Acute Kidney Injury

 Acute Kidney Injury (AKI)  

Definition

Acute kidney injury (AKI), previously known as acute renal failure, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys.

The clinical context, careful history taking, and physical examination often narrow the differential diagnosis for the cause of AKI. Prerenal azotemia should be suspected in the setting of vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs. Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia. A history of prostatic disease, nephrolithiasis, or pelvic or paraaortic malignancy would suggest the possibility of postrenal AKI. Whether symptoms are present early during obstruction of the urinary tract depends on the location of obstruction. Colicky flank pain radiating to the groin suggests acute ureteric obstruction. Nocturia and urinary frequency or hesitancy can be seen in prostatic disease. Abdominal fullness and suprapubic pain can accompany massive bladder enlargement. Definitive diagnosis of obstruction requires radiologic investigations.

2 Causes

A. Prerenal (impaired renal perfusion)

Mechanism: decreased renal blood flow → reduced glomerular filtration (functional decline without initial structural damage). Common settings: hypovolemia (bleeding, dehydration), decreased effective circulating volume (heart failure, cirrhosis), sepsis (vasodilation), and drugs that lower renal perfusion (e.g., high-dose diuretics, NSAIDs, ACE inhibitors/ARBs in volume-depleted patients). If prolonged, prerenal AKI can progress to ischemic intrinsic injury (ATN).

B. Intrinsic renal (direct kidney parenchymal damage)

Mechanism: injury to renal structures — glomeruli, tubules, interstitium, or vessels. Major types:

• Acute tubular necrosis (ATN) — ischemic or nephrotoxic (myoglobin, aminoglycosides, contrast).
• Acute interstitial nephritis (AIN) — often drug-induced (antibiotics, PPIs) or immune-mediated.
• Acute glomerulonephritis — inflammatory glomerular injury (eg, rapidly progressive GN).
• Vascular causes — thrombotic microangiopathy, malignant hypertension.
  Urine sediment, urine indices (FeNa/FeUrea) and biomarkers can help differentiate causes.

C. Postrenal (obstructive)

Mechanism: obstruction to urine outflow (anywhere from ureter to urethra) → back pressure and falling GFR. Causes: ureteric stones, prostatic obstruction, malignancy, retroperitoneal fibrosis, or ureteral ligation after surgery. Bilateral obstruction (or obstruction of a solitary functioning kidney) is usually required to cause AKI. Bedside bladder scan/renal ultrasound are key early tests.

3 Symptoms

AKI presentations vary from asymptomatic laboratory abnormalities to life-threatening metabolic derangements. Common features:

• Oliguria or anuria (reduced or absent urine output) — direct marker of decreased renal filtration.
• Fluid overload / peripheral & pulmonary edema — from impaired sodium/water excretion. May present with shortness of breath.
• Fatigue, nausea, anorexia, confusion, reduced consciousness — manifestations of uremia (accumulation of nitrogenous wastes) and electrolyte/acid-base disturbances.
• Electrolyte abnormalities: hyperkalemia (may cause muscle weakness, arrhythmia), metabolic acidosis, hyperphosphatemia, and hypocalcemia. Rapid potassium rises can cause ECG changes and are medical emergencies.
• Symptoms related to the cause: e.g., fever/rash with drug-related AIN, flank pain in obstruction, hypotension in prerenal states.

4 Treatment

Overarching approach

1. Identify and treat the underlying cause (restore perfusion for prerenal; remove obstruction for postrenal; stop offending drugs for intrinsic causes). Early cause-directed therapy often reverses AKI.
2. Supportive care / organ stabilization: monitor urine output, daily weights, fluid balance, serial labs (SCr, electrolytes, acid-base), and hemodynamics. Avoid or adjust nephrotoxins and renally cleared drugs.

Specific interventions

• Volume management / fluids

Give isotonic fluid resuscitation for hypovolemia (guided by hemodynamics). Avoid unnecessary fluid overload  careful reassessment is essential. In septic shock, use vasopressors (norepinephrine) if fluids are insufficient to maintain perfusion targets.

• Diuretics (e.g., IV loop diuretics)

Useful to manage volume overload when kidneys remain responsive; they do not improve AKI recovery per se and should not be used solely to “treat” AKI. Use for symptomatic relief of pulmonary edema or refractory fluid accumulation.

• Correct hyperkalemia and acid-base disorders

Immediate measures for life-threatening hyperkalemia: IV calcium (stabilize myocardium), insulin + dextrose (shift K⁺ into cells), nebulized β-agonist, and consider sodium bicarbonate if acidotic. For ongoing or recurrent hyperkalemia, potassium binders (newer agents like patiromer or sodium zirconium cyclosilicate (SZC)) can lower serum K⁺ and help avoid or delay dialysis in some settings  though their primary evidence is in chronic/ambulatory hyperkalemia and their role in acute, life-threatening AKI is evolving and should be used judiciously. Traditional sodium polystyrene sulfonate (SPS) is still used in many settings but has safety concerns.

• Renal Replacement Therapy (RRT, dialysis)

Indications for urgent/acute dialysis include life-threatening hyperkalemia (eg, K⁺ ≥ ~6.5 mmol/L or ECG changes), severe metabolic acidosis refractory to medical therapy (pH often cited <7.1–7.2), pulmonary edema/volume overload refractory to diuretics, and overt uremic complications (encephalopathy, pericarditis, bleeding). RRT is also used for some drug/toxin removal. The decision to start RRT depends on clinical context, hemodynamic status, and resources.

Timing of RRT (early vs delayed) has been extensively studied (AKIKI, IDEAL-ICU, STARRT-AKI). Large randomized trials (e.g., STARRT-AKI) found no overall mortality benefit to accelerated universal early initiation; many patients in “delayed” strategies never required dialysis. Current practice favors using standard urgent indications rather than automatic early initiation, while individualizing decisions.

Other practical steps

• Renal ultrasound to look for obstruction (postrenal cause).
• Urine studies: urinalysis, microscopy, urine electrolytes (FeNa/FeUrea)  to help separate prerenal from intrinsic causes.
• Avoid nephrotoxins (NSAIDs, aminoglycosides where possible, IV contrast unless necessary; use preventive measures if contrast needed)

  Summary
 
Acute Kidney Injury is a sudden, potentially reversible condition that requires prompt medical attention. Understanding its causes, symptoms, and early warning signs helps prevent complications and improve outcomes. Supporting hemodynamics and electrolytes, avoiding nephrotoxins, and using dialysis when life-threatening electrolyte, acid-base, volume, or uremic complications occur.  

FAQ on Acute Kidney Injury (AKI)

1. What is Acute Kidney Injury (AKI)?

Acute Kidney Injury (AKI) is a sudden decline in kidney function that occurs over hours to days. It means the kidneys are no longer able to efficiently remove waste products, balance fluids, or regulate electrolytes in the body.
Doctors usually diagnose AKI by checking:

• A rise in blood creatinine (a waste product that the kidneys normally remove).
• A drop in urine output (less than 0.5 mL per kg body weight per hour for 6 hours or more).

2. What causes AKI?

AKI can result from various conditions that affect blood flow, kidney tissue, or urine flow. Doctors group the causes into three categories:

• Prerenal (before the kidney) – Caused by reduced blood flow to the kidneys, such as from dehydration, severe bleeding, heart failure, or low blood pressure.
• Intrinsic (within the kidney) – Occurs due to direct damage to the kidney tissue, such as from infections, toxins, inflammation, or certain drugs (like some antibiotics or painkillers).
• Postrenal (after the kidney) – Happens when urine flow is blocked by stones, an enlarged prostate, or tumors that compress the urinary tract.

3. What are the symptoms of AKI?

Some people with AKI have no noticeable symptoms at first, but laboratory tests reveal the problem. When symptoms appear, they may include:

• Reduced urine output or complete absence of urination
• Swelling in the legs, feet, or around the eyes (fluid retention)
• Fatigue, confusion, or drowsiness from toxin buildup
• Shortness of breath due to fluid in the lungs
• Nausea, vomiting, or loss of appetite
• Irregular heartbeat or muscle weakness, often caused by high potassium levels

Because these symptoms can worsen quickly, AKI is considered a medical emergency.

4. How is AKI diagnosed?

Diagnosis involves:

• Blood tests – especially serum creatinine and blood urea nitrogen (BUN) levels. Complete kidney function test with electrolytes.
• Urine tests – to check for protein, blood, or abnormal sediment under a microscope.
• Ultrasound or CT scan – to rule out urinary blockages or kidney abnormalities.
• Medical history review – to look for dehydration, infections, medications, or other illnesses that may have triggered AKI.

5. Can AKI be reversed?

Yes — in many cases, AKI is reversible, especially when identified and treated early. The key is to remove or correct the underlying cause (for example, giving fluids for dehydration or removing a kidney stone). However, if the damage is severe or prolonged, some people may develop chronic kidney disease (CKD) later on.

6. How is AKI treated?

Treatment depends on the cause and severity:

• Restore blood flow to the kidneys if reduced (through IV fluids, medications, or treating heart failure).
• Stop harmful medications or toxins that may have injured the kidneys.
• Manage fluid balance — use of diuretics if there’s swelling or overload.
• Control high potassium using potassium binders (like patiromer or sodium zirconium cyclosilicate) or emergency measures if levels are dangerously high.
• Dialysis may be needed temporarily if:
• Waste products or potassium become dangerously high,
• There’s severe swelling or shortness of breath,
• Or symptoms of uremia (like confusion or pericarditis) appear.

7. Is AKI the same as chronic kidney disease (CKD)?

No.

• AKI happens suddenly and may be reversible with prompt treatment.
• CKD develops slowly over months or years and usually causes permanent loss of kidney function.
  However, people who have experienced AKI are at higher risk of developing CKD later in life, especially if the injury was severe.

8. What lifestyle changes help recovery from AKI?

After recovery, it’s important to:

• Stay well-hydrated (unless restricted by a doctor).
• Avoid unnecessary painkillers (NSAIDs) and other nephrotoxic drugs.
• Monitor blood pressure and blood sugar closely.
• Eat a kidney-friendly diet — limit salt, potassium, and processed foods if advised by your doctor or dietitian.
• Follow up regularly with kidney function tests to ensure recovery is stable.

9. Who is at higher risk for developing AKI?

People most at risk include:

• Elderly individuals
• Those with diabetes, high blood pressure, or heart failure
• Patients undergoing major surgery or taking contrast dye for scans
• Individuals on nephrotoxic medications (like NSAIDs, ACE inhibitors, or certain antibiotics)

10. What recent research is improving AKI care?

Recent studies are exploring:

• Early biomarkers (like NGAL, KIM-1, and TIMP-2·IGFBP7) to detect AKI before creatinine rises.
• Improved dialysis timing — research shows not all patients benefit from early dialysis, emphasizing individualized care.
• New protective drugs and therapies to reduce kidney inflammation and injury.
• Artificial intelligence tools that predict AKI risk in hospitalized patients, helping doctors intervene sooner.

11. Can AKI lead to death?

Severe AKI can be life-threatening if not recognized and treated quickly. The risks are higher in critically ill or elderly patients, those with sepsis, or people who already have chronic kidney problems. With early medical attention and appropriate treatment, however, many patients recover completely.

12. When should someone seek medical attention?

You should contact a doctor or visit an emergency room immediately if you experience:

• Sudden drop in urine output
• Swelling, shortness of breath, or unexplained fatigue
• Severe vomiting, confusion, or chest discomfort
• Recent dehydration, infection, or use of kidney-impacting medicines followed by feeling unwell

Prompt evaluation can make the difference between full recovery and lasting damage.

13. How can AKI be prevented?

While not all cases are preventable, risk can be reduced by:

• Staying hydrated, especially during illness or heat exposure.
• Avoiding overuse of painkillers (NSAIDs) and nephrotoxic drugs.
• Controlling chronic diseases like diabetes and hypertension.
• Regular kidney checkups if you are at higher risk.
• Alerting healthcare providers before scans or surgeries so they can take kidney-protective measures (e.g., IV fluids before contrast dye).