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Pathophysiology - Urinary Tract > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is hydronephrosis characterized by? What typically causes it?

A

Distention / dilation of the renal pelvis / calyces with possible atrophy of the renal cortex and medulla

Caused by urinary obstruction, VUR, or retroperitoneal fibrosis.

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2
Q

What is the most common congenital cause of hydronephrosis?

A

Ureteropelvic junction stenosis (small opening of proximal ureter in renal pelvis)

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3
Q

What is the definition of acute kidney injury?

A

Abrupt decrease in GFR occurring over hours to days which leads to accumulation of nitrogenous compounds in the body (azotemia), including urea and creatinine

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4
Q

What are the urinary output classifications of acute kidney injury?

A

Non-oliguric: >500 mL/day
Oliguric: <500 mL / day
Anuric: < 50 mL/day

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5
Q

What are the three major categories of acute renal failure (acute kidney injury)/

A
  1. Pre-renal -> renal hypoperfusion
  2. Post-renal -> obstruction
  3. Intra-renal -> intrinsic renal disease
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6
Q

What does RIFLE stand for in the RIFLE criteria for acute kidney injury?

A 
R - Risk
I - Injury
F - Failure
L - Loss
E - End Stage Kidney Disease
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7
Q

What are the GFR criteria for RIF of the RIFLE criteria?

A

Risk - Serum creatinine is 1.5x, or GFR decreases by 25%

Injury - Serum creatinine is 2x or GFR decrease by 50%

Failure - Serum creatinine is 3x
or GFR decrease by 75%.

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8
Q

What are the absolute diagnostic criteria for acute renal FAILURE (F of RIFLE)?

A

Serum creatinine is >4 mg/dL
Acute rise in serum creatinine >0.5 mg/dL

Or

Urinary output <0.3 mg/kg/h x24 hours, or anuria x 12 hours.

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9
Q

What are the general urinary criteria for RI?

A

Urinary output decreases to less than 0.5 mL/kg/hr for 6 or 12 hours

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10
Q

What is the definition of Loss or ESKD?

A

Loss - persistent ARF –> complete loss of kidney function for >4 weeks

ESKD - >3 months of ARF = CKD endstage, dialysis required

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11
Q

What is the most common cause of acute renal failure?

A

Pre-renal AKI -> decreased perfusion of kidneys

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12
Q

What will happen if pre-renal azotemia is not corrected promptly?

A

Ischemic-type acute tubular necrosis

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13
Q

How do cyclosporin / tacrolimus (calcineurin inhibitors) cause renal injury?

A

Vasoconstriction of afferent arteriole

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14
Q

What are the categories of causes of prerenal acute renal failure and some examples within each?

A
  1. Hypovolemia -> hemorrhage, GI loss, burns
  2. Hypotension -> antihypertensives, sepsis
  3. Low cardiac output -> heart failure, MI
  4. Increased renal vascular resistance -> excessive pressors
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15
Q

How will urine production be in pre-renal and post-renal azotemia? Will tubular function remain intact?

A

Pre-renal -> typically oliguria

Post-renal -> typically anuria

Tubular function should remain intact, so urine sodium and water reabsorption should be adequate

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16
Q

How does pre-renal azotemia due to decreased true / effective circulatory volume tend to perpetuate more pre-renal azotemia?

A

Decreased BP -> increased firing of central baroreceptors

-> increased sympathetic tone, restoring blood volume, but reducing blood flow to the glomerulus (via epinephrine)

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17
Q

How does post-renal azotemia lead to reduced GFR?

A

Blockage of flow leads to increased intratubuar pressure, which leads to renal vasoconstriction as well as parenchymal destruction due to infection

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18
Q

Is post-renal azotemia common, and who tends to get it?

A

No - because it required bilateral obstruction to produce azotemia

Newborns - congenital anomalies
Older males - BPH
Females - pelvic malignancy

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19
Q

What are the vascular disease causes of ARF?

A

Large vessel diseases - i.e. renal artery thrombosis or vein thromobosis (bilateral), thromboembolism, vasculitis

Microvascular disease - Lupus, malignant HTN, TTP/HUS

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20
Q

What are glomerular diseases which cause ARF and what will the urinalysis show?

A

Post-streptococcal GN, hemolytic uremic syndrome, RPGN (crescentic), anti-GBM disease

-> urinalysis shows RBC casts

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21
Q

What drugs commonly cause acute interstitial nephritis?

A 
Remember the P's
Pee - diuretics
Pain-free - NSAIDs
Pencillins and cephalosporins
Proton pump inhibitors
RifamPin

Sulfa drugs in general + ciprofloxacin

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22
Q

What will urinalysis show for acute interstitial nephritis?

A

WBC casts with numerous eosinophils

23
Q

What accounts for 90% of intrinsic renal injury and what will appear in the urine?

A

Acute Tubular Necrosis - Brown casts / muddy casts

24
Q

What are the endogenous, toxic causes of ATN?

A

Hemoglobinuria (intravascular hemolysis)
Myoglobinuria - very common, due to severe muscle trauma / rhabdomyolysis
Endotoxemia - cytokine overproduction

25
Q

What are the exogenous toxic causes of ATN?

A

Aminoglycosides, radiocontrast media, lead, cisplatin (gyno malginancies), ethylene glycol (oxalate crystals), amphotericin B

26
Q

How does the damage appear in ATN and where is it worst?

A

Appears patchy

Worst in proximal tubule and outer medullary segment of TALH

27
Q

What happens to the serum BUN/Cr ratio in intrarenal vs extrarenal causes of ATN and why?

A

serum BUN/Cr ratios -> increases above 15 in extrarenal causes, as tubules try to preserve volume and are functioning properly, and BUN can be reabsorbed while Cr cannot.

Ratio falls below 15 in intrarenal AKI (i.e. ATN) because tubules are not functioning properly in reabsorption of BUN.

28
Q

What happens to the FENa in intrarenal vs extrarenal causes of ATN and why?

A

FENa = fractional excretion of sodium

Extrarenal - will be below 1% -> proper reabsorption of Na (until damage causes tubular failure)

Intrarenal - tubules failing - will be above 1%

29
Q

What are the consequences of short vs medium vs prolonged hypoxia to renal tubular cells?

A

Short - Sublethal injury

Medium - induction of apoptosis

Prolonged - tubular necrosis -> sloughing off of necrotic cells can lead to acute tubular necrosis / obstruction

30
Q

Why does renal ischemia or toxic injury lead to intrarenal vasoconstriction, worsening ischemia?

A

Ischemia -> sublethal endothelial injury

Injury to endothelial cells causes increased endothelin release (potent vasoconstrictor) and reduced nitric acid production (vasodilator)

  • > this is intended to cause thrombosis and repair of injury, but just worsens existing ischemia
  • > thrombosis and procoagulation also causes congestion inducing hypoxia
31
Q

What is the inciting event in the dysfunction of tubular epithelial cells following ischemia?

A

ATP depletion causes actin binding proteins to induce disassembly of actin bundles

Actin cytoskeleton becomes disrupted

32
Q

How does actin cytoskeleton disruption disrupt the function of tubular cells?

A
  1. Loss of polarity -> impaired solute transport, with Na/K ATPase and integrins moving to apical surface
  2. Tubular obstruction -> due to brush border injury and detachment of epithelial cells, forming casts
  3. Backleak of glomerular filtrate into interstitium -> due to loss of cells and impaired tight junction function
33
Q

How does tubular injury and dysfunction in ATN cause afferent arteriolar vasoconstriction?

A

Tubular damage reduces reabsorption of NaCl

-> increased delivery of NaCl to macular densa, and activation of tubuloglomerular feedback

34
Q

How does glomerular permeability change in ATN?

A

Decreased -> likely due to ATII-induced glomerular size reduction, as well as mesangial changes and contraction.

35
Q

How does tubular obstruction contribute to injury in ATN?

A

Tubular obstruction with cellular debris leads to an increase in intratubular pressure
-> inappropriate opposes GFR, reducing it -> maintains ATN

36
Q

What are the causes of oliguria ARF vs anuria ARF?

A

Oliguria - pre-renal and renal

Anuria - postrenal, complete renal artery occlusion (i.e. thromboembolus)

37
Q

What happens to urinary sodium in pre-renal vs intrinsic renal? Urinary osmolality?

A

Urinary sodium: <20 mEq/L in pre-renal, >40 in intrinsic renal

Urinary osmolality: >500 mOsm/kg in pre-renal, <350 in intrarenal

38
Q

How is FENa calculated?

A

(Urinary / Plasma [Sodium]) / (Urinary / Plasma [Creatinine]) * 100%

Normal: <1% Na excreted -> creatinine excretion approximates GFR

39
Q

What will be seen in the urine in pre-renal ARF vs intrinsic renal failure? When should this sample be taken?

A

Pre-renal - benign (no changes)

Intrarenal - coarse granular casts; renal tubular epithelial cell casts

Take urine sample BEFORE giving diuretics

40
Q

Why is ultrasound always needed in ARF workup?

A

Need to rule out kidney stones / hydronephrosis causing post-renal azotemia
-> the values of post-renal azotemia can look like prerenal (if mild) or post-renal (if severe, causing tubular damage)

41
Q

What are the three distinct phases of ATN?

A
  1. Initiation phase - potentially reversible period if insult is corrected
  2. Maintenance period - irreversible loss of renal function lasting 1-3 weeks, as tubular cells take time to re-enter cell cycle / regenerate
  3. Recovery phase - renal function returning to normal, marked by polyuria
42
Q

What happens when renal blood flow returns to normal in the maintenance period?

A

Nothing really -> the tubules are damaged and have not had time to regenerate. The maintenance period is a period of irreversible damage where supportive care is needed until the patient’s tubules can regrow

43
Q

What are the metabolic risks in the maintenance phase of acute renal failure?

A

Oliguria -> hyperkalemia, metabolic acidosis (unable to excrete daily produced acids), uremia

44
Q

What happens to urine production, electrolytes, and nitrogenous substances during the recovery period of ARF?

A

Polyuria -> BUN and serum creatinine fall as GFR recovers

Risk of hypokalemia from overexcretion

45
Q

What injury is most likely to result in acute tubular necrosis?

A

Severe burns -> dehydration + increased catabolism

46
Q

Do small changes in creatinine affect mortality?

A

Yes

47
Q

What factors are indicative of a poor prognosis in ATN?

A

Old age, oliguria (vs non-oliguric ATN), infection, GI bleeding, severity of initial insult

48
Q

How much protein should a patient in ARF have per day?

A

1 gm/kg/day, because patient is hypercatabolic and losing body weight

49
Q

At what threshold should hyperkalemia be treated and how should it be done?

A

> 5.3 mEq/L

Calcium gluconate for membrane stabilization, sodium bicarbonate (correct acidosis), B-agonists, hypertonic glucose with insulin, Keyexalate (resin), dialysis -> all from potassium lecture

50
Q

When should metabolic acidosis be treated in AKI?

A

When serum bicarbonate falls below 15 mEq/L

51
Q

What is the leading cause of death in AKI?

A

Infections -> avoid Foley catheters and IV’s if possible

52
Q

What are the indications for dialysis in ARF?

A
  1. Fluid overload which is refractory to diuretics
  2. Persistent hyperkalemia
  3. Severe metabolic acidosis refractory to treatment, especially methanol / ethylene glycol poisoning
  4. Uremic symptoms, and automatically if BUN>100.
  5. GI bleeding
53
Q

What are uremic symptoms, and why does GI bleeding occur in ESRD?

A

Pericarditis, encephalopathy, peripheral neuropathy, nausea / anorexia, asterixis

GI bleeding occurs due to platelet dysfunction induced by uremia

Pathophysiology - Urinary Tract (14 decks)

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