Studying the Relationship Between Mean Platelet Volume and Neutrophil/ Lymphocyte Ratio With Inflammation and Proteinuria in Chronic Kidney Disease

NCT ID: NCT03149068

Last Updated: 2017-05-16

Basic Information

• Recruitment Status: UNKNOWN
• Total Enrollment: 100 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2017-07-01
• Study Completion Date: 2018-05-01

Brief Summary

Inflammation begins during early stages of CKD in which neutrophil counts are increased, whereas lymphocyte counts are decreased during inflammation. In addition to known conventional indications of inflammation such as C-reactive protein (CRP), fibrinogen, erythrocyte sedimentation rate, several interleukins and tumor necrotizing factor alpha, Neutrophil-to-lymphocyte ratio (NLR) has increasingly been reported as a measure of systemic inflammation (Okyay G U et al 2013 and Yilmaz G et al ,2017) Several recent studies have shown that mean platelet volume (MPV) is also increased during inflammation and may be associated with poorer prognosis in CKD (Yilmaz G et al ,2017).

Detailed Description

Chronic kidney disease (CKD) is a worldwide problem and its incidence is steadily increasing. Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation (NKF) defines chronic kidney disease as either kidney damage or a decreased kidney glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months (Levey AS.,2011). Whatever the underlying etiology, the destruction of renal mass with irreversible sclerosis and loss of nephrons leads to a progressive decline in GFR. CKD progression is associated with high morbidity and mortality (Sanz AB.,2014) .The early detection of CKD is important and early treatment may reduce adverse outcomes associated with CKD and slow or even prevent the progression of the disease. Therefore, the detection of CKD at early stages is an important public health issue (Katherine T.,2015).

Cardiovascular disease is a leading cause of death in patients with chronic kidney disease (CKD), for whom the cardiovascular mortality rate is 15 to 30 times higher than in the general population. The underlying pathological state is caused by a complex interplay of traditional and nontraditional risk factors that results in atherosclerosis, arteriosclerosis, and altered cardiac morphological characteristics. (Effat et al 2012) Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Inflammation actively participates in the mechanisms of renal damage progression in diseases of several etiologies (Akchurin OM and Kaskel F, 2015). In glomerular diseases, for example, the following sequence is believed to occur: 1) persistent glomerular injury produces capillary hypertension, with increased glomerular filtration and passage of proteins into the tubular fluid; 2) glomerular proteinuria increases the production of angiotensin II and promotes liberation of inflammatory mediators (cytokines and chemokines), which induce the renal interstitial build-up of mononuclear cells; 3) the initial neutrophil recruiting is replaced by macrophages and T lymphocytes, which unleash the immune response producing interstitial nephritis; 4) tubular cells respond to this inflammatory process with injury to their basement membrane and with the epithelial-mesenchymal transition, becoming interstitial fibroblasts; 5) The formed fibroblasts produce collagen which, in turn, injuries the renal vessels and tubules, eventually generating a cellular scar (Vianna H R et al 2011).

Inflammation begins during early stages of CKD in which neutrophil counts are increased, whereas lymphocyte counts are decreased during inflammation. In addition to known conventional indications of inflammation such as C-reactive protein (CRP), fibrinogen, erythrocyte sedimentation rate, several interleukins and tumor necrotizing factor alpha, Neutrophil-to-lymphocyte ratio (NLR) has increasingly been reported as a measure of systemic inflammation (Okyay G U et al 2013 and Yilmaz G et al ,2017) . It is a simple parameter to assess easily the inflammatory status of a subject and has proven its usefulness in the stratification of mortality in major cardiac events, as a strong prognostic factor in several types of cancers , or as a predictor and a marker of inflammatory or infectious pathologies (ex., pediatric appendicitis) and postoperative complications (Forget P et al 2017). Recent studies have emphasized that NLR could be used as an indication for inflammation and may be associated with poorer prognosis in CKD (Yilmaz G et al ,2017) .

Several recent studies have shown that mean platelet volume (MPV) is also increased during inflammation and may be associated with poorer prognosis in CKD (Yilmaz G et al ,2017). Platelet activation in patients with chronic kidney disease (CKD) may contribute to cardiovascular mortality. The relationship between mean platelet volume (MPV) and coronary artery disease, atherosclerotic vascular pathologies, and platelet aggregation in CKD is not well established (Altun E et al 2016).

Conditions

Evaluation of Early Inflammatory Process in CKD

Study Design

• Observational Model Type: CASE_CONTROL
• Study Time Perspective: PROSPECTIVE

Study Groups

75 patient

Seventy five (75) CKD patients in different stages will be included in our study from Nephrology unit, Internal Medicine department, Assuit University Hospital

No interventions assigned to this group

25 healthy control

twenty five (25) age and sex matched apparently healthy individuals will be enrolled as controls

No interventions assigned to this group

Eligibility Criteria

Inclusion Criteria

• Patients are eligible for participation in the study if :

1. Patients between the ages of 19-65 years

2. CKD patient in stages 2,3,4

3. GFR values of 15-89 mL/min/1.73 m2

4. Body mass index ( BMI ) <35 kg/ m2

Exclusion Criteria

• Patients were excluded from the study if :

1. Diabetes Mellitus patients,

2. Patients with any active infection,

3. Patients with any malignancy,

4. Patients with coronary artery disease ,

5. Patients on steroids and , or immunosuppressive drugs

• Minimum Eligible Age: 19 Years
• Maximum Eligible Age: 65 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Assiut University

OTHER

Sponsor Role: lead

Responsible Party

walaa soliman

assuit

Responsibility Role: PRINCIPAL_INVESTIGATOR

Other Identifiers

Assuit University 96

Identifier Type: -

Identifier Source: org_study_id