History and exam

Key diagnostic factors

common

reduced urine production

Oliguria and anuria are common in AKI. They are not suggestive of a particular etiology.

vomiting

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

dizziness

Orthostatic symptoms support prerenal azotemia.

orthopnea

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

paroxysmal nocturnal dyspnea

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

pulmonary edema

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

hypotension

Supports prerenal azotemia that may progress to acute tubular necrosis.

tachycardia

Supports prerenal azotemia.

orthostatic hypotension

Orthostatic symptoms support prerenal azotemia.

hypertension

Suggests intravascular volume expansion.

peripheral edema

May result from impaired renal salt excretion.

uncommon

muscle tenderness

Suspect rhabdomyolysis and pigment-induced AKI.

limb ischemia

Suspect rhabdomyolysis and pigment-induced AKI.

seizures

Suspect rhabdomyolysis and pigment-induced AKI.

prostatic obstructive symptoms

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

hematuria

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

fever

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

rash

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

arthralgia/arthritis

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

altered mental status

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

signs of uremia

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

Other diagnostic factors

common

nausea

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

uncommon

thirst

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

flank pain

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

abdominal distention

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

abdominal bruit

Presence of renal bruits suggests renovascular disease.

livedo reticularis

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

petechiae

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

ecchymoses

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

Risk factors

strong

advanced age

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]

underlying renal disease

Associated with increased susceptibility to AKI, particularly contrast-related AKI. Risks increase with increasing severity of chronic kidney disease.[5]

malignant hypertension

Malignant hypertension may cause AKI.[5]

diabetes mellitus

AKI incidence rates of 9% to 38% have been reported in patients with diabetes and chronic kidney disease undergoing contrast exposure.[44]​ There is evidence to suggest that diabetes mellitus is an independent risk factor for contrast-induced AKI.[45]

myeloproliferative disorders, such as multiple myeloma

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]

connective tissue disease

May present with AKI (e.g., systemic lupus erythematosus, scleroderma, antineutrophil cytoplasmic antibody-associated glomerulonephritis, antiglomerular basement membrane disease).[5]

sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome)

Associated with chronic kidney disease, but may present with AKI.[5]

radiocontrast

Exposure may cause AKI.[5] However, the association is controversial because population studies do not replicate risk.[33][34][35]

exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-tazobactam, cancer therapies, nonsteroidal anti-inflammatory drugs, or ACE inhibitors)

May precede and lead to AKI.[5][47][48][49]

trauma

There may be impaired renal perfusion causing prerenal azotemia, rhabdomyolysis predisposing to pigment-induced injury, or ischemia causing acute tubular necrosis.[50]

hemorrhage

The resulting impaired renal perfusion supports prerenal azotemia as cause of AKI or ischemia resulting in acute tubular necrosis.

sepsis

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.[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]​ 

pancreatitis

There may be severe third spacing of fluid leading to intravascular volume depletion resulting in prerenal failure.

drug overdose

May precede AKI due to direct toxicity, rhabdomyolysis, and volume depletion.

surgery

May precede AKI from prerenal, intrinsic, or postrenal causes.[52]​ Cardiothoracic surgery is particularly high risk, although off-pump approaches may limit this risk.[53]

cardiac arrest

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

recent vascular intervention

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

excessive fluid loss

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

nephrolithiasis

May lead to AKI if significant obstruction occurs, especially with one functioning kidney.

weak

drug abuse

AKI from nephrotoxicity, ischemia.

alcohol abuse

Suspect pigment-induced AKI if rhabdomyolysis is present (e.g., after prolonged loss of consciousness).

excessive exercise

Suspect pigment-induced AKI due to rhabdomyolysis.[54]

recent blood transfusion

AKI may be present from intravascular hemolytic transfusion reaction, deposition of immune complexes.

malignancy

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.

genetic susceptibility

There is preliminary evidence that a genetic predisposition for AKI may exist, especially with apolipoprotein E (APO-E) genes.[41] Genome-wide searches have found other protective candidates, but much more work is needed to validate these findings.[42]

use of renin-angiotensin system inhibitors

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]​ 

proton pump inhibitors

Proton pump inhibitors likely increase risk of AKI; however, more studies are needed to clarify this association.[57][58]

herbal therapy

Case reports suggest that herbs and dietary supplements could potentially contribute to kidney injuries.[59]

Use of this content is subject to our disclaimer