Download Chronic Renal Failure (CRF)

RENAL FAILURE
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Classifications
 Acute
versus chronic
 Pre-renal, renal, post-renal
 Anuric, oliguric, polyuric
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Renal Physiology Review
a.
b.
c.
d.
e.
f.
The Kidneys:
Control the fluid/electrolyte balance for the
body
Remove metabolic wastes from the blood &
excrete them to the outside
Regulate red-blood cell production
Regulate blood-pressure
Important in calcium ion absorption
Control volume, composition and pH of the
blood
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Renal Hormone Regulation
Synthesis and activation of hormones by
the kidney include:
•
Active form of Vitamin D
•
Erythropoietin
Renal blood flow regulated by:
Renin-angiotensin aldosterone system
(RAAS)
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Fluid and Electrolyte Control
Mechanisms
– Renin-Angiotensin Aldosterone
System
 Aldosterone
 ADH – Anti-Diuretic Hormone
 RAAS
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Aldosterone
 Increases
rate of sodium ion absorption
 Chloride moves along with sodium
because of + charge of sodium
 Increases rate of potassium & hydrogen
ion secretion
Result:
Fluid and sodium retention increases bloodpressure
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ACUTE RENAL FAILURE
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Acute Renal Failure
 Definition


The loss of renal function (measured as GFR)
over hours to days
Expressed clinically as the retention of
nitrogenous waste products in the blood
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Acute Renal Failure
 Definitions




Azotemia - the accumulation of nitrogenous
wastes
Uremia - symptomatic renal failure
Oliguria - urine output < 400-500 mL/24 hours
Anuria - urine output < 100 mL/24 hours
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Causes of ARF

Pre-renal =



Intrinsic


vomiting, diarrhea, poor fluid intake, fever, use of
diuretics, and heart failure
cardiac failure, liver dysfunction, or septic shock
Interstitial nephritis, acute glomerulonephritis, tubular
necrosis, ischemia, toxins
Post-renal =



prostatic hypertrophy, cancer of the prostate or cervix, or
retroperitoneal disorders
neurogenic bladder
bilateral renal calculi, papillary necrosis, coagulated
blood, bladder carcinoma, and fungus
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Symptoms of ARF



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
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

Decrease urine output (70%)
Edema, esp. lower extremity
Mental changes
Heart failure
Nausea, vomiting
Pruritus
Anemia
Tachypenic
Cool, pale, moist skin
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Hyperkalemia Symptoms


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

Weakness
Lethargy
Muscle cramps
Paresthesias
Dysrhythmias
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Hyperkalemia Treatment
 Calcium
gluconate (carbonate)
 Sodium Bicarbonate
 Insulin/glucose
 Diuretics (Furosemid)
 Albuterol
 Hemodialysis
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Prerenal Acute Renal Failure

Volume Depletion
 Decreased effective blood volume





congestive heart failure
cirrhosis
nephrotic syndrome
sepsis
Renal vasoconstriction



hepatorenal syndrome
hypercalcemia
nonsteroidal anti-inflammatory drugs
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Prerenal Acute Renal Failure:
Clinical Presentation
 History







volume loss (e.g., diarrhea, acute blood loss)
heart disease
liver disease
evidence of infection
diuretic use
thirst
orthostatic symptoms
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Prerenal Acute Renal Failure:
Clinical Presentation
 Physical



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


Examination
Blood pressure and pulse
Orthostatic changes in blood pressure
Skin turgor
Dryness of mucous membranes and axillae
Neck veins
Cardiopulmonary exam
Peripheral edema
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Prerenal Acute Renal Failure:
Clinical Presentation

BUN:Creatinine ratio


> 20:1
Urine indices

Oliguria
• usually < 500 mL/24 hours; but may be non-oliguric

Elevated urine concentration
• UOsm > 700 mmol/L
• specific gravity > 1.020

Evidence of high renal sodium avidity
• UNa < 20 mmol/L
• FENa < 0.01

Inactive urine sediment
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Fractional Excretion of Sodium
 Etiologies
of a fractional excretion of
sodium <0.01




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

normal renal function
prerenal azotemia
hepatorenal syndrome
early obstructive uropathy
contrast nephropathy
rhabdomyolysis
acute glomerulonephritis
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Treatment of
Prerenal Acute Renal Failure
 Correction
of volume deficits
 Discontinuation of antagonizing
medications


NSAIDs/COX-2 inhibitors
Diuretics
 Optimization
of cardiac function
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Postrenal Acute Renal Failure
 Urinary

tract obstruction
level of obstruction
• upper tract (ureters)
• lower tract (bladder outlet or urethra)

degree of obstruction
• partial
• complete
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Pathophysiology of Renal Failure in
Obstructive Uropathy
 Early


Increased intratubular pressure
Initial increase followed by decrease in renal
plasma flow
 Late


Normal intratubular pressure
Marked decrease in renal plasma flow
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Etiologies of Postrenal
Acute Renal Failure

Upper tract
obstruction

Intrinsic
•
•
•
•

nephrolithiasis
papillary necrosis
blood clot
transitional cell cancer
Extrinsic
• retroperitoneal or pelvic
malignancy
• retroperitoneal fibrosis
• endometriosis
• abdominal aortic
aneurysm

Lower tract
obstruction
• benign prostatic
hypertrophy
• prostate cancer
• transitional cell cancer
• urethral stricture
• bladder stones
• blood clot
• neurogenic bladder
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Postrenal Acute Renal Failure:
Clinical Presentation
 History

Symptoms of bladder outlet obstruction
•
•
•
•
•
•
urinary frequency
urgency
intermittency
hesitancy
nocturia
incomplete voiding
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Postrenal Acute Renal Failure:
Clinical Presentation
 History

Changes in urine volume
• anuria
• polyuria
• fluctuating urine volume
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Flank pain
Hematuria
History of pelvic malignancy
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Postrenal Acute Renal Failure:
Clinical Presentation
 Physical
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Examination
Suprapubic mass
Prostatic enlargement
Pelvic masses
Adenopathy
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Postrenal Acute Renal Failure:
Clinical Evaluation
 Diagnostic



studies
BUN: Creatinine ratio > 20:1
Unremarkable urine sediment
Variable urine chemistries
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Postrenal Acute Renal Failure:
Clinical Evaluation
 Diagnostic

studies
Post-void residual bladder volume
• > 100 mL consistent with voiding dysfunction

Radiologic studies
•
•
•
•
•
Ultrasound
CT scan
Nuclear medicine
Retrograde pyelography
Antegrade nephrostograms
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Treatment of
Postrenal Acute Renal Failure
 Relief

of obstruction
Lower tract obstruction
• bladder catheter

Upper tract obstruction
• ureteral stents
• percutaneous nephrostomies
 Recovery
of renal function dependent
upon duration of obstruction
 Risk of post-obstructive diuresis
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Intrinsic Acute Renal Failure
 Acute
tubular necrosis (ATN)
 Acute interstitial nephritis (AIN)
 Acute glomerulonephritis (AGN)
 Acute vascular syndromes
 Intratubular obstruction
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Acute Tubular Necrosis

Ischemic
• prolonged prerenal
azotemia
• hypotension
• hypovolemic shock
• cardiopulmonary
arrest
• cardiopulmonary
bypass

Sepsis

Nephrotoxic

drug-induced
•
•
•
•
•

radiocontrast agents
aminoglycosides
amphotericin B
cisplatinum
acetaminophen
pigment nephropathy
• hemoglobin
• myoglobin
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Pathophysiology of
Acute Tubular Necrosis
 Mechanisms



of decreased renal function
Vasoconstriction
Tubular obstruction by sloughed debris
Backleak of glomerular filtrate across
denuded tubular basement membrane
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Acute Tubular Necrosis:
Clinical Presentation

History
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Physical examination

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
Acute illness
Exposure to nephrotoxins
Episodes of hypotension
Hemodynamic status
Volume status
Features of associated illness
Laboratory data


BUN:Creatinine ratio < 10:1
Evidence of toxin exposure
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Acute Tubular Necrosis:
Clinical Presentation

Urine indices

Urine volume
• may be oliguric or non-oliguric

Isosthenuric urine concentration
• UOsm  300 mmol/L
• specific gravity  1.010

Evidence of renal sodium wasting
• UNa > 40 mmol/L
• FENa > 0.02

Urine sediment
• tubular epithelial cells
• granular casts
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Acute Tubular Necrosis:
Treatment
 Supportive
therapy
 No specific pharmacologic treatments
 Acute dialysis for:




volume overload
metabolic acidosis
hyperkalemia
uremic syndrome
• pericarditis
• encephalopathy

azotemia
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Prognosis of
Acute Tubular Necrosis

Mortality dependent upon comorbid conditions
 overall mortality ~ 50%
 Recovery of renal function seen in ~ 90% of
patients who survive - although not necessarily
back to prior baseline renal function
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Acute Interstitial Nephritis
 Acute
renal failure due to lymphocytic
infiltration of the interstitium
 Classic triad of



fever
rash
eosinophilia
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Acute Interstitial Nephritis

Drug-induced
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

penicillins
cephalosporins
sulfonamides
rifampin
phenytoin
furosemide
NSAIDs
Malignancy
Idiopathic

Infection-related

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bacterial
viral
rickettsial
tuberculosis
Systemic diseases
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SLE
sarcoidosis
Sjögren’s syndrome
tubulointerstitial nephritis
and uveitis
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Acute Interstitial Nephritis:
Clinical Presentation

History
 preceding illness or drug exposure
 Physical examination
 fever
 rash
 Laboratory Findings
 eosinophilia
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Acute Interstitial Nephritis:
Clinical Presentation

Urine findings
 non-nephrotic protinuria
 hematuria
 pyuria
 WBC casts
 eosinophiluria
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Acute Interstitial Nephritis:
Treatment

Discontinue offending drug
 Treat underlying infection
 Treat systemic illness
 Glucocorticoid therapy may be used in patients
who fail to respond to more conservative therapy
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Acute Glomerulonephritis

Nephritic presentation
 proteinuria
• may be in nephrotic range (> 3 g/day)
hematuria
 RBC casts
 Diagnosis usually requires renal biopsy

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Acute Glomerulonephritis

Etiologies
 poststreptococcal glomerulonephritis
 postinfectious glomerulonephritis
 endocarditis-associated glomerulonephritis
 systemic vasculitis
 thrombotic microangiopathy
• hemolytic-uremic syndrome
• thrombotic thrombocytopenic purpura

rapidly progressive glomerulonephritis
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Acute Vascular Syndromes

Renal artery thromboembolism
 Renal artery dissection
 Renal vein thrombosis

Atheroembolic disease
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Intratubular Obstruction
 Intratubular

crystal deposition
tumor lysis syndrome
• acute urate nephropathy

ethylene glycol toxicity
• calcium oxylate deposition
 Intratubular

protein deposition
multiple myeloma
• -Bence-Jones protein deposition
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Differential Diagnosis of
Acute Renal Failure
 Prerenal
ARF
 Postrenal ARF
 Intrinsic ARF





acute tubular necrosis
acute interstitial nephritis
acute glomerulonephritis
acute vascular syndromes
intratubular obstruction
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Acute Renal Failure:
Diagnostic Evaluation
 Evaluate

for prerenal causes
clinical exam
• blood pressure
• orthostasis




– skin turgor
– mucosal membrane hydration
central venous pressures and cardiac
output
intake/output record
urine sediment
– FENa < 0.01
urine sodium
• UNa < 20 mmol/L

therapeutic trial of volume replacement
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Acute Renal Failure:
Diagnostic Evaluation
 Evaluate


for postrenal causes
bladder catheterization
renal ultrasound
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Acute Renal Failure:
Diagnostic Evaluation
 Evaluation

for intrinsic ARF
clinical history
• medications
• hypotension


– radiocontrast agents
– sepsis
physical exam
urinalysis
• crystals
• paraproteins
– cells
– casts
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Diagnostic Evaluation of ARF
Form of ARF
BUN:Cr UNa (mEq/L) FENa
Urine Sediment
Prerenal
>20:1
<20
< 1%
Normal
Postrenal
>20:1
>20
variable
Normal or RBC’s
ATN
<10:1
>40
> 2%
Muddy brown casts;
tubular epithelial cells
AIN
<20:1
>20
>1%
WBC’s WBC casts,
RBC’s, eosinophils
AGN
variable
<40
<1%
RBC’s, RBC casts
Vascular
variable
>20
variable
Normal or RBC’s
Intrinsic
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Acute Renal Failure:
Management
 Prerenal



ARF
volume repletion
inotropic support
discontinue diuretics
 Postrenal



ARF
bladder catheterization
percutaneous nephrostomy or ureteral stents
fluid management during post-obstructive
diuresis
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Acute Renal Failure:
Management
 Intrinsic

ARF
General supportive care
•
•
•
•
•
•
•
fluid management
diuretics
bicarbonate supplementation
potassium
phosphate
drug dosing
nutrition
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Acute Renal Failure: Management
 Indications




for dialysis
volume overload
metabolic acidosis
hyperkalemia
uremic syndrome
• pericarditis
• encephalopathy

azotemia
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Dialysis Indications
 Refractory
 Metabolic
 Volume
 Mental
hyperkalemia
acidosis
overload
status changes
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CHRONIC RENAL FAILURE
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Pathophysiology of CRF
What is Chronic Renal Failure?
It is progressive tissue destruction with
permanent loss of nephrons and renal
function.
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Risk Factors


Age > 60 years
Race or ethnic background
African-American
Hispanic
American Indian
Asian
 History of exposure to chemicals/toxins
Cigarette smoke
Heavy metals
 Family history of chronic kidney disease
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Chronic vs. Acute Renal Failure

a.
b.

a.
b.
Acute Renal Failure (ARF):
Abrupt onset
Potentially reversible
Chronic Renal Failure (CRF):
Progresses over at least 3 months
Permanent- non-reversible damage to
nephrons
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Pathophysiology of CRF
Progressive destruction of nephrons leads to:
a. Decreased glomerular filtration, tubular
reabsorption & renal hormone regulation
b. Remaining functional nephrons compensate
c. Functional and structural changes occur
d. Inflammatory response triggered
e. Healthy glomeruli so overburdened they
become stiff, sclerotic and necrotic
Lippincott Williams & Wilkins (2005). Pathophysiology A 2-1 reference
for nurses (1st ed.) Ambler, Pa.:Lippincott Williams & Wilkins
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Functional Changes of CRF

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The Kidneys are unable to:
Regulate fluids and electrolytes
Balance fluid volume and renin-angiotensin
system
Control blood pressure
Eliminate nitrogen and other wastes
Synthesize erythropoietin
Regulate serum phosphate and calcium levels
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4 Stages of CRF
1.
2.
3.
4.
Reduced Renal Reserve (Silent): no
symptoms evident- GFR up to 50ml/min
Renal Insufficiency: ½ function of both
kidneys lost- GFR 25-50 ml/min
Renal Failure: GFR 5-25 ml/min
End Stage Renal Disease: GFR less
than 5 ml/min
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Causes of CRF
1)
2)
3)
4)
5)
6)
7)
Diabetic Nephropathy
Hypertension
Vascular Disease
Polycystic Kidney Disease/Genetics
Chronic Inflammation
Obstruction
Glomerular Disorders/
Glomerulonephritis
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SIGNS & SYMPTOMS
Lab Value Cues
1.
2.
3.
Anemia’s - d/t decreased erythropoietin secretion
& uremic toxin damage to RBC’s
Azotemia – (elevated nitrogen) d/t retention of
nitrogenous wastes
Creatinine – a component of muscle & it’s nonprotein waste product. Normally filtered in the
glomerulus & lost in the urine. Glomerular damage
increases reabsorption into the blood. Serum
creatinine 3 x normal shows a 75% loss of renal
function.
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SIGNS & SYMPTOMS
Lab Value Cues
4.
5.
Hypocalcemia – impaired
regulation of Vitamin D
leads to decreased
absorption & low calcium
levels. High phosphorus
levels also cause low
serum calcium levels.
Hyperkalemia – impaired
excretion of potassium by
the kidneys leads to
elevated potassium levels.
6.
7.
Hyperlipidemia –
decreased serum albumin
leads to increased
synthesis of LDL’s &
cholesterol by the liver,
contributing to elevated
lipid levels
Proteinuria – increased
protein filtration d/t
glomeruli damage
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SIGNS & SYMPTOMS
Visual / Verbal Cues
1)
2)
3)
4)
Dry mouth, fatigue,
nausea – d/t
hyponatremia & uremia
Hypertension – d/t
sodium & water
retention
Hypervolemia – d/t
sodium & water
retention
Gray/yellow skin – d/t
accumulated urine
pigments
5)
6)
7)
8)
Cardiac irritability – d/t
hyperkalemia
Muscle cramps – d/t
hypocalcemia
Bone & muscle pain – d/t
hypocalcemia /
hyperphosphatemia
Restless leg syndrome –
d/t toxins’ effects on the
nervous system
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Genetics of Kidney Disease
Genetic diseases that
cause CRF:

Polycystic Kidney
Disease (PKD)

Nephropathic Cystinosis
(Fanconi’s Syndrome)

Alport Syndrome
Sanford, R. (2004). Autosomal dominant polycystic kidney disease.
Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/camgenetics/sanford.htm
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Metabolic Impact
 Hyperlipidemia
common in CRFespecially in Nephrotic Syndrome
 Excessive lipids accelerate progression of
renal disease
 Cholesterol increases glomerular injury
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Contributing Mechanisms
Two known paths of hyperlipidemia
progression in CRF:
 Hyperlipidemia
activates LDL receptors in
mesangial cells
 Increased synthesis of lipoproteins in the
liver related to increased albumin
production
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Albumin Contribution
Normal glomeruli structure limits proteins from filtering
through the urine

Progression of glomeruli injury leads to increased
capillary filtration of albumin
 The liver compensates and increases albumin
production - to replace albumin lost in urine
 This leads to increased synthesis of lipoproteins by the
liver secondary to the compensatory increase in albumin
production.
 Results in increased LDL levels – predisposing to
atherosclerosis
 Atherosclerosis further increases glomeruli injury
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Inflammation
 Inflammatory
response can be triggered
by: tissue injury, infections, toxins, immune
responses and/or Angiotensin II
 Can be acute or chronic
 Can affect the renal pelvis and interstitial
tissue as in pyelonephritis
 Can affect the glomeruli as in
glomerulonephritis
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Inflammation- (Cont.)
Renal Failure- prolongs inflammatory reactions
 Adverse effects of chronic inflammation=
Decreased appetite
Muscle and fat wasting
Endothelial damage
Atherosclerosis
Hypoalbuminemia
Increased cardiovascular disease risk
Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50
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Causes of Inflammation
in CRF
 Infection
 Anemia
– increases oxidation of proteins,
lipids & carbohydrates, leading to vascular
inflammation
 Malnutrition – decreases antioxidants
 Low serum albumin – decreases
antioxidants
 Uremia
Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50
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Angiotensin II in the
Inflammatory Process
Inflammatory mediator causing:
•
•
•
Increased vascular permeability
Increased leukocyte infiltration
(monocytes, macrophages)
Cell proliferation & hypertrophy
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Glomerular Inflammatory
Disorders
Reminder:
The glomeruli filter blood & form urine filtrate. The
selectively permeable, capillary membrane
allows H2O and small particles (i.e. glucose) to
leave the capillary membrane. Large particles
(i.e. proteins & blood cells) stay in the blood.
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Nephrotic vs. Nephritic
Syndromes
 Nephrotic
Syndromes - glomerular
disorders that affect the glomerular
capillary membrane & increases
permeability to plasma proteins
 Nephritic Syndromes – glomerular
disorders that initiate the inflammatory
response within the glomeruli & initially
decreases permeability of the membrane
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Nephritic Syndromes
Glomerulonephritis
• An inflammatory response in the endothelial,
epithelial & mesangial cells of the glomeruli
• Inflammatory process damages the capillary
wall-allowing RBCs into the urine
Symptoms:
• 1st oliguria, followed by hematuria, azotemia,
low GFR (d/t hemodynamic changes),
hypertension
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Nephrotic Syndromes
Primary causes:
 Lipoid Nephrosis
 Focal Segmental
glomerulosclerosis
 Membranous
glomerulonephritis
Secondary causes:
 Diabetes Mellitus
 SLE
 Amyloidosis
Characterized by:
 Proteinuria > 3.5g/day
 Lipiduria
 Hypoalbuminemia
 Hyperlipidemia
Increased permeability of
glomerular membrane
allows proteins to escape
into the filtrate
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Chronic Glomerulonephritis






A slow, progressive disease that can be caused
by primary ( Nephrotic & Nephritic Syndromes)
or secondary disorders ( SLE, Good pasture's)
Typically develops asymptomatically over many
years
Hypertension, proteinuria and hematuria
exhibited with progression of disease
Late stages display uremic symptoms of
azotemia, nausea, vomiting, dyspnea and
pruritis
Leads to CRF
Treatment includes: control of hypertension,
control of fluid/electrolyte imbalances, reduce
edema, prevent heart failure
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Pharmacology in CRF
Pharmacokinetics –
drug absorption, distribution, metabolism &
excretion
Pharmacodynamics –
A drug’s mechanism of action and effect at
the target site
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Alterations in Drug Responses in
CRF

Gastrointestinal impairments affect absorption of
medications
 Volume of distribution (Vd) – the availability of a
drug distributed in body tissues is increased or
decreased by alterations in body composition or
protein binding
 Metabolism of medications altered -the kidneys
produce many enzymes involved in drug
metabolism including cytochrome P-450
 Decreased glomerular filtration rate affects drug
excretion
Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.
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Medication Considerations in
CRF
Dilantin – increased Vd related to protein binding
changes and low albumin, increasing risk of
drug toxicity
 Digoxin – increased Vd leading to toxicity due to
decreased renal excretion
 Insulin – metabolism of insulin decreases,
requiring dose reduction
 Tylenol and procainamide – liver metabolized
drugs with metabolites that are excreted renally,
can accumulate leading to drug toxicity

Campoy, S, Elwell, R.(2005). Pharmacology &
CKD. AJN, 105(9),60-72.
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Medication Considerations
(Cont.)
Impaired renal excretion leads to toxic drug accumulations
with:
Aminoglycoside antibiotics (tobramycin & gentamycin)
Atenolol
AIEC
Lithium
Vancomycin
Metformin
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Over-the-Counter Medications
and CRF
NSAIDS – inhibit prostaglandins decreasing GFR
and reduced sodium excretion
Antacids and laxatives (containing magnesium &
aluminum) – causes mineral accumulation and
metabolic complications
Campoy, S, Elwell, R.(2005). Pharmacology & CKD.
AJN, 105(9),60-72.
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Acute Problems in CRF
 Relating
to underlying disease
 Relating to ESRD
 Dialysis related problems
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Problems Related to ESRD
– K/Ca
 Volume overload
 Anemia, platelet disorder, GI bleed
 HTN, pericarditis
 Peripheral neuropathy, dialysis dementia
 Abnormal immune function
 Metabolic
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Dialysis
½
of patients with CRF eventually require
dialysis
 Diffuse harmful waste out of body
 Control BP
 Keep safe level of chemicals in body
 2 types


Hemodialysis
Peritoneal dialysis
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Hemodialysis
 3-4
times a week
 Takes 2-4 hours
 Machine filters
blood and
returns it to
body
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Types of Access

Temporary site
 AV fistula



Surgeon constructs by combining an artery and a vein
3 to 6 months to mature
AV graft


Man-made tube inserted by a surgeon to connect
artery and vein
2 to 6 weeks to mature
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What This Means
 No
BP on same arm as fistula
 Protect arm from injury
 Control obvious hemorrhage


Bleeding will be arterial
Maintain direct pressure
 No
IV on same arm as fistula
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Access Problems
 AV
graft thrombosis
 AV fistula or graft bleeding
 AV graft infection
 Steal Phenomenon


Early post-op
Ischemic distally
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Peritoneal Dialysis
 Abdominal
3



lining filters blood
types
Continuous ambulatory
Continuous cyclical
Intermittent
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Dialysis Related Problems
 Lightheaded
–give fluids
 Hypotension
 Dysrhythmias
 Disequilibration



Syndrome
At end of early sessions
Confusion, tremor,
Due to decrease concentration of blood
versus brain leading to cerebral edema
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