Download Referral History

SMOKESCREEN
DR EM Klaus
31st May 2010
Department Internal Medicine
Division Nephrology
Consultant : Prof B van Rensburgh
Case Presentation:
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14y Female
Secondary School Student
Nigeria
Father recent immigrant to RSA
Referral from Nephrologists in Rumuigbo,
Port Harcourt, Nigeria for renal biopsy
Referral History:
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Illness started end March 2010:
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Fever
Progressive facial, leg swelling
Oliguria
No antecedent history:
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No skin sepsis, no sore throat
No arthralgia, skin rash or mouth ulcers
Referral History:
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Ill with facial and gross bipedal pitting oedema
Pyrexia; Temp axillary 38°C
Episodes of rigor, pallor was anicteric
Respiratory:
 Rate: 24bpm
 Chest clear
Cardio:
 P=68bpm;
BP=110/80
 Normal heart sounds; no murmurs or friction rub
heard
Referral History:
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Abdominal:
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Minimal Ascites
No organomegaly
Sideroom: Urinalysis
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3+ proteinuria
Numerous RBC, leukocytes and epithelial cells
Granular casts
Referral History:
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Lab:
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Na= 127.9 mmol/l
K=
4.5
Cl=
97.2
BUN = 13.8 mmol/l
Creat =159 umol/l
eGFR=35 ml/min
Total chol =7 mmol/l
Referral History:
Referral History:
 Lab:
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Peripheral Blood smear =
P. falciparum malaria
Referral History:
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Management:
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Hospitalized 2 – 21 April 2010
Rx:
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Quinine IVI
Rocephin & Ciprofloxacin IVI
Renal function not improved. Diagnosed as acute GN
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Fluid restrict
Furosemide IVI
Single Dialysis
Prednisolone & Azathioprine
History:
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Medication on arrival Universitas:
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Proguanil 50mg BID PO
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Prednisone 30mg BID PO
Azathioprine 50mg BID PO
Lasix 100mg BID PO daily
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ASA 75mg OD PO
Norvasc 10mg OD PO
Simvastatin 20mg OD PO
Examination: 4th May 2010
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Mass=54kg;
Apyrexial
General:
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L=155cm
BP=130/80
BMI=22,5 kg/m²
P=78
Bipedal oedema and peri-orbital oedema
No jaundice, anemia
Bilateral Malar rash – involving nasolabial folds
Resp: Left pleural effusion
Abdom: Ascites
CVS: normal
Neuro: normal
MS: No vasculitis, synovitis
Examination: 4th May 2010
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Side room:
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Urine Dipstix:
Urinalysis:
3+ prot; 4+blood; 3+ Leucocytes;
WBC casts; Granular casts
Na=125 K=3.5 C02=17
BUN=64.8
Creat=894
CRP=6.2
Alb=12
Chol=8,6
Urine Prot: Creat = 0.22mg/mg
Examination: 4th May 2010
 Renal
U/S=
 Left=13,9cm
Right=15,1cm
 Grade 2 hyperechoic with NO
hydronephrosis
 Left pleural effusion + Ascites in pelvis
Special Investigations:
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Urine (5th May) = Burkholderia Cepacia
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Sensitive to Ciprofloxacin, Bactrim
Sputa MCS = Negative
 24 hr Urine (6th May) =
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Volume = 566ml
Creat Clearance = 8,7 ml/min
Prot = 0,31g/24 hr
Special Investigations:
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Malaria =
Negative
HIV =
Negative
RPR =
Negative
Hep B/C =
Negative
ASOT =
<50
ANCA =
Negative
C3 = Negative; C4 = Negative
ANA = Positive, Speckled, Titre 1:640
Anti ds DNA Positive
Renal Biopsy: 13th May
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Immuno Florescence:
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Granular positivity with IgA, IgG, IgM, C1q, C3 and C4
Light Microscopy:
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All 9 glomeruli had extracapillary proliferation with
formation of fibrocellular cresents compatible with
CLASS IV LUPUS NEPHRITIS.
Activity score 18/24
Chronicity 4/12.
Problem Statement:
14 y Female
1. Class IV Lupus Nephritis
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Complication:
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Nephrotic Syndrome
Renal Failure
UTI
Malaria- Associated
Renal Disease
Malaria:
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Protozoan
Genus Plasmodium
Acquired:
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Sting of infected Anopheles mosquito
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Blood transfusions (Prevalence amongst blood donors in a teaching hospital in Nigeria 32%)
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Infected vector introduced in aircraft (“aircraft malaria”)
Malaria:
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Protozoan
Genus Plasmodium
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Falciparum
Malariae
Vivax
Ovale
RBC any age
Aging RBC
Young RBC
Young RBC
Malaria:
Reported malaria cases (annual), By Country, Total, 2003 Source: WHO and UNICEF.
World Malaria Report 2005.
Malaria immune status:
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NB in assessing suspected severe malaria
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Individuals might have partial immunity (i.e. grown
up in areas with malaria transmission throughout
the year)
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Could have asymptomatic parasitaemia with P. falciparum
Presenting illness may be due to another cause (e.g. meningococcal
meningitis in an older child with possible cerebral malaria).
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In patients without malaria immunity diagnosis
established if parasitaemia present.
Life Cycle:
Pathogenesis:
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Antigen-monocyte interaction
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↑ expression intracellular adhesion molecule-1 and CD 14
Interaction Th1 and Th2 cytokines
TNF α secretion
Infected RBC express surface antigens (Pf155/RESA)
favouring Th2 lymphocyte response
P. falciparum activates the alternative Complement
pathway + intrinsic coagulation cascade
Pathogenesis: Plasmodium falciparum
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Infection induces changes RBC that
cause them to :
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Adhere to each other and to the endothelium.
Changes in RBC deformability
Sequestered in the microcirculation
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Maturation of the parasite occurs prior to haemolysis
and infection of new red blood cells.
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Blockage of the microcirculation → organ dysfunction
and failure
Pathogenesis:
Microvascular sequestration of P. falciparum in the human
brain. (Photo by Kamolrat Silamut, Wellcome Mahidol University Oxford Tropical Medicine Programme)
WHO criteria for severe malaria:
One or more of the following clinical
or laboratory features
Laboratory test
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Hyperparasitemia
Clinical manifestations
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Acidosis
Hyperlactatemia
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Prostration (Defined as the inability to sit
upright in a child normally able to do so, or to drink in the
case of children too young to sit.)
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Impaired consciousness
Multiple convulsions
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Renal impairment
Hypoglycemia
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Severe anemia
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Respiratory distress (acidotic breathing)
Pulmonary oedema (radiological)
Circulatory collapse
Abnormal bleeding
Jaundice
Hemoglobinuria
Taken from WHO Guidelines for the Treatment of Malaria. (WHO, Geneva Switzerland: 2006). Full details of the definitions can
be found in “WHO severe falciparum malaria” (Trans R Soc Trop Med Hyg 2000; 94 (Suppl. 1): 1–90).
Classic presentation of severe
malaria is:
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Discoloured urine due to
haemoglobinuria from severe
intravascular haemolysis:
‘blackwater fever’
Classic presentation of severe
malaria is:
Acute Renal Failure:
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Fluid, electrolyte disturbance and Renal
Failure
common esp P falciparum
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Mortality: 15 – 45%
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Untreated mortality:
> 70%
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Acute Renal Failure Treatment:
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Common complication of severe malaria
(non-immune adults and children)
Treatment:
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Renal replacement therapy — preferably by
hemofiltration when available
HD superior to PD
(in terms of mortality and cost-effectiveness)
Nicholas Day, Arjen M. Dondorp, The Management of Patients with Severe Malaria. Am. J. Trop.
Med. Hyg., 77(Suppl 6), 2007, pp. 29–35
Metabolic Acidosis Treatment:
Common complication of severe malaria
Strong associated with mortality
Lactic acid, impaired renal bicarbonate handling
and other unidentified acids play major roles
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Hemofiltration
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rapidly eliminate acidosis in malaria patients with renal
failure, even in the presence of lactic acidosis.
Early hemofiltration may be a useful in acidosis
and renal impairment (NO trial data yet)
Nicholas Day, Arjen M. Dondorp, The Management of Patients with Severe Malaria. Am. J. Trop.
Med. Hyg., 77(Suppl 6), 2007, pp. 29–35
Glomerulonephritis
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Acute Transient GN
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Chronic GN
Acute Transient GN:
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P.ovale, P. vivax,
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P.falciparum
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Acute nephritic / nephrotic syndrome
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Microscopic hematuria, mild proteinuria
Low C3 and C4
Circulating immune complexes
Mesangial proliferation
Fine granular deposits of IgM and C3
Chronic GN:
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P. malariae
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Clinical:
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(P. vivax)
Nonspecific, quartan malaria
Heavy proteinuria, nephrotic syndrome
Hypertension (late finding)
Lab:
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Complement normal
Cholesterol normal (nutritional deficiency)
Chronic GN:
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P. falciparum
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Infects all RBC
Severe Malaria
Th1 response
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P. malariae
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Senescent RBC
Indolent infection
Th2 response
Prolonged
parasitemia,
increased humoral
and cell-mediated
response
Prognosis of Chronic GN :
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Despite successful treatment of malaria:
ESKD in 3 -5 years
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Unmodified by steroids, immunosuppressive
agents
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Progression:
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Genetics
Malnutrition
EBV
Autoimmunity
References:
1.
Nicholas Day, Arjen M. Dondorp, The Management of Patients with
Severe Malaria. Am. J. Trop. Med. Hyg., 77(Suppl 6), 2007, pp. 29–
35
2.
WHO Guidelines for the Treatment of Malaria. “WHO severe
falciparum malaria” Trans R Soc Trop Med Hyg 2000; 94 (Suppl. 1):
1–90).
3.
Gary Maartens Severe malaria. CME June 2008 Vol.26 No.6
4.
Johnson , Feehaly. Comprehensive Nephrology -3rd edition
Disclosure Statement:
No conflict of interest to be declared with this presentation