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Autoantibody prevalence and clinical outcomes in Omani chronic kidney disease patients: A retrospective cohort study
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Received: ,
Accepted: ,
How to cite this article: Alghailani HH, Salmi I, Ahmad AlShahri HA, Al Shidi S, Soliaman MM, Elias F, et al. Autoantibody prevalence and clinical outcomes in Omani chronic kidney disease patients: A retrospective cohort study. World Adv Renal Med. doi: 10.25259/WARM_6_2026
Abstract
Objectives:
The incidence and prevalence of chronic kidney disease (CKD) are rising globally, driven by an increase in non-communicable diseases and autoimmune disorders. While the role of autoimmunity in CKD is recognized, its specific impact on the Omani population is not well understood. This study aimed to determine the prevalence of various autoantibodies in clinically suspected Omani CKD patients and to evaluate their association with disease progression and mortality.
Material and Methods:
We conducted a retrospective cohort study at a major tertiary hospital in Oman, including 800 CKD patients who attended the adult nephrology outpatient clinic between July 2016 and July 2020. Autoantibody testing was performed based on specific clinical indications. Clinical and laboratory data were collected at the first encounter, with a mean follow-up period of 5.5 years. The primary outcomes were the rate of estimated glomerular filtration rate (eGFR) decline and all-cause mortality.
Results:
The study population consisted of 53.4% males, with a mean age of 45.2 years. The prevalence of autoantibodies was 26.7% among tested CKD patients, with a higher prevalence in younger females. The most common autoantibodies were lupus anticoagulant (39.3%), anti-nuclear antibody (ANA) (23.5%), anti-SSA-RO (14.8%), anti-double stranded DNA (13.6%), and anti-Ro52 (10.8%). Multivariate regression analysis revealed a significant association between the presence of autoantibodies, particularly ANA, and a more rapid decline in eGFR (R2 = 38%). Furthermore, autoantibody positivity was associated with an increased risk of all-cause mortality, even after adjusting for baseline covariates in multivariable Cox regression analysis.
Conclusion:
Autoimmune antibodies are highly prevalent in clinically suspected Omani CKD patients and are significantly associated with disease progression and mortality. These findings underscore the importance of targeted screening for autoimmunity in this patient population to facilitate early intervention and improve clinical outcomes. Further research is needed to explore the underlying mechanisms and to develop targeted therapeutic strategies.
Keywords
Autoantibodies
Autoimmune
Chronic kidney disease
Non-communicable diseases
INTRODUCTION
Chronic kidney disease (CKD) represents a growing public health challenge worldwide, with its incidence and prevalence steadily increasing.[1-3] This trend is largely fueled by the global epidemic of non-communicable diseases such as diabetes and hypertension.[4] In addition to these well-established risk factors, there is mounting evidence that various autoimmune disorders are significantly associated with the development and progression of CKD.[5,6]
Immunological disorders can trigger inflammatory processes within the kidneys, leading to glomerular and tubulointerstitial damage.[7,8] A number of autoantibodies have been identified in association with kidney diseases, some of which are directly implicated in the pathogenesis of renal injury.[9-12] Glomerulopathies, which are often immune-mediated, are a significant cause of progression to end-stage kidney disease (ESKD).[9,10,13] In the United States, glomerulonephritis is the third leading cause of CKD, although its true burden is likely underestimated.[14]
While the association between autoimmunity and CKD is well-documented in many populations, the prevalence and clinical impact of autoantibodies in CKD patients in Oman remain unknown. Although diabetes and hypertension are recognized as major contributors to CKD in Oman,[3] the role of autoimmunity has not been systematically investigated. This knowledge gap limits the ability to accurately diagnose, manage, and prognosticate for Omani patients with immune-mediated kidney disease.
This study, therefore, is the first to evaluate the prevalence of a comprehensive panel of autoantibodies in a large cohort of Omani CKD patients who underwent clinically indicated testing. We also aimed to examine the clinical impact of these autoantibodies on the progression of CKD and patient survival. By providing region-specific data, we hope to improve the understanding of CKD pathogenesis in this population and to inform the development of more effective clinical management strategies.
MATERIAL AND METHODS
Study design and population
We conducted a retrospective cohort study at the Royal Hospital in Muscat, Sultanate of Oman, a major tertiary care center. The study population included all adult patients (≥18 years of age) with a diagnosis of CKD who attended the nephrology outpatient clinic between July 2016 and July 2020. Patients were identified through the hospital’s electronic medical record system (Al Shifaa). Of the 1100 patients initially screened, 800 met the inclusion criteria and were included in the final analysis.
Exclusion criteria were clearly defined and included patients with a primary diagnosis of inherited kidney disease (e.g., polycystic kidney disease), congenital renal anomalies, or CKD primarily caused by specific medications known to be nephrotoxic. Patients who were being followed for acute kidney injury without evidence of chronic disease were also excluded from the study.
Data collection and variables
All clinical and laboratory data were collected from the electronic medical records. Baseline data included demographic information (age, gender), primary cause of CKD, and a comprehensive panel of laboratory tests. Laboratory data included hematological parameters (hemoglobin, white cell count), biochemical profiles (serum urea, creatinine, albumin), and inflammatory markers (erythrocyte sedimentation rate, C-reactive protein). The estimated glomerular filtration rate (eGFR) was calculated using the modification of diet in renal disease equation. CKD staging was performed according to the Kidney Disease: Improving Global Outcomes guidelines.
Immunological assays
Autoantibody testing was performed based on clinical suspicion of an underlying autoimmune disease or in cases of unexplained CKD progression. Testing was not performed systematically across the entire cohort. Indications for testing included: unexplained rapid decline in eGFR, active urinary sediment (hematuria or cellular casts), systemic symptoms suggestive of an autoimmune disorder, or atypical presentations of suspected diabetic nephropathy. Patients with classic, slowly progressive diabetic nephropathy without atypical features were generally not tested. The immunological data collected included:
Anti-nuclear antibody (ANA): Detected by indirect immunofluorescence. A titer of ≥1: 80 was considered positive
Anti-neutrophil cytoplasmic antibodies: Detected by indirect immunofluorescence
Extractable nuclear antibodies: Including anti-double stranded DNA (anti-dsDNA), anti-Smith,Anti-Sjögren’s-syndrome-related antigen A (Ro) antibody (Anti-SSA/Ro), Anti-Sjögren’s-syndrome-related antigen B (La) antibody (Anti-SSB/La), Anti-ribonucleoprotein (U1-RNP) antibody (Anti-RNP), and anti-Scl-70, were identified using an immunoblot assay
Other markers: Rheumatoid factor and lupus anticoagulant were also measured.
All tests were performed using commercial kits, and the assays were standardized and validated according to the manufacturer’s protocols. Positivity for each autoantibody was defined based on the reference ranges provided by the clinical laboratory.
Outcomes
The primary outcomes of the study were the rate of eGFR decline and all-cause mortality. The rate of eGFR decline was calculated as the difference between the first and last recorded eGFR values, annualized over the follow-up period. All-cause mortality was ascertained from the electronic medical records.
Statistical analysis
Data were analyzed using STATA 13/SE statistical software (Stata Corp, College Station, Texas, USA). Continuous variables were presented as mean ± standard deviation for normally distributed data or as median and interquartile range (IQR) for non-normally distributed data. Categorical variables were presented as frequencies and percentages (%). To compare groups, the Student’s t-test or Mann–Whitney U test was used for continuous variables, and the Chi-squared test was used for categorical variables. A univariate regression analysis was performed to identify variables associated with eGFR decline. To avoid prematurely excluding potentially important variables, a p ≤ 0.2 was used as the cutoff for inclusion in the multivariate regression model. A multivariate linear regression analysis was then used to determine the independent predictors of eGFR decline.
To assess autoantibody positivity as an independent predictor of mortality, a multivariable Cox proportional hazards regression analysis was performed, adjusting for baseline covariates including age, gender, baseline eGFR, diabetes status, and proteinuria.
Missing data were minimal (<5% for all variables) and were handled by complete-case analysis. A p < 0.05 was considered statistically significant for all final analyses. Model assumptions, including linearity, normality of residuals, and homoscedasticity, were checked.
RESULTS
Baseline characteristics
A total of 800 patients with CKD were included in the analysis. The baseline demographic and clinical characteristics of the study cohort are presented in Table 1. The study population consisted of 428 males (53.4%) and 372 females (46.6%), with a mean age of 45.2 (±14.6) years for males and 45.3 (±15.7) years for females. The mean follow-up period was 5.5 years.
| Characteristic | Males (n=428) | Females (n=372) | p-value |
|---|---|---|---|
| Demographics | |||
| Age (years), mean±SD | 45.2±14.6 | 45.3±15.7 | 0.94 |
| Renal function parameters | |||
| Baseline eGFR (mL/min/1.73 m2), median (IQR) | 42 (25–62) | 40 (20–55) | 0.18 |
| Baseline serum creatinine (µmol/L), median (IQR) | 285 (175–430) | 275 (170–410) | 0.42 |
| Baseline serum urea (mmol/L), median (IQR) | 12.5 (8.8–17.0) | 11.5 (8.0–16.0) | 0.31 |
| Follow-up renal function (at 5.5 years) | |||
| Final eGFR (mL/min/1.73 m+2), median (IQR) | 35 (18–52) | 32 (15–48) | 0.15 |
| Final serum creatinine (µmol/L), median (IQR) | 320 (180–480) | 310 (170–470) | 0.38 |
| Final serum urea (mmol/L), median (IQR) | 13.5 (9.0–19.0) | 12.0 (8.5–17.0) | 0.25 |
| Inflammatory markers | |||
| ESR (mm/h), median (IQR) | 28 (15–45) | 32 (18–52) | 0.08 |
| CRP (mg/L), median (IQR) | 8.5 (3.2–18.0) | 9.2 (3.5–20.0) | 0.42 |
| Hematological parameters | |||
| Hemoglobin (g/dL), mean±SD | 11.2±2.1 | 10.8±2.3 | 0.02 |
| White cell count (×109/L), median (IQR) | 6.8 (5.2–8.5) | 7.0 (5.5–8.8) | 0.31 |
| Platelet count (×109/L), median (IQR) | 215 (170–270) | 225 (180–280) | 0.18 |
| Biochemical parameters | |||
| Albumin (g/L), mean±SD | 38.5±5.2 | 37.8±5.8 | 0.08 |
| Urinary parameters | |||
| Proteinuria (g/24 h), median (IQR) | 1.2 (0.3–3.5) | 1.5 (0.4–4.0) | 0.22 |
| Hematuria, n (%) | 95 (22.2) | 78 (21.0) | 0.65 |
| Complement levels | |||
| C3 (mg/dL), mean±SD | 98±28 | 95±32 | 0.35 |
| C4 (mg/dL), mean±SD | 22±8 | 20±9 | 0.09 |
Data are presented as mean±SD for normally distributed variables and median (IQR) for non-normally distributed variables. SD: Standard deviation, eGFR: Estimated glomerular filtration rate, IQR: Interquartile range, ESR: Erythrocyte sedimentation rate, CRP: C-reactive protein. A p-value of 0.05 or less was considered statistically significant.
At the final follow-up, the median serum urea was 12.0 (IQR: 8.5–16.5) mmol/L, the median serum creatinine was 280 (IQR: 180–420) μmol/L, and the median eGFR was 38 (IQR: 22–58) mL/min/1.73 m2.
The primary causes of CKD in this cohort were diabetes mellitus (42%), hypertension (26%), and established autoimmune diseases (16%). immunoglobulin A nephropathy (IgAN) was the cause in 5% of patients, and other miscellaneous causes accounted for the remaining 11%. The distribution of primary causes is illustrated in Figure 1.
Prevalence of autoantibodies
Overall, 214 patients (26.7%) of those tested had at least one positive autoantibody. The prevalence of specific autoantibodies among tested patients is detailed in Table 2. The most frequently detected autoantibodies were lupus anticoagulant (39.3%), ANA (23.5%), anti-SSA-RO (14.8%), and anti-dsDNA (13.6%). Autoantibody positivity was significantly more common in females compared to males (p = 0.016 for ANA) and was more prevalent in younger patients, with a mean age of 25 years for the autoantibody-positive group. The gender-specific prevalence of all autoantibodies is shown in Figure 2.
| Autoantibody | Total tested | Total positive n (%) | Males tested | Males positive n (%) | Females tested | Females positive n (%) | p-value |
|---|---|---|---|---|---|---|---|
| Anti-nuclear antibody | 800 | 188 (23.5) | 428 | 68 (15.9) | 372 | 120 (32.3) | <0.001 |
| Lupus anticoagulant | 800 | 314 (39.3) | 428 | 144 (33.6) | 372 | 170 (45.7) | 0.001 |
| ANCA | 800 | 70 (8.8) | 428 | 26 (6.1) | 372 | 44 (11.8) | 0.005 |
| Anti-dsDNA | 800 | 109 (13.6) | 428 | 18 (4.2) | 372 | 91 (24.5) | <0.001 |
| Anti-SSA-RO | 800 | 118 (14.8) | 428 | 12 (2.8) | 372 | 106 (28.5) | <0.001 |
| Anti-RO52 | 800 | 87 (10.9) | 428 | 0 (0) | 372 | 87 (23.4) | <0.001 |
| Anti-Smith | 800 | 27 (3.4) | 428 | 0 (0) | 372 | 27 (7.3) | <0.001 |
| Anti-RNP | 800 | 26 (3.3) | 428 | 0 (0) | 372 | 26 (7.0) | <0.001 |
| Anti-histone | 800 | 42 (5.3) | 428 | 37 (8.6) | 372 | 5 (1.3) | <0.001 |
| Rheumatoid factor | 800 | 42 (5.3) | 428 | 42 (9.8) | 372 | 0 (0) | <0.001 |
Prevalence rates are calculated as a percentage of total patients tested within each gender group. Anti-dsDNA: Anti-double stranded DNA, ANCA: Anti-neutrophil cytoplasmic antibodies, Anti-SSA-RO: Anti-Sjögren’s syndrome-related antigen A/Ro antibodies, Anti-RNP: Anti-ribonucleoprotein antibodies. A p-value of 0.05 or less was considered statistically significant.
Association of autoantibodies with clinical outcomes
To assess the impact of autoantibodies on disease progression, we compared clinical outcomes between patients with and without a positive autoantibody test [Table 3]. Patients in the autoantibody-positive group had a significantly lower baseline eGFR and experienced a more rapid decline in renal function over the follow-up period. The annualized rate of eGFR decline was −5.2 mL/min/1.73 m2 in the positive group compared to −2.1 mL/min/1.73 m2 in the negative group (p < 0.001). Furthermore, all-cause mortality was significantly higher in the autoantibody-positive group (18.7% vs. 10.9%, p = 0.008).
| Outcome variable | Autoantibody positive (n=214) | Autoantibody negative (n=586) | p-value |
|---|---|---|---|
| Baseline renal function | |||
| eGFR (mL/min/1.73 m2), median (IQR) | 48 (28–68) | 58 (35–78) | <0.001 |
| Serum Creatinine (µmol/L), median (IQR) | 310 (180–480) | 245 (150–380) | <0.001 |
| Serum Urea (mmol/L), median (IQR) | 14.2 (9.5–20.0) | 11.0 (7.8–15.5) | <0.001 |
| Follow-up renal function (at 5.5 years) | |||
| eGFR (mL/min/1.73 m2), median (IQR) | 28 (12–48) | 42 (25–62) | <0.001 |
| Serum creatinine (µmol/L), median (IQR) | 380 (220–580) | 280 (160–420) | <0.001 |
| Serum urea (mmol/L), median (IQR) | 16.5 (11.0–24.0) | 12.0 (8.5–16.5) | <0.001 |
| Disease progression | |||
| Annualized eGFR decline (mL/min/year), median (IQR) | −5.2 (−8.5–−2.1) | −2.1 (−4.2–−0.5) | <0.001 |
| Patients with eGFR decline >5 mL/min/year, n (%) | 128 (59.8) | 185 (31.6) | <0.001 |
| Mortality | |||
| All-cause mortality, n (%) | 40 (18.7) | 64 (10.9) | 0.008 |
| Cardiovascular mortality, n (%) | 18 (8.4) | 28 (4.8) | 0.042 |
| Renal-related mortality, n (%) | 15 (7.0) | 22 (3.8) | 0.052 |
Data are presented as median (IQR) for continuous variables and n (%) for categorical variables. eGFR: Estimated glomerular filtration rate, IQR: Interquartile range. A p-value of 0.05 or less was considered statistically significant.
Predictors of eGFR decline and mortality
A comparison of key clinical variables between patients with eGFR <60 and ≥60 mL/min/1.73 m2 is presented in Figure 3. Univariate and multivariate regression analyses identified several independent predictors of eGFR decline [Tables 4 and 5].
| Variable | Coefficient | 95% CI | p-value | R2 |
|---|---|---|---|---|
| Age (years) | −0.551 | −0.882–−0.221 | 0.001 | 0.069 |
| Gender (female) | 5.047 | 15.28–2.193 | 0.132 | 0.0064 |
| ANA positive | 4.988 | 17.175–1.199 | 0.120 | 0.004 |
| ANA titer | −4.850 | −19.947–−01.248 | 0.156 | 0.015 |
| ANCA positive | 2.454 | 10.810–2.808 | 0.155 | 0.010 |
| Lupus Anticoagulant | 10.439 | 3.011–27.889 | 0.136 | 0.025 |
| ESR (mm/hr) | −0.396 | −0.233–−0.560 | 0.001 | 0.148 |
| CRP (mg/L) | −0.397 | −0.140–−0.656 | 0.003 | 0.064 |
| Hemoglobin (g/dL) | 6.990 | 8.910–5.070 | 0.001 | 0.260 |
| Albumin (g/L) | 1.017 | 1.691–0.344 | 0.003 | 0.057 |
| Proteinuria (g/24 h) | −0.285 | −0.512–−0.058 | 0.014 | 0.032 |
| C3 (mg/dL) | −0.042 | −0.078–−0.006 | 0.022 | 0.028 |
| C4 (mg/dL) | −0.156 | −0.298–−0.014 | 0.031 | 0.022 |
Variables with p≤0.2 were selected for inclusion in the multivariate model. eGFR: Estimated glomerular filtration rate, IQR: Interquartile range, CI: Confidence interval, ANA: Anti-nuclear antibody, ESR: Erythrocyte sedimentation rate, CRP: C-reactive protein, ANCA: Anti-neutrophil cytoplasmic antibodies, ANA: Antinuclear antibody. A p-value of 0.05 or less was considered statistically significant.
| Variable | Coefficient (β) | 95% CI | p-value | Standardized β |
|---|---|---|---|---|
| Age (years) | −0.485 | −0.758–−0.212 | 0.001 | −0.285 |
| ANA positive | −2.845 | −4.512–−1.178 | 0.001 | −0.158 |
| ESR (mm/h) | −0.312 | −0.485–−0.139 | 0.001 | −0.198 |
| CRP (mg/L) | −0.218 | −0.398–−0.038 | 0.018 | −0.095 |
| Hemoglobin (g/dL) | 4.225 | 2.891–5.559 | <0.001 | 0.285 |
| Albumin (g/L) | 0.642 | 0.285–0.999 | 0.001 | 0.142 |
| Proteinuria (g/24 h) | −0.198 | −0.385–−0.011 | 0.038 | −0.078 |
| Complement C3 (mg/dL) | −0.028 | −0.052–−0.004 | 0.024 | −0.082 |
The model explains 38% of the variance in eGFR decline (R2=0.38). eGFR: Estimated glomerular filtration rate, CI: Confidence interval, ANA: Anti-nuclear antibody, ESR: Erythrocyte sedimentation rate, CRP: C-reactive protein. A p-value of 0.05 or less was considered statistically significant.
To further evaluate the impact of autoantibodies on survival, we performed a multivariable Cox proportional hazards regression analysis for all-cause mortality [Table 6]. After adjusting for age, gender, baseline eGFR, diabetes status, and proteinuria, autoantibody positivity remained an independent predictor of mortality (Hazard Ratio 1.65, 95% confidence interval 1.12–2.43, p = 0.011).
| Variable | Hazard ratio | 95% CI | p-value |
|---|---|---|---|
| Age (per 10 years) | 1.42 | 1.21–1.67 | <0.001 |
| Gender (Female) | 0.88 | 0.62–1.25 | 0.480 |
| Baseline eGFR (per 10 mL/min) | 0.78 | 0.69–0.88 | <0.001 |
| Diabetes mellitus | 1.55 | 1.08–2.22 | 0.018 |
| Proteinuria (>1 g/day) | 1.35 | 0.95–1.92 | 0.095 |
| Autoantibody positive (Any) | 1.65 | 1.12–2.43 | 0.011 |
Hazard ratio >1 indicates increased risk of mortality. Adjusted for age, gender, baseline eGFR, diabetes status, and proteinuria. eGFR: Estimated glomerular filtration rate, CI: Confidence interval. A p-value of 0.05 or less was considered statistically significant.
DISCUSSION
To the best of our knowledge, this is the first study to comprehensively evaluate the prevalence and clinical impact of a broad panel of autoantibodies in a large cohort of Omani patients with CKD. Our findings reveal a significant prevalence of autoantibodies (26.7%) in this clinically tested population and demonstrate a strong association between autoantibody positivity, particularly ANA, and adverse clinical outcomes, including a more rapid decline in eGFR and increased all-cause mortality. These results highlight the critical role of autoimmunity in the progression of CKD in the Omani population and underscore the need for increased clinical awareness and screening.
Our study found that patients with positive autoantibodies had a more severe clinical presentation at baseline and experienced a more aggressive disease course. This is consistent with previous research that has linked autoimmunity to more severe renal damage and a higher risk of progression to ESKD.[15-17] The independent association of ANA positivity with eGFR decline in our multivariate analysis suggests that ANA may be a valuable prognostic marker in this patient population, even in the absence of a definitive diagnosis of a systemic autoimmune disease.
It is important to distinguish between autoantibody positivity as a marker of a specific autoimmune disease (e.g., lupus nephritis) and non-specific immune activation that can occur in the context of chronic inflammation and uremia.[18-25] While a significant proportion of our autoantibody-positive patients had a confirmed diagnosis of an autoimmune disease, a subset had positive autoantibodies without clear clinical evidence of a systemic rheumatic condition. This phenomenon of “non-specific” autoantibody positivity in CKD is increasingly recognized and may reflect a state of chronic immune dysregulation driven by the uremic environment itself.[19-28] Future studies are needed to elucidate the pathogenic significance of these non-specific autoantibodies and to determine whether they warrant a different clinical management approach.
We also noted that IgAN accounted for 5% of our cohort. While IgAN is an immune-mediated disease characterized by the deposition of IgA immune complexes, it is generally not associated with the classic systemic autoantibodies measured in our panel. This highlights the distinction between kidney-specific immune complex disease and systemic autoimmunity, and explains why this subgroup largely fell into the autoantibody-negative category in our analysis.
Strengths and limitations
This study has several strengths, including its large sample size, the comprehensive panel of autoantibodies assessed, and the long-term follow-up of a well-characterized patient cohort. By focusing on the Omani population, we provide novel, region-specific data that can inform clinical practice in the Middle East and beyond.
However, we also acknowledge several limitations. First, the retrospective, single-center design may limit the generalizability of our findings. Second, and most importantly, autoantibody testing was based on clinical suspicion rather than systematic screening of all patients. This introduced a significant selection bias, as patients with a higher a priori likelihood of autoimmunity were more likely to be tested. Consequently, the reported prevalence of 26.7% reflects the prevalence among suspected cases and significantly inflates the true population prevalence. These figures should not be extrapolated to the general CKD population. Third, kidney biopsies were not performed in all patients, which limits our ability to definitively establish the underlying renal pathology in all cases and means our findings largely represent clinical associations rather than proven histological immune dysfunction. Finally, while we controlled for a number of potential confounders, residual confounding cannot be entirely excluded.
Clinical implications and future research
The findings of this study have several important clinical implications. First, they suggest that targeted screening for autoantibodies should be considered in Omani patients with CKD, particularly those with unexplained disease progression or atypical presentations. Second, the presence of autoantibodies, especially ANA, should alert clinicians to a higher risk of adverse outcomes and may warrant more aggressive management and closer monitoring. Finally, our findings highlight the need for a multidisciplinary approach to the management of CKD, involving both nephrologists and rheumatologists.
Future research should focus on prospectively validating our findings in a multicenter cohort of Omani patients using systematic screening protocols. Further studies are also needed to investigate the underlying mechanisms by which autoantibodies contribute to CKD progression and to explore the potential of targeted immunomodulatory therapies in this high-risk patient population.
CONCLUSION
Our study demonstrates that autoimmune antibodies are highly prevalent in clinically suspected Omani patients with CKD and are independently associated with a more rapid decline in renal function and increased mortality. These findings underscore the significant role of autoimmunity in the pathogenesis of CKD in this population and highlight the importance of early detection and management. Further research is needed to translate these findings into improved clinical care and to develop novel therapeutic strategies for this growing patient population.
Acknowledgment:
We would like to thank our patients and all the staff responsible for the delivery of patient care.
Availability of data and material
Data from this study are not publicly available but can be requested from the corresponding author upon reasonable request.
Author contributions:
HHA: Conceived the study, developed the study protocol, supervised the research, drafted the initial manuscript, and contributed substantially to the interpretation of the results; IAS: Contributed to the study design and methodology, drafted the initial manuscript, and contributed substantially to the interpretation of the results; HAAA: Responsible for data collection and data management; SAS: Responsible for data collection and data management; MMS: Conducted the statistical analyses and contributed to data interpretation; FE: Participated in data validation, interpretation of the findings, and critical revision of the manuscript; AAA: Provided overall supervision, methodological oversight, and critical review of the manuscript. All authors contributed substantially to the interpretation of the results, critically revised the manuscript for important intellectual content, approved the final version for publication, and agree to be accountable for all aspects of the work.
Ethical approval:
The research/study was approved by the Institutional Review Board at the Scientific Research Committee at the Royal Hospital, Muscat, Oman, number 27428, dated 28th August, 2023.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
Issa Al Salmi is on the Editorial Board of the Journal.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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