDCH enabling our access to all relevant
records, a thorough profile could be constructed for the majority of patients.
In some cases, the diagnosis of lupus could be confirmed only after combining
data from several hospitals or physicians. Third, as noted above, the use of 2
analytical case definitions (ACR and rheumatologist definitions) independently
confirmed the diagnoses in the majority of patients and accommodated the
clinical uncertainty of classifying SLE. The rheumatologist rates may be
considered to yield conservative estimates and, thus, serve as a validated
“lower bound” for the estimation of SLE. Fourth, the collaboration with
colleagues from the CDC, the Georgia Lupus Registry, and the respective state
health departments for the methods and infrastructure development can serve as
a prototype for the implementation of other SLE registries, which will enhance
opportunities for comparison of SLE statistics across sites. Indeed, new
registries based on this framework have been initiated in regions with greater
representation of other minority groups (Asian/Pacific Islander,
Hispanic/Latino, and American Indian/Alaska Native groups).

on this comprehensive, population-based surveillance program, our data
underscored substantial levels of confirmed systemic lupus erythematosus cases
which of course influenced frequency of lupus nephritis. Our purpose to mention
the above study in detail was to depict that even in such a well-equipped setup
as United States they had limitations in their study.  Such data support a focus of medical resources
on early diagnosis and improved treatment of lupus nephritis.

 We also need to have specific SLE/LUPUS
registry such as Georgia lupus registry. In the 1950’s, systemic lupus
erythematosus (SLE) was thought to be rare, predominantly affecting females
with light hair, fair skin, and “inability to tan”. An epidemiologic study from
1956–65 showed for the first time the higher burden of disease in black women
compared to their white counterparts. We now appreciate the disproportionate
burden of SLE on women, particularly in their childbearing years, and in
certain racial groups. These epidemiologic studies advanced our understanding
of the burden of SLE but were limited in their ability to find all cases in the
population and thus describe the full spectrum of diagnosed systemic lupus

the recent significant increase in awareness of and research in SLE and LN,
along with the availability of innovative techniques, the purpose of this Georgia
Lupus Registry (GLR) study was to advance the epidemiologic understanding of
SLE by doing more complete case finding in a targeted population, avoiding
referral bias in a particular institution, using available case definitions to
better define the incidence and prevalence of diagnosed SLE, and characterizing
individuals with this disease from a population perspective. The GLR is one of
two recently completed Centers for Disease Control and Prevention (CDC) funded
population-based lupus registries designed to minimize many of the limitations
of previous studies. An innovative tool in this approach is the use of the
state public health surveillance exemption to the Health Insurance Portability
and Accountability Act (HIPAA) to obtain greater access to protected health
information without requiring individual patient consent, a limitation that can
bias findings. This new and powerful approach allows for an unprecedented
completeness of case finding from multiple sites of ascertainment throughout
the targeted community. Coupled with detailed training of abstractors, strict
quality control of data gathering and processing, many sources of case
ascertainment that reduced bias from a consent process or institution type, and
the high number of cases, this study provided more reliable population-based
estimates of true incidence and prevalence of SLE than previously reported.

 The frequency and severity of lupus nephritis
may be related to the patients’ racial background and studies have suggested
that there are certain nephropathy susceptibility genes that predisposing to
lupus nephritis 134. Although all of the evidence suggests
that a genetic predisposition plays a major role in development of systemic
lupus erythematosus (SLE) and/or lupus nephritis (LN), the susceptibility genes
are mostly unknown. The problem in identifying susceptibility genes is due in
part to multiple genes with variable genetic effects and the diverse genetic
backgrounds of human populations. In human SLE, genes of early components of
complements as well as many polymorphic genes (including the MHC class II and
class III, Fc?R, mannose-binding protein, IL-6, Bcl-2, and IL-10 genes) have
been linked with SLE or LN by population-based case-control or within-case
studies. The contribution of some of these disease-associated genes to the presence
or absence of clinical manifestations has been further tested in mice with
targeted alteration of the specific candidate gene. In addition to SLE
susceptibility genes, there may be a separate set of nephropathy susceptibility
genes predisposing to LN as suggested by the familial clustering of end stage
renal disease in African-Americans with Lupus Nephritis. The availability of tightly
packed genetic markers spanning the entire genome has enabled the
identification of chromosomal regions linked to disease susceptibility genes
without previous knowledge of the gene function. Our group has used known
murine lupus susceptibility loci as a guide, and conducted linkage analysis of
genetic markers located within a specific, possibly syntenic human chromosomal
region. Evidence for linkage of a chromosome 1q41-42 region was observed in
SLE-affected sib pairs from multiple ethnic groups. More recently, several
groups have reported results of genome scans of SLE-affected sib pairs or
pedigrees. Given the morbidity associated with LN, the ability to accurately
identify SLE patients destined to develop LN could shift the current management
paradigm from treatment to prevention. Although it is not likely that CKD and
ESRD can be avoided completely, because many patients present with LN as the
initial manifestation of their SLE, a preventative management strategy could
significantly reduce CKD and ESRD. For example, SLE patients destined to
develop LN could be followed much more closely, perhaps with home monitoring of
the urine so kidney biopsy and treatment could be started without delay.
Alternatively, such patients could be considered for pre-emptive therapy to
attenuate autoimmunity before any clinical manifestations of kidney involvement
are apparent. Although it is currently not possible to determine a priori who with SLE will develop
LN, several investigations of lupus genetics have approached this question.

 Lupus Nephritis remains also major cause of
morbidity and mortality particularly among patients of Hispanic and
African-American ethnicity SLE patients with renal involvement are at a higher risk
of dying of this disease 135,136. Generally renal involvement is more common
in Blacks, Indians and Chinese, with lesser prevalence in Caucasians and Arabs
137, 138.

our study showed a frequency of renal involvement (86%) as compared to the
Indians (73%) 137, Blacks (78%) 140, Chinese (54%) 138 and Arabs 12 (54%)
139. The mean age of the study group patients at presentation was 27.31 ± 7.45
years. Our study also showed LN class 4 being the most common histopathological
finding diagnosed when patients underwent renal biopsy. A similar finding was
observed by Vineeta Shobha ET, al. 141. There has been a recent update
regarding renal biopsy 145. Although the decision to perform a kidney biopsy
in SLE patients when there is clinical evidence of renal involvement seems straightforward,
it has become somewhat controversial because of a prevailing view that all
forms of LN can be adequately treated with corticosteroids plus mycophenolate
mofetil (MMF). As the therapy of LN moves beyond the currently available non targeted
immunosuppressive regimens of high-dose corticosteroids plus cyclophosphamide
or MMF to interventions that focus on specific immune pathways, a more
comprehensive picture of renal pathology through molecular imaging of the
kidney biopsy may be desirable. The immune pathways active in the kidney at the
time of lupus nephritis diagnosis vary considerably between patients.
Nonetheless, the kidney biopsy is important to define the nature of renal
involvement. Although immune-complex–mediated GN is the most common cause of
kidney disease in systemic lupus erythematosus, there are other mechanisms that
result in renal injury which can only be diagnosed with a biopsy, and require a
different approach to management than immune-complex LN 145. There was a
preponderance of female patients in the study. This finding is similar to most
of the studies of SLE that have shown a predominance of females 142,143.  The
limitation of our study were that it was a single center study and may if
plenty of systemic lupus erythematosus patients were screened the actual
frequency would have been different