Comparative study of extrapolative factors linked with oxidative injury and anti-inflammatory status in chronic kidney disease patients experiencing cardiovascular distress.
BACKGROUND
Chronic kidney disease (CKD) is a group of heterogeneous abnormalities affecting the function and structure of the kidney and mostly further proceeds to cardiovascular damage prior to end stage renal disease (ESRD). The oxidative insult and inflammatory mediators have some undefined role in CKD and cardiovascular complications. It is therefore, aimed at to pin point the predictive factors in the development of cardiovascular disorder in patients with chronic kidney disease.


METHODS
Fifty patients of CKD experiencing cardiovascular distress and twenty normal individuals having same age and sex acted as control during these observations. Blood samples (Each 5 ml) were drawn and subjected to centrifugation for 10-15 minutes to separate the serum at 4000-5000rpm. The levels of MDA, GSH, SOD, CAT, VIT C, VIT E, IL-1, TNF-alpha, nitric oxide (NO) and advanced oxidation protein products (AOPPs) were estimated and analyzed.


RESULTS
The nitric oxide levels in the CKD patients decreased significantly (13.26±1.25 ng/ml) compared to controls (42.15±5.26 ng/ml). The serum vitamin E and C levels in these patients recorded 2.15±0.25 μg/ml and 0.97±0.09 μg/ml respectively as against their assigned controls which read 6.35±1.22 μg/ml and 3.29±0.25 μg/ml. Furthermore, a significantly higher level of Malondialdehyde (MDA) as1.25±0.07 nmol/ml was observed in CKD patients viz-a-viz relevant control. However, the serum SOD, catalase (CAT) and GSH levels in the same patients registered a significant decline as evident from respective figures 0.07±0.002 μg/dl, 1.22±0.012 μmol/mol, and 3.25±1.05 μg/dl. The control for these was observed as0.99±0.06 μg/dl, 3.19±0.05 μmol/mol, and 8.64±0.03 μg/dL. On the other hand, the IL-1 levels in the CKD patients found quite higher (402.5±18.26 pg/ml). This clearly points to substantial increase in oxidative insult and reduced NO levels leading to the renal and cardiovascular damage.


CONCLUSIONS
Observations support the fact that the decrease in anti-oxidative capacity accompanied by higher inflammatory mediators in CKD is indicative of oxidative stress, consequently leading to CKD progression, in all probability to cardiovascular insult. The outcome reiterates that strategies be designed afresh to contain CKD progression to cardiovascular complications and ESRD. One way could be to focus on early detection of stress related to the disease. It requires analyzing the factors related to stress, such as the one reported here. Linking these factors with the symptoms could be a crucial step forward. And further, the disease could be monitored in a more disciplined manner.
Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.
Mahmood
M
Rasool
Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Lahore, Pakistan.
Muhammad Abdul Basit
MA
Ashraf
Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Lahore, Pakistan.
Arif
A
Malik
Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Lahore, Pakistan.
Sulayman
S
Waquar
King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Shahida Aziz
SA
Khan
Center for Research in Molecular Medicine (CRiMM), The University of Lahore, Lahore, Pakistan.
Mahmood Husain
MH
Qazi
Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.
Waseem
W
Ahmad
Department of Biotechnology and Informatics, BUITEMS, Quetta, Pakistan.
Muhammad
M
Asif
Department of Botany, Women University of Azad Jammu & Kashmir, Bagh, Pakistan.
Sami Ullah
SU
Khan
National Institute for Biotechnology and Genetic Engineering (NIBGE), Faisalabad, Pakistan.
Ahmad
A
Zaheer
Department of Botany, Ghazi University, Dera Ghazi Khan, Pakistan.
Muther Mansoor
MM
Qaisrani
Obesity & Diabetes Research Laboratory, Department of Chemistry, University of Azad Jammu & Kashmir, Muzaffarabad, Pakistan.
Abdul Rehman
AR
Khan
National Institute for Biotechnology and Genetic Engineering (NIBGE), Faisalabad, Pakistan.
Aamir
A
Iqbal
National Institute for Biotechnology and Genetic Engineering (NIBGE), Faisalabad, Pakistan.
Amir
A
Raza
Bolan Medical Hospital, Quetta, Pakistan.
Saima
S
Iram
Faculty of Life Sciences, University of Balochistan, Quetta, Pakistan.
Kashif
K
Kamran
Faculty of Life Sciences, University of Balochistan, Quetta, Pakistan.
Asim
A
Iqbal
CASVAB, University of Balochistan, Quetta, Pakistan.
Mohammad Zahid
MZ
Mustafa
Department of Biochemistry, Cancer Metabolism and Epigenetic Unit, Faculty of Science, Center of Innovation in Personalized Medicine, Cancer and Mutagenesis Unit, King Fahd Center for Medical Research, King Abdulaziz University, Jeddah, Saudi Arabia.
Hani
H
Choudhry
Department of Biochemistry, Cancer Metabolism and Epigenetic Unit, Faculty of Science, Cancer and Mutagenesis Unit, King Fahd Center for Medical Research, King Abdulaziz University, Jeddah, Saudi Arabia.
Mazin A
MA
Zamzami
Department of Biochemistry, Cancer Metabolism and Epigenetic Unit, Faculty of Science, Cancer and Mutagenesis Unit, King Fahd Center for Medical Research, King Abdulaziz University, Jeddah, Saudi Arabia.
Wesam H
WH
Abdulaal
King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Mohammad Sarwar
MS
Jamal
D062107:Advanced Oxidation Protein Products / Q000097:blood; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000209:etiology*; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000175:diagnosis / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000097:blood; D014810:Vitamin E / Q000097:blood
D062107:Advanced Oxidation Protein Products; D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; D014810:Vitamin E; D009569:Nitric Oxide; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D001205:Ascorbic Acid