Hematuria
Dr. Mansour Alzahrani
Assistant Professor of Family Medicine
College of Medicine
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Slide 001
What is the definition of hematuria?
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The Correct Answer
American Urological Association (AUA)
definition - ≥ 3 intact red blood cells visible
per high-powered field (RBC/HPF) on
microscopic exam of urine sediment from 2
of 3 properly collected urine specimens.
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Take more details
• Gross vs microscopic
• Symptomatic vs Asymptomatic
• Transient vs Persistent
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Question
Where are the blood came from (source)?
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Acute Glomerulonephritis
Background:
Glomerulonephritis is defined here as a
disease characterized by intraglomerular
inflammation and cellular proliferation
associated with hematuria.
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• Hematuria in patients with glomerulonephritis
is typified by the presence of dysmorphic red
cells or red-cell casts in the urine, findings that
differentiate hematuria of glomerular origin from
extraglomerular bleeding.
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• Acute glomerulonephritis is a syndrome
characterized by the abrupt onset of
macroscopic hematuria; oliguria; acute
renal failure
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Acute Glomerulonephritis
• Currently described as a clinical syndrome that
frequently manifests as a sudden onset of
hematuria, proteinuria, and red cell casts.
• This clinical picture often is accompanied by
hypertension, edema, and impaired renal
function( sudden
GFR, HTN, Edema).
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Pathophysiology
• Glomerular lesions in acute glomerulonephritis
are the result of glomerular deposition or in situ
formation of immune complexes. On gross
appearance, the kidneys may be enlarged up to
50%.
• Histopathologic changes include swelling of the
glomerular tufts (network) and infiltration with
polymorphonucleocyte. Immunofluorescence
reveals deposition of immunoglobulins and
complement.
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Frequency
• In the US, glomerulonephritis represents
10-15% of glomerular diseases. Variable
incidence has been reported due in part to
the subclinical nature of the disease in
more than one half the affected
population.
• Remains much more common in regions
such as Africa, the Caribbean, India,
Pakistan, Malaysia, Papua New Guinea,
and South America.
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Mortality/Morbidity, Sex, Age
• Most epidemic cases follow a course ending in complete
patient recovery
• Sporadic cases often progress to a chronic form.
• The mortality rate of acute glomerulonephritis in the most
commonly affected age group, pediatric patients, has
been reported at 0-7%.
• A male-to-female ratio of 2:1 has been reported.
• Most cases occur in patients aged 5-15 years.
• Only 10% occur in patients older than 40 years.
• Acute nephritis may occur at any age, including infancy.
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Clinical
• History
– suddenly onset of puffiness of the eyelids, facial
edema and dark and scanty urine; with the elevated
blood pressure.
– Nonspecific symptoms include weakness, fever,
abdominal pain, and malaise.
– In the setting of postinfectious acute nephritis, a latent
period of up to 3 weeks occurs before onset of
symptoms.
– The latent period generally is 1-2 weeks for the
postpharyngitis form of the disease and 2-4 weeks in
the case of postdermal infection.
– Onset of nephritis within 1-4 days of streptococcal
infection suggests preexisting renal disease.
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Physical
• Edema, frequently including the face, specifically
the periorbital area
• Hypertension in as many as 80% of patients in
all populations affected
• Gross hematuria
• Skin rashes
• Abnormal neurologic examination or altered
level of consciousness
• Hypocomplementemia
• Pharyngitis
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Causes
• Postinfectious etiologies
– The most common cause is
postinfectious Streptococcus species
(ie, group A, beta-hemolytic). Two types
have been described:
1. attributed to serotype 12,
poststreptococcal nephritis due to an
upper respiratory infection occurring
primarily in the winter months, and
2. attributed to serotype 49,
poststreptococcal nephritis due to a
skin infection
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Causes
– Other specific agents include viruses and
parasites, systemic and renal disease,
visceral abscesses, endocarditis, infected
grafts or shunts, and pneumonia.
– Bacterial causes other than group A
streptococci may be diplococcal,
streptococcal, staphylococcal, or
mycobacterial. Salmonella typhosa,
Brucella suis, Treponema pallidum,
Corynebacterium bovis, and actinobacilli
also have been identified
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Causes
• Viral: Cytomegalovirus, coxsackievirus, EpsteinBarr virus, hepatitis B, rubella, rickettsial scrub
typhus, and mumps are accepted as viral
causes*
• Fungal and parasitic: Identified organisms
include Coccidioides immitis and the following
parasites: Plasmodium malariae, Plasmodium
falciparum, Schistosoma mansoni, Toxoplasma
gondii, filariasis, trichinosis, and trypanosomes.*
* only if it can be documented that a recent group
A beta-hemolytic streptococcal infection did not
occur.
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Systemic causes
• Wegener granulomatosis causes
glomerulonephritis that combines upper and
lower granulomatous nephritises.
• Hypersensitivity vasculitis encompasses a
heterogeneous group of disorders featuring
small vessel and skin disease.
• Cryoglobulinemia causes abnormal quantities of
cryoglobulin in plasma that result in repeated
episodes of widespread purpura and cutaneous
ulcerations upon crystallization.
• Systemic lupus erythematosus causes
glomerulonephritis through renal deposition of
immune complexes.
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Systemic causes
• Polyarteritis nodosa causes nephritis from a
vasculitis involving the renal arteries.
• Henoch-Schönlein purpura causes a
generalized vasculitis resulting in
glomerulonephritis.
• Goodpasture syndrome causes circulating
antibodies to type IV collagen and often
results in a rapidly progressive oliguric renal
failure (weeks to months).
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Renal diseases
• Membranoproliferative glomerulonephritis is due
to the expansion and proliferation of mesangial
cells as a consequence of the deposition of
complements.
– Type I refers to the granular deposition of C3;
– Type II refers to an irregular process.
• Berger disease (IgG-immunoglobulin A [IgA]
nephropathy) glomerulonephritis results from a
diffuse mesangial deposition of IgA and IgG.
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Renal diseases
• Idiopathic rapidly progressive
glomerulonephritis is a form of
glomerulonephritis characterized by the
presence of glomerular crescents. Three
types have been distinguished. Type I is
an antiglomerular basement membrane
disease, type II is mediated by immune
complexes, and type III is identified by
antineutrophil cytoplasmic antibody.
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Lab Studies
• Complete blood count
– CBC may demonstrate dilutional anemia.
– In a setting of infectious etiology, pleocytosis may be
evident.
• Electrolytes including BUN and creatinine: BUN
and creatinine exhibit a degree of renal
compromise.
• Urinalysis
–
–
–
–
Urine is dark.
Specific gravity is greater than 1020 osm.
Proteinuria is indicated.
RBCs and red cell casts are present.
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Lab Studies
• Antistreptolysin O
– This quantitative titer is increased in 60-80%
of patients.
– Increase begins in 1-3 weeks, peaks in 3-5
weeks, and returns to normal in 6 months.
– Unrelated to severity, duration, or prognosis
of renal disease.
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Lab Studies
• Serum complement (C3, C4)
– Low serum complement levels suggest the following
systemic diseases: cryoglobulinemia, systemic lupus
erythematosus, bacterial endocarditis, & shunt
nephritis.
– Under the same conditions, renal diseases
characteristic of membranoproliferative or
poststreptococcal glomerulonephritis also may be
considered.
– Normal serum complement levels suggest a visceral
abscess, polyarteritis nodosa, Goodpasture
syndrome, or Henoch-Schönlein purpura. In addition,
normal complement levels suggest renal diseases
such as immune complex disease, idiopathic rapidly
progressive glomerulonephritis, and IgG or IgA
nephropathy.
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Lab Studies
• Renal biopsy
– Acute glomerulonephritis usually has a selflimited course with a good prognosis.
– Candidates for biopsy are patients with an
individual or family history of renal disease
and patients with atypical presentation,
including massive proteinuria, nephrotic
syndrome, or a rapid rise in creatinine without
resolution
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Therapeutics
• Consider admission for patients with the
following conditions:
– Compromised renal function or
immunosuppression.
– Anuria, nephrotic syndrome, massive proteinuria,
significant hypertension, or pulmonary symptoms.
– Oliguria and renal failure.
– Severe hypertension associated with signs of
cerebral dysfunction is a hypertensive emergency
requiring immediate aggressive treatment.
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Therapeutics
• Poststreptococcal
– Eradicate streptococcal causes by oral antibiotic
therapy.
• Restrict fluids for acute nephritic syndrome
• Hypertension
– Use anti HTN medications.
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Therapeutics
• Nonstreptococcal glomerulonephritis: Steroids
and cytotoxic agents may be indicated in the
following conditions:
– Glomerulonephritis secondary to hypersensitivity
– Vasculitis
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Therapeutics
(Nonstreptococcal glomerulonephritis)
• Systemic lupus erythematosus: Pulse therapy with
methylprednisolone
• Systemic lupus erythematosus: Pulse therapy with
methylprednisolone
• Idiopathic rapidly progressive glomerulonephritis: Pulse
intravenous methylprednisolone is used to reduce risk of
progression to end-stage renal disease.
Cyclophosphamide also is used in conjunction with
steroids.
• Goodpasture syndrome: Plasmapheresis is combined
with immunosuppression. High-dose pulse steroids are
effective for pulmonary hemorrhage.
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Complications
• 0.5-2% of patients with acute glomerulonephritis
progresses toward renal failure, resulting in
kidney death in a short period.
• Abnormal urinalysis may persist for years
(microhematuria).
• Marked decline in glomerular filtration rate is
rare.
• Other complications, include the following:
–
–
–
–
–
Hypertensive retinopathy
Hypertensive encephalopathy
Rapidly progressive glomerulonephritis
Chronic renal failure
Nephrotic syndrome
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Prognosis
• In poststreptococcal nephritis, long-term prognosis
generally is good. > 98% of individuals are
asymptomatic after 5 years, with chronic renal
failure 1-3% of the time.
• The prognosis for nonstreptococcal postinfectious
glomerulonephritis depends on the underlying
agent, which must be identified and addressed.
• Other causes of acute glomerulonephritis have
outcomes varying from complete recovery to
complete renal failure. Prognosis depends on the
underlying disease and the overall health of the
patient.
• Occurrence of cardiopulmonary or neurologic
complications worsens the prognosis.
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Kidney stones
• Also known as nephrolithiasis,
urolithiasis or renal calculi.
• Solid concretions ( crystal
aggregations) of dissolved minerals in
urine
• found inside the kidneys or ureters.
They vary in size from as small as a
grain of sand to as large as a grapefruit
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Cont.
• Kidney stones (calculi) are hardened
mineral deposits that form in the kidney.
They originate as microscopic particles
and develop into stones over time. The
medical term for this condition is
nephrolithiasis, or renal stone disease.
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Location of Renal stones
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• A vast majority of stones will contain
elements of calcium within them and
therefore are easily seen on x-ray having
the same density as bone.
• Depending on the size, number, and the
location of the stone(s) as well as it's
composition guides initial and then further
management can be implemented.
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Renal stones
• Kidney stones occur in 1 in 20 people at
some time in their life.
• Urolithiasis is rare in children. When
present, it is often associated with
specific metabolic disorders or anatomic
abnormalities .
• For precipitation of crystals in urine to
occur, the urine must be "supersaturated"
for the precipitating crystal.
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Stone Formation
•
•
•
Kidney stones form when there is a high level
of mineral (s) ; i.e. calcium (hypercalciuria),
oxalate (hyperoxaluria), or uric acid
(hyperuricosuria) in the urine;
a lack of citrate in the urine; or insufficient
water in the kidneys to dissolve waste
products.
Urine normally contains chemicals—citrate,
magnesium, pyrophosphate—that prevent the
formation of crystals.
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Cont.
• Low levels of these inhibitors can contribute to
the formation of kidney stones.
• Citrate is thought to be the most important
• The chemical composition of stones depends
on the chemical imbalance in the urine.
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Types of renal stones
1.
2.
3.
4.
Calcium oxalate
Phosphate
Uric acid
Cystine
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Calcium Stones:
• Approximately 85% of stones are composed
predominantly of calcium compounds.
• The most common cause of calcium stone
production is excess calcium in the urine
(hypercalciuria).
• In hypercalciuria, excess calcium builds up in
the kidneys and urine, where it combines with
other waste products to form stones.
• Low levels of citrate, high levels of oxalate and
uric acid, and inadequate urinary volume may
also cause calcium stone formation.
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Cont.
• Calcium stones are composed of oxalate (calcium
oxalate) or phosphate (calcium phosphate).
• Calcium phosphate stones typically occur in patients
with metabolic or hormonal disorders such as
hyperparathyroidism and renal tubular acidosis.
• These stones come in 2 different types - monohydrate
and dihydrate.
• Calcium oxalate dihydrate stones usually break
easily with lithotripsy.
• Monohydrate stones are among the most difficult
stones to fragment.
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Calcium oxalate monohydrates
Calcium
oxalate dihydrates
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Uric Acid Stones
• Digestion produces uric acid.
• If the acid level in the urine is high or too much
acid is excreted, the uric acid may not dissolve
and uric acid stones may form.
• They are not visible on X-rays.
• Patients with gout often develop these stones.
• Uric acid stones form in acidic urine and often
dissolve when the urine is alkalinized.
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Cont.
• Genetics may play a role in the
development of uric acid stones, which are
more common in men.
• Approximately 10% of patients with kidney
stone disease develop this type of stone.
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Uric acid
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Aetiopathogenesis
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•
•
•
•
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Infections
Hot climate
Dietary factors
Metabolic factors
Immobilization
Decreased urinary citrate
Inadequate urinary drainage
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Staghorn Calculus
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Clinical Features
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•
•
•
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Renal pain
Ureteric colic
Haematuria
Recurrent UTI
Guarding and Rigidity
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Complications
1. Calculus hydronephrosis
2. Calculus pyonephrosis
3. Renal failure
4. Squamous cell carcinoma
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Investigations
1. Blood urea and creatinine
2. Plain x-ray
3. IVP
4. Urine
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X-ray renal stone
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Intravenous Pyelogram
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Treatment
A. Non-operative
• Conservative
• ESWL
B.
Operative
• Endoscopy
• Open surgery
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ESWL Machine
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Renal endoscope
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