Presentations
Approach to acute kidney injury
The same eight steps, every presentation: threats first, then the history and exam that discriminate, one honest sentence, a mechanism-grouped differential, and the tests read in order.
Immediate threats
- Hyperkalemia with ECG changes
- Refractory volume overload
- Uremic encephalopathy or pericarditis
- Severe acidosis
History that discriminates
- The trend: baseline creatinine, and when it left it
- Intake, losses, and thirst; urine output honestly quantified
- The medication interrogation: NSAIDs, RAAS blockade, diuretics, contrast, new antibiotics
- Obstructive symptoms; systemic features (rash, arthralgia, fever)
Examination
- Volume status: JVP, orthostatics, edema, weight trend
- Bladder scan on everyone
- Skin: rash (interstitial nephritis, vasculitis), livedo
Problem representation
Oliguric creatinine rise after diarrheal losses on ramipril and naproxen (prerenal setup) versus AKI with a nephritic sediment and hemoptysis (pulmonary-renal emergency).
Differential, by mechanism
Prerenal
- Volume depletion
- Sepsis and vasodilation
- Cardiorenal
- Hepatorenal
- RAAS/NSAID physiology
Intrinsic
- ATN (ischemic, toxic, pigment)
- Glomerulonephritis
- Interstitial nephritis
- Vascular (vasculitis, TMA)
Postrenal
- Bladder outlet obstruction
- Bilateral ureteric obstruction
- Obstructed solitary kidney
Investigations
- Urinalysis with microscopy: the kidney's own biopsy-lite
- Urine electrolytes (FENa, FEUrea on diuretics)
- Bladder scan, then renal ultrasound
- Targeted serologies when the sediment is nephritic
Interpretation
- FENa below 1 percent with bland sediment: intact tubules under hypoperfusion
- Muddy brown casts: tubular injury
- Red cell casts: glomerular inflammation, and a faster phone call
Next steps
- Stop the nephrotoxins and dose-adjust everything renally cleared
- Match volume therapy to the examined volume state
- Define dialysis triggers out loud before they are needed
Connected
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