8-1: 10/13: Renal Perfusion/acute Kidney Injury

Front 1

Post-Renal AKI:
Definition
Causes

Back 1

Obstructive uropathy; interruption of urine outflow

Causes:
Children: congenital
Males: Prostate disorder
Females: Gynecological tumors

Front 2

Post-Renal Obstruction:
Partial vs Complete Obstruction

Back 2

Partial:
Continued filtration and preservation of GFR due to PGs (vasodilation of afferent arteriole)
If prolonged and high grade (>4-5hrs): Thromboxane (vasoconstriction)-->Decline in GFR

Complete obstruction:
Filtration continues initially
Increased tubular pressure
Cessation of filtration-->Anuria

Front 3

What post-renal changes are required for a decline in GFR?

Back 3

Blockage of BOTH kidneys

Severity of decline depends on duration of blockage and degree of obstruction

Front 4

______ present with post-renal obstruction is a medical emergency.

Back 4

Infection

Front 5

Post-Renal AKI:
Treatment
Complications

Back 5

Relieve obstruction at site of blockate (foley--bladder outlet obstruction, nephrostomy tube--ureter, ureteral stent--ureter, ureteropelvic junction)

Replace fluid losses if pt has large volume diuresis (polyuria due to loss of tubular concentrating ability)

Complications:
Distal tubular injury:
Post-obstructive diuresis (impaired Na+ reabsorption, insensitive to ADH)
Inability to excrete H+ (normal AG metabolic acidosis)

Front 6

What is the degree of recovery expected in a patient with post-renal obstruction? Provide answers by DURATION of obstruction.

Back 6

<2 weeks: Complete recovery
Up to 3 mos: Residual impairment
>3 months: No recovery

Front 7

What ultrasound finding indicates a poorer prognosis in patients with post-renal AKI?

Back 7

Thin renal cortex

Front 8

Pre-Renal AKI:
Definition
Causes

Back 8

No intrinsic renal pathology

Decline in GFR due to poor blood flow through kidneys

Causes:
Volume depletion
Systemic decline in renal perfusion
Selective decline in renal perfusion

Front 9

Systemic Hypoperfusion

Back 9

Hypotension in setting of shock (sepsis, anaphylaxis)
CHF
Cirrhosis (hepatorenal syndrome, decreased intravascular volume)

Front 10

Hepatorenal Syndrome

Back 10

Decreased intravascular volume due to poor oncotic pressure; results in poor renal perfusion in otherwise normal kidney (dec GFR)

Poor perfusion despite volume repletion bc splanchnic vasodilation due to low systemic vascular resistance (blood diverted away from kidneys)

Front 11

Selective Renal Hypoperfusion

Back 11

Afferent arteriolar vasoconstriction (NSAIDs)

Efferent arteriolar dilatation (ACEI, ARBs)

Front 12

Effects of Renal Artery Stenosis

What medicines should be avoided in its treatment?

Back 12

Not AKI, this is a chronic process

Results in chronically constricted efferent arteriole; ARF induced in setting of ACEI or ARB administration

Front 13

Pre-Renal AKI:
Treatment
Prognosis

Back 13

Tx: removal or treatment of inciting event

EXCELLENT PROGNOSIS (unless can't make precipitating event go away, e.g., cirrhosis)

Front 14

Intrinsic Renal Disease:
Definition
Causes

Back 14

Renal parenchymal dz
Renal failure due to pathology of any portion of filtering unit (vascular dz, glomerular dz, interstitial inflammn, tubular dz: ischemic or toxic insult)

Cause:
Most common = ACUTE TUBULAR NECROSIS
Others: vasculitis, GN, interstitial nephritis

Front 15

Why are renal tubules so prone to ischemic injury? Which region of the kidney is most susceptible?

Back 15

Medulla is hypoxic and prone to ischemia due to hairpin loop structure

Ascending LOH most susceptible to ischemia

Also affected by reperfusion injury (Ca2+, oxygen radicals_

Front 16

Why are the kidney tubules so prone to toxic injury?

What substances cause tubular necrosis?

Back 16

Tubular cells are exposed to drugs/toxin levels far exceeding plasma levels:

20% of CO allocated to kidney; high renal blood flow-->inc'd exposure to drugs/toxin

High intracellular and intraluminal concentrations

Toxic injury substances:
Aminoglycoside abx
Heme pigments (Hg, myoglobin)
Cis platinum
IV contrast dye

Front 17

In intrinsic AKI:
Mechanisms of GFR reduction
Mechanisms of Tubular Obstruction

Back 17

GFR reduction: tubular injury, but intact glomerulus

Tubular obstruction:
Accumulation of damaged membrane fragments and cast formation

Front 18

How does back leak of glomerular filtrate occur?

Back 18

In intrinsic AKI, injured tubules are no longer impermeable to filtrate and allow indiscriminate reabsorption of filtered substances; results in minimal clearance

Front 19

Risk factors for intrinsic AKI.

Back 19

**DM
**Cirrhosis
Chronic Kidney Dz
Heart Surgery (hypoperfusion)
IV contrast dye

Front 20

Intrinsic AKI:
Prognosis

Back 20

50% mortality

Recovery usually occurs w/resoln of primary illness

Not a risk factor for chronic kidney dz

Most have COMPLETE recovery

Poorer prognosis with repeated insults of poor systemic hemodynamics; with pts with persistent oliguria (low urine output)

Front 21

Acute Interstitial Nephritis:
Causes
Onset
Presentation
Lab Findings

Back 21

Causes:
Infections
Medications (most common cause): cephalosporins, PCNs; NSAIDS including COX-2 inhibitors (celecoxib), diuretics

Onset:
2-3 weeks (rapid onset with allergic reaction; delayed onset--months--with diuretics, NSAIDs)
Not dose dependent; recurrent with re-exposure

Presentation: Fever, constitutional syx, rash

Lab:
Eosinophilia, eosinophilURIA, WBC casts and WBCs in urine
(mild proteinuria)

Front 22

Acute Interstitial Nephritis:
Treatment
Prognosis

Back 22

Tx: Withdrawal of medication, treatment of underlying cause, corticosteroid therapy

Most recover after cessation of medication

Front 23

Nephrotic vs Nephritic Syndrome:
Physical exam and lab findings

Back 23

Nephrotic:
>3g proteinuria daily
Hypoalbuminemia
Edema

Nephritic:
Hematuria
HTN (hypervolemia)
Azotemia

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Front 29

Causes of glomerular disease with low complement. Provide primary and secondary causes.

Back 29

Low complement:
Primary Renal Dz: Membranoprolif GN

Systemic/Secondary:
These are all immune mediated:

Post Strep/Infectious GN
Lupus Nephritis
Hep B/C related GN
Cryoglobulinemia

Front 30

Causes of glomerular disease with normal complement. Provide primary and secondary causes.

Back 30

Primary: AntiGBM dz, Minimal Change Dz, IgA nephropathy

Secondary:
These are all systemic dz's w/glomerular dz:
Goodpastures, Microscopic polyangitis, HIC assoc nephropathy

Front 31

Formula for fractional excretion of substance X.

Back 31

FEx = Clx/GFR x 100%
= (Ux/Px)/(Ucr/Pcr) x 100%

Front 32

Pre-Renal vs Intrinsic Renal Disease:
BUN/Cr Ratio
Uosm
Urinary Na
FE Na
Urinalysis

Back 32

Pre-Renal; Renal
BUN/Cr: 20:1; 10-15:1
Uosm: >500; <350
Urinary Na: <10-20; >40
FE Na: <1%; >2%
Urinarlysis: Normal; ATN: muddy brown granular casts, tubular epithelial cells, AIN: WBC casts, GN: RBC casts, dysmorphic RBCs

Front 33

Complications of AKI

Back 33

Volume overload
Hyperkalemia
Metabolic Acidosis
Uremia
Hypocal, Hyperphos

Front 34

Low urine sodium is indicative of ______-renal injury.

Back 34

Pre-renal

Front 35

Calculate FeNa for:
Urine Na: 10
Serum Na: 140

Urine Cr: 20
Serum Cr: 2.0

Is this pre-renal or intrinsic-renal?

Back 35

FeNa = (UNa/PNa)/(UCr/PCr)x100%
=(10/140)/(20/2.0)x100%
=0.7%

This is pre-renal (<1%)

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