AKI – The Basics
________ azotemia is most commonly due to acute tubular necrosis
Intrarenal/intrinsic
These cylindrical structures seen in urine are formed in the tubules and can help identify the type of AKI.
urinary casts
The first stage of AKI, where injury is occurring but not yet fully established.
Initiation phase
The two major mechanisms of ATN.
A high five if you can list causes for each mechanism
What are ischemia and toxins
Draw a basic nephron and label the proximal tubule, loop of Henle, distal tubule, and collecting duct.
Reference iPad
Two lab values that rise in AKI and are used to monitor kidney function.
BUN and creatinine?
These “muddy brown” casts are a hallmark of ATN
granular casts
Define the maintenance phase
The stage where oliguria, azotemia, and electrolyte imbalances dominate
Which nephron segment(s) is the most vulnerable to ischemic ATN? You can receive a high five if you tell us why
Proximal tubule and medullary segment of thick ascending limb
(Because of high metabolic demand for active transport)
Draw a patient silhouette and mark the clinical findings of AKI
Edema in legs, nausea, metallic taste, Chapman point,
Explain why patients with AKI often develop edema and shortness of breath.
Fluid retention due to decreased filtration and sodium excretion, leading to volume overload
A patient with AKI has FeNa (fractional excretion of Na) >2%. Explain what this means.
Seen in intrinsic AKI (such as ATN); value is seen due to the damaged tubules not being able to reabsorb sodium
A patient in recovery after AKI suddenly develops polyuria. Why?
Filtration is restored before full concentrating ability, leading to osmotic diuresis
Which nephron segment(s) is most affected by aminoglycoside-induced ATN?
Proximal convoluted tubule
Draw hilum of kidney
Contents (anterior → posterior):
Renal vein (most anterior)
Renal artery (middle)
Renal pelvis (posterior, becomes the ureter)
This BUN/creatinine ratio value suggests intrinsic renal damage rather than prerenal AKI.
less than 15
A patient with suspected prerenal AKI has urine osmolality of 550 mOsm/kg. How does this help distinguish prerenal from intrinsic AKI?
Intact tubules in prerenal AKI can concentrate urine (>500), while in intrinsic AKI urine is dilute (~300)?
Explain how tubular obstruction and back-leak reduce effective urine output in ATN.
Casts and dead cells block tubules, while filtrate leaks back into interstitium instead of being excreted
Steps for managament of AKI
Hold potentially nephrotoxic substances, ACE-Is, ARBs, NSAIDs, and nonessential medications.
Adjust the dosing of essential renally cleared medications.
Manage volume status and blood pressure to optimize kidney perfusion.
Identify and manage complications (e.g., electrolyte disturbances, acidosis, fluid overload).
Consider additional supportive care measures (e.g., nutritional support, VTE prophylaxis).
Draw out alpha-intercalated cell (include co-transporters/exchangers in luminal and basolateral membrane) :0
Reference iPad
A patient’s creatinine rose from 0.9 to 2.5 mg/dL in 2 weeks. Integrate the mechanism of GFR changes and tubular injury that explains this.
Reduced filtration is due to tubular obstruction, back-leak of filtrate, and loss of autoregulation lowering GFR
A patient with AKI has hyperkalemia, hypocalcemia, and metabolic acidosis. Integrate how tubular dysfunction explains these findings
Impaired Na⁺ reabsorption and distal K⁺/H⁺ secretion → hyperkalemia and acidosis, plus loss of Ca²⁺ reabsorption → hypocalcemia
In the recovery (polyuric) phase of AKI, patients are at risk of hypovolemia and shock. Explain the mechanism.
Increased GFR with impaired tubular reabsorption leads to excessive loss of water and electrolytes, which causes dehydration and hypotension?
Cisplatin can cause nephrotoxic ATN. What drug class does it belong to?
Platinum analog
Draw the RAAS pathway and show how reduced renal perfusion activates it.
Renin release → angiotensin II → efferent arteriole constriction + aldosterone/ADH release to preserve GFR and volume