Chronic kidney disease (CKD) is defined by a reduction in the kidney function (shown by
reduced estimated glomerular filtration rate (eGFR) or markers of kidney damage, or both,
for at least three months). It varies depending on the amount of blood pressure control,
the degree of proteinuria, the previous rate of decline in GFR, and the underlying renal
disease, including diabetes.
Phosphorus excretion decreases in many kidney disorders, and as a result, the amount of
fibroblast growth factor 23 (FGF-23) rises.FGF-23 levels have appeared to predict risk of
death in individuals with chronic renal disease as the estimated glomerular filtration
rate declines, and a corresponding increase in FGF-23 can be noted.
FGF-23 is a hormone with a molecular weight of 30 kDa works on fibroblast growth factor
receptors (FGFR1-4) in the kidney, heart, colon, and parathyroid gland. It is secreted by
osteocytes and, to a lesser extent by osteoblasts into the bloodstream. A rise in FGF-23
could indicate kidney dysfunction, and concurrent bone disease. Patients with CKD are
well known to have greater risk for developing bone fractures.
The term "chronic kidney disease-mineral bone disorder" (CKD-MBD) refers to the decline
in bone quality and the subsequent development of disorders in bone and mineral
metabolism caused by impaired kidney function. In addition to PTH, vitamin D, calcium and
phosphorus, fibroblast growth factor-23 (FGF-23) play a role in CKD-MBD.
Treatment of the underlying disease, if possible, and treatment of secondary factors,
such as increased blood pressure and proteinuria, are the two main ways to limit the rate
of CKD progression. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II
receptor blockers (ARBs) are renin-angiotensin system (RAS) inhibitors that are more
effective than other antihypertensive medications in reducing proteinuria and slowing the
rate of progression of proteinuria during CKD, regardless of the etiology.
Ramipril inhibits ACE, which lowers FGF-23 expression in the kidney and attenuates
proteinuria. Angiotensin inhibition frequently causes mild to moderate decrease in GFR
and hyperkalemia following the treatment initiation or following dose escalation. If CKD
is progressive, hyperkalemia may develop quickly after the start of treatment or at a
later time.
Coenzyme Q10 (CoQ10) is an organic molecule can be found in both reduced (ubiquinol) and
oxidised (ubiquinone) forms in mitochondria and cell membranes. Patients with CKD have
been found to have considerably reduced plasma CoQ10 levels. CoQ10 lowers the level of
aldosterone and modifies the angiotensin effect on sodium retention. An increase in CoQ10
availability may have altered renin-angiotensin-aldosterone action resulting in a
decrease in ACE level. Additionally, the endothelium appears to be directly affected by
CoQ10, causing vasodilation and reducing blood pressure. High dose CoQ10 supplementation
in cases where the condition is treated early resulted in an improvement in renal
function and a reduction in proteinuria.CoQ10 prevent an increase of FGF-23 and also
provides a reduction in cardiovascular risk.The aim of this work is to evaluate the role
of Coenzyme Q10 (CoQ10) as adjuvant therapy to angiotensin converting enzyme inhibitor on
blood pressure, proteinuria and bone metabolism in patients with chronic kidney disease
(CKD).
All the participants will be subjected to the following:
- Demography, History and Physical Examination
Age, sex, sex distribution ratio (M/F) will be determined. Measurement of weight in
nearest kilogram and height in nearest centimeter will be measured using Detecto
Scale with subsequent calculation of body mass index according to the following
formula: BMI= [Weight (kg) ÷ Height2 (m)]. Full medical history will be taken to
avoid inclusion of any patient with confounding disease or medication in the study.
Measurement of blood pressure will be done using a mercury sphygmomanometer in
accordance with recommendations of the American Heart Association and standardized
office blood pressure measurements. The mean values of the duplicate measurements
will be recorded. The blood pressure will be assessed at baseline and every 4 weeks.
Measurements of routine parameters at baseline, through evaluation of:
Fasting blood glucose
Alanine aminotransferase (ALT)
Serum total bilirubin
In addition, prothrombin time or international normalization ratio (INR) will be
also assessed. Assessment of Proteinuria at the time of enrollment, 3 and 6 months
after intervention. Proteinuria will be assessed using urine dipstick test.
Albumin-to-creatinine ratio will be calculated by dividing the urinary albumin
concentration by the urinary creatinine concentration. Assessment of kidney
functions at baseline, 4 weeks, 3 and 6 months after initiation of ACEI by
assessment: Serum creatinine, Estimated glomerular filtration rate (eGFR) in
mL/min/1.73m2 which will be calculated using the Chronic Kidney Disease Epidemiology
Collaboration (CKD-EPI) creatinine equation, 2021, blood urea nitrogen and serum
potassium Evaluation of Chronic Kidney Disease-Mineral and Bone Disorder Chronic
Kidney Disease-Mineral and Bone Disorder (CKD MBD) will be assessed at baseline and
at the end of intervention through evaluation of: - Serum level of Fibroblast growth
factor-23 (FGF-23)
Serum Parathyroid hormone (PTH) level .
Serum concentration of 25 (OH) vitamin D.
Serum calcium
Serum phosphorus
Clinical outcome will be assessed at baseline and 6 months after Intervention through:
- Evaluation of Health Related Quality of Life (HRQOL) using the validated Arabic
version of -Kidney Disease and Quality of Life- Short Form (KDQOL-SF™) version 1.3
questionnaire which was formerly used in Egypt for patients with CKD.