CONTORA, ISAH D.

NMD-2B
TBL ON RENAL

1: PATIENT’S PROBLEM
1. Describe the patient’s characteristics
A. An 11-year-old boy came in to the ER: hypertensive with edematous face (puffiness).

2. Enumerate the pertinent findings in the history and physical examination

A. PERSONAL INFORMATION: 11-year-old boy
B. HISTORY: He had impetigo and sore throat 2 weeks previously with complete treatment
by his pediatrician.
C. PHYSICAL EXAM: Hypertensive (135/90), edematous, puffy face.
D. LAB RESULTS:
TESTS RESULTS INTERPRETATION
ASO- Anti- 487 IU/ml (below 200) High
streptolysin O
Serum Creatinine 110 µmol/L (53–106 μmol/L) High
Urinalysis: Hematuria, Proteinuria, Pyuria
• RBC TNTC
• PROTEIN MODERATE
• WBC 8-10/HPF (<2-5/HPF)
C3 <0.2gm/L (0.83-2.02) High
CBC NORMAL Normal
KIDNEY BIOPSY was found to be compatible
with APSGN
He was given Furosemide as medication for his hypertension and showed good control in
BP he also had a good urine output. He was place under fluid and salt restricted diet. And
upon discharge, he followed up his urinalysis for proteinuria and hematuria and it resolved
early, C3 normalize after 2 months. Patient still continued to monitor his urinalysis for 3-6
months. The patient did not develop long-term complications

3. Diagnosis (Cite your basis/ criteria)

A. This is a case of Acute Post-Streptococcal Glomerulonephritis (APSGN)
• Based on HISTORY/PE
1. Patient had Impetigo sore throat 2 weeks previously (APSGN
develops 1-2 weeks after recovery and 6 weeks from skin
impetigo)
2. His Age 11 (APSGN is common among age 4-12 years old)
3. The Patient is Male (APSGN is common among male 2:1)
• Based on Signs and Symptoms:
1. The patient presented with the classic triad of APSGN
1. Hematuria (microscopic)- tea cola urine
2. Edema (face puffiness)- last between 7-10 days
3. Elevated Blood pressure/ hypertension- acute phase usually last
for 10 days

• Based on laboratory findings:

Renal Biopsy: APSGN
1. High total WBC counts-ongoing inflammation process
CONTORA, ISAH D.
NMD-2B
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2. High Creatinine-rise during acute phase indicate Renal Impairment
3. Urine Exam: High WBC, proteinuria, hematuria
4. ASO Titer Positive-confirms serological evidence of antecedent
streptococcal infection
5. Serum C3 level low-significantly reduced in more than 90% of the patients
in acute phase.

4. Discuss briefly the pathophysiology and complications of APSGN.

PATHOPHYSIOLOGY:
The disease is immunological; representing a type III hypersensitivity reaction. The exact
mechanism by which PSGN occurs is not fully determined. The body responds to nephrogenic
streptococcal infection by forming immune complexes containing the streptococcal antigen with a
human antibody. Some theories suggest that these immune complexes become deposited in kidney
glomeruli reaching through the circulation. Others claim that the condition results from an “in situ”
formation of the antigen-antibody complex within the kidney glomeruli. This “In situ immune complex
formation” is either due to a reaction against streptococci antigens deposited in the glomerular
basement membrane or, according to other theories, due to an antibody reaction against glomerular
components that cross-react with streptococcal antigen due to molecular mimicry.

COMPLICATIONS:
The presence of immune complexes leads to the activation of the alternate complement
pathway causing infiltration of the leukocytes, and proliferation of the mesangial cells in the
glomerulus thus impairing the capillary perfusion and glomerular filtration rate (GFR). Reduction
in GFR can lead to renal failure (oliguria or anuria), acid-base imbalance, electrolyte
abnormalities, volume overload, edema, and hypertension.

2: THERAPEUTIC OBJECTIVE.
A. Curative
Antibiotic therapy with PENICILLIN
• 10 days course is advised to limit the transmission of nephritogenic organism

B. Symptomatic
1. DIURETICS
• eg. Intravenous FUROSEMIDE to resolve edema

2. Calcium channel antagonist, vasodilators or angiotensin-converting enzyme inhibitor

• used to treat hypertension

C. Preventive
IMPROVE HEALTH / HYGIENIC CONDITION
• usually occurs as sporadic cases
• epidemic outbreak has taken place in crowded population with:
• poor hygiene and high incidence of malnutrition, anemia and intestinal parasites
CONTORA, ISAH D.
NMD-2B
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Long term monitoring for AGN complications

• Hypertension and acute renal dysfunction
• monitoring BP & urine examination for blood and protein x 1 year

Risk of developing encephalopathy & heart failure as complication of hypertension

• watch out for diagnosed in patients with blurred vision, severe headache, altered mental
status or new seizure.

3: TREATMENT CHOICE
A. Make a drug study of Furosemide using the following table:

DRUG FUROSEMIDE
BRAND NAME LASIX
DOSAGE 40 mg once or twice daily
(Larger initial dose maybe necessary in
patients with advance CHF and azotemia)
ADMINISTRATION Oral, IV
ONSET Oral: 1 hour
IV: 5 mins
DURATION Oral: 6-8 hours diuresis
IV: 2 hours
Pharmacokinetics 40-70% oral bioavailability; short elimination t
Absorption ½ (1.5 hrs.)
Distribution Tightly bound to plasma proteins so delivery
Metabolism to tubules by filtration is limited;
Excretion secreted efficiently by the organic acid
transport system in the proximal tubule, and
thereby gain access to their binding sites on
the NKCC2 symport in the luminal membrane
of the thick ascending limb.
occurs predominantly in the kidney (35%)
renal excretion (65%)
SPECIAL PRECAUTIONS hypokalemia; Oliguric ARF; osteopenic
postmenopause women
Contraindication: severe sodium and volume
depletion, hypersensitivity to sulfonamides
and anuria unresponsive to a trial dose of loop
diuretic.
SIDE EFFECTS / ADVERSE REACTIONS Fluid and electrolyte imbalance ototoxicity,
hyperuricemia, Hyperglycemia, increases LDL
and triglycerides, lowers HDL.
DRUG INTERACTIONS • aminoglycosides, carboplatin,
paclitaxel (synergism of ototoxicity)
• anticoagulants (increased
anticoagulant activity)
CONTORA, ISAH D.
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• digitalis glycosides (increased digitalis-
induced arrhythmias)
• lithium (increased plasma levels of
lithium)
• propranolol (increased plasma levels
of propranolol)
• sulfonylureas (hyperglycemia)
• cisplatin (increased risk of diuretic-
induced ototoxicity)
• NSAIDs (blunted diuretic response and
salicylate toxicity when given with
• high doses of salicylates)
• probenecid (blunted diuretic response)
• thiazide diuretics (synergism of
diuretic activity of both drugs leading
to profound diuresis)
• amphotericin B (increased potential for
nephrotoxicity and toxicity and
• intensification of electrolyte imbalance
MECHANISM OF ACTION Inhibit the activity of Na+-K+-2Cl-(NKCC2)
symporter in the thick ascending limb of the
loop of Henle.

Pregnancy
Pregnancy Category C -Furosemide has been shown to cause unexplained maternal deaths and
abortions in rabbits at 2, 4 and 8 times the maximal recommended human dose. There are no
adequate and well-controlled studies in pregnant women. LASIX should be used during pregnancy
only if the potential benefit justifies the potential risk to the fetus.
CONTORA, ISAH D.
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B. Enumerate the types of diuretics and give examples of each type. Illustrate the
nephron and indicate sites of action of each type of diuretics.

1. Proximal Convoluted Tubule

• Carbonic Anhydrase Inhibitors (Acetazolamide, Methazolamide)
• Osmotic diuretics (oral/IV) (Glycerin / Isosorbide)
• (Mannitol / Urea)
2. Medullary Ascending Limb of the Loop of Henle
• Loop diuretics (Furosemide, Bumetanide)
• Osmotic Diuretic
3. Distal Convoluted Tubule
• Thiazides /Thiazide -like (chlorothiazide, Metolazone)
4. Cortical Collecting Tubule
• K+ sparing
• block ENaC /Antagonize
• aldosterone (Amiloride, Triamterene)
• (Spironolactone, Eplerenone)

STEP 4: START TREATMENT. How then will you write your medication orders?

Name : HP Age/Sex : 11/M

Address : Davao City Date : March 5, 2022

RX
Furosemide 40 mg (Lasix) tab # 2
Sig. 1/2 tablet 2x a day for 2 days

Isah D. Contora, RMT

Lic No.: 0089438
PTR No.: 0001

STEP 5: GIVE PATIENT FURTHER INFORMATION AND INSTRUCTION. Write (bullet format)
further information and warnings with the treatment that will be given to the patient and
family/caregivers

1. Patient education:
✓ Avoidance of overcrowding
✓ Maintain good personal hygiene
CONTORA, ISAH D.
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✓ Proper antibiotic therapy if positive for bacterial infection
2. Antibiotic Treatment:
✓ Penicillin G or erythromycin if with allergy to Penicillin

STEP 6: MONITOR TREATMENT. How do you monitor treatment based on effect? When
do you continue, adjust or stop the medications?

✓ Early systemic antibiotic therapy for streptococcal throat and skin infections does
not eliminate the risk of glomerulonephritis.
o Family members of patients with acute glomerulonephritis should be:
▪ cultured for group A hemolytic streptococci and treated if culture
positive
CONSISTS OF:
1. blood pressure measurements and urine examinations for protein and blood
• In general, examinations are performed at
• 4- to 6-week intervals for the first 6 months
• and at 3- to 6-month intervals thereafter,
• until both hematuria and proteinuria have been absent and the blood pressure has been
normal for 1 year.
• Documenting that the low C3 has returned to normal after 8-10 weeks may be useful.

2. Follow up at 0-6 weeks as frequently as necessary to determine the following:

• Hypertension has been controlled.
• Edema has started to resolve.
• Gross hematuria has resolved.
• Azotemia has resolved.

3. Follow up at 8-10 weeks after onset to assess the following:

• Azotemia has subsided.
• Anemia has been corrected.
• Hypertension has resolved.
• C3 and C4 concentrations have returned to normal.

4. Follow up at 3, 6, and 9 months after onset to check the following:

• Hematuria and proteinuria are subsiding gradually.
• Blood pressure is normal

5. Follow up at 12 months after onset to evaluate that proteinuria and microscopic

hematuria has disappeared.

6. Follow up at 2, 5, and 10 years after onset to check the patient's urine, blood pressure,
CONTORA, ISAH D.
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and serum creatinine level are normal.

7. Indications for doing Renal Biopsy:

• Renal function is worsening
• Patient has anuria
• There is no latent period between the acute glomerulonephritis and streptococcal
infection
• Complement levels are normal
• There is no rise in antistreptococcal antibodies
• There is persistent hypertension

8. Prompt address of hypertension and complications are the mainstay of treatment.

• Immediate outcome is excellent at expert hand
• and 1% can develop chronic kidney disease in long-term
• Recurrence is very rare (<1%).
• Prognosis: most recover completely
• One attack confers lifelong immunity