 AKI is common, affecting up to 20% of hospital inpatients and between 30% to 60% of critically ill patients [3] with a rising incidence worldwide. Hospital-acquired AKI is 5 to 10 times more common than community-acquired AKI. AKI has a significant impact on patient morbidity and mortality with increased health care costs. AKI may be reversible or can lead to CKD. AKI is often multifactorial but generally categorized as prerenal, renal, or postrenal. Prerenal factors include impaired blood flow from any cause including hypotension, hypovolemia, decreased cardiac output, or renal artery occlusion. Renal causes include any disease that damages renal parenchyma, such as vasculitis, acute tubular necrosis, glomerulonephritis, interstitial nephritis, renal infection or infiltration, drugs, and toxins. Postrenal AKI results from ureteral, bladder, or urethral obstruction. Renal and prerenal etiologies far outweigh obstruction as a cause of AKI, accounting for >97% of AKI [4]. For appropriate intervention, identification of the specific cause of AKI is critical, as there are different treatments for diseases such as glomerulonephritis, vasculitis, and ureteral obstruction. Evaluation of the patient with AKI includes a thorough history, physical examination, and laboratory analysis of blood (for serum creatinine, blood urea nitrogen, complete blood count, and differential) and urine (microscopy for casts and epithelial cells, chemistry, and biomarkers) [3]. Renal biopsy may be indicated for differentiation of nephritic and nephrotic syndromes [3]. CKD is common, affecting 10% of the world population. It is defined as an abnormality of kidney structure or function, present for >3 months, with health consequences [5]. The definition requires knowledge of laboratory values in the preceding 3 months. Hypertension and diabetes are the predominant risk factors for CKD [6].
Renal Failure.  AKI is common, affecting up to 20% of hospital inpatients and between 30% to 60% of critically ill patients [3] with a rising incidence worldwide. Hospital-acquired AKI is 5 to 10 times more common than community-acquired AKI. AKI has a significant impact on patient morbidity and mortality with increased health care costs. AKI may be reversible or can lead to CKD. AKI is often multifactorial but generally categorized as prerenal, renal, or postrenal. Prerenal factors include impaired blood flow from any cause including hypotension, hypovolemia, decreased cardiac output, or renal artery occlusion. Renal causes include any disease that damages renal parenchyma, such as vasculitis, acute tubular necrosis, glomerulonephritis, interstitial nephritis, renal infection or infiltration, drugs, and toxins. Postrenal AKI results from ureteral, bladder, or urethral obstruction. Renal and prerenal etiologies far outweigh obstruction as a cause of AKI, accounting for >97% of AKI [4]. For appropriate intervention, identification of the specific cause of AKI is critical, as there are different treatments for diseases such as glomerulonephritis, vasculitis, and ureteral obstruction. Evaluation of the patient with AKI includes a thorough history, physical examination, and laboratory analysis of blood (for serum creatinine, blood urea nitrogen, complete blood count, and differential) and urine (microscopy for casts and epithelial cells, chemistry, and biomarkers) [3]. Renal biopsy may be indicated for differentiation of nephritic and nephrotic syndromes [3]. CKD is common, affecting 10% of the world population. It is defined as an abnormality of kidney structure or function, present for >3 months, with health consequences [5]. The definition requires knowledge of laboratory values in the preceding 3 months. Hypertension and diabetes are the predominant risk factors for CKD [6].