Acute Kidney Injury (AKI) and Electrolyte Management

Comprehensive vocabulary flashcards covering the definition, KDIGO staging, etiologies, diagnostic distinctions, clinical evaluation, hyperkalaemia ECG features, and acute management of Acute Kidney Injury (AKI).

Acute Kidney Injury (AKI)

A rapid reduction in kidney function occurring over hours to days, as measured by serum urea and creatinine, leading to the failure of maintaining fluid, electrolyte, and acid-base balance.

KDIGO Stage 1 AKI

Serum creatinine rise of $>26\,\text{mcmol/L}$ within $48\,\text{h}$ OR $>1.5\times$ baseline, OR urine output $<0.5\,\text{ml/kg/hr}$ for $>6$ consecutive hours.

KDIGO Stage 2 AKI

Serum creatinine rising to $2\text{--}2.9\times$ baseline, OR urine output $<0.5\,\text{ml/kg/hr}$ for $>12$ consecutive hours.

KDIGO Stage 3 AKI

Serum creatinine $\ge 3\times$ baseline, OR $>354\,\text{mcmol/L}$, OR commenced on renal replacement therapy (RRT) irrespective of stage, OR urine output $<0.3\,\text{ml/kg/hr}$ for $>24\,\text{hrs}$, OR anuria for $>12\,\text{h}$.

Pre-renal AKI

A category of AKI caused by reduced renal perfusion leading to a fall in glomerular filtration rate (eGFR), initially occurring without structural kidney damage.

Intrinsic Renal AKI

Kidney failure resulting from direct structural damage to the renal tubules, interstitium, glomeruli, or renal blood vessels.

Post-renal AKI

Kidney dysfunction resulting from obstruction anywhere along the urinary tract, increasing upstream pressure and decreasing eGFR; commonly due to surgical or obstructive causes.

Acute Tubular Necrosis (ATN)

A tubular intrinsic renal pathology caused by ischaemia (when renal autoregulation fails in uncorrected pre-renal AKI) or direct tubular toxins, damaging epithelial cells and impairing reabsorption and secretion.

Direct Tubular Toxins

Nephrotoxic agents that directly damage tubular cells, including amphotericin B (Ampho B), aminoglycosides, radiocontrast, and myoglobin from crush syndrome.

Acute Interstitial Nephritis (AIN)

Intrinsic renal inflammation of the interstitium commonly caused by drugs (NSAIDs, cephalosporins, PPIs, diuretics), infections (pyelonephritis), infiltration (sarcoidosis, lymphoma), or idiopathic etiologies.

Renal Microangiopathies

Vascular causes of intrinsic renal failure that include haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).

Urine Specific Gravity in AKI

A diagnostic indicator that is $>1.020$ in pre-renal dysfunction (as the kidney retains fluid and concentrates solutes) and $>1.010$ in intrinsic renal disease.

Urine Osmolarity in AKI

A laboratory parameter measuring solute concentration that is $>500\,\text{mOsm/kg}$ in pre-renal failure and $<350\,\text{mOsm/kg}$ in intrinsic renal injury.

Urine Sodium (Na) in AKI

A diagnostic marker that is $<10\,\text{mmol/L}$ in pre-renal dysfunction due to active sodium retention to restore perfusion, compared to $>20\,\text{mmol/L}$ in intrinsic renal disease.

Clinical Signs of Volume Depletion

Physical signs indicating hypovolaemia, including reduced urine output, non-visible JVP, poor skin turgor, decreased blood pressure, and increased pulse.

Clinical Signs of Volume Overload

Physical signs of fluid excess, including lung crepitations, raised JVP, peripheral oedema, increased blood pressure, and an $S_3$ gallop.

Von Willebrand Factor (vWF)

A plasma protein whose primary function is binding to other proteins, particularly factor VIII, and promoting platelet adhesion to wound sites; its impaired endothelial release in uraemia contributes to haemorrhage.

Hyperkalaemia

A medical emergency defined as a plasma potassium level $>6.5\,\text{mmol/L}$, which causes myocardial hyperexcitability and can lead to ventricular fibrillation and cardiac arrest.

Calcium Gluconate 10%

A cardioprotective emergency agent given as a slow IV bolus of $10\,\text{mL}$ over $10\,\text{min}$ (maximum dose $40\,\text{mL}$) that increases the action potential threshold in cardiac conduction tissue to prevent fatal arrhythmias.

Dextrose with Actrapid

An emergency potassium-shifting regimen of $100\,\text{mL}$ of $50\%$ dextrose with $10\,\text{units}$ of Actrapid infused intravenously over $15\text{--}30\,\text{min}$, accompanied by hourly blood glucose monitoring.

Sodium Polystyrene Sulfonate (Kayexelate)

A potassium-binding resin given as $15\,\text{g}$ orally with $15\,\text{mL}$ lactulose every $6\,\text{hours}$; releases sodium or calcium in the stomach for hydrogen ions and subsequently exchanges hydrogen for free potassium in the colon for faecal elimination.

Peaked T Waves

An electrocardiographic manifestation associated with mild hyperkalaemia ($5.5\text{--}6.5\,\text{mmol/L}$).

Moderate Hyperkalaemia ECG Features

Electrocardiographic changes seen with serum potassium levels of $6.6\text{--}8\,\text{mmol/L}$, characterized by prolongation of the QRS complex, ST elevation, ectopic beats, and escape rhythms.

Sine Wave Pattern

A severe hyperkalaemia ($>8\,\text{mmol/L}$) ECG abnormality marked by progressive and extreme widening of the QRS complex merging into the T wave, which can precede ventricular fibrillation and asystole.

AEIOU Indications for Dialysis

The clinical criteria for initiating renal replacement therapy in AKI: Acidosis ($\text{pH} < 7.2$ or base deficit $>10$), Electrolyte disturbance ($K > 7\,\text{mmol/L}$), Intoxication (e.g., lead), Overload (persistent pulmonary oedema), and Uraemic complications (encephalopathy, pericarditis, or gastritis).