![]() The providers need to look for inciting events such as diarrhea, nausea, vomiting, which may have caused volume loss, or any over-the-counter drugs such as NSAIDs or other nephrotoxins. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. The history and physical exam should focus on determining the etiology of AKI and the timeline of progression. AKI is thus an important contributor to more extended hospital stays and patient morbidity. Furthermore, a huge percentage, approximately 95%, of nephrologist consultations are related to AKI. Sometimes, it may even necessitate frequent monitoring of drug levels, for example, vancomycin. Most of the drugs are renally excreted, and dosages might need to be adjusted on account of the reduced renal function. Most drugs or procedures that use contrast media may need to be delayed due to co-existent AKI. AKI is one of the most clinically impactful diseases since it affects patient management to a great extent in terms of the treatment options for their primary disease. During hospitalization, the approximate incidence rate of acute kidney injury is 2% to 5% and it develops in up to 67% of patients admitted in the intensive care unit. It is often an important factor in making the decision to hospitalize for other conditions, if not being the sole reason for hospitalization. In the United States, 1% of all hospital admissions have AKI on admission. Few examples with the mechanism of prerenal AKI are listed below:ĪKI is very commonly seen in patients admitted to the hospital. However, tubular and glomerular function tends to stay normal. This may be part of systemic hypoperfusion resulting from hypovolemia or hypotension, or maybe due to selective hypoperfusion to the kidneys, such as those resulting from renal artery stenosis and aortic dissection. The prerenal form of AKI is because of any cause of reduced blood flow to the kidney. Each of these categories has several different causes associated with it. Pathophysiology of AKI has always been traditionally divided into three categories: prerenal, renal, and post-renal. Nevertheless, whatever the cause of AKI, renal blood flow reduction is a common pathologic pathway for declining glomerular filtration rate. This pressure gradient is affected by the renal blood flow and is under the direct control of the combined resistances of afferent and efferent vascular pathways. The impetus for glomerular filtration is the difference in the pressures between the glomerulus and the Bowman space. According to KDIGO, AKI is the presence of any of the following: Among these, KDIGO is the most recent and most commonly used tool. There is no clear definition of AKI however, several different criteria have been used in research studies such as RIFLE, AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease: Improving Global Outcomes) criteria. It can be seen in up to 7% of hospital admissions and 30% of ICU admissions. It is a very common condition, especially among hospitalized patients. It can also result in several electrolyte disturbances. AKI can lead to the accumulation of water, sodium, and other metabolic products. The only sign of acute kidney injury may be a decline in urine output. Although, immediately after a renal insult, blood urea nitrogen (BUN) or creatinine levels may be within the normal range. Acute kidney injury (AKI), previously called acute renal failure (ARF), denotes a sudden and often reversible reduction in kidney function, as measured by glomerular filtration rate (GFR).
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