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PDAT3 > 20 - AKI > Flashcards

20 - AKI Flashcards

1
Q

AKI vs CKD

A

AKI = Acute Decline in Kidney Function
we look at
Serum Creatinine +/- Urine Output

CKD
renal dysfunction for 3+ months

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2
Q

Preventable & Non-Preventable
Risk Factors for AKI

A

Not Preventable
CKD / >75yo
Peripheral Vascular Dz / HF / Liver Disease / Diabetes

  • *Preventable**
  • *Nephrotoxins** = NSAIDs / AminoGlycosides
  • Hypo*Tension = HypoVolemia / Cardiac Disease
  • *Sepsis**
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3
Q

Causes of PRE-RENAL AKI

A

IVF Volume Depletion
hypovolemia / hemorrhage / GI losses / Urinary Losses
Cirrhosis / HF / sepsis / vasodilators

  • *Reduced Cardiac Output**
  • HypoTension / HF / MI / Drugs = CCBs*

Vascular Obstruction
BILATERAL renal artery stenosis
Renal A-fferent Arteriol Vasoconstriction = NSAIDs / Vasopressors / TAC+CSA
VVVV
all leads to
Decreased Renal Blood flow –> ↑SCr

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4
Q

Pre-Renal AKI
Diagnosis & Evaluation

A

History
Dehydration / Diarrhea / Diuresis

Physical Exam
Orthostatic Hypotension + TACHYcardia

Labs:
BUN:SCr >20 // USG > 1.015
Urine >500 mOsm/L // Urine Na Conc < 20
FENa < 1%

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5
Q

Diagnostic Challenge

Post-Renal AKI
is NOT likely without what?

A

complaints of

URINARY FREQUENCY
or
BLADDER FULLNESS

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6
Q

Diagnosisng PRE-RENAL AKI

History & Physical Exam

A

“EASY WAY”

Is the patient HypoVolemic (dry) ?

Low BP // HIGH HR

Dry oral mucosa

Poor Skin Turgor

Dry Underarms

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7
Q

FLUID CHALLENGE

Used for WHAT & how is it done?

A

If OVERT HypoVolemia….

Give bolus fluid +/- start maintenance IV fluids

VVV

if SCr significantly IMPROVES = PRE-RENAL AKI

  • if it does not:*
  • *AKI = likely intrinsic**
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8
Q

FENa of 1-2%
means WHAT?

A
  • EITHER*
  • *Pre-Renal** or Intrinsic

Limitations:
Only Accurate in OLIGURIC AKI (UOP<400-500 mL/d)
will be FALSELY HIGH in patients on Diuretics

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9
Q

FENa of >2%
means WHAT?

A

INTRINSIC
Renal Disease

Limitations:
Only Accurate in _OLIGURIC AK_I (UOP <400-500mL/d)
will be FALSELY HIGH in patients on Diuretics​

if on DIURETICS & >2%** –> **use FEUrea

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10
Q

FENa of <1%
means WHAT?

A

PRE-RENAL AKI

Limitations:
Only Accurate in OLIGURIC AKI​ (UOP <400-500mL/d)
will be FALSELY HIGH in patients on Diuretics​

  • *if FENa is LOW despite being on DIURETICS**
  • *likely PRE-RENAL AKI**
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11
Q

FEUrea of 50-65%%

Means WHAT?
&
When do we use FEUrea?

A

INTRINSIC AKI

Used when taking DIURETICS
because FENA will be FALSELY ELEVATED

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12
Q

FEUrea of <35%

Means WHAT?
&
When do we use FEUrea?

A

PRE-RENAL AKI

Used when taking DIURETICS
because FENa will be FALSELY ELEVATED

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13
Q

Intrinsic Renal Disease

Causes

A

GlomeruloNephropathy = GNs
damage to glomerulus generally due to AUTOIMMUNE disease
since it acts a a filter –> allows PROTEINS –> tubules
Characteristic Finding is PROTEINURIA

Also:
Tubular Nephropathy
Most commonly - ATN (Acute Tubular Necrosis)
also AIN (Acute Interstitial Nephritis)

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14
Q
  • *Nephrotic Range Proteinuria**
  • *Typically Caused by? & range?**
A

Intrinsic AKI from GNs (glomerulonephropathies)

By definition:

  • *Urine Protein** > 3.5 gm/d
  • normal is <80 mg/d for 24 hr sample*

Typically done with:
24 Urine collection (gold standard but difficult)
Random = Spot​
Protein to Creatinine Ratio

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15
Q

Nephrotic Syndome

From what & Features?

A

NOT a disease, but a Group of Signs + Symptoms
seen in patients with
NEPHROTIC RANGE PROTEINURIA (Intinsic AKI)

Hallmark features
FACIAL EDEMA** + **FROTHY URINE

Loss of Antithrombin –> risk of DVTs & PEs
Loss of LMW complements + ABs –> increased risk of INFECTION
Increased:
Cholesterol / LDL / VLDL / TGs

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16
Q

Treatment Approach for GNs
Intrinsic AKI

A

IMMUNOSUPRESSIVE THERAPY

Also, Supportive Therapy for:
Proteinuria / Clots / Edema
+
HYPERlipidemia + HT

17
Q

Treatment for PROTEINURIA

Nephrotic Range Proteinurea –> Intrinsic AKI

A

ACE** or **ARB
may reduce proteinuria by up to 40-50%
also improved with salt restriction
a rise of 10-20% in SCr –> should NOT cause cessation of treatment

Causes:
INDUCED E-fferent Vasodilation
AC-E

18
Q

ACE-I / ARB

MoA for Proteinuria
caused by Glomerulonephopathies = GNs –> Intrinsic AKI

A

Induced E-ferrent VasoDilation
AC-E

Opens up –> Exit Arteries
VVV
Reduction in Arteriolar Pressure
VVV
less Protein Filtration –> INCREASE SCr

19
Q

Which Type of Tubular Nephropathy?

UNCOMMON

AUTOIMMUNE RELATED

Caused by:
DRUG ALLERGY - 75%
or SLE / Sarcoidosis

May present with
STERILEPURIEA
rash / fever / eosinophilia

A

AIN
Acute Interstitial Nephropathy

cause of
INTRINSIC RENAL DISEASE

20
Q

Which Type of Tubular Nephropathy?

Due to:
Prolonged or Severe PRE-RENAL AKI –> ischemia

Results in the:
Necrosis of the tubules –> MUDDY BROWN granular CASTS

A

ATN
Acute Tubular Necrosis
cause of
​INTRINSIC RENAL DISEASE

MOST COMMON CAUSE of AKI

21
Q

Goals + Mangement

of INTRINSIC AKI

A

Goal:
prevent progression of AKI & need for Dialysis

Management:
Removal of cause if possible / known
IMS if autoimmune
Prevent HypoTension & HypoVolemia
AVOID Nephrotoxins

22
Q

EDEMA

Management & Values

A

SODIUM RESTRICTION
to PREVENT edema: < 2gm/d

  • If SIGNIFICANT Edema:*
  • *Sodium Restriction to 1-1.5gm/d**
  • *Loop Diuretis**

Monitor Weight Daily
with goal loss of 1 kg/day

23
Q

Indications for DIALYSIS

Starting dialysis EARLIER
in the course of renal failure
does NOT improve Outcomes

A

A E I O U

Metabolic Acidosis pH <7.1

Electrolytes: K > 6.5 or rapidly rising K

Intoxication

Refractory Fluid Overload

Uremia - ConfUsion

24
Q

Pathogenesis of AKI
from POST-RENAL Obstruction

A

Interstitial Damage to Kidneys

INCREASED RISK of:
UTIs** + **PYELONEPHRITIS

25
Q

Post-Renal Kidney Diseases

A

CALCULI = Kidney Stones
Common in YOUNG ADULTS

Congenital Abnormalities
common in CHILDREN

BPH + Prostate Cancer
older ment

26
Q

2 Sub-Types of Urolithiasis

A

Urolithiasis = Stones that form in URINARY SYSTEM

2 Types:

Nephrolitiasis = stones in KIDNEY

Uretherolithiasis = stones in the URETERS

27
Q

Pathogenesis of Stone Formation

& Composition

A

HIGH RECURRENCE

80% are Calcium Oxalate / Phosphate
Risk factors:
Increased: Calcium / oxylate / phosphate / uric Acid
decreased: urinary CITRATE / urine VOLUME

20% are Uric Acid** or **STRUVITE (Mg+Ammonium Phos)
risk factor is acidic urine
Struvite caused by Chronic UTIs
formed by urease-producing Bacteria (yeast / proteus)

28
Q

Diagnosis of Kidney Stones

A

Imaging Studies
done to dertermine Size & Composition

Stones >10 mm & PROXIMAL (close to kidney) ureteral stones
unlikely to pass spontaneously

Stones <5mm
likely to pass spontaneously

29
Q

Treatment for Kidney Stones

A

If stones are <5 mm –> allow it to pass

HYDRATE
with PO or IV fluids

Pain Control:
NSAIDs or short course of Opiods

  • *Medical Expulsive Therapy = MET**
  • efficacy is conflicting, likely BETTER with a LARGER stone*
  • *TAMSULOSIN**
  • nifedipine - lowers BP*
30
Q

DIETARY PREVENTION
of CALCIUM STONES

A

Increase FLUID intake
target urine volume = 2-2.5 L/day

avoid CALCIUM & VIT-C supplements

avoid DARK colas
they contain phosphoric acid

  • Sodium Restriction*
  • decreases calcium & oxalate xcration*

low protein diet –> increases oxalate production
reduce OXALATE rich food

31
Q

MEDICATIONS
for Prvention of CALCIUM stones

A
  • *Thiazide Diuretics**
  • lowers calcium concentration* in the urine
  • *Potassium Citrate**
  • *Citric acid** binds to Calcium
  • but is MUCH MORE SOLUBLE than Calcium OXALATE / PHOSPHATE*
  • *30-60 mEq/d** to a urine pH of 6.5 (more basic, normally 6.0)

PDAT3 (23 decks)

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