Epidemiology
The reported incidences of AKI vary, and are confounded by differences in diagnosis, definition criteria, or hospital discharge coding.[6][7] The rate of hospitalizations for AKI in US Medicare patients increased by approximately 35% between 2010 and 2019.[8] Patients with diabetes were hospitalized with AKI at a greater than 2-fold higher rate compared with those without diabetes, and patients with chronic kidney disease (CKD) and diabetes were hospitalized with AKI at a more than 7.5-fold higher rate compared with patients with neither preexisting condition.[8] Overall incidence of AKI among hospitalized patients ranges from 13% to 22%.[3][9] In the intensive care unit (ICU), the incidence of AKI is higher.[10] Prediction scores have been developed for outcomes of AKI, but have had variable success in terms of reproducibility or utility.[11][12]
Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in approximately 20% of ICU patients. Prerenal azotemia, obstruction, glomerulonephritis, vasculitis, acute interstitial nephritis, acute on chronic kidney disease, and atheroembolic injury account for most of the remainder.[13][14]
The incidence of contrast nephropathy varies, and is reported to be the third most common cause of AKI in hospitalized patients. One large systematic review and meta-analysis reported a 9% incidence of contrast-induced nephropathy in patients undergoing angiography for any reason, including percutaneous intervention for coronary artery disease, with 0.5% of patients requiring dialysis.[15]
Up to 7% of patients hospitalized with AKI require renal replacement therapy.[16] In the ICU, the mortality rate exceeds 50% in patients with multiorgan failure who require dialysis.[13][14][16] Minor rises in creatinine (≥0.3 mg/dL) are associated with an increased risk of hospital mortality, increased risk of chronic kidney disease, and higher odds of progressing to end-stage renal failure.
Risk factors
Advanced age is associated with chronic kidney disease, underlying renal vascular disease, and other comorbid medical conditions that predispose to AKI. Older patients with frailty appear to be at particular risk for AKI.[43]
Associated with increased susceptibility to AKI, particularly contrast-related AKI. Risks increase with increasing severity of chronic kidney disease.[5]
Malignant hypertension may cause AKI.[5]
May present with AKI (e.g., systemic lupus erythematosus, scleroderma, antineutrophil cytoplasmic antibody-associated glomerulonephritis, antiglomerular basement membrane disease).[5]
Associated with chronic kidney disease, but may present with AKI.[5]
There may be impaired renal perfusion causing prerenal azotemia, rhabdomyolysis predisposing to pigment-induced injury, or ischemia causing acute tubular necrosis.[50]
The resulting impaired renal perfusion supports prerenal azotemia as cause of AKI or ischemia resulting in acute tubular necrosis.
May result in acute tubular necrosis, infectious glomerulonephritis, prerenal azotemia from hypotension, or drug-induced injury from drugs used in treatment. Highest risk with bacteremia.[50] Coronavirus disease 2019 (COVID-19), which is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, is strongly associated with AKI via several proposed pathophysiologic mechanisms, some being similar to those of non-COVID sepsis.[51]
There may be severe third spacing of fluid leading to intravascular volume depletion resulting in prerenal failure.
May precede AKI due to direct toxicity, rhabdomyolysis, and volume depletion.
May precede prerenal azotemia or acute tubular necrosis, especially if there is severe and prolonged renal ischemia.
May be associated with atheroembolic injury, perioperative ischemia, or contrast-induced AKI.
From hemorrhage, vomiting, diarrhea, or sweating; hospitalized patients may have insufficient replacement fluids.
May lead to AKI if significant obstruction occurs, especially with one functioning kidney.
AKI from nephrotoxicity, ischemia.
Suspect pigment-induced AKI if rhabdomyolysis is present (e.g., after prolonged loss of consciousness).
Suspect pigment-induced AKI due to rhabdomyolysis.[54]
AKI may be present from intravascular hemolytic transfusion reaction, deposition of immune complexes.
May lead to postrenal AKI if mass effect is causing outflow obstruction, or AKI may result in association with myeloproliferative disorders or chemotherapy-related toxicities (i.e., tumor lysis). Immune complex glomerulonephritis may result from the malignancy.
Found to be a predictor of risk of postoperative AKI, but may be a marker rather than a mediator of risk. It is unclear whether there is any benefit to stopping agents prior to surgery in high-risk patients.[55] Patients previously taking renin-angiotensin system inhibitors should restart them following an episode of AKI, as there is evidence that they lower risk of death in this group.[56]
Case reports suggest that herbs and dietary supplements could potentially contribute to kidney injuries.[59]
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