History and exam

Key diagnostic factors

Oliguria and anuria are common in kidney injury, but are not diagnostic. They are not suggestive of a particular etiology.

May precede AKI and suggest prerenal azotemia, or be a later manifestation resulting from uremia.

Orthostatic symptoms support prerenal azotemia.

Symptoms of volume overload may result from impaired salt and volume regulation and decreased urine production.

Symptoms of volume overload may result from impaired salt and volume regulation and decreased urine production. Congestive heart failure increases risk for prerenal azotemia.

Evidence of pulmonary edema (e.g., rales on exam) suggest volume overload resulting from impaired salt and volume regulation.

Supports prerenal azotemia that may progress to acute tubular necrosis.

Supports prerenal azotemia.

Orthostatic symptoms support prerenal azotemia.

Suggests intravascular volume expansion.

May result from impaired renal salt excretion.

Suspect rhabdomyolysis and pigment-induced AKI.

Suspect rhabdomyolysis and pigment-induced AKI.

Suspect rhabdomyolysis and pigment-induced AKI.

Postrenal failure more common in older men with prostatic obstruction and symptoms of urgency, frequency, or hesitancy.

May indicate obstruction caused by renal calculi, papillary necrosis, infection, tumor, or acute glomerulonephritis.

If present, suspect interstitial nephritis, systemic disease, infectious complication, or vasculitis.

If present, suspect interstitial nephritis, systemic disease, infectious complication, or vasculitis.

If present, suspect interstitial nephritis, systemic disease, infectious complication, or vasculitis.

May be due to underlying illness; will also be seen in AKI when uremia ensues.

Although more often seen in chronic renal failure, symptoms and signs may be seen in AKI prior to dialysis initiation (e.g., asterixis).

Other diagnostic factors

May precede AKI and suggest prerenal azotemia, or be a later manifestation resulting from uremia.

Suggests prerenal azotemia if normal physiologic responses and drives are present in a conscious patient.

May indicate infection, obstruction caused by renal calculi, or papillary necrosis.

Bladder outlet obstruction may manifest as distention and pain. Severe intra-abdominal pressure can lead to abdominal compartment syndrome.

Presence of renal bruits suggests renovascular disease.

The presence of classic findings for systemic diseases may suggest renal manifestations.

The presence of classic findings for systemic diseases may suggest renal manifestations.

The presence of classic findings for systemic diseases may suggest renal manifestations.

Risk factors

Advanced age is associated with chronic kidney disease, underlying renal vascular disease, and other comorbid medical conditions that predispose to AKI.

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]

AKI incidence rates of 9% to 38% have been reported in patients with diabetes and chronic kidney disease undergoing contrast exposure.[45]

Intratubular precipitation of light chains in times of volume contraction is associated with renal injury, especially in cases of contrast exposure with volume contraction in myeloma patients. Hypercalcemia predisposes to prerenal azotemia.[5][46]

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]

Exposure may cause AKI.[5] However, the association is controversial because population studies do not replicate risk.[36][37][38]

May precede and lead to AKI.[5][47][48]

There may be impaired renal perfusion causing prerenal azotemia, rhabdomyolysis predisposing to pigment-induced injury, or ischemia causing acute tubular necrosis.

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 medications used in treatment. Highest risk with bacteremia.

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 AKI from prerenal, intrinsic, or postrenal causes. Cardiothoracic surgery is particularly high risk, although off-pump approaches may limit this risk.[49]

May precede prerenal azotemia or acute tubular necrosis, especially if there is severe and prolonged renal ischemia.

May be associated with atheroembolic injury or contrast-induced AKI.

From hemorrhage, vomiting, diarrhea, or sweating; hospitalized patients may have insufficient replacement fluids.

May lead to AKI if significant obstruction is present.

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.

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.

There is preliminary evidence that a genetic predisposition for AKI may exist, especially with apolipoprotein E (APO-E) genes.[43] Genome-wide searches have found other protective candidates, but much more work is needed to validate these findings.[44]

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.[50]

Proton pump inhibitors may increase risk of AKI; however, more studies are needed to clarify this association.[51]

Case reports suggest that herbs and dietary supplements could potentially contribute to kidney injuries.[52]

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