Acute Kidney Injury (AKI) is defined as an abrupt cessation in renal function. Specifically, it can be defined as a reduction in urine volume below 0.5 ml/kg/h for a period of 6 hours or an abrupt rise in serum creatinine to more 0.3 mg/dl within a period of 2 days. Acute Kidney injury can also be defined as a rise in serum creatinine to a value above 1 and a half times the baseline under a period that is assumed to be a week. The condition can also be characterized by a rise in the blood urea nitrogen. Nevertheless, a rise in creatinine may not be apparent within the first few days of AKI onset and the only sign of the condition may be a sudden and apparent drop in the level of urine.

An increase in blood creatinine levels can be due to other factors such as drugs like trimethoprim, which interferes with renal tubular function. Similarly, an increase in the blood urea nitrogen can also be due to other reasons such as from gastrointestinal bleeding. Therefore, thorough investigations ought to be carried out before the diagnosis of acute kidney injury is made.

CLASSIFICATIONS

Acute Kidney Injury can be classified into three main categories based on the etiology. These three categories are pre-renal AKI, intrinsic or renal AKI, and post-renal AKI. The pathology behind pre –renal AKI revolves around an acute reduction in the intravascular volume. There is also a correspondent reduction in the cardiac output of the heart. This is immediately followed by systemic vasodilation and renal vasoconstriction. Pre-renal AKI is usually the most common form of acute kidney injury. In most instances, the systemic reduction in volume is from events such as bleeding (hemorrhage), vomiting and diarrhea, burns, or pancreatitis. The reduced cardiac output can also be from cardiogenic shock and myocardial infarction, which eventually results in reduced renal perfusion. The reduced cardiac output can also be from states of shock such as anaphylaxis or sepsis. There are also drugs which induce vasoconstriction and thus lead to pre-renal AKI. These drugs include NSAIDs, norepinephrine, and amphotericin.

Structural compromise of the kidney can also lead to acute kidney injury. This type of acute kidney injury is referred to as intrinsic or renal kidney injury. The most common cause of renal AKI is acute tubular necrosis. Renal AKI can be as a result of the occlusion of both renal vein or artery from conditions such as thrombosis, emboli or conditions that lead to vasculitis such as hemolytic uremic syndrome. Renal AKI can also be from interstitial causes such as infections (pyelonephritis), drugs (penicillins, rifampin, cephalosporins, sulfonamides, and PPIs), and systemic diseases such as lymphomas, SLE, uveitis, and Sjogren syndrome.

The third type of AKI is usually due to obstruction in the post-renal tract. The obstruction can be at the level of the bladder, ureters, pelvis, or the urethra. Ureteric obstruction can be due to stones, local malignancy, fibrosis, or adhesions after surgery. Obstructions at the level of the urethra can be due to phimosis, strictures, or malignancy. Mechanical obstructions at the neck of the bladder may be caused by prostate cancer, malignancy of the bladder, benign prostatic hypertrophy, or a neurogenic bladder.

DIFFERENTIAL DIAGNOSES & WORK-UP

There are several differentials to consider in the diagnosis of acute kidney injury. They include renal calculi, urinary tract infections, diabetic ketoacidosis, chronic renal failure, heart failure, sickle cell anemia, and metabolic acidosis. The diagnostic workup for the disease includes renal function tests which are likely elevated, urinalysis, complete blood count, and peripheral smears. In some instances. Renal biopsy, nuclear scanning, and renal artery angiography may be necessary diagnostic workups.

MANAGEMENT

The management of Acute Kidney Injury should be at the earliest denotation of renal function abnormality. A rise in the serum creatinine may only be apparent after a large amount of the renal parenchyma has been injured. Currently, there is no therapeutic treatment of the disease and that the modalities used are mainly for supportive care. The main goals of treatment revolve around ratification of biochemical abnormalities and volume homeostasis. The correction of fluid overload is usually achieved through the administration of furosemide a loop diuretic. Severe metabolic acidosis is usually corrected using the administration of bicarbonate which is also supplementary to renal dialysis. The correction of hyperkalemia entails a dietary reduction of potassium intake, the use of potassium-binding resins to allow for potassium exchange in the gut lumen, the use of beta agonists and dextrose to boost intracellular movement of potassium, and finally initiating dialysis. Finally, some of the hematological abnormalities in acute kidney injury such as uremia, platelet abnormalities, and anemia can be managed through elements such as desmopressin, transfusions, and the use estrogens.