Acute Kidney Injury

Acute Kidney Injury (aka Acute Renal Failure) definition + Lab Indicators

An abrupt decrease in GFR resulting in accumulation of nitrogenous waste products (like urea and creatinine) as well as inflammatory components.

Labs: Increase BUN, Increased Cr

Concepts of prerenal, intrinsic, and postrenal AKI

Prerenal = decreased renal perfusion with intact parenchyma

Intrinsic= primary kidney lesion, parenchyma is not intact

Post renal= impediment to urine flow due to functional or structural obstruction

Prerenal AKI pathophysiology

Reduced renal perfusion → intact kidney responds with Na/H2O retention, low urine Na, concentrated urine

Intrinsic AKI pathophysiology

Direct injury to renal parenchyma (ATN, AIN, GN, vascular injury) → tubular necrosis, loss of polarity, back‑leak, casts, impaired concentrating ability.

Postrenal AKI pathophysiology

Obstruction anywhere from renal pelvis to urethra → ↑ hydrostatic pressure proximal to obstruction → ↓ GFR

Major causes of prerenal AKI

True volume depletion(DI, diarrhea, vomiting, blood loss), CHF/cirrhosis (low effective circulation), NSAIDs/ACEi/ARBs, renal artery stenosis, hypercalcemia, vasoconstrictive drugs.

Major causes of intrinsic AKI

Acute Tubular Necrosis(ATN) (ischemic or toxic), Acute Interstitial Nephritis (AIN)(drug/infection/autoimmune), Glomerulonephritis (nephritic syndromes), vascular causes (TMA, atheroemboli).

Major causes of postrenal AKI

BPH, urethral stricture, stones, tumors, neurogenic bladder, papillary necrosis, retroperitoneal fibrosis.

Diagnosis of prerenal AKI

BUN/Cr >20:1, FENa <1%, FEUrea <35% (if on diuretics), Una <20, Uosm >500, bland sediment.

Diagnosis of intrinsic AKI

BUN/Cr <20:1, FENa >2%, Una >40, Uosm <350, muddy brown casts (ATN), WBC casts (AIN), RBC casts (GN).

Diagnosis of postrenal AKI

BUN/Cr >15:1, FENa >2–4%, hematuria or crystals possible, imaging shows hydronephrosis or obstruction. TX: Relieve obstruction

Etiology of Acute Tubular Necrosis (ATN)

Ischemia (prolonged prerenal states, shock, surgery), endogenous toxins (myoglobin, hemoglobin, uric acid, light chains), exogenous toxins (contrast, aminoglycosides, amphotericin, heavy metals).

What is AIN and Causes of Acute Interstitial Nephritis (AIN)

Inflammation and swelling of interstitial tissue where nephron sits→Causes: Allergic drug reaction (β‑lactams, sulfa, NSAIDs, PPIs), infections (pyelo, CMV, EBV), autoimmune (sarcoid, TINU).

Treatment of prerenal AKI

Restore perfusion: isotonic fluids, blood products, pressors if needed

Treatment of intrinsic AKI

Supportive care: maintain SBP >100, correct electrolytes, treat acidosis, avoid nephrotoxins, adjust drug dosing, dialysis if needed.

Treatment of postrenal AKI

Relieve obstruction: Foley catheter, remove stones/clots, stents or nephrostomy for extrinsic compression.

Indications for dialysis in AKI (AEIOU)

AEIOU: Acidosis (pH <7.2), Electrolytes (refractory hyperkalemia), Intoxications, Uremia (AMS/pericarditis), Overload (refractory).

Acute Interstitial Nephritis (AIN) Clinical Triad

Rash, Fever, Eosinophilia

Acute Interstitial Nephritis (AIN) Diagnosis + Tx

Increased white cells and white cell casts. Tx: Discontinue agent, corticosteroids

Serum BUN/Cr >20:1 suggests AKI where

Prerenal AKI

Serum BUN/Cr <20:1 suggests AKI where

Intrinsic

Muddy Brown Casts think:

Acute Tubular Necrosis

How do NSAIDs affect autoregulation of GFR with decreased renal perfusion?

They inhibit prostaglandins compensation/correction (normally vasodilating afferent arteriole and increasing GFR)→causes decreased GFR(worse kidney function)

How do ACEi/ARB affect autoregulation of GFR when there is decreased renal perfusion?

Normally in decreased perfusion Angiotensin release will constrict efferent arteriole to increase GFR, BUT ACEi/ARBs inhibit this»cause efferent vasodilation and decreased GFR(worse kidney function in hypoperfusion)

Acute Tubular Necrosis (ATN) Phases (pee related)

Initiation (peeing very little due to tubular damage and water retention)

Maintenance (pee a lot more as tubular epithelium regenerates)
Recovery (peeing normal and regenerated epithelium but cant reabsorb H20 and electrolytes)

Contrast Induced Nephropathy (cause, timing, tx)

Type of ATN caused by constrast induced renal artery constriction and direct tubular injury; AKI is apparent within first 24-48hrs after contrast

Tx: Prevention is key, use fluids before, during and after to volume expand

Pigment Induced Acute Tubular Necrosis (cause, labs)

Caused by Rhabdomyolysis (seen with trauma or statins)→ muscle breakdown increases Cr, heme (+) in urine with NO RBCs, hyperkalemia/hyperphosphatemia/hyperuricemia

Nephrotoxin Drug Induced Acute Tubular Necrosis DRUGS (3)

Aminoglycosides, Amphotericin B, Vancomycin

Mechanism of Aminoglycosides causing ATN

Accumulates in lysosomes of nephrons and taken up in PT» and interferes with normal cell function→cell death

Mechanism of Amphotericin B Drug Induced ATN

It directly binds to tubular epithelial cells and punches holes into the proximal tubule»causes Na, K, Mg wasting