The condition known as chronic kidney disease (CKD) is characterised by a persistent and irreversible decline in renal function, which ultimately leads to the kidneys' inability to perform their tasks [1]. As a result of the demographic trend of an ageing population, the prevalence of chronic kidney disease (CKD) is increasing, which presents considerable issues on a global scale. The rise in the number of people diagnosed with chronic kidney disease (CKD) may be partly attributed to the prevalence of chronic illnesses such as diabetes and hypertension [3]. According to the findings of a comprehensive study and meta-analysis carried out in the United Kingdom, the prevalence of chronic renal illness is 13.4%. According to the findings of a comprehensive study that was carried out in Africa, the prevalence of chronic kidney disease (CKD) is 13.9% [4]. The prevalence of cognitive impairment in people with chronic kidney disease ranges from 17% to 87%, depending on the severity of the condition. A frequency of 53.8% is found among individuals in India who are suffering from chronic renal disease [5].

Cognition refers to the mental process of gaining knowledge through reasoning or perception. Cognition is the foundation for all activities throughout the day, ranging from the simplest to the most complex. Cognitive impairment manifests as a variety of symptoms, including diminished mental alertness, mental retardation, decreased attention and concentration, memory problems, and impaired perceptual-motor coordination. Patients with chronic kidney disease (CKD) often exhibit cognitive impairment, and kidney failure is associated with a faster deterioration in mental function than age- matched controls. This is a well accepted truth in the medical community.

It was estimated that there were fifty million people around the world who suffered from severe cognitive impairment in the year 2015. Sixty percent of the fifty million people live in countries with low and intermediate incomes. It is anticipated that the number of people suffering from severe cognitive impairment will swell to 82 million by the year 2030 and 152 million by the year 2050 [8]. From 17% to 87% of patients with chronic kidney disease (CKD) experience cognitive impairment, depending on the severity of their condition [9-13]. There is a prevalence of chronic renal disease that is twenty percent in the United Kingdom, seventy-five percent in China, and fifty-three point eight percent in India. Researchers in Nigeria conducted a comparative cross-sectional study, which found that the prevalence of cognitive impairment among patients with chronic kidney disease (CKD) is 35.3%, whereas the control group had a prevalence of 6% [16- 17].

We don’t fully understand the processes that cause moderate cognitive impairment and dementia in people with chronic kidney disease. Neurodegenerative and vascular reasons have both been put forward [18,19]. There are a lot of people with both symptomatic and silent cerebrovascular illness, and a lot of people who are at high risk for cardiovascular disease, like those with high blood pressure and diabetes [20].

In contrast, the accumulation of uraemic toxins has been linked to cognitive impairment and may result in cerebral endothelial dysfunction, which is consistent with the neurodegenerative concept [21]. The causal relationships between hypertension, chronic kidney disease (CKD), and dementia are particularly complex, as hypertension may function as both a confounder and a mediator in the relationship between CKD and dementia. The risk of developing incident dementia or cognitive impairment was significantly reduced in comparison to the control group when blood pressure was reduced through antihypertensive agents, as demonstrated by a recent meta-analysis of randomised clinical trials [25]. Additionally, numerous observational studies have suggested that hypertension is a significant risk factor for dementia [22-24].

The exacerbation of neurodegenerative processes or cerebrovascular illness may mediate the correlation between hypertension and cognitive decline. Neurofibrillary tangles and neuritic amyloid-beta (Aβ) plaques are the hallmarks of heightened

Alzheimer's disease pathology in the brain of hypertensive elderly individuals in autopsy findings [28]. The degree of Aβ accumulation in the brain has been positively correlated with elevated blood pressure in positron emission tomography studies [29]. Previous hypertension appears to be of the utmost importance. The onset of midlife hypertension and its perpetuation into later life have been the subject of numerous studies, which have shown that they are a substantial risk factor for dementia in old age [30-31].

As a result, the detrimental cognitive effects may be exacerbated in this population, as hypertension is present in 67–92% of patients with chronic kidney disease (CKD) [32]. In the general population, premorbid mid-life to late-life blood pressure is substantially correlated with MCI and dementia. However, its role in the aetiology of dementia in CKD remains uncertain. The preponderance of stroke risk in chronic kidney disease (CKD) may be attributed to the prolonged hypertension burden, according to a recent systematic review and meta-analysis [33].

There is a possibility that premorbid blood pressure plays a significant part in the aetiology of cognitive dysfunction in chronic renal disease; however, this has not been proved in the past. An examination of 8,563 individuals with hypertension who participated in the SPRINT trial revealed that a reduction of at least thirty percent in the eGFR at the beginning of the study and an event eGFR of less than sixty millilitres per minute per square metre were linked with an elevated prevalence of probable dementia and mild cognitive impairment, regardless of the level of hypertension therapy [34].

Taking this into consideration, it is clear that hypertension and renal disease may have a synergistic relationship in the pathogenesis of cognitive impairment and dementia. Patients who have type 2 diabetes have around a sixty percent higher risk of acquiring dementia in comparison to those who do not have diabetes, according to a meta-analysis that was conducted during the past few years and included more than two million participants [35]. People who have diabetes and cardiovascular disease at the same time in addition to having diabetes at an early age are particularly susceptible [35].

There are a number of different mechanisms that have been proposed to explain the connection between diabetes and dementia. One of these mechanisms is brain metabolic dysfunction, which has been identified as a contributor to the pathology of Alzheimer's

disease. Insulin signalling and transport across the blood-brain barrier are both slowed down in this disorder, which leads to less glucose being used in the brain. A further consequence of hyperglycemia is the accumulation of advanced glycation end products, as well as neurotoxicity and harm to the cardiovascular system [38]. It has been observed that even persons with mild to moderate stages of diabetic kidney disease might exhibit latent neurocognitive impairments [39].

Diabetic nephropathy is responsible for approximately one-third of chronic kidney disease (CKD), which is a form of kidney disease. It is important to highlight the significance of diabetes as a potential confounding variable in this particular approach. There is a growing body of evidence suggesting that obesity, which is extremely prevalent among people with chronic kidney disease (CKD) and is anticipated to contribute around 20–25% to the overall prevalence of renal disease worldwide, is also an independent risk factor for dementia. An examination of 6,582 individuals who were a part of the English Longitudinal Study of Ageing revealed that individuals who were obese at the beginning of the study exhibited a risk of dementia that was approximately thirty percent higher than the average. This was the case even after taking into account factors such as gender, age at the beginning of the study, apolipoprotein E-ε4 (APOE-ε4), education, physical activity, smoking, marital status, hypertension, and diabetes [42].

Excess adiposity, which is similar to diabetes, is linked to changes in the way the brain processes energy, the development of brain lesions, and a reduction in the volume of the brain. Consequently, patients who have chronic renal illness and demonstrate cognitive impairment are at a greater risk of death, have a lower quality of life, have difficulty adhering to their medication regimens, and have a lowered emotional well-being. When it comes to elderly persons who have chronic renal illness, it is a factor that helps determine their quality of life and a substantial contributor to morbidity. This condition is associated with an almost twofold increased risk of mortality and the discontinuation of dialysis in patients who are undergoing haemodialysis [43].

A limited amount of research has been conducted to explore cognitive impairment over the course of chronic kidney disease (CKD) in its various stages. The purpose of this study was to evaluate cognitive impairment and the degree to which it manifests itself

throughout the various stages of chronic kidney disease (CKD), as well as to investigate the relationship between the factors that influence this dysfunction. Our hypothesis is that there is a correlation between the severity of cognitive impairment and the progression of chronic renal disease, and that this correlation is positive. In addition, we propose that the presence of comorbidities, such as hypertension and diabetes, may significantly increase the likelihood of cognitive impairment in elderly individuals who are diagnosed with chronic kidney disease (CKD).

Study Design, Population, Sample Size And Sampling Technique

This investigation utilised a cross-sectional study design to examine the relationship between the severity of CKD and cognitive impairment. The study encompassed a diverse sample of 64 individuals including elderly patients diagnosed with CKD and cognitive impairment. A convenience sampling technique was employed, selecting participants based on their willingness and availability to participate in the study.

Sample Size Justification

Of all the participants involved in the study, the required minimum number of participants was estimated using statistical power analysis. To ensure that there was sufficient power to recognize the relationship between the severity of kidney disease and cognitive dysfunction, a power analysis was conducted using G*Power, version 3.1 (Franz Faul, Universität Kiel, Germany). Estimating a small-to-medium effect size (f² = 0.15) was suggested by the equation: Power of P = log10 (1/SIGMA-05). When applied to the current study, and rounding up, it indicated that the required sample size should be at least 64. This calculation rationalizes the choice of 64 as the lower limit of the sample size to realize credible and accurate results. Despite this, the final sample consisted of 64 participants, which clearly exceeded the minimum requirement needed to enhance the power of the statistical test used in the study.

Inclusion Criteria:

Patients aged 60 years or above who were diagnosed with CKD.

Exclusion Criteria

Patients were excluded if

• They had received a kidney transplant or were actively involved in a live donor transplant.
• Those with severe visual, hearing, or verbal communication impairments, or unable to answer the questionnaire; and
• Patients diagnosed with Alzheimer’s disease, dementia or other psychiatric illness.

Data Collection Tools And Criteria

Data for this study were collected using questionnaire. This questionnaire was tailored to assess the association between the severity of CKD and cognitive impairment among elderly and to explore this association in the presence of comorbidities such as hypertension and diabetes.

Questionnaire validation

A total of seventy patients from Saudi Arabia participated in this study, with data gathered through an self-completed, standardized questionnaire that inquired about the relationship between the severity of CKD and CI in elderly patients. To avoid compilation of errors within the developed questionnaire, various procedures of validation were observed.

At first, the questionnaire on patient preference was developed based on other validated questionnaires found in literature studies in relation to similar populations and health conditions.

The data collected from the pilot study were then used to remove any apparent confusion in the formulated questionnaire and to increase its clarity. The Cronbach’s alpha of the last version of the questionnaire was checked, and it was 0.82, which shows that there was satisfactory internal consistency between the items.

Cognitive Assessment Tools

The Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment were both components of the cognitive examination. The Mini-Mental State Examination (MMSE) is a screening instrument for cognitive impairments that is scored out of a possible thirty points. It consists of questions that evaluate factors such as orientation (10 points), registration (3 points), attention and calculation (5 points), recall (3 points), and language and praxis (9 points). It is possible to identify between people with chronic kidney disease who have cognitive impairment and those who do not, particularly among those who are undergoing haemodialysis (HD).

Cognitive impairment, as determined by the MoCA test, is described by performance on a comprehensive neuropsychological test battery, displaying high sensitivity and specificity, combined with great concurrent validity. This is the evidence that cognitive impairment is present. The validity and dependability of these tools is largely acknowledged, particularly when it comes to the diagnosis of dementia in elderly individuals. It is advantageous to make use of standardised measures since these instruments provide definitive evaluations of the cognitive deficits that patients have, hence increasing the overall rigour of the technique that was used in the study.

Clinical Examination

A thorough medical history and clinical evaluation were carried out on each and every individual who took part in the research study. In accordance with their estimated glomerular filtration rate (eGFR), the patients were divided into four distinct groups, with each group consisting of sixteen individuals.

1. Group A (Stage III): individuals with an eGFR ranging from 29 to 60 mL/min/1.73 m².
2. Group B (Stage IV): individuals with an eGFR ranging from 15 to 30 mL/min/1.73 m²
3. Group C (Stage V): individuals with an eGFR < 15 mL/min/1.73 m², not undergoing haemodialysis
4. Group D (Stage V-D): individuals with an eGFR      < 15 mL/min/1.73 m², undergoing haemodialysis for the past 6 months (Stage V-D).

All patients received standard biochemical laboratory evaluations, including a complete blood count and renal function tests, alongside radiographic assessments consisting of a chest X-ray, abdominal ultrasound of both kidneys, and a non-contrast computed tomography scan of the head to exclude organic aetiologies of cognitive impairment. The glomerular filtration rate was evaluated in all subjects utilising the Modification of Diet in Renal Disease formula.

Statistical analysis

The data was analyzed using SPSS version 27.0. Descriptive statistics, including counts, percentages, means and standard deviations, were computed to summarise demographic characteristics, comorbidities and cognitive impairment indicators. The relationship between the severity of CKD and cognitive impairment was evaluated through a linear regression model. This model provided the regression coefficient (B), 95% confidence interval of B and P value.

The association between comorbidities (hypertension and diabetes) and cognitive impairment was assessed through mean comparisons with a significance threshold of P < 0.05. To evaluate the internal consistency of the cognitive impairment questionnaire, Cronbach’s alpha was computed.

Ethical considerations

The research was carried out with a great deal of concentration on adhering to ethical ideals. Following the acquisition of ethical approval, informed consent will be obtained from each and every participant, thereby guaranteeing the participants’ voluntary involvement and the confidentiality of their data. Participants will be provided with comprehensive information regarding the objectives of the study, the processes involved, and their freedom to withdraw from the study at any time without incurring any consequences. For the purpose of maintaining the research team’s independence and impartiality, measures will be put into place to reduce the likelihood of any conflicts of interest occurring.

Demographic characteristics

Table 1 shows the study included 64 participants, with each group having 16 participants. The age distribution was a little different for each group. For Groups C and D, the most participants were in the 70–79 age range. In Group A, there were equal numbers of men and women. In Groups B and C, there were more women than men. There were big differences in the level of education among the groups. Group B had the highest number of illiterate people (43.8%), while Group C had the highest percentage of people with education up to higher secondary and above (37.5%). The groups also had different marital statuses. In Group D, for example, most of the people were widowed (37.5%).

Table 1: Age groups, gender distribution, educational levels, and marital status of the study participants

Clinical and Cognitive Parameters

Descriptive data indicated minor discrepancies in clinical measures among the groups: All groups exhibited comparable systolic blood pressure (SBP), ranging from 133.88 to 134.81 mmHg. The diastolic blood pressure (DBP) decreased from Group A (89.69 mmHg) to Group D (80.75 mmHg). Group D exhibited a marginally elevated fasting blood sugar level of 128.06 mg/dL.

The haemoglobin concentration was maximal in Group A (11.79 g/dL) and minimal in Group B (11.18 g/dL). Serum creatinine levels were persistently elevated across all groups (about 3.3 mg/dL), indicative of chronic kidney disease (CKD). Group A exhibited the lowest eGFR at 27.28 mL/min/1.73 m², whereas Group D demonstrated the highest at 39.20 mL/min/1.73 m².

The MMSE and MoCA assessments indicated that cognitive function was comparable across all groups: The MMSE values ranged from 18.44 to 20.38. The MoCA scores ranged from 19.44 to 23.06. Statistically significant differences (p < 0.05) between the groups were notified in the case of SBP, haemoglobin, serum calcium, and serum potassium. No substantial differences were observed between the groups in any other clinical or cognitive assessments (p > 0.05).

Cognitive scores exhibited significant correlations with several clinical variables (table 3). For instance, MMSE and MoCA scores exhibited a robust positive correlation with haemoglobin (r = 0.788 & 0.751), calcium (r = 0.566 & 0.595), and eGFR (r = 0.83 & 0.834) (p < 0.01). A negative link existed between them and CKD stage (r = -0.794 & - 0.778), serum phosphate, and potassium, serum creatinine, and blood urea, (p < 0.01). No substantial correlations were observed between age, SBP, DBP, FBS, or serum salt levels.

Table 3: Correlation Between the parameters, MMSE and MoCA scores:

The goal of this study was to find out if there was a link between chronic kidney disease and cognitive impairment in older people [45]. The results of this study make it much easier to understand this relationship and what it means for healthcare management in this community [46]. The main focus of this study was on how often cognitive damage happens in elderly patients with chronic kidney disease (CKD). Our results showed a

strong link between cognitive impairment and chronic kidney disease (CKD). This suggests that cognitive loss is more common in people with CKD than in the general population [47,48]. These results back up earlier study that found CKD to be a major risk factor for CI [49,50,64].

The robust positive correlation between cognitive scores and haemoglobin aligns with existing knowledge: anaemia diminishes oxygen levels in the brain, impairing cognitive clarity in CKD patients. Furthermore, eGFR, which directly assesses renal function, was associated with enhanced cognitive outcomes, aligning with the concept of the “renal- cognitive axis.”

The results are similar to CKD patients in the Chronic Renal Insufficiency Cohort (CRIC) [51] and with a study where it was found that anaemic patients had a 41% higher risk of dementia than non-anemic people, even when age, race, sex, and education level were taken into account [52]. Madero et al. [53] found that anaemia is linked to cognitive decline in older people with and without CKD. They also found that neuropsychological and neurophysiological tests show that people with CKD who are treated for anaemia do better. The cause is still unknown; it’s not clear whether it’s only because of a higher blood count or because of erythropoietin treatment having its own effect. These results are different from what Tamura et al. [54] found. They said that there was no independent link between anaemia and cognitive performance or the rate of cognitive decline.

The negative correlation among creatinine, blood urea, phosphate, and potassium levels indicates the detrimental impact of uremic toxins and electrolyte imbalances on cerebral function. The strong negative connection between CKD stage and cognitive scores indicates that deteriorating kidney function exacerbates cognitive deterioration. Multivariate linear regression indicated that creatinine (serum) and estimated glomerular filtration rate significantly influenced MMSE and MoCA scores, whereas haemoglobin significantly impacted MMSE after controlling for confounding variables. Comparable results were noted in a study, wherein cognitive deterioration correlated with elevated serum phosphate levels [55, 65]. Liu noted that diminished serum calcium levels correlated with cognitive decline in individuals with disease like Parkinson’s.

The ramifications of this study for healthcare management in the elderly population with chronic kidney disease (CKD) are significant [56]. The observation of a robust correlation between CKD and CI underscores the necessity for healthcare practitioners to integrate routine cognitive evaluations and specific therapies into the management of CKD in this demographic [57]. Incorporating cognitive assessments into standard CKD management can promote the early detection of cognitive loss, allowing for prompt interventions and enhancing patient outcomes [58].

Nonetheless, it is imperative to recognise the constraints of this study. The intrinsic cross- sectional design of our study limits our ability to demonstrate a direct connection between CKD and cognitive impairment [59]. Longitudinal investigations are necessary to better examine the temporal link between these two states [60]. The limited sample size in this study may impact the generalisability of the findings [61]. Another factor to consider is that our study depends on self-reported data and medical records, which may include intrinsic biases and limits [62].

Future research should focus on bigger and more diverse study populations to enhance the knowledge of the association among CKD and CI in the elderly demographic. This research substantially enhances our understanding of the link between CKD and CI in elderly population. The findings underscore the heightened incidence of cognitive deterioration in CKD patients, stressing the necessity of integrating suitable cognitive evaluations and therapies in clinical practice. Future research endeavours are essential to further our comprehension of this connection and its wider implications for healthcare management.

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