A client has developed acute kidney injury (AKI) as a complication of glomerulonephritis. Which would the nurse expect to observe in the client?

In acute kidney injury (AKI) complicating glomerulonephritis, the kidneys lose their ability to excrete sodium and water adequately, leading to fluid retention and volume overload. This excess intravascular volume directly increases preload and peripheral vascular resistance, resulting in hypertension. Hypertension is therefore a hallmark expected finding in AKI, particularly when the underlying cause is glomerulonephritis, which impairs glomerular filtration and promotes sodium and water retention. Bradycardia is not a typical finding; in fact, the hyperkalemia that often accompanies AKI can cause dysrhythmias, and patients are more likely to experience tachycardia as a compensatory mechanism. Decreased cardiac output would be unusual because volume overload tends to increase preload and initially maintain or elevate cardiac output, though prolonged dysfunction can impair it. Decreased central venous pressure is also incorrect; fluid retention and volume overload raise central venous pressure rather than lowering it. A decreased CVP would suggest hypovolemia, which is the opposite of what occurs when the kidneys fail to excrete fluid. Therefore, hypertension is the most expected clinical observation in a client with AKI secondary to glomerulonephritis, reflecting the underlying pathophysiology of impaired renal excretion and resulting volume overload.