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Epidemiology: Glomerulonephritis Represents 10-15% of Glomerular Diseases.
Epidemiology: Glomerulonephritis Represents 10-15% of Glomerular Diseases.
Mortality/Morbidity
• Most epidemic cases follow a course ending in complete patient recovery (as
many as 100%).
• Sporadic cases of acute nephritis often progress to a chronic form. This
progression occurs in as many as 30% of adult patients and 10% of pediatric
patients.
• Glomerulonephritis is the most common cause of chronic renal failure (25%).
• The mortality rate of acute glomerulonephritis in the most commonly affected age
group, pediatric patients, has been reported at 0-7%.
Sex
• A male-to-female ratio of 2:1 has been reported.
Age
• 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.
Etiology:
Immunoglobulin A (IgA) nephropathy glomerulonephritis (ie, Burger disease) is
the most common cause of glomerulonephritis worldwide.
• Postinfectious etiologies
○ The most common cause is postinfectious Streptococcus species (ie, group
A, beta-hemolytic). Two types have been described as (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 usually
observed in the summer and fall and more prevalent in southern regions of
the United States.
○ 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 have also been identified.
○ Cytomegalovirus, coxsackievirus, Epstein-Barr virus, hepatitis B rubella,
rickettsial scrub typhus, and mumps are accepted as viral causes only if it
can be documented that a recent group A beta-hemolytic streptococcal
infection did not occur. Acute glomerulonephritis has been documented as
a rare complication of hepatitis A.3
○ Fungal and parasitic: Attributing glomerulonephritis to a parasitic or
fungal etiology requires the exclusion of a streptococcal infection.
Identified organisms include Coccidioides immitis and the following
parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma
mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes.
• Systemic causes
○ Vasculitis (ie, Wegener granulomatosis causes glomerulonephritis that
combines upper and lower granulomatous nephritides).
○ Collagen vascular diseases (ie, systemic lupus erythematosus causes
glomerulonephritis through renal deposition of immune complexes).
○ 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.
○ Polyarteritis nodosa causes nephritis from a vasculitis involving the renal
arteries.
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○ 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).
○ Drug-induced (ie, gold, penicillamine)
• 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.
○ 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.
Definition:
Patients Profile
Name: Avila, Sonny Sarmiento
Age: 39 years old
Address: Sta, Ana Bulacan, Bulacan
Birthdate: May 22,1970
Religion: Roman Catholic
Race: Filipino
Place of admission: Gregorio del Pilar District Hospital
Date of admission: Dec. 03,2009
Chief Complaint: Fever and frequent urination for 2 weeks
Admitting Diagnosis: Acute Glumerulonephritis
Sonny S. Avila is 39 years old, single and a service driver. He lives at Sta. Ana Bulacan,
Bulacan. He used to smoke a pack of cigarette a day and used to drink 2 to 3 bottles at
least twice a week.
On his father side there was a history of having Hypertension and Diabetes.
Present Illness
Sonny S. Avila came to the hospital with the chief complaint of fever and frequent
urination for 2 weeks. He under gone some specific medical diagnostic test such as CBC
and Urinalysis.
Physical Assessment
1.Hematuria
2.Oliguria
3.Edema
✔ Pitting edeme
✔ Starts in the eyelids and face then the lower and upper limbs then
generalized.
✔ It may be migratory ; appear in eyelid in tne morning , disappear in the
afternoon and reappear around the ankle in the ambulant patients by the
end of the day.
4.Hypertension
5. General
✔ Pallor due to edema and/or anemi
.
The whole blood supply passes through the kidneys every 5 minutes, ensuring that waste
materials don't build up. The renal artery carries blood to the kidney, while the renal vein
carries blood, now with much lower concentrations of urea and mineral ions, away from
the kidney. The urine formed passes down the ureter to the bladder.
The work of the kidneys is much more than just the removal of waste, however. Other
functions of the kidneys include:
• Helping control the amount of water lost to the outside world – most important in
land animals.
• Helping regulate the pH (i.e., level of acidity or alkalinity) of the blood and the
general balance of ions in the blood, and hence in the body fluid as a whole.
• Conserving essential substances such as glucose and amino acids.
Location, shape, and size of the kidneys
The kidneys are paired, bean-shaped organs. Adult human kidneys, are approximately 12
cm long, 6 cm wide, and 3 cm thick. They are situated in the abdominal cavity, just
below the rib-cage, one on either side of the spine. More specifically, they lie between the
twelfth thoracic vertebra and third lumbar vertebra.
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• The right kidney usually is slightly lower than the left because the liver displaces
it downward.
• The kidneys, protected by the lower ribs, lie in shallow depressions against the
posterior abdominal wall and behind the parietal peritoneum. This means they are
retroperitoneal.
• Each kidney is held in place by connective tissue, called renal fascia, and is
surrounded by a thick layer of adipose tissue, called perirenal fat, which helps to
protect it. A tough, fibrous, connective tissue known as the renal capsule closely
envelopes each kidney and provides support for the soft tissue that is inside.
Urinalysis
Albumin - +2
Bile
Pregnancy Test
Others
HEMATOLOGY
Differential Count
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DRUG STUDY
Generic Anti- Anti- • Analgesic- •Contrain • CNS: Increased Inter- • Assess for
name: pyretic pyretic: Antipyretic dicated Headache toxicity ference allergy to
Acetamino- Reduces in patients with with long with acetami-
phen/Para- Anal- fever by with aspirin allergy to • CV: term, Dextrostix nophen/para
cetamol gesic acting allergy, acetami- Chest pain, excessive cetamol,
directly hemostatic nophen/ dyspnea, ethanol pregnancy,
Brand on the distur- parace- myocardial ingestion lactation,
name: hypothal bances. tamol damage chronic
Biogesic amic Possible alcoholism
heat- • arthritis •Use • GI: decreased
regula- and cau- Hepatic effec- • Do not
ting rheumatic tiously toxicity and tiveness exceed the
center to disorders with failure, of zidovu- recom-
cause involving impaired jaundice dine mended
vasodi- musculo- hepatic dosage
lation skeletal function, • Hyper-
and pain. chronic sensitivity: • Consult
sweating alcoho- Rash, fever physician if
which • Common lism, needed for
helps cold, flu, preg- children <3
dissipate other viral nancy, yrs.
heat. and lactation
bactericidal •Disconti-
Analge- infections nue if
sic: with pain hypersen-
Site and and fever. sitivity
mecha- occurs
nism of
action
unclear.
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DRUG STUDY
• Periopera- Parenteral
tive Drug
prophylaxis
• Avoid
alcohol
while taking
this drug
and for 3
days later
bec. Severe
reactions
often occur.
• You may
experience
these side
effects:
stomach
upset or
diarrhea
Day 1
Last December 3.2009 at around 5:30pm, the patient consulted at Gregorio del
Pilar District Hospital because of 5 days fever. Consent for admission and management
was secured and the patient was hence admitted to patient`s room of choice under the
supervision of Dr. Maria Rhina R. Uy. Then, assessment for Temperature, Blood
Pressure, and Respiratory every shift. Administration of D5LR 1L to run for 8 hours. Dr.
Maria Rhina R. Uy prescribed Cefuroxime 100mg and Ranitidine 1 ampule to be given
Intravenously to run for 8 hours and Paracetamol 500mg tab. Round the clock every 6
hours. And also ordered to monitor Vital signs every 6 hours and record all the
assessment findings. An order for Complete Blood Count, Platelet Count and urinalysis
was also given for Kidney, Ureter, Bladder – Ultrasound. Repeat Complete Blood count
and Platelet Count tomorrow as ordered.
Day 2
The next day, December 4,2009, Complete Blood Count/kidney, Ureter, Bladder
– Ultrsound repeated. Then, the following drugs were given at 1:00pm and mnonitoring
the Vital signs.
Day 3
The following day, December 5,2009, Dr. Maria Rhina R. Uy, ordered to repeat
Urinalysis prior to discharge. Dr, Maria Rhina R. Uy prescribed Lefuroxime 50mg,
Rowatinex 1 tab and relief forte 1 tablet two times a day for Home Medication. The
Patient will come back on Friday 1pm referred to Dr.Acob.
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Discharge Planning
R – egular check-up
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OUR LADY OF FATIMA UNIVERSITY
A CASE PRESENTATION
PRESENTED
BY
MEMBERS:
Sario, Jefherson
DECEMBER 2009
TABLE OF CONTENTS
PATHOPHYSIOLOGY ---------------------------------------------------------------- 8