Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

Acute kidney injury is a sudden decline in kidney function, which is usually reversible. This process can occur within hours to days.

Acute kidney injury (AKI) is a syndrome with varying severity, going through different stages. The main characteristic of AKI is a sudden decrease in glomerular filtration rate (increased BUN and serum creatinine) within hours to days.

Definition of AKI:

• Rapid decrease in glomerular filtration rate (GFR) within hours to days.

• Retention of nitrogenous waste products such as urea and creatinine.

• Progression through multiple stages in terms of time, severity, onset, progression, and recovery.

• Recovery depends on the cause, underlying kidney disease, and treatment.

AKI Classification:

• Non-oliguric: Urine volume > 500ml/24h, rapid decrease in GFR.

• Oliguric: Urine volume < 400ml/24h.

• Anuric: No urine production < 100ml/24h.

Causes of AKI:

• Pre-renal (70%):

• Decreased effective intravascular volume:

• Hemorrhage.

• Fluid loss through the gastrointestinal tract, through the kidneys (diuretics, osmotic diuretics).

• Third-space fluid loss: burns, pancreatitis, decreased albumin, systemic inflammatory response syndrome.

• Loss through the skin: burns, sweating, hyperthermia.

• Decreased intake: poor diet.

• Decreased effective intravascular volume:

• Decreased cardiac output: congestive heart failure, cardiac shock, acute cardiac tamponade, severe pulmonary embolism.

• Peripheral vasodilation: sepsis, anaphylaxis, antihypertensive medications, anesthesia.

• Hemodynamic changes in the kidneys:

• Constriction of afferent arterioles.

• Dilation of efferent arterioles.

• Renal (35-40%):

• Vascular:

• Large and medium-sized vessels: renal artery embolism or thrombosis, renal artery clamping, bilateral renal artery embolism, polyarteritis nodosa.

• Small vessels: microvascular thrombosis, malignant hypertension syndrome, HELLP syndrome, HUS/TTP, atheroembolic diseases, atherosclerosis, scleroderma.

• Glomerulus:

• Nephrotic syndrome.

• Acute glomerulonephritis.

• Rapidly progressive glomerulonephritis.

• Interstitium:

• Drug-induced interstitial nephritis: antibiotics (methicillin, cephalosporin, rifampicin, sulfonamide, erythromycin, ciprofloxacin), diuretics (furosemide, thiazide, chlorthalidone), anticonvulsants (phenytoin, carbamazepine), allopurinol.

• Interstitial nephritis associated with infection: bacteria (Streptococcus, Staphylococcus), viruses (CMV, EBV), tuberculosis.

• Tubules:

• Renal ischemia: shock, hemorrhage, trauma, septic shock, acute pancreatitis, hypotension.

• Toxins:

• Exogenous: drugs, myoglobin released from rhabdomyolysis, hemolytic hemoglobin, uric acid.

• Endogenous:

• Aminoglycoside, amphotericin B, acyclovir, indinavir, pentamidine, foscarnet, contrast media, cisplatin, enflurane, phosphate soda.

• Post-renal (<5%):

• Bilateral or unilateral obstruction of the urinary tract above a single kidney:

• Within the ureter: stones, blood clots, pus, or renal papilla, edema after retrograde ureterography, transitional cell carcinoma.

• Outside the ureter: abdominal tumor, pelvis, retroperitoneal fibrosis, ureteral or pelvic injury during abdominal surgery.

• Urethral or bladder neck obstruction:

• Benign prostatic hypertrophy.

• Bladder or prostate cancer.

• Neurogenic bladder, or use of anticholinergics causing urinary retention.

• Urethral stricture.

• Bladder stones.

• Fungal infection.

• Blood clots.

Markers in AKI:

• Serum creatinine:

• Filtered through the glomerulus.

• Excreted by the renal tubules.

• Not reabsorbed.

• Urea, BUN:

• Increased reabsorption when dehydrated.

• Increased without affecting kidney function: increased catabolism, high protein intake, gastrointestinal bleeding, high doses of corticosteroids.

• Decreased in: low protein diet, malnutrition, severe liver disease.

• Cystatin C:

• Protein produced by nucleated cells.

• Freely filtered at the glomerulus.

• Completely reabsorbed in the proximal renal tubules.

• Not excreted.

• Overcomes the limitations of creatinine: related to muscle mass, changes more than creatinine in AKI.

• Other AKI biomarkers:

• Urinary Interleukin 18 (IL18), NGAL, Kim-1: increase earlier than BUN and creatinine by 1-2 days when ischemia is present.

• Characteristics: secreted into blood and urine when AKI is present (similar to troponin after myocardial infarction), higher sensitivity and specificity than urea and creatinine.

Diagnosis of AKI:

• KDIGO 2012: at least one of the following criteria:

• Increase in Cr > 0.3mg/dl within 48h.

• Increase in Cr > 1.5 times compared to baseline 7 days ago.

• Urine volume < 0.5ml/kg/h for 6h.

• RIFLE:

• Risk: Creatinine increased 1.5 times or GFR decreased > 20%, urine < 0.5ml/kg/h for 6h.

• Injury: Creatinine increased 2 times or GFR decreased > 50%, urine < 0.5ml/kg/h for 12h.

• Failure: Creatinine increased 3 times or GFR decreased 75%, urine < 0.3ml/kg/h for 24h or anuria for 12h.

• Loss: Complete loss of kidney function lasting 4 weeks.

• End stage: End-stage kidney disease.

AKI in the community:

• Accounts for 1%.

• Often accompanied by chronic kidney disease.

• Causes: pre-renal 70%, post-renal 17%.

AKI acquired in hospital:

• According to RIFLE, 20% of hospitalized patients experience AKI.

• Causes: hypovolemia, sepsis, medications, contrast media.

• Pre-renal damage is common in general wards.

• Acute tubular necrosis is common in the ICU.

Acute kidney injury is an independent risk factor for in-hospital mortality and is associated with length of stay.

Differentiating acute and chronic kidney failure:

• History: urea creatinine levels, ultrasound showing kidney atrophy, loss of corticomedullary differentiation.

• Normocytic, normochromic anemia unexplained by other causes, with GFR < 30.

• Hypocalcemia.

Causes of acute kidney injury:

• Pre-renal (50-60%):

• Decreased effective intravascular volume.

• Decreased effective intravascular volume.

• Hemodynamic changes in the kidneys.

• Renal (35-40%):

• Vascular.

• Glomerulus.

• Interstitium.

• Tubules.

• Post-renal (<5%):

• Bilateral or unilateral obstruction of the urinary tract above a single kidney.

• Urethral or bladder neck obstruction.

Pre-renal acute kidney injury:

• Also known as pre-renal azotemia.

• Includes: decreased effective intravascular volume, decreased effective intravascular volume, hemodynamic changes in the kidneys.

Autoregulation mechanism in the kidney:

• When blood pressure drops to 70-80mmHg, the afferent arterioles dilate and the efferent arterioles constrict to maintain GFR.

Diagnosis of pre-renal acute kidney injury:

• Clinical presentation suggestive of dehydration, heart failure.

• Laboratory tests: BUN/Creatinine blood ratio > 20, U Na < 20 meq/L, FE Na < 1%, concentrated urine, specific gravity 1.018, osmolality > 500 mOsmol/kg H2O, clean urine sediment, no casts.

Post-renal acute kidney injury:

• Due to bilateral or unilateral obstruction of the urinary tract above a single kidney.

• Urethral or bladder neck obstruction.

Diagnosis of post-renal acute kidney injury:

• Clinical presentation.

• Ultrasound: hydronephrosis, cause of obstruction.

• Non-contrast CT scan.

• MRI of the urinary system.

Renal acute kidney injury:

• Vascular.

• Glomerulus.

• Interstitium.

• Tubules.

Renal acute kidney injury due to acute tubular necrosis:

• The most common cause of renal acute kidney injury.

• Mechanism: tubular damage, hemodynamic disturbances in the kidney, inflammatory response in the kidney, vasoconstriction in the kidney.

• Clinical presentation: onset, spreading, maintenance, recovery.

• Treatment goals: reduce tubular damage, treat and prevent complications from high urea syndrome during oliguria and anuria, timely adjust changes in progression during polyuria until complete recovery.

AKI Treatment:

• Pre-renal:

• Dehydration: 0.9% NaCl, infuse 1000ml in 1h or 250ml/h, monitor urine output, carotid pulse, lung auscultation, blood pressure.

• Heart failure: diuretics, preload reducers, afterload reducers, inotropes, antiarrhythmics, refractory cases can be treated with ultrafiltration.

• Cirrhosis: differentiate between dehydration or hepatorenal syndrome, diuretics, paracentesis, albumin replacement, portacaval shunt, vasopressin analogs.

• Malignant hypertension syndrome: diuretics, albumin replacement if hypotension occurs, treat the underlying disease (corticosteroids, cytotoxic agents).

• Renal:

• Interstitial nephritis: remove the causative agent, antibiotic treatment if infected, consider corticosteroids.

• Acute tubular necrosis: use diuretics cautiously, when adequate hydration has been achieved and in oliguric stage (80-500mg/24h), low-dose dopamine is not beneficial, avoid nephrotoxic drugs and adjust medications that are excreted by the kidneys.

• Post-renal:

• Remove the cause of obstruction: place a urinary catheter, place a JJ stent, bring the ureter out.

Supportive treatment:

• Nutrition 30-35 kcal/kg/day, protein restriction 0.8g/kg/day, adjust medications according to glomerular filtration rate, renal replacement therapy.

Indications for emergency renal replacement therapy:

• Manifestations of hyperuremic syndrome: tremors, pericardial friction rub, neurological symptoms, nausea, vomiting.

• Oliguria or anuria.

• Severe hyperkalemia unresponsive to medical management.

• Acute pulmonary edema unresponsive to medical management.

• Acidosis unresponsive to medical management.

• BUN > 100 mg/dl, creatinine > 10 mg/dl.

• Drug overdose: removal through renal replacement therapy.

Dialysis should be initiated earlier in the presence of severe underlying medical conditions:

• Drug overdose.

• Severe burns.

• Obstetric complications.

• Bee stings.

• Polytrauma.

Factors contributing to more severe hyperkalemia:

• Acidosis, insulin deficiency.

• Potassium release from destroyed tissues: severe trauma, rhabdomyolysis, hemolysis, tumor lysis syndrome.

• Medications, potassium-containing products: IV fluids, potassium-sparing diuretics, NSAIDs, beta blockers, calcium channel blockers, ACE inhibitors.

Dangerous effects of hyperkalemia:

• Toxicity to the heart: tall T wave, prolonged PR, QRS, slowed AV conduction, loss of P wave, eventually ventricular fibrillation, asystole.

Treatment of hyperkalemia:

• Stop sources of increased potassium: diet, medication, remove tissues, treat infection.

• Calcium Gluconate.

• Insulin.

• Blood alkalization.

• Beta 2 stimulation.

• Actual potassium removal from the body: diuretics, ion exchange resin Kayexalate, renal replacement therapy.

Anuria:

• No urine production < 100ml/24h.

• Complete anuria: < 50ml/24h.

• Non-oliguria: > 400ml/24h.

• Oliguria: < 400ml/24h.

Acute kidney injury (AKI):

• Glomerular filtration rate < 60 ml/minute/1.73m2.

• Decrease in glomerular filtration rate > 35%.

• Increase in creatinine > 50% compared to baseline.

• Structural kidney damage within < 3 months.

Note:

• This article is for informational purposes only.

• Please consult a doctor for an accurate diagnosis and treatment.