Acute Kidney Injury (AKI): Symptoms, 3 Stages & Treatment

Acute Kidney Injury (AKI): Symptoms, 3 Stages & Treatment

Medically Reviewed by Dr. Andrew Stein MD, Consultant Nephrologist (Hospital Kidney Specialist). Last updated: June 2026

Acute Kidney Injury (AKI) is a clinical syndrome characterised by a rapid deterioration in renal function, typically occurring over hours to days.

It is extremely common, affecting 20% of hospital admissions, and is usually reversible if treated promptly.

1. Definition and KDIGO Staging

AKI (formerly known as Acute Renal Failure, ARF):

• Defined by: a rapid decline in kidney function, leading to impaired regulation of fluid, electrolytes, and acid–base balance
• Detected by: a rise in serum creatinine, reduced urine output, or both
• Develops: over hours to days
• Often reversible: with timely treatment

KDIGO Staging

Establishing Baseline Creatinine 

This is important. When baseline kidney function is unknown:

• Review previous blood tests (GP, hospital records)
• If unavailable, estimate baseline using back‑calculation from an assumed eGFR of 75 mL/min/1.73m² (KDIGO guidance)
• Reassess once the patient stabilises

AKI vs CKD

• AKI differs from CKD by its rapid onset and potential reversibility
• AKI patients usually look unwell, whereas CKD patients look well
• Most AKI patients require hospital admission. CKD do not

2. Epidemiology

• 20% of hospital admissions
• >50% of ICU patients
• Contributes to 1.7 million deaths globally per year
• Major economic burden due to prolonged admissions and dialysis
• In a US cohort of 2,214 AKI patients: mean age 67 years; 41% women; 54% white; only 41% achieved full recovery

3. High‑Risk Groups

• Age >65
• Pre‑existing CKD, diabetes, heart failure, chronic liver disease
• Severe infections, dehydration, major surgery (especially cardiac)
• NSAID use, ACE inhibitors/ARBs during illness
• Recent vomiting/diarrhoea, sepsis, reduced urine output, unexpected creatinine rise

4. Causes of AKI

AKI is traditionally classified into prerenal, intrinsic, and postrenal causes. In practice, in most cases, causes are multifactorial.

A. Prerenal (≈80%)

Kidneys structurally normal but under‑perfused.

• Hypovolaemia (dehydration, haemorrhage, diuretics)
• Sepsis‑induced hypotension
• Heart failure, renal artery stenosis
• NSAIDs, ACE inhibitors/ARBs
• Surgery, infections (including COVID‑19)

B. Intrinsic (≈10%)

Structural damage within the kidney.

• Acute Tubular Necrosis (ATN) — ischaemia or toxins
• Nephrotoxicity — aminoglycosides, IV contrast
• Glomerulonephritis — autoimmune (SLE, vasculitis)
• Acute Interstitial Nephritis (AIN) — drug‑induced (PPIs, penicillins)

C. Postrenal (≈10%)

Mechanical or functional obstruction.

• Tumours, prostate cancer, bilateral stones
• BPH, urethral strictures

Notes

Sepsis is one of the leading causes of AKI in hospitalised patients, often through a combination of hypotension, inflammation, microvascular injury and its treatment (e.g. antibiotics).

AKI also frequently occurs on a background of pre-existing CKD (‘AKI-on-CKD’), where relatively minor insults such as dehydration or infection can produce substantial deterioration in renal function.

Data Insight: In one clinical study, the most common breakdown of causes in hospitalised patients showed:

1. Prerenal disease, ATN, and AKI superimposed on CKD (80%)
2. Urinary tract obstruction (10%)
3. Glomerulonephritis, vasculitis, AIN, or atheroemboli (10%; with 1 in 10 of those being atheroemboli).

5. Symptoms and Signs

AKI is often asymptomatic early. Suspect AKI in any acutely unwell patient with:

• Oliguria or anuria
• Volume overload (hypertension, oedema, pulmonary oedema)
• Uraemia (confusion, nausea, asterixis, bruising)
• Hypovolaemia (tachycardia, low BP, dry mucosa)

Note. Clinical signs are heavily dominated by the underlying cause and the clinical setting (e.g. post-cardiac surgery).

Red Flags Requiring Urgent Care

• Oliguria (<400 ml/day) or oligo-anuria (<100 ml/day)
• Severe electrolyte imbalance
• Severe dehydration or collapse
• New confusion
• Fluid overload (breathlessness, severe swelling)
• Sepsis symptoms (fever, rigors, tachypnoea)

Note. Complete anuria (no urine) is rare – and strongly points to total urinary tract obstruction, severe acute glomerulonephritis, or a major vascular catastrophe like an abdominal aortic aneurysm affecting the renal arteries.

6. Investigation and Diagnosis

A rapid, multidisciplinary diagnostic approach is required to differentiate between ‘simple’ AKI (like dehydration) and ‘complex’ intrinsic or obstructive causes.

Key Tests for AKI

• Serum creatinine. A byproduct of muscle metabolism. This remains the gold-standard blood marker used to stage the severity of the injury
• Urinalysis. Checking for protein, blood, and nitrites. It detects active urinary tract infections or ‘active sediment’ indicating intrinsic glomerular damage
• Mid-Stream Urine (MSU): Sent for microscopy and culture to pinpoint specific bacteria for targeted antibiotic therapy
• Urine Albumin-Creatinine Ratio (uACR): Quantifies protein leakage. High levels indicate glomerular disease and help predict future long-term CKD risk

Additional Tests – in all patients with Stage 3 AKI 

• Renal immunology. Blood tests looking for specific autoantibodies (such as ANCA or ANA) to diagnose underlying autoimmune vasculitis/glomerulonephritis or Lupus
• Renal Ultrasound. Evaluates kidney size and anatomy. It is the primary tool used to urgently rule out postrenal obstruction (showing as hydronephrosis).

Typical Laboratory Abnormalities in AKI

• Rising urea/creatinine
• Hyperkalaemia
• Metabolic acidosis
• Hyperphosphataemia
• Hypocalcaemia (occasionally)

Urine Microscopy Patterns

• Muddy brown casts → ATN
• RBC casts → glomerulonephritis
• WBC casts → interstitial nephritis
• Crystals → obstruction or drug toxicity

Fractional Excretion Tests (FENa / FEUrea) – not often done

• FENa <1% → prerenal
• FENa >2% → ATN
• FEUrea <35% → preferred if on diuretics

7. Treatment and Management

Management focuses on treating the underlying cause, preventing further injury, and supporting organ function.

General Measures

• Stop nephrotoxic drugs (see DAMN drugs below)
• Adjust doses of renally cleared medications (see below)
• Initiate Sepsis Six if infection suspected. This is an important part of AKI care in many patients

Fluid Balance Correction (very variable)

• If dry:
  • Use balanced crystalloids (Hartmann’s, Plasma‑Lyte)
  • Give 250–500 mL boluses, reassessing frequently
  • Avoid fluid overload (monitor JVP, lungs)
• If wet
  • Give diuretics (+/- dialysis)

Electrolyte Correction

Emergency treatment for hyperkalaemia to prevent cardiac arrest.

Medication

Commonly Withheld Drugs (‘DAMN’)

• Diuretics
• ACE inhibitors/ARBs
• Metformin
• NSAIDs

Medication Dosing in AKI

• Adjust antibiotics (vancomycin, gentamicin)
• Avoid morphine (use oxycodone/fentanyl)
• Reduce LMWH dose
• Avoid potassium‑sparing agents

Renal Replacement Therapy (RRT; i.e. dialysis)

Initiated for ‘AEIOU indications’:

• Acidosis
• Electrolyte abnormalities (refractory hyperkalaemia)
• Intoxication (e.g. lithium, aspirin, ethylene glycol)
• Overload (pulmonary oedema)
• Uraemia (encephalopathy, pericarditis)

U&E Monitoring Frequency

• Stage 1: U&Es every 24 h
• Stage 2: Every 12–24 h
• Stage 3: Every 4–12 h; consider HDU/ICU
• Hourly urine output if oliguria

Urgent Nephrology Review

• Stage 3 AKI
• Suspected GN or vasculitis
• Refractory hyperkalaemia/acidosis
• Unexplained AKI
• Dialysis requirement

8. Complications

Short‑Term

• Hyperkalaemia → fatal arrhythmias
• Severe acidosis → impaired cardiac contractility
• Pulmonary oedema → respiratory failure
• Uraemia → encephalopathy, pericarditis

Long‑Term

• CKD or ESRF
• Increased risk of heart failure, stroke, hypertension
• High risk of recurrent AKI

9. Prognosis: Renal Recovery and Mortality

Renal Recovery

Recovery Phase

A polyuric phase is common as tubules recover.

3‑Month Rule

If kidney function has not returned to baseline within 90 days → CKD. If dialysis‑dependent at 90 days → ESRF.

Recovery Statistics

• Mild AKI: usually resolves within 10–14 days (this is the natural history of ATN)
• Dialysed patients: 50% recover within 3 months
• Overall: 15% remain permanently dialysis‑dependent

Factors Associated with Better Recovery

• Younger age
• Higher baseline eGFR
• Higher haemoglobin
• No heart failure or liver disease

This information comes from a prominent US study of 2,214 patients (Lee, 2019) demonstrates that patients who successfully recover baseline kidney function tend to share specific clinical characteristics.

Mortality

• Hospital mortality — Death rates rise sharply with severity:
  • Overall – 20%
  • Dialysis-dependent – 50%
  • ICU (if ventilated) – 70%
• ICU impact — In the ICU, where AKI affects over 50% of patients, mortality is often driven by multi‑organ failure rather than kidney injury alone.
• Long‑term mortality — Even after apparent recovery, AKI survivors face a persistently elevated risk of cardiovascular death, heart failure, stroke, and progression to CKD/ESRF, reflecting the systemic impact of the initial injury.
• Risk factors for death — Older age, sepsis, hypotension, pre‑existing CKD, liver disease, and delayed recognition of AKI all significantly increase mortality risk.

10. Prevention and Post‑Discharge Care

With strict clinical vigilance and proactive education, approximately 30% of all hospital-acquired AKI cases are entirely preventable.

Community Prevention – Sick Day Rules

Pause ACE inhibitors, ARBs, diuretics, and metformin during vomiting, diarrhoea, or fever.

Hospital Prevention – Contrast‑Induced AKI 

• Pre‑ and post‑hydration
• Use low‑osmolar contrast
• Avoid nephrotoxins 48 hours before/after
• Check creatinine 48–72 hours post‑contrast in high‑risk patients

Hospital Vigilance

Patients should ask: “What is my urine output today, and has my creatinine changed?”

Post‑Discharge Follow‑Up

Creatinine and eGFR at 1–3 months after discharge.

Nutrition in AKI

• Limit potassium‑rich foods during hyperkalaemia risk
• Moderate protein intake (0.8 g/kg/day unless on dialysis)
• Avoid high‑phosphate foods