It is imperative to look for any radiologic studies involving the use of iodinated contrast agents, a common cause of AKI. For example, if a sudden creatinine rise is noted, an inciting factor usually occurs in the 24 to 48 hours preceding this onset. Noting the time of onset of AKI can be useful when dealing with hospitalized patients. The most common causes of AKI in hospitalized patients are as follows:Įvaluation of AKI should include a thorough search for all possible etiologies of AKI, including prerenal, intrarenal, and postrenal disease. History and physical examination are essential in AKI because labs often cannot provide a clear answer as to the etiology of AKI.

Moreover, a careful review of past medical history may reveal comorbid conditions that can help narrow down the etiology of AKI, such as cirrhosis or a history of blood clots requiring anticoagulation. A history suggestive of CKD can include symptoms such as chronic fatigue, anorexia, nocturia, disturbed sleep-wake cycle, polyuria, and pruritis. Differentiating between AKI and chronic kidney disease (CKD) is essential, as CKD itself is not an uncommon risk factor for AKI. Providers should look for inciting events such as diarrhea, nausea, vomiting, which may have caused volume loss, or any over-the-counter drugs such as NSAIDs. 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 progression timeline. The most common etiology of postrenal AKI is bladder outlet obstruction, which is often due to prostatic hypertrophy in older men, pelvic masses in older women, and nephrolithiasis in younger patients. Once obstruction is released, post-obstructive diuresis occurs in up to 50% of patients and should be monitored for severe complications of hypovolemia and electrolyte abnormalities. Weeks or months of obstruction can lead to ESRD. Eventually, bladder atony, periglomerular fibrosis, chronic interstitial nephritis, and secondary FSGS can develop. This results in decreased renal perfusion, inflammation, tubular atrophy, and interstitial fibrosis.

Pathological disturbances can occur within 2 hours of obstruction, starting with decreased filtration at the level of the glomerulus due to increased upper urinary tract pressure. Postrenal etiology for AKI includes obstructive causes, which lead to congestion and urinary backflow of the filtration system, leading to a shift in the filtration driving forces. A noteworthy fact is that a unilateral obstruction may not always present as AKI, especially if the obstruction is gradual, because a normal working contralateral kidney may compensate for the function of the affected kidney. Intratubular obstruction: monoclonal gammopathy (such as in multiple myeloma), tumor lysis syndrome, hemolytic anemia, and toxins such as ethylene glycol. A few examples of prerenal AKI mechanisms are listed below: However, tubular and glomerular function tends to be initially normal. This may be part of systemic hypoperfusion resulting from hypovolemia or due to selective hypoperfusion of the kidneys, such as resulting from renal artery stenosis or aortic dissection. The prerenal form of AKI is due to any cause of reduced blood flow to the kidney. Each of these categories has many different associated causes, and some causative factors of AKI have overlapping mechanisms of injury. The pathophysiology of AKI has traditionally been divided into three categories: prerenal, intrinsic renal (ie, intrarenal), and postrenal. For most causes of AKI, renal blood flow reduction is a common pathologic pathway for declining GFR. 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 pressure difference between the glomerulus and Bowman's space.

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