Chapter 36
Alterations of Renal and Urinary
Tract Function
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Urinary Tract Obstruction

Blockage of urine flow within the urinary tract


Obstruction can be caused by an anatomic or
functional defect
• Obstructive uropathy
Severity based on:
• Location
• Completeness
• Involvement of one or both upper urinary tracts
• Duration
• Cause
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Urinary Tract Obstruction



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Hydroureter
Hydronephrosis
Tubulointerstitial fibrosis
Apoptosis
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Urinary Tract Obstruction
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Urinary Tract Obstruction

Compensatory hypertrophy
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

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Obligatory growth
Compensatory growth
Postobstructive diuresis
Low bladder wall compliance
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Kidney Stones

Other factors affecting stone formation


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Crystal growth–inhibiting substances
Particle retention
Matrix
Stones

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Calcium oxalate or calcium phosphate
Struvite stones
Cystinuric stones
Uric acid stones
Indinavir
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Kidney Stones

Manifestation


Evaluation
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

Renal colic
Stone analysis
Kidney-ureter-bladder (KUB)
Intravenous pyelogram
Spiral abdominal computed tomography (CT)
Treatment

Stone removal
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Kidney Stone Formation

Supersaturation of one or more salts
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
Precipitation of a salt from liquid to solid state


Presence of a salt in a higher concentration than
the volume able to dissolve the salt
Temperature and pH
Growth into a stone via crystallization or
aggregation
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Kidney Stones: Calculi


Masses of crystals, protein, or other
substances that form within and may obstruct
urinary tract
Risk factors

Male
 Age 20-40 years
 Inadequate fluid intake (biggest contributor)
 Living in desert or tropical region
• Temperature, humidity, fluid, and dietary patterns
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Kidney Stones: Calculi

Composition of mineral salts
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

Calcium oxalate/phosphate (70%-80%)
Struvite (magnesium, ammonium, phosphate,
15%)
Uric acid (7%)
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Lower Urinary Tract Obstruction
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


Bladder neck dyssynergia
Prostate enlargement
Urethral stricture
Severe pelvic organ prolapse
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Lower Urinary Tract Obstruction

Neurogenic bladder
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
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Neurogenic detrusor overactivity
• Detrusor sphincter dyssynergia
• Overactive bladder syndrome
Obstruction
Low bladder wall compliance
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Neurogenic Bladder
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Tumors

Renal tumors
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

Renal adenomas
Renal cell carcinoma
Bladder tumors



Papillary tumors
Nonpapillary tumors
Metastasis to lymph nodes, liver, bone, lungs
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Urinary Tract Infection (UTI)
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



Inflammation of the urinary epithelium
following invasion and colonization by some
pathogen within the urinary tract
Complicated UTI
Uncomplicated UTI
Persistent UTI
Interstitial cystitis
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Urinary Tract Infection (UTI)

Most common pathogens
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Escherichia coli
Staphylococcus saprophyticus
Enterobacter spp
Virulence of uropathogens

Host defense mechanisms
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Urinary Tract Infection (UTI)

Cystitis


An inflammation of the bladder
Manifestations
• Frequency, dysuria, urgency, and lower abdominal and/or
suprapubic pain

Treatment
• Antimicrobial therapy, increased fluid intake, avoidance
of bladder irritants, urinary analgesics
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Pyelonephritis

Acute pyelonephritis


Acute infection of the ureter, renal pelvis, and/or renal
parenchyma
Contributing factors
• Cystitis
• Urinary tract obstruction with reflux infection
• Women are 5 times more likely to develop pyelonephritis
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Pyelonephritis
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Clinical manifestations
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Flank pain
Fever
Chills
Costovertebral tenderness
Purulent urine
Treatment
Chronic pyelonephritis
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Glomerular Disorders


Glomerulopathies are disorders that directly
affect the glomerulus
Urinary sediment changes
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

Nephrotic sediment
Nephritic sediment
Sediment of chronic glomerular disease
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Glomerular Disorders


Glomerular disease has sudden or insidious
onset of hypertension, edema, and an
elevated blood urea nitrogen (BUN)
Decreased glomerular filtration rate


Elevated plasma creatinine, urea, and reduced
creatinine clearance
Glomerular damage causes decreased
glomerular membrane surface area,
glomerular capillary blood flow, blood
hydrostatic pressure
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Glomerular Disorders


Increased glomerular capillary permeability and
loss of negative ionic charge barrier result in
passage of plasma proteins into the urine
Resulting hypoalbuminemia encourages plasma
fluid to move into the interstitial spaces

Edema
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Glomerular Disorders

Glomerulonephritis
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Inflammation of the glomerulus
• Immunologic abnormalities (most common)
• Drugs or toxins
• Vascular disorders
• Systemic diseases
• Viral causes
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Acute Glomerulonephritis
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Pathophysiology
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Formation of immune complexes
(antigen/antibody) in the circulation with
subsequent deposition in glomerulus
Antibodies produced against the strep organism
cross-react with the glomerular endothelial cells
(may be related to inadequately treated strep)
Activation of complement
Recruitment/activation of immune cells and
mediators
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Glomerulonephritis
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Glomerulonephritis
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Acute poststreptococcal glomerulonephritis
IgA nephropathy (Berger disease)
Crescentic glomerulonephritis
Membraneous nephropathy
Membranoproliferative glomerulonephritis
Antiglomerular basement membrane disease
(Goodpasture syndrome)
Chronic glomerulonephritis
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Glomerulonephritis
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Acute Glomerulonephritis
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Decreased GFR
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
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Decreased glomerular perfusion (glomerular blood
flow) due to inflammation
Glomerular sclerosis (scarring)
Thickening of the glomerular basement membrane
(but increased permeability to proteins)
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Clinical Manifestations of
Acute Glomerulonephritis
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Hematuria
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Proteinuria
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Smoky, brown-tinged urine
Red blood cell casts
Low serum albumin
Edema
Eventual oliguria

Oliguria: urine output <30 ml/hour or <400 ml/day
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Nephrotic Syndrome
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

Excretion of 3.5 g or more of protein in the urine
per day
Protein excretion is due to glomerular injury
Findings

Hypoalbuminemia, edema, hyperlipidemia, and
lipiduria
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Causes of Nephrotic Syndrome
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
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Glomerulonephritis
Genetic defects that alter the glomerular
membrane
Systemic diseases (diabetes, SLE)
Drug/toxin injury
Infections (especially chronic and/or
recurrent)
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Nephrotic Syndrome
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Renal Dysfunction
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Renal insufficiency
Renal failure
End-stage renal failure
Uremia
Azotemia
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Renal Failure
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Acute


Sudden and rapidly progressive within hours (often
reversible); abrupt reduction in renal function
Chronic

Chronic, slowly progressing to end-stage renal failure
over months or years
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Renal Failure


Azotemia: increased urea and frequently
creatinine levels
Uremia: elevated urea and creatinine levels
with fatigue, anorexia, nausea, vomiting,
diarrhea, weight loss, pruritus, edema,
neurologic changes (all related to retention of
toxic wastes, deficiency states, and
electrolyte disorders)
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Prerenal ARF


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Most common cause of ARF
Caused by impaired renal blood flow (sudden
reduction of perfusion to the kidneys)
GFR declines due to the decrease in filtration
pressure (results in oliguria)
Ischemia leads to hypoxic injury and acute
tubular necrosis (ATN)
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Intrarenal ARF

Damage to the renal parenchyma
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
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

ATN (most common cause)
• Postischemic
• Nephrotoxic injury
Corticol necrosis
Acute glomerulonephritis
Vascular disease (i.e., malignant hypertension)
Toxic injury (drugs, such as antibiotics;
nephrotoxins)
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Postrenal ARF

Occurs with urinary tract obstructions that
affect the kidneys bilaterally and increase the
intraluminal pressure upstream (thus a fall in
GFR)

Prostatic hypertrophy
 Bladder outlet obstruction
 Bilateral ureteral obstruction
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Clinical Manifestations of ARF
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Oliguria/anuria
Elevated BUN and creatinine
Hyperkalemia
Metabolic acidosis
Hypertension (volume overload)
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Acute Renal Failure (ARF)
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Initiation phase
Maintenance phase
Recovery phase
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Chronic Renal Failure


The irreversible loss of renal function that
affects nearly all organ systems
Progression

Reduced renal reserve
 Renal insufficiency
 Renal failure
 End-stage renal disease
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Chronic Renal Failure
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Creatinine and urea clearance
Sodium and water balance
Phosphate and calcium balance
Potassium balance
Acid-base balance
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Chronic Renal Failure
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Skeletal and bone alterations
Cardiopulmonary system
Neural function
Endocrine and reproduction
Hematologic alterations
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Chronic Renal Failure
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Immunologic
Gastrointestinal
Integument
Alterations in proteins, carbohydrates, and
lipids
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Progression of
Chronic Renal Failure
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Decreasing renal function




Reduced renal reserve (GFR reduced to 50%)
Renal insufficiency (GFR declines to 25%)
Renal failure: significant loss of function (GFR
<20% of normal)
End-stage renal failure (near absence of GFR)
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Reduced Renal Reserve

GFR reduced to 50%


No clinical symptoms
BUN may be elevated
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Renal Insufficiency

GFR reduced to 25%
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Compensation of remaining nephrons
Mild clinical symptoms (mild uremia)
Increased BUN/creatinine
Mild anemia
Impaired renal function during stress
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Renal Failure



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GFR <20%
Increased BUN/creatinine
Oliguria
Metabolic acidosis
Electrolyte imbalances



Hyperkalemia, hypernatremia
Severe anemia
Increasing uremia and affects nonrenal
organs
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End-Stage Renal Disease
(ESRD)




GFR = 0%
Severe uremia
Severe water, electrolyte, acid-base
imbalances
Multiorgan/multisystem failures
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Multiorgan/Multisystem Failures

Cardiovascular

Hypertension, congestive heart failure
• Volume overload, hyperactivity of renin system
 Atherosclerosis, stroke, coronary artery disease
• Dyslipidemia

Hematologic


Anemia (lack of erythropoietin)
Platelet defects—bleeding disorders
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Multiorgan/Multisystem Failures

Neurologic



Neuropathies
Encephalopathy
Gastrointestinal


Nausea, vomiting, anorexia
Uremic fetor
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Multiorgan/Multisystem Failures

Endocrine



Insulin resistance
Decreased sex hormones
Metabolic

Altered protein, lipid, carbohydrate metabolism
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Multiorgan/Multisystem Failures

Integumentary, bone, mineral





Hyperphosphatemia
Hypocalcemia
Hyperparathyroidism; brittle bones
Skin changes (bruises, itching, uremic frost,
yellowing)
Immune dysfunction

Immunosuppression
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Dialysis or Transplant?



Immediately life threatening: hyperkalemia
Severe uremia and multi-organ effects
Metabolic acidemia
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