Role of oxidative stress in aggravating kidney dysfunction in coronary artery disease patients- A laboratory finding

Acute cardiac decompensation results in activation of hemodynamic and neurohormonal factors that lead to an acute drop in glomerular filtration rate (GFR) resulting in acute kidney injury. This relationship is referred to as cardiorenal syndrome type 1 (CRS), which usually goes unnoticed. The present study was designed to evaluate the occurrence of kidney dysfunction in coronary artery disease (CAD) patients visiting the clinical biochemistry laboratory. Ninety percent (90%) of CAD patients were observed to have stage 3 chronic kidney disease (CKD) on the basis of their GFR. They had significantly raised (p < 0.05) blood urea and serum creatinine levels as compared to those without kidney dysfunction and healthy controls. Renal dysfunction was more pronounced in CAD patients suffering from congestive heart failure along with hypertension. All these patients were advised serum uric acid estimations by the clinician. A close look at serum uric acid levels interestingly showed that levels were significantly low (p < 0.05) in CAD patients having kidney dysfunction as compared to those without kidney disease and healthy controls. Uric acid is an important antioxidant molecule in the body. CAD patients with stage 3 CKD had relatively increased oxidative stress as revealed from their low serum superoxide dismutase (SOD) and catalase activity which might lead to quenching of uric acid resulting in its low concentrations. It was proposed that the reduced free radical scavenging capacity of the body may be responsible for inflammatory conditions prevailing in the body in response to the injury to the cell membrane and hence causing organ dysfunction which could be the involvement of kidneys in CAD patients leading to CRS type1. Hence it is very important to check the pro-oxidant-antioxidant balance at the very initial stages.