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MALARIA

Malaria
Malaria is an infectious disease which
is transmitted by the bite of female
anopheline mosquitoes.
Human malaria can be caused by
four species of the genus
Plasmodium: P. falciparum, P. vivax,
P. ovale, P. malariae.
Among all the stated genuses, P.
falciparum is the most deadly.

According to WHO report:


malaria prevalence in the world
ranges between 300-500 million per
year.
Mortality rate : 1.5 2.7 million per
year.
: 90% in Africa
: mostly affecting
children
below 5 yrs old.

Clinical Features
Fever
Headache
General malaise
Shivering
Myalgia

Clinical Examination
Tachycardia
Fever
Anemia
Splenomegaly

Affected renal function in P. falciparum

Definition
Affected renal function draws a wide
picture in red blood cell
abnormalities with the activation of
TH1 and TH2.
It includes hemodynamic which
direct to acute tubular necrosis.

LITERATURE REVIEW

Definition
Malaria caused by parasite in tropical
area transmitted by female
anopheline mosquitoes.
Malaria is known as the main cause
of acute kidney injury in South East
Asia, Vietnam, Peninsular India, and
Africa.

Clinical manifestations
Fever at first the fever may be continual or
erratic: the classical tertian or quartan fever
only appears after some daysn and it is
accompanied by rigors and drenching sweats.
Physical examination: tachycardia, fever,
anemia, hepatomegaly and splenomegaly.
P. falciparum infected: anemia, diarrhoea,
jaundice, acute kidney injury, acute coma
respiratory distress, disseminated
intravascular coagulation (DIC), breathlessnes.

Pathophysiology

Acute Tubular Necrosis


Incidence : 1-4% from P. falciparum
malaria.
Oliguria is common in early age:
typically occurs in few days until few
weeks.
Factors postulated to be involved is
intrarenal microvascular
vasoconstriction.

Acute Interstitial Nephritis


Acute interstitial inflammation
found in histopatology examination
of acute tubular necrosis and acute
glomerulonephritis P. falciparum.

Glomerulonephritis
Histological patterns: mononuclear
cell in infiltration, ( mesangial
hyperplasia and endothelial) , and
the thickness of basal membrane.

Immunological Mechanism

Clinical Manifestation
ATN microcircular destruction.
Massive hemolysis from
intravascular.
Imunne reaction towards the
parasites.
Fluid and electrolit disturbances.

Acute Kidney Injury


Definition
Compilation of clinical manifestations
marked functional decrease and the
increasing of creatinine serum or
decreasing of urine output.

Pathophysiology

Labarotorium Examination

Parasitology

Microscopic examination
QBC (semi quantitative buffy coat)
Rapid Manual Test
PCR ( Polymerase Chain Reaction)

Immunological Examination
C3 and C4 almost low in most
patients in early 2 weeks.
C3 loss in P. falciparum, around 44
60%, 20-40mg/dl (normal: 80-170
mg %)

Radiologic Examination
Chest X-ray cardiomegaly, %), lung
congestion, and pleural effusion.
Albar study: cardiomegaly (84,1%),
congested circulation (68,2%), pleura
effusion (65,9%) and lungs edema
(48,9%).

Diagnosis
Originated or living in an endemic
area.
Fever or history of high fever
Manifestations of affected renal; fluid
and electrolit disturbances,
glomerulonephritis
Malaria parasites findings in blood
culture
Other causes eliminated

Differential Diagnosis
APSGN occurs after certain latent period

If onset of hematuria occurs at the same time


or only within 2 5 days after respiratory
infection, IgA nephropathy should be
suspected

Presence of arthralgia, arthritis, carditis, hepatic


involvement or gastrointestinal bleeding is not
characteristic of APSGN.

Those conditions may be present in lesions such as


lupus nephritis or Henoch-Schonlein Nephritis

MPGN has similar features compared to


APSGN, but initial manifestation usually
more severe with renal function that is
greatly compromised.
The disease will progress into chronic stage

Management
Mild P. falciparum without
complication :
first line treatment - combined
artesunate and amodiaquin.
Second line - kina and tetracycline or
doxycycline
Severe malaria depends on
artemeter and injection of kina.

First line treatment for P. falcifarum

Second line treatment for


P.falcifarum

Amodiaquin
Antipirectic and anti inflamatory
Not recommended for prophylaxis
treatment
Present in 200-600mg per tablet of
amodiaquin hidroclorida or 151,1 mg
amodiaquin clorohidrat.
Amodiaquin dosage 10 mg /kg /3
days.

Artemisinin derivatives or
qinghaosu
Antimalaria for P. falciparum and P.
vivax
Derivatives: artesunat, artemeter,
dihidroartemisinin, artemisinin,
arteeter, and artelinic acid.
Mechanism interact with Fe and
heme in malaria hemozoin

Recommendation of WHO
2001
Combination of:
Artemeter and Lumefantrine
Artesunat and Amodiaquine
Artesunat and PirimetaminSufadoksin
Amodiaquine and PirimetaminSufadoksin
Artesunat and Meflokuin

Artesunate or artesunic
acid
Present in :
Tablet - 50 mg of artesunat
Ampule - 60 mg of artesunat
Artesunate is used 4 mg/kg /3 days
per dosage

Fluid, calorie and electrolyte


treatment
Insensible water loss (IWL) + urine
quantity 1 day before + water loss
from vomit, stool, and NGT

Hyponatremia
Sodium < 130 mEq/L
Common : overload of previous fluid
restriction
Dosage : (140-Na serum)x BW x 0,6=
mEq
Another opinion : Na=(125-Na
serum) x 0,6 x BW

Hypocalcemia
Does not need therapy unless tetanic
If tetanic: Ca-gluconase 10% dosage
0.5-1 ml/kgBW iv slowly

Diuretic challenge:
Furosemid 1 mg/kg BW
Increases urine output in kidney
failure

Anemia
Transfusion is needed if Hb<6g% or
Ht < 20%
PRC (10cc/kgBW) is given to increase
blood volume

FOLLOW UP
Days 4,7,14,28
Parasitemia might increased in first
12-24 hours after receving
antimalaria therapy
Diuresis monitoring : ureum and
creatinine rate 2-3 x/week, Na+, K+,
HCO3, PH.
ECG and Xray on indication

Prognosis
Morbidity : increase 45% if kidneys
affected, hence increasing mortality
rate by three times