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Renal II: Renal Failure and Bladder Function

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His medical history was notable for recurrent pyelonephritis on the right side. ... blockage, or a risk of kidney damage, a stone should always be removed. – PowerPoint PPT presentation

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Title: Renal II: Renal Failure and Bladder Function


1
Renal Pathophysiology and Bladder Dysfunction
2
Clinical Assessment of Renal Function
3
Clinical Assessment of Renal Function
  • Glomerular Filtration Rate
  • Blood urea nitrogen
  • Serum creatinine
  • Creatinine clearance
  • Renal Tubular Function and Integrity
  • Urine Concentrating Ability
  • Proteinuria
  • Urinary Sodium Excretion

4
Clearance
5
Clearance
  • An imaginary quantity
  • Physical there is no such thing as clearance
  • Normally performed as a 24-hour urine collection
  • The clearance of a solute - the virtual volume
    of blood that would be totally cleared of a
    solute in a given time.
  • The rate at which the kidneys excrete solute into
    urine rate at which solute disappears from
    blood plasma.
  • Solutes come from the blood perfusing the
    kidneys.
  • For solute X

Conc. of X in urine
Volume of urine formed in given time
?
Cx Ux x V
Conc. of X in systemic blood plasma
Px
Clearance
6
Measurement of GFR
7
Measurement of GFR
  • GFR is also assessed using principles of
    clearance.
  • As the solute, we use creatinine because all of
    the creatinine that is filtered ends up in the
    urine and none of it is reabsorbed
  • GFR - volume of fluid filtered into Bowmans
    capsule per unit time.
  • Same equation, GFR is Cx if X has certain
    required properties (i.e. Ccreatinine).

Conc. of X in urine
Volume of urine formed in given time
?
GFR Ux x V
Conc. of X in systemic blood plasma
Glomerular filtration rate
Px
8
Clinical Assessment of Renal Function Metabolism
of Blood Urea Nitrogen (BUN)
9
Clinical Assessment of Renal Function Metabolism
of Blood Urea Nitrogen (BUN)
  • Major nitrogenous end product of protein and
    amino acid catabolism
  • Produced by liver and distributed throughout
    intracellular and extracellular fluid
  • In kidneys almost all urea is filtered out of
    blood by glomerular function. Some urea
    reabsorbed with water (50) but most is removed
    in urine

10
Increased BUN
11
Increased BUN
  • Dehydration
  • There is a lack of fluid volume to excrete waste
    products
  • High protein diet
  • GI bleed
  • Equivalent to a high protein diet because there
    are a lot of red blood cells
  • Digested blood is a source of urea
  • Anabolic Steroid use
  • Impaired renal function
  • The kidneys are less able to clear urea from the
    bloodstream
  • CHF - poor renal perfusion
  • Shock
  • MI
  • Excess protein catabolism

12
Decreased BUN
13
Decreased BUN
  • Fluid excess - especially a concern with IV
    fluids
  • SIADH
  • Excess water is retained in the bloodstream
    inappropriately
  • Trauma, surgery, opioids,
  • Liver failure
  • Urea is synthesized by the liver so liver
    problems lead to decreased synthesis
  • If the liver is not working well, ammonia is high
  • Malnutrition
  • Anabolic steroid use
  • Pregnancy - dilutional effects of having a
    higher blood volume

14
BUN Bottom Line
15
BUN Bottom Line
  • Bottom line BUN is not really a good indicator
    of renal function since many other things can
    influence its levels.
  • Multiple variables can interfere with the
    interpretation of a BUN value
  • GFR and creatinine clearance are more accurate
    markers of kidney function.
  • Age, sex, and weight will alter the "normal"
    range for each individual, including race.
  • In renal failure or chronic kidney disease (CKD),
    BUN will only be elevated outside "normal" when
    more than 60 of kidney cells are no longer
    functioning.
  • More accurate measures of renal function are
    generally preferred to assess the clearance for
    purposes of medication dosing.

16
Serum Creatinine
17
Serum Creatinine
  • Normal values
  • Men  0.8-1.3 mg/dL
  • Women 0.6-1.0 mg/dL
  •  
  •  
  •  

18
Creatinine Metabolism
19
Creatinine Metabolism
  • Creatinine is a waste product of creatine
    phosphate metabolism by skeletal muscle tissue. 
  • The amount of muscle that a person has is
    proportional to muscle mass.

20
Increased Creatinine
21
Increased Creatinine
  • Occurs only with a loss of more than 50 of
    nephrons
  • Impaired renal function
  • Chronic nephritis
  • Urinary tract obstruction
  • Muscle diseases such as gigantism, acromegaly,
    and myasthenia gravis because there are issues
    with muscles breaking down and releasing a lot of
    creatinine
  • Congestive heart failure
  • Shock

22
Decreased Creatinine
23
Decreased Creatinine
  • Elderly
  • Persons with small stature, decreased muscle mass
  • Inadequate dietary protein
  • Muscle atrophy

24
Serum Creatinine Bottom Line
25
Serum Creatinine Bottom Line
  • Serum creatinine measurements are a good first
    approximation of renal function. It is better
    than BUN but is not as good as creatinine
    clearance

26
Creatinine Clearance Test
27
Creatinine Clearance Test
  • Normal values
  • 110-115 mL/min
  •  
  • Creatinine clearance - the total amount of
    creatinine excreted in urine in a 24 hour period
  • Creatinine is excreted entirely by the kidneys
    and is not reabsorbed in the tubules.
  • Therefore, it is directly proportional to the
    glomerular filtration rate (GFR). 
  • So clinically it can be seen as a measure of
    GFR. 

28
Changes in Creatinine Clearance
29
Changes in Creatinine Clearance
  • With unilateral kidney disease or nephrectomy, a
    decreased creatinine clearance is NOT expected if
    the other kidney is normal
  • During renal failure, diminished glomerular
    filtration occurs
  • Increases the retention of creatinine in the
    serum.
  • When chronic renal failure and uremia becomes
    very severe, an eventual reduction occurs in the
    excretion of creatinine by both the glomeruli and
    the tubules.
  • Bottom line Creatinine clearance is the gold
    standard measurement of renal function because
    it is a measure of the GFR.

30
Assessment of Renal Tubular Function and Integrity
31
Assessment of Renal Tubular Function and Integrity
  • The tubules are responsible for urine
    concentration
  • Resorb a lot of solutes and a lot of water
  • Does this to control the ECF, not to produce
    urine
  • Urine specific gravity 1.003-1.030

32
Factors that Can Influence the Concentration
Gradient
33
Factors that Can Influence the Concentration
Gradient
  • 1) Decreased sodium absorption
  • Chronic polyuria (e.g. diabetes insipidus,
    diabetes mellitus)
  • Altered sodium resorption (e.g. Addison's
    disease).
  • 2) Lack of ADH
  • ADH increases the permeability of the tubules to
    water and urea
  • A lack of ADH decreases the permeability of the
    tubules
  • Hypokalemia
  • Hypercalcemia
  • 3) Increased medullary blood flow
  • Causes medullary solute washout, because the vasa
    recta is critical in maintaining the medullary
    interstitial gradient
  • Hypokalemia
  • Hypercalcemia
  • Thyroid hormone

34
Assessment of Glomerular Function and Integrity
35
Assessment of Glomerular Function and Integrity
  • Proteinuria- protein in the urine
  • Types
  • Transient
  • Orthostatic
  • Persistent

36
Transient Proteinuria
37
Transient Proteinuria
  • Transient- resolves with treatment of underlying
    condition
  • May occur with fever, CHF, seizure, exercise
  • This is of no consequence
  • Single tests need to be repeated to verify
    findings

38
Orthostatic Proteinuria
39
Orthostatic Proteinuria
  • Not associated with deteriorating renal function.
  • Increased protein excretion in the upright
    position and normal protein excretion in the
    supine position

40
Persistent Proteinuria
41
Persistent Proteinuria
  • Persistent- indicates significant renal disease
  • Glomerular- alterations in basement membrane
    filtration
  • Due to increased filtration of albumin and other
    macromolecules across the glomerular basement
    membrane
  • Occurs because of an alteration in the charge
    selectivity and size selectivity of the
    glomerular barrier
  • Tubular- impairment of tubular reabsorption
    (amino acid nuria)

42
Types of Dysfunctions that Cause Renal Disease
43
  • Types of Dysfunctions that Cause Renal Disease
  • First question when you have a patient with renal
    problems
  • Pre-renal
  • Intra-renal (Intrinsic)
  • Post-renal

44
Pre-Renal Dysfunction
45
Pre-Renal Dysfunction
  • Decreased blood flow to kidney (most common form)
  • If the kidney does not get enough blood, it
    cannot function properly
  • Causes
  • Hemorrhage
  • ? Cardiac Output (CO)
  • Dehydration
  • Loss of fluids
  • Shock

46
Intra-Renal Dysfunction
47
Intra-Renal Dysfunction
  • Disorders that disrupt the structures of the
    kidney
  • Causes
  • Ischemia
  • Drugs
  • Glomerular disease
  • Intratubular obstruction
  • Toxins from infection

48
Post-Renal Dysfunction
49
Post-Renal Dysfunction
  • Disorders that impair urine outflow from the
    kidneys
  • Ureteral obstruction
  • Obstruction of the ureters or the urethra

50
Pre-renal Causes of Kidney Dysfunction
51
Pre-renal Causes of Kidney Dysfunction
  • Kidneys receive 25 of CO to filter blood they
    regulate fluids and electrolytes.
  • ?Renal Blood Flow (RBF) ?
  • ? Glomerular Filtration Rate (GFR) ? ? urine
    output (u/o)
  • ?RBF ? ?02 delivery to tubular cells ? cell death
  • The glomeruls efferent arteriole leads to another
    capillary bed that nourishes the tubule
  • ?RBF ? ? GFR, ? filtration of substances,
    ?substances in blood ???Cr, ?BUN

52
Intrinsic Causes of Renal Dysfunction
53
Intrinsic Causes of Renal Dysfunction
  • Conditions that cause damage to structures within
    kidney
  • glomeruli, interstitium, tubules
  • Injury to tubules most common
  • Injury to glomeruli

54
Intrinsic Causes of Renal Dysfunction Injury to
Tubules
55
Intrinsic Causes of Renal Dysfunction Injury to
Tubules
  • Ischemia
  • Toxic insult (drugs)
  • Obstruction

56
Intrinsic Causes of Renal Dysfunction Injury to
Glomeruli
57
Intrinsic Causes of Renal Dysfunction Injury to
Glomeruli
  • Diabetes
  • The most common cause of glomerular disease
  • Autoimmune disease

58
Immune Mechanisms of Glomerular Disease
59
Immune Mechanisms of Glomerular Disease
Antigens Exogenous or endogenous to the
kidney. Immune complexes set up intense
inflammation that damages the BM.
Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 550
60
Anti-Glomerular Membrane Antibodies
61
Anti-Glomerular Membrane Antibodies
  • Antiglomerular antibodies leave circulation,
    react with antigens present in BM of glomerulus.
  • Autoantibodies react to structures of the
    glomerulus, most commonly the basement membrane

62
Circulating Antigen-Antibody Complex Deposition
63
Circulating Antigen-Antibody Complex Deposition
  • Antigen-antibody complexes circulating in
    blood become trapped as they are filtered in
    glomerulus.
  • Circulating immune complexes are bound to an
    antigen
  • Because they are bound to antigen, they have the
    capability of evoking an immune response
  • Clogged up and lodge in the kidney, leading to an
    inflammatory response in the glomeruls

64
End Result of the Immune Mechanisms of Glomerular
Disease
65
End Result of the Immune Mechanisms of Glomerular
Disease
  • The end result is the same...the only difference
    is the location of the antigen
  • Left part of the kidney, right can be anywhere,
    circulating
  • The commonality is that inflammation occurs,
    damaging the basement of the glomerulus

66
Intrinsic Glomerular Disorders
67
Intrinsic Glomerular Disorders
  • Glomerular disorders affect glomerular capillary
    structures that filter material from the blood.
  • Nephritic syndromes
  • Nephrotic syndromes

68
Nephritic Syndromes
69
Nephritic Syndromes
  • Nephritic syndromes are caused by diseases that
    produce proliferative inflammatory responses that
    decrease the permeability of the capillary
    membrane.
  • This is usually because the membrane thickens

70
Nephrotic Syndromes
71
Nephrotic Syndromes
  • The nephrotic syndrome is caused by disorders
    that increase the permeability of the glomerular
    capillary membrane, causing massive loss of
    protein in the urine.
  • This makes the membrane too porous
  • Disorders may be nephritic and then nephrotic or
    nephrotic and then nephritic

72
Acute Proliferative Glomerulonephritis
73
Acute Proliferative Glomerulonephritis
Hematuria Proteinuria RBC Casts shape of the
tubule because so many rbcs were in the tubule
nephrotic syndrome
Infection with streptococci
Edema Hypertension, HF Encephalopathy Renal
Failure
Immune complexes/antigens glom onto the strep,
creating circulating complexes that become
entrapped in the glomerular membrane
Oliguria, Na and H2O retention Hypervolemia
nephritic syndrome
Activation of complement Recruitment of leukocytes
Inflammation and Swelling Of capillary membrane
74
Other Nephritic Syndromes
75
Other Nephritic Syndromes
  • Rapidly Progressive Glomerulonephritis
  • IgA Nephropathy (i.e. Buerger disease)
  • As nephritic syndromes worsen, they may progress
    to nephrotic syndromes and vice versa.

76
Rapidly Progressive Glomerulonephritis
77
Rapidly Progressive Glomerulonephritis
  • Caused by a number of immunologic disorders
  • Systemic lupus erythematosis
  • Goodpasture syndrome
  • The antibody-antigen complex leads to
    inflammation, which then destroys the glomerulus

78
IgA Nephropathy (i.e. Buerger disease)
79
IgA Nephropathy (i.e. Buerger disease)
  • Deposition of IgA immune complexes in mesangium

80
Symptoms of Nephrotic Syndromes
81
Symptoms of Nephrotic Syndromes
  • Proteinuria
  • Lipiduria
  • Hypoalbuminemia
  • Edema
  • Hyperlipidemia
  • The hallmark of a nephrotic syndrome is
    proteinuria
  • When proteins pass into the urine, their
    concentration decreases in the blood, leading to
    edema
  • This is because there is not enough osmotic
    pressure pulling the fluid back into the venous
    capillary

82
Nephrotic Disorders
83
Nephrotic Disorders
  • Membranous Glomerulonephritis
  • Thickening of GBM due to immune complexes
  • Minimal Change Disease (Lipoid Nephrosis)
  • Diffuse loss of foot processes from the
    epithelial layer of the glomerular membrane.
  • Focal Segmental Glomerulosclerosis
  • Sclerosis of some glomeruli. (Alonzo Mourning)

84
Diabetic Nephropathy
85
Diabetic Nephropathy
Hyperglycemia
Hyperfiltration Hyperperfusion
Microalbuminuria
Increased messangial cell matrix production
hypertrophy
GBM thickens
Glomerular sclerosis
Renal Failure
86
Diabetic Nephropathy Description
87
Diabetic Nephropathy Description
  • Diabetes damages the basement membrane because of
    the high glucose
  • Glucose can attach itself to proteins
  • One of the first signs is microalbuminuria caused
    by increased permeability of the basement
    membrane
  • This is an increase in GFR
  • Can test the urine for small amounts of albumin
  • Treat this by putting them on an ACE inhibitor in
    order to retard the nephropathy
  • Then GBM thickens, leading to renal failure
  • Occurs when the kidney leaks small amounts of
    albumin into the urine
  • In other words, when there is an abnormally high
    permeability for albumin in the renal glomerulus.
  • An important prognostic marker for kidney disease
    in diabetes mellitus

88
Hypertensive Glomerular Disease
89
Hypertensive Glomerular Disease
  • Hypertension is a cause and effect of kidney
    disease
  • Everyone with renal failure has hypertension
  • ? glomerular structure (sclerosis) ? thick vessel
    walls ? ? perfusion of the nephron ? ?BUN and
    proteinuria
  • BUT as RBF declines, the kidney secretes renin,
    activating the RAAS, thereby raising BP further.

90
Hypertension and the Kidneys
91
Hypertension and the Kidneys
  • Hypertension causes renal failure
  • High pressure on the glomerulus causes it to
    thicken, which decreases perfusion of the nephron
    and increases the BUN
  • Because the glomerulus is damaged, there will be
    proteinuria
  • Kidney senses damage and secretes renin
  • Creates angiotensin II, which raises the blood
    pressure
  • May restore renal blood flow for a while but then
    destroys the kidney further as well
  • The RAAS will become more active and lead to
    higher blood pressure

92
Intratubular Obstruction
93
Intratubular Obstruction
  • Myoglobin
  • Hemoglobin
  • Large amounts of uric acid or protein

94
Myoglobin
95
Myoglobin
  • Myoglobin stores oxygen for the skeletal muscle
    to use
  • Rhabdomyolosis leads to liberation of the
    myoglobin, which will clog up the tubules
  • Skeletal muscle breakdown from trauma, exertion,
    hyperthermia, prolonged seizures, statins and
    fibrin derivatives.

96
Hemoglobin
97
Hemoglobin
  • Hemolysis, including blood transfusion reactions,
    liberates the hemoglobin and causes tubular
    obstruction

98
Large Amounts of Uric Acid or Protein
99
Large Amounts of Uric Acid or Protein
  • Widespread cancer, such as leukemia and multiple
    myeloma
  • Massive tumor destruction with chemotherapy
    liberates all of the contents of the blood cells
    into the blood
  • Radiation (tumor lysis syndrome)

100
Postrenal Causes of Renal Failure
101
Postrenal Causes of Renal Failure
  • Obstruction of urine outflow from kidneys
  • Ureters
  • Calculi, strictures
  • Bladder
  • Tumors, neurogenic bladder
  • Urethra
  • Prostatic hypertrophy may lead to urine backing
    up into the kidneys
  • Strictures

Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 540
102
Mechanisms of Renal Damage Due to Obstruction
103
Mechanisms of Renal Damage Due to Obstruction
  • For the post-renal causes and pre-renal causes,
    if you reverse the cause pretty quickly, the
    kidney can get back to normal fairly quickly
  • Kidney damage depends on
  • Degree of obstruction
  • Partial vs. complete unilateral vs. bilateral
  • Duration of the obstruction

104
Most Damaging Effects of Obstruction
105
Most Damaging Effects of Obstruction
  • Stasis of urine, bacteria ascend urethra?
    infection, stone formation
  • Development of back pressure ?Decreased renal
    blood flow, destroys kidney tissue

106
Obstruction Diagram
107
Hydronephrosis is distention (dilation) of the
kidney with urine, caused by backward pressure on
the kidney when the flow of urine is obstructed.
  • Marked/complete obstruction ? ? back pressure due
    to continued glomerular filtration, impedance to
    urine flow
  • Hydroureter
  • Obstruction in distal ureter ? ? pressure above
    it ? dilation of ureter
  • Hydronephrosis
  • Urine-filled dilatation of renal pelvis

Merck Manual
The panels show the right and left kidneys of a
patient. Note the dilated pelvis and calyces on
the right compared to the left. A tumor caused
an outflow obstruction on the right, resulting in
hydronephrosis.
108
Manifestations of Obstruction
109
Manifestations of Obstruction
  • Pain
  • Usually the reason for seeking medical care
  • Result of distention of bladder, collecting
    system, renal capsule.
  • Signs of urinary tract infection

110
Nephrolithiasis
111
Nephrolithiasis
  • The fancy name for kidney stones
  • Crystalline structures made up of materials the
    kidney normally excretes in urine
  • The etiology of stone formation is complex and
    not well understood
  • Usually people who get one stone usually get
    multiple ones
  • ? Why usually unilateral?
  • ? Urine is saturated with stone components?
  • Calcium salts, Magnesium-ammonium phosphate,
    cystine, uric acid
  • ? Organic materials produced by epithelial cells?
  • ? Lack of proteins that inhibit crystallization?

112
Stones
113
Stones
  • Calcium oxalate, calcium phosphate
  • Associated with hypercalcemia
  • Hyperparathyroidism
  • Vitamin D intoxication
  • Diffuse bone disease
  • Immobility
  • Renal tubular acidosis will favor stone formation

114
A 58-year-old man presented with a 1 year history
of dysuria
115
A 58-year-old man presented with a 1 year history
of dysuria
Rajaian S and Kekre N. N Engl J Med 20093611486
Rajaian S and Kekre N. N Engl J Med 20093611486
116
Manifestations of Stones
117
Manifestations of Stones
  • Renal Colic
  • Noncolicky Renal Pain

118
Renal Colic
119
Renal Colic
  • Stretching of the collecting system/ureter.
  • Stones (1-5mm) move into ureter, obstruct flow.
  • Acute, intermittent, excruciating pain in flank
    on affected side.

120
Noncolicky Renal Pain
121
Noncolicky Renal Pain
  • Not as much pain
  • Stones that produce distention of the renal
    calyces/pelvis.
  • Dull ache in flank, mild to severe
  • Worsens with fluid intake.

122
Treatment of Small Stones
123
Treatment of Small Stones
  • Treatment depends on the type and cause of the
    stone. Most stones can be treated without
    surgery. Stones less than 5 mm in size usually
    will pass spontaneously.
  • Drinking lots of water (two and a half to three
    liters per day) and staying physically active are
    often enough to move a stone out of the body.
  • However, if there is infection, blockage, or a
    risk of kidney damage, a stone should always be
    removed. Any infection is treated with
    antibiotics first. Nonsteroidal anti-inflammatory
    drugs or opioids are used for pain control, along
    with a stool softener.

124
Treatment of Larger Renal Stones
125
Treatment of Larger Renal Stones
  • Stones greater than 6 mm will require some form
    of intervention, especially if the stone is
    stuck, causing obstruction and infection of the
    urinary tract.
  • Extracorporeal Shock Wave Lithotripsy (ESWL)
  • Ureteroscopic Stone Removal
  • Percutaneous Nephrolithotomy (PCNL)

126
Extracorporeal Shock Wave Lithotripsy (ESWL)
127
Extracorporeal Shock Wave Lithotripsy (ESWL)
  • This is the most common method
  • Does not involve a surgical operation.
  • Ultrasound waves are used to break the stones
    into crystals small enough to be passed in the
    urine.
  • The shock waves do not hurt
  • Some people feel some discomfort at the time of
    the procedure and shortly afterwards.

128
Ureteroscopic Stone Removal
129
Ureteroscopic Stone Removal
  • If a stone is lodged in the ureter, a flexible
    narrow instrument called a cystoscope can be
    passed up through the urethra and bladder.
  • The stone is "caught" and removed, or shattered
    into tiny pieces with a shock wave.
  • This procedure is usually done under a general
    anesthetic.

130
Percutaneous Nephrolithotomy (PCNL)
131
Percutaneous Nephrolithotomy (PCNL)
  • If ESWL does not work or a stone is particularly
    large, it may be surgically removed under general
    anesthetic.
  • The surgeon makes a small cut in the back and
    uses a telescopic instrument called a nephroscope
    to pull the stone out or break it up with shock
    waves.

132
Renal Failure
133
Renal Failure
  • Condition in which the kidneys fail to remove
    metabolic end products from the blood and
    regulate the fluid, electrolyte, and pH balance
    of the extracellular fluids.
  • Underlying cause may be renal disease or systemic
    disease.
  • Can occur as acute or chronic

134
Types of Renal Failure
135
Types of Renal Failure
  • Acute
  • Abrupt in onset
  • Usually reversible with early treatment
  • Chronic
  • End result of irreparable damage to the kidneys
  • Develops over the course of years

136
Acute Renal Failure (ARF)
137
Acute Renal Failure (ARF)
  • Azotemia
  • Accumulation of nitrogenous waste products (urea)
    in blood.
  • Urea, nitrogen, creatinine
  • Both the BUN and the creatinine would go up
  • ?GFR ? ? urine excretion of wastes? ? Blood
    urea nitrogen (BUN), ? Blood Creatinine (Cr).
  • Many causes
  • Acute tubular necrosis is one

GFR
  • BUN
  • Cr

McCance (2002) Figure 34-6 pg. 1175
138
Acute Tubular Necrosis (ATN)
139
Acute Tubular Necrosis (ATN)
  • Very common in hospitalized patient
  • Characterized by destruction of tubular
    epithelial cells ? ? tubular functions
  • Most common cause of intrinsic renal failure
  • Risk
  • Elderly, diabetics, poor renal perfusion
  • Tubular injury is usually reversible

140
Causes of Acute Tubular Necrosis
141
Causes of Acute Tubular Necrosis
  • Ischemia, such as from shock
  • Nephrotoxic drugs
  • Tubular obstruction
  • Ex. myoglobin and hemoglobin
  • Toxins from infectious agents

142
Three Phases of ATN
143
Three Phases of ATN
  • Onset/initiating
  • Maintenance Phase
  • Recovery Phase

144
Onset/Initiating Phase
145
Onset/Initiating Phase
  • Hours/days from onset of insult
  • Gradual
  • Urine output will decrease slowly

146
Maintenance Phase
147
Maintenance Phase
  • ? GFR
  • Retention of metabolites (urea, K, sulfate, Cr),
    ? U/O
  • Generalized edema
  • Pulmonary edema
  • Metabolic acidosis
  • Because the kidney is not working to rid the body
    of acid
  • Everything is clogged up and a lot of times the
    person will not produce any urine at all

148
Recovery Phase
149
Recovery Phase
  • Repair of renal tissues
  • Gradual improvement in U/O, BUN, and creatinine

150
Chronic Renal Failure
151
Chronic Renal Failure
  • Progressive, irreversible destruction of nephrons
    over many years.
  • Requires dialysis, kidney transplants.
  • Causes
  • Diabetes, hypertension, glomerulonephritis
  • Signs and symptoms are not evident until disease
    is advanced.

Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p.564
152
Chronic Renal Failure Stages of Progression
153
Chronic Renal Failure Stages of Progression
  • Diminished Renal Reserve
  • Renal Insufficiency
  • Renal Failure
  • End-Stage Renal Disease (ESRD)

154
Diminished Renal Reserve
155
Diminished Renal Reserve
  • GFR 50 of normal and BUN/Cr are normal
  • No signs/symptoms

156
Renal Insufficiency
157
Renal Insufficiency
  • GFR 20-50 of normal
  • Azotemia
  • Anemia
  • Hypertension

158
Renal Failure
159
Renal Failure
  • GFR lt 20
  • ? fluid/electrolyte regulation
  • Metabolic acidosis
  • Other systems fail

160
End-stage Renal Disease
161
End-stage Renal Disease
  • GFR lt 5 normal
  • Atrophy/fibrosis of kidneys
  • Dialysis or transplant required

162
Signs and Symptoms of Renal Failure
163
Signs and Symptoms of Renal Failure
  • Fluid and electrolyte imbalance
  • Increase in blood levels of metabolic acids and
    other small, diffusible particles (e.g. urea)
  • Anemia - erythropoietin is missing
  • Hyperparathyroidism
  • Vitamin D and calcium in the kidney are not
    working so the parathyroid gland secretes more
  • Cardiovascular effects
  • Activation of renin-angiotensin mechanism,
    leading to increased vascular volume
  • Fluid retention and hypoalbuminemia
  • Excess extracellular fluid volume, left
    ventricular hypertrophy and anemia
  • Body fluids
  • Hematologic

164
Signs/Symptoms of Renal Failure Fluid and
Electrolyte Imbalance
165
Signs/Symptoms of Renal Failure Fluid and
Electrolyte Imbalance
  • Fluid and electrolyte imbalance
  • Increases in blood levels of metabolic acids and
    other small, diffusible particles (urea)
  • Signs of uremic encephalopathy
  • Lethargy
  • Decreased alertness
  • Loss of recent memory
  • Delirium
  • Coma
  • Seizures
  • Asterixis
  • Muscle twitching
  • Tremulousness
  • Signs of neuropathy
  • Restless leg syndrome
  • Paresthesias
  • Muscle weakness and atrophy

166
Signs/Symptoms of Renal Failure Anemia,
Hyperparathyroidism, High Concentrations
167
Signs/Symptoms of Renal Failure Anemia,
Hyperparathyroidism, High Concentrations
  • Anemia
  • Because erythropoietin is missing
  • Hyperparathyroidism
  • Vitamin D and calcium in the kidney are not
    working so the parathyroid gland secretes more
  • High concentration of metabolic end products in
    body fluids
  • Pale, sallow complexion
  • Pruitus
  • Uremic frost and odor of ammonia on skin and
    breath

168
Consequences of Renal Failure Cardiovascular
169
Consequences of Renal Failure Cardiovascular
  • Activation of the RAAS and increased vascular
    volume
  • Hypertension that must be treated
  • Everybody with kidney failure has hypertension
    because the RAAS is working over time
  • Fluid retention and hypoalbuminemia
  • Leads to edema
  • Dialysis is required
  • Excess extracellular fluid volume
  • Left ventricular hypertrophy and anemia
  • CHF
  • Pulmonary edema
  • Dialysis is required

170
Consequences of Renal Failure Body Fluids
171
Consequences of Renal Failure Body Fluids
  • Decreased ability to synthesize ammonia and
    conserve bicarbonate
  • Metabolic acidosis
  • Dialysis is required
  • Inability to excrete potassium
  • Hyperkalemia and dialysis
  • Inability to regulate sodium excretion
  • Salt wasting or sodium retention and dialysis
  • Impaired ability to excrete phosphate
  • Hyperphosphatemia and dialysis
  • Osteoporosis
  • Impaired phosphate excretion and inability to
    activate vitamin D
  • Hypocalcemia and increased levels of PTH

172
Consequences of Renal Failure Hematologic
173
Consequences of Renal Failure Hematologic
  • Impaired synthesis of erythropoietin and effects
    of uremia
  • Anemia
  • Impaired platelet function
  • Bleeding tendencies

174
Dialysis
175
Dialysis
176
Renal Failure and the Elimination of Drugs
177
Renal Failure and the Elimination of Drugs
  • Kidneys are responsible for elimination of drugs
    and their metabolites
  • Renal failure and its treatment interfere with
    elimination of drugs
  • Decreased elimination allows some drugs to
    accumulate in blood dosages may need to be
    adjusted
  • A type 2 diabetes drug that is eliminated
    completely by the kidney is metformin
  • People with renal failure cannot take metformin

178
The maintenance phase of acute tubular necrosis
(ATN) is characterized by
179
The maintenance phase of acute tubular necrosis
(ATN) is characterized by
  1. Hypokalemia
  2. Diuresis
  3. Edema
  4. Discolored urine

180
Control of Urine Elimination and Disorders of
the Bladder
181
Control of Urine Elimination
182
Control of Urine Elimination
  • Urine formation is a by-product of the normal
    functioning of the kidneys, whose main function
    is to maintain the acid-base balance and ion
    concentrations in the blood.
  • The urine is whatever is left over from the
    processes of the kidney
  • The bladder stores urine and controls its
    elimination from the body

183
Alterations in Urine Elimination
184
Alterations in Urine Elimination
  • Neurogenic bladder an inability to urinate
  • The bladder does not contract properly
  • Incontinence urinate too much, in the wrong
    place, or at the wrong time

185
Four Layers of Bladder
186
Four Layers of Bladder
  • Outer serosal layer
  • Detrusor muscle
  • Network of smooth muscle fibers
  • Submucosal layer of loose connective tissue
  • Inner mucosal lining of transitional epithelial
    cells
  • Acts as a barrier to prevent the passage of water
    between the bladder contents and blood

Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 576
187
Description of the Bladder
188
Description of the Bladder
  • The bladder has a lot of layers that expand as it
    fills with urine
  • The urine is propelled down the ureters by
    peristalsis
  • When it gets to the bladder, the bladder squeezes
    the ureters
  • The bladder is made of smooth muscle lined by
    epithelium (transitional epithelium)
  • The area at the bladder neck is called the
    trigone
  • There is an internal sphincter (smooth muscle)
    and an external sphincter (skeletal muscle,
    voluntary control)

189
Motor Control of Bladder Function
190
Motor Control of Bladder Function
  • Detrusor muscle
  • Muscle of micturition (smooth muscle)
  • Contracts?urine is expelled from bladder under
    ANS control
  • Abdominal muscles
  • Contraction ? ? intra-abdominal pressure ? ?
    bladder pressure
  • Internal sphincter
  • Circular smooth muscles in bladder neck
    continuation of detrusor. Bladder relaxed, these
    fibers are closed and act as sphincter. When
    detrusor contracts, sphincter is pulled open by ?
    in bladder shape under ANS control
  • External sphincter
  • Circular skeletal muscle that surrounds urethra,
    acts as a reserve mechanism to stop micturition
    maintains continence despite ? bladder pressure
    skeletal muscle is under voluntary control

191
Neural Control of Bladder Function Nervous System
Control
192
Neural Control of Bladder Function Nervous System
Control
  • ANS and Voluntary control
  • Parasympathetic Nervous System (PSNS)
  • Sympathetic Nervous System (SNS)

193
Parasympathetic Nervous System
194
Parasympathetic Nervous System
  • Excitatory input to the bladder ?bladder emptying
  • Relaxes internal sphincter
  • The PNS is the mechanism for emptying the bladder

195
Sympathetic Nervous System
196
Sympathetic Nervous System
  • Relaxes bladder smooth muscle
  • Contracts internal sphincter
  • The SNS is the mechanism for not emptying the
    bladder

197
Levels of Neurogenic Control of Bladder Function
198
Levels of Neurogenic Control of Bladder Function
  • Three main levels of neurologic control for
    bladder function
  • Spinal cord reflex centers (involuntary/parasympat
    hetic)
  • Micturition center in the pons
  • Cortical and subcortical centers


(Voluntary Control)
199
Spinal Cord Centers
200
Spinal Cord Centers
  • The centers for reflex control of micturition are
    located in S2-S4 (PSNS) and T11-L1 (SNS)
  • Afferent (sensory) input from bladder and urethra
    is carried to CNS by fibers that travel with PSNS
    (pelvic), somatic (pudendal), and SNS
    (hypogastric) nerve.

Porth, (2005) Pathophysiology Concepts of
Altered Health States, Lippincott, p. 853.
201
Pelvic Nerves and Muscles
202
Pelvic Nerves and Muscles
  • Pelvic nerve carries sensory fibers from stretch
    receptors in bladder wall
  • Pudendal nerve carries sensory fibers from the
    external sphincter
  • Pelvic muscles and the hypogastric nerve carry
    sensory fibers from the trigone area.

203
Bladder Emptying and Urine Storage Diagram
204
Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 578
205
Developmental Micturition
206
Developmental Micturition
  • In infants/children micturition is involuntary,
    triggered by spinal cord reflex.
  • Bladder fills, detrusor contracts, and internal
    sphincter relaxes.
  • As bladder ? in capacity ? ? tone of internal
    sphincter.
  • At 2-3 yrs, child becomes conscious of the need
    to urinate and can learn to contract pelvic
    muscles to maintain closure of external sphincter
    and delay urination.
  • As nervous system continues to mature, inhibition
    of involuntary detrusor muscle activity takes
    place.
  • After child achieves continence, micturition
    becomes voluntary.
  • There is a cortical input to the sympathetic
    neurons

207
Disorders in Bladder Function
208
Disorders in Bladder Function
  • Urinary tract infection (UTI)
  • Urinary obstruction and stasis
  • Urinary incontinence
  • Neurogenic bladder disorders

209
Urinary Tract Infection (UTI)
210
Urinary Tract Infection (UTI)
  • Normally, urine is sterile. An infection occurs
    when bacteria from the stool cling to the opening
    of the urethra and begin to multiply.
  • Women, especially young women, have more UTIs
    than men because their urethra is shorter
  • Bacteria travel up the urethra and multiply. An
    infection of the urethra is urethritis. A
    bladder infection is called cystitis. If the
    infection is not treated promptly, bacteria may
    then travel further up the ureters to cause a
    kidney infection, called pyelonephritis

211
Structure of the Urinary System and Infection
212
Structure of the Urinary System and Infection
  • The urinary system is structured in a way that
    helps ward off infection. The ureters and bladder
    prevent urine from backing up toward the kidneys
    because it is tunneling, and the flow of urine
    from the bladder helps wash bacteria out (as long
    as you void completely).

Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 576
213
UTI Symptoms
214
UTI Symptoms
  • A frequent urge to urinate with a painful,
    burning in the bladder or urethra during
    urination.
  • The urine itself may look milky or cloudy, even
    reddish if blood is present (because the bladder
    is so irritated by the infection).

215
UTI Diagnosis
216
UTI Diagnosis
  • Made by urinalysis (U/A)
  • The urine is examined for white and red blood
    cells and bacteria.
  • A culture may be done to identify the organism.
  • E. coli is the most frequent infecting organism

217
UTI Treatment
218
UTI Treatment
  • UTIs are treated with antibacterial drugs.
  • Drug choice and length of treatment depend on the
    patient history and U/A results.
  • The drug most often used to treat routine,
    uncomplicated UTIs is trimethoprim/
    sulfamethoxazole (Bactrim, Septra, Cotrim)
  • Often, a UTI can be cured with 1 or 3 days of
    treatment if not complicated by an obstruction or
    other disorder

219
Acquired Urethral Obstruction
220
Acquired Urethral Obstruction
  • External compression of urethra caused by benign
    or malignant enlargement of prostate gland
  • The prostate becomes larges and can squeeze the
    urethra
  • Gonorrhea, STDs ? infection produces urethral
    strictures
  • Bladder tumors surround bladder, urethra
  • Constipation, fecal impaction

Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 580
221
Signs of Outflow Obstruction and Urine Retention
222
Signs of Outflow Obstruction and Urine Retention
  • Bladder distention
  • Hesitancy
  • Straining when initiating urination
  • Small and weak stream
  • Frequency
  • Feeling of incomplete bladder emptying
  • Overflow incontinence

223
Urinary Incontinence
224
Urinary Incontinence
  • An involuntary loss of urine
  • ? Frequency in elderly
  • A shorter urethra in women means that there is
    less resistance to flow and incontinence is more
    likely
  • Stress incontinence
  • Urge incontinence, overactive bladder
  • Overflow incontinence
  • Mixed (stress and urge)

225
Stress Incontinence
226
Stress Incontinence
  • Involuntary loss of urine associated with
    activities, such as coughing
  • Associated with activities that increase
    intra-abdominal pressure

227
Overactive Bladder (Urge Incontinence)
228
Overactive Bladder (Urge Incontinence)
  • Urgency and frequency associated with activation
    of the detrusor muscle in response to low levels
    of PNS stimulation
  • May or may not involve involuntary loss of urine

229
Overflow
230
Overflow
  • Involuntary loss of urine when bladder pressure
    is greater than urethral presence in the absence
    of detrusor activity

231
Neurogenic Bladder Disorders
232
Neurogenic Bladder Disorders
  • Neural control of bladder function can be
    interrupted at any level (sensory, CNS, or motor)
  • Neurogenic disorders
  • 1. Failure to store urine spastic bladder
    dysfunction (automatic bladder)
  • 2. Failure to empty flaccid bladder dysfunction

233
Neurogenic Bladder Failure to Store Urine
234
Neurogenic Bladder Failure to Store Urine
  • Results from neurogenic lesions above the level
    of the sacral cord (spinal cord injuries or
    stroke) that allow neurons in the micturition
    center in the SC to function reflexively without
    control from higher CNS centers

235
Neurogenic Bladder Failure to Empty Bladder
236
Neurogenic Bladder Failure to Empty Bladder
  • Results from neurologic disorders affecting motor
    neurons in SC or peripheral nerves that control
    detrusor muscle contraction or bladder emptying
  • Peripheral neuropathies

237
The micturation center in the brain stem
coordinates the action of the detrusor muscle
and
238
The micturation center in the brain stem
coordinates the action of the detrusor muscle
and
  1. External sphincter
  2. Conscious control
  3. Bladder pressure
  4. Neuromediators
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