Acute Kidney Injury And Renal Failure Flashcards Preview

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Flashcards in Acute Kidney Injury And Renal Failure Deck (27)
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What is a AKI?

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)


Prerenal causes

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**


Intrinsic renal causes

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


Postrenal causes

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


Complications of AKI

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


Prerenal lab values

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


What is the most common cause of renal AKI?

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)


Intrinsic renal AKI lab values

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


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

Hyaline casts

** granular or RBC cell casts = intrinsic renal cause


Children vs children renal failure causes

- 90% ATN
- 10% other

- 50% ATN
- 50% other


Rhabdomyolysis and AKI

Common cause of AKI that causes ATN.
- hyperthermia
- crush injuries
- extreme working out


PSGN lab values

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


Acute interstital nephritis

**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

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


Treatment of AIN induced medication

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


Contrast induced nephropathy

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


Aminoglycoside antibiotics in AKI

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


Renal ATN lab values

Is intrinsic cause:
-FENa = high
-BUN: creatinine ratio is low
-Urine sodium is high

***Granular casts injuries = always ATN***



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


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

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

- 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

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


What does chronic kidney disease as a child produce?

Growth retardation and developmental delay


What are the effects of renal osteodystrophy from renal failure?


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***


what are the three phases of ATN?

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**



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**


Diffuse cortical necrosis

A cause of intrinsic AKI

Caused by cortical infraction of the arcuate arteries of the kidney

Associated with sepsis, obstetric complications, vasospasm and DIC


Renal papillary necrosis

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

Associated with sickle cell disease and pyelonephritis


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

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

More than 2 mg/dL with anuria = rhabdomyolysis


What are the leading causes of ATN

Trauma and sepsis