Acute Kidney Injury And Renal Failure Flashcards

1
Q

What is a AKI?

A

Caused by progressive azotemia (abnormally high levels of nitrogen-containing compounds in blood)
- kidney is injured and cant get rid of the nitrogen waste properly
Occurs over a few days

All AKI shows oligouria/anuria

  • *usually shows BUN:creatinine increases**
  • normal ratio is 5-20:1

3 main types

  • prerenal
  • intrinsic renal
  • postrenal

** can be compound (multiple causes) or just one)

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2
Q

Prerenal causes

A

Almost always caused by hypovolemia in some way shape or form

  • sepsis
  • diabetes mellitus
  • GI losses
  • Renal losses
  • hemorrhages

the one exception is severe systolic HF which produces cardiorenal syndrome

results in decreased GFR rates, activations of RAAS and elevated BUN:creatinine ratio of 20

*urine levels of sodium will be <20 mEq/L, urine will be >500 oSmoles, and FENa = <1%. (Because the kidney has less filtrate and chronic stimulation of the RAAS system

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3
Q

Intrinsic renal causes

A

Most commonly caused by acute tubular necrosis (ATN)

  • death and physiological damage caused by ischemia from a prerenal AKI
  • most common damaged cells = PCT/TAL cells

Additional causes:

1) nephrotoxicity via:
- contrast
- Aminoglycosides
- cisplatin
- heavy metals
- rhabdomyolysis (myoglobin)
- poisons
- hemolytic anemia (hemaglobinuria)

Shows BUN:creatinine ratio of less <20

  • high FENa = 2%
  • high urine Na+ > 40 mEq/L
  • urine osmolality <350 mEq/L
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4
Q

Postrenal causes

A

Is always a blockage of some sort

  • kidney stones
  • prostate hypertrophy/cancer
  • overplayed bladder

#1 is always prostate hypertrophy in men

Variable lab values**
- but urine will always be <350 osmolarity

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5
Q

Complications of AKI

A

Massive amounts of different complications Includes:

1) metabolic
- hyperkalemia, hyponatremia, hypocalcemia, hyperphosphatemia, hyperuricemia, metabolic acidosis

2) cardiovascular
- pericardial effusion, HTN, MIs, arrhythmias, pulmonary edema

3) GI
- N/V, malnutrition, GI hemorrhages

4) CNS
- AMS, asterixis, seizures

5) infectiosn
- pneumonia, sepsis

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6
Q

Prerenal lab values

A

BUN:creatine ratio is almost always >20
- if GI bleed present also = > 40

FRNa (fractional excretion of sodium) will be very low <1%

  • also low urine sodium <20 mEq/L
  • ** this is because the kidney is trying to conserve sodium to retain water
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7
Q

What is the most common cause of renal AKI?

A

Acute tubular necrosis

  • also is 90% the cause of renal failure
  • almost always caused by ischemia or shock of some sort (usually trauma or infectious shock/sepsis)
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8
Q

Intrinsic renal AKI lab values

A

FENa = high (>1%)

  • high urine sodium concentration also (kidney isnt working)
  • *however if the patient is taking diuretics (especially loop) the FENa looks normal or low.

Urine sodium = > 40

BUN:creatinine ratio is low <20

Very high water in urine

**FEurea will be high and 100% needs to be monitored if patient is taking diuretics

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9
Q

What kind of casts in urine would signal a pre renal or post renal cause of AKI?

A

Hyaline casts

** granular or RBC cell casts = intrinsic renal cause

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10
Q

Children vs children renal failure causes

A

Adults

  • 90% ATN
  • 10% other

Children

  • 50% ATN
  • 50% other
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11
Q

Rhabdomyolysis and AKI

A

Common cause of AKI that causes ATN.

  • hyperthermia
  • crush injuries
  • extreme working out
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12
Q

PSGN lab values

A

Intrinsic cause of ATI:

  • FENa is high
  • BUN:creatinine ratio will be low
  • Urine sodium will be high

shows red blood cell casts and RBCs in the urine

Treatment = antibiotics for past infection (if you still think its around). give fluids and electrolytes and HTN treatment short term

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13
Q

Acute interstital nephritis

A
  • *WBC casts with eosinophils and direct RBCs and WBCs will be in the urine**
  • **if it was pylonephritis/ infectious it would show NO eosinophils in the urine

Is believed to be type 1 or type 4 hypersensitivity reaction to some drugs (such as NSAIDs, PPIs, rifampin, penicillins and sulfa drugs are MOST common)**
- can also be caused by systemic infections, autoimmune reactions (SLE and sarcoidosis are most common) coagulopathies, and mycoplasma infections as well as pyelonephritis and diabetes mellitus

Intrinsic cause of AKI:

  • BUN: creatinine ratio is low
  • **however creatinine is high
  • FENa = 2.5% roughly with high sodium in urine >40 mEq/L

Symptoms:

  • fever
  • rash
  • hematuria
  • Pyuria
  • costovertebral tenderness
  • **eosinophils in urine and eosinophilia = drug-induced AIN needs to be #1
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14
Q

Treatment of AIN induced medication

A

Usually self-limiting and just stop the meds and symptomatically treat via palliative care

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15
Q

Contrast induced nephropathy

A

giving IV contrast can cause nephropathy, however it is less dangerous as literature implies

Risk factors:

  • diabetes
  • multiple myeloma
  • hypovolemia
  • > 60 yrs
  • high loads of contrast
  • previous renal injuries/insufficiency **most important

treatment = fluids and monitor
- *N-Acetyl-cystine before IV contrast tanks the risk % of getting this

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16
Q

Aminoglycoside antibiotics in AKI

A

Most common antibiotic associated with ATN
- dose dependent and length (need to measure and monitor you dont give them too much)

Treatment = discontinue meds
- rarely progresses CKI

17
Q

Renal ATN lab values

A

Is intrinsic cause:

  • FENa = high
  • BUN: creatinine ratio is low
  • Urine sodium is high

Granular casts injuries = always ATN

18
Q

Oliguria

A

Urine output 100/400 mL/24 hrs
- low levels of urine overall

Not a good indicator or specific cause of AKI, but is sensitive for general AKIs

19
Q

What are the most common physiological pathologies that are present in renal failure?

A

Metabolic acidosis
- cant excrete H+ ions, but excretes/ doesnt reabsorb HCO3-

Hyperkalemia
- as a result of combating metabolic acidosis, the body moves potassium inside cells and pumps potassium into the blood via H+/K+ exchangers

Periorbital edema
- retention of H20/Na+ since it cant excrete things easily

Uremia

  • retention of toxins since the kidneys cant get rid of them
  • causes nausea/anorexia/ easy bleeding/ anemia/neuropathy/encephalopathy and pericarditis
20
Q

What does chronic kidney disease as a child produce?

A

Growth retardation and developmental delay

21
Q

What are the effects of renal osteodystrophy from renal failure?

A

Hyperphosphatemia

Vitamin D deficiency/ calcitrol
- leads to hypocalcemia

both of these two combined leads to osteoporosis and increased levels of PTH hormone

also can lead to calcium stones and plaques throughout vasculature

22
Q

what are the three phases of ATN?

A

1) inciting event

2) maintenance phase
- 1-3 weeks after #1
- induces hyperkalemia and metabolic acidosis
- uremia is also produced
- creatinine:BUN >20

3) recovery phase
- 4 weeks after #1
- re-epithlialization occurs
- polyuria and hypokalemia can occur
- Creatinine:Bun ratio = <20
- at this phase you will see granular cell casts and renal tubular epithelial cells in urine

23
Q

HUS

A

Is hemolytic uremic syndrome of:

1) acute kidney injury
2) thrombocytopenia
3) hemolytic anemia

Also shows oliguria

most common caused 1-3 weeks after a GI infection (E. Coli is most common). Patient may or may not complain of past bloody diarrhea also

24
Q

Diffuse cortical necrosis

A

A cause of intrinsic AKI

Caused by cortical infraction of the arcuate arteries of the kidney

Associated with sepsis, obstetric complications, vasospasm and DIC

25
Q

Renal papillary necrosis

A

A cause of intrarenal AKI
- causes renal papillae sloughing via ischemia

Associated with sickle cell disease and pyelonephritis

26
Q

What is the tell tale sign for a 0 GFR in a patient?

A

If serum creatinine is increasing 1-2 mg/dL per day

More than 2 mg/dL with anuria = rhabdomyolysis

27
Q

What are the leading causes of ATN

A

Trauma and sepsis