Acute kidney injury is defined as an abrupt (within hours) decrease in kidney function, which encompasses both injury (structural damage) and impairment (loss of function). According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, AKI can also be defined by an increase in serum creatinine (SC) by more than or equal to 0.3 mg per dl within 48 h or an increase in SC more than or equal to 1.5 times baseline within 7 days. Urine output was not used to define AKI since most records were inaccurate and would not portray a reliable source of results. Severity of AKI was calculated as the ratio between maximum SC during hospitalization and baseline SC, and staged according to KDIGO recommendations, with stage 2 comprising increases in SC of 2 to 2.9 times baseline and stage 3 of more than or equal to 3 times baseline or more than or equal to 4 mg per dl and or need for hemodialysis. According to the World Health Organization, approximately 850,000 patients develop ESRD every year. It has a serious medical, social, and financial impact on patients’ lives.

The International Society of Nephrology launched the Initiative that aims to eliminate preventable deaths from AKI by 2025. The American Society of Nephrology has launched a new initiative (AKI! Now) to promote excellence in the prevention and treatment of AKI by building a foundational program, to reduce morbidity and associated mortality and to improve long-term outcomes.

The causes of AKI are usually divided into three broad pathophysiologic categories: Prerenal AKI diseases characterized by effective hypoperfusion of the kidneys in which there is no parenchymal damage to the kidney. Intrinsic AKI diseases involving the renal parenchyma. Postrenal (obstructive) AKI diseases associated with acute obstruction of the urinary tract. Acute tubular necrosis (ATN) is the term used to designate AKI resulting from damage to the tubules. It is the most common type of intrinsic kidney injury. AKI from glomerular damage occurs in severe cases of acute glomerulonephritis (GN). 

Approximately a third of patients with AKI in hospital develop AKI during their stay in hospital, two-thirds of patients with AKI in hospital have AKI at the time of admission3. So, there is an opportunity to prevent the development of AKI in a large number of patients: in cases of AKI developed whilst in hospital, 20% are avoidable. Estimates of the incidence of AKI are highly dependent on the case definition used, with rates among hospitalized patients ranging from as high as 44percent when defined based on a change in serum creatinine level of atleast 0.3 mg per dL to as low as 1percent using an increase in serum creatinine level of at least 2.0 mg per dL. Approximately 3 percent to 7 percent of hospitalized patients and 25 percent to 60 percent of intensive care unit patients develop AKI, with 5 percent  to 6 percent of the ICU population requiring renal replacement therapy after developing AKI. 

When diagnosed late, AKI has adverse effects for the individual in general. It is associated with increased length of hospital stay and higher health-care costs4. The duration and severity of AKI is a risk factor for the development of complications such as a 10-fold increase in the risk of CKD and a 3-fold risk of end-stage kidney disease. Moreover, a multicentre survey conducted in China revealed that when defining AKI by both standard and extended KDIGO criteria its prevalence was  3 percent, but only 25.8 percent of AKI cases were formally identified and documented within hospital records. 

Acute kidney injury (AKI) is a leading cause of in-hospital death worldwide, with a prevalence of about one-fifth in hospitalized patients. A previous meta-analysis of more than 77 million hospitalized patients from 952 studies showed that the pooled incidence of AKI was 21 percent, and the in-hospital mortality rate of AKI patients was approximately 21 percent. Among them, patients with AKI stage 3 and those receiving renal replacement treatment had a mortality rate of 42 percent and 46 percent, respectively.

Pharmacists play crucial roles, such as educating patients on medication management throughout the course of AKD; calibrating drug dosages; ensuring no unnecessary nephrotoxic drug exposure in the post-AKI phase; exercising caution in reintroducing indispensable drugs with potential nephrotoxic effects during acute illness settings, such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs); managing comorbidities; and monitoring patients and collaborating with their care teams8. Pharmacist interventions have been effective in enhancing medication adherence among both patients with CKD and those with AKD.

Pharmaceutical services led by clinical pharmacists play an important role in the prevention and treatment of nosocomial infections. As a member of the medical team, clinical pharmacists play an important role in drug use, especially in drug concentration monitoring and drug monitoring9. During the treatment of AKI patients, clinical pharmacists assist physicians in formulating treatment plans, strengthen pharmaceutical care for hospitalized patients, and provide targeted suggestions and improvement measures, including adjustment of concomitant drugs and drug doses .