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MALARIA ASSOCIATED RENAL FAILURE. Common in the tropics Plasmodium falciparum Renal tubules Acute intravascular hemolysis Heavy parasitic infection. INTRAVASCULAR HEMOLYSIS. Malarial infection Antimalarial drugs G-6-P-D Deficiency Quinine, Phosphates, Pyrimethamine. BLACKWATER FEVER.

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malaria associated renal failure
MALARIA ASSOCIATED RENAL FAILURE

Common in the tropics

Plasmodium falciparum

Renal tubules

Acute intravascular hemolysis

Heavy parasitic infection

intravascular hemolysis
INTRAVASCULAR HEMOLYSIS
  • Malarial infection
  • Antimalarial drugs
  • G-6-P-D Deficiency
  • Quinine, Phosphates, Pyrimethamine
blackwater fever
BLACKWATER FEVER
  • Hemoglobinemia
  • Hemoglobinuria
  • Exclude drug causation
  • Scanty parasitemia
  • Re-infection in non-immune immigrants
  • Acute renal failure
  • Uncommon in Kenya
renal histopathology of blackwater fever
RENAL HISTOPATHOLOGY OF BLACKWATER FEVER
  • Tubular Atrophy
  • Interstitial Lymphocyte infiltration
  • Focal fibrosis
  • Iron pigments in fibroblasts and tubules
  • Heme casts in tubular lumen
causes of hemolysis in falciparum malaria
CAUSES OF HEMOLYSIS IN FALCIPARUM MALARIA
  • Impairment in physiologic deformity
  • Increased mechanical fragility
  • Interference with RBC ATP
  • Interference with Na-K RBC ATP
  • Altered charges on RBC surface
  • Immunologic reactions
malaria associated acute renal failure
MALARIA ASSOCIATED ACUTE RENAL FAILURE
  • Common cause of MARF
  • Heavy parasitemia
  • 1% to 4% develop ARF
  • 60% in Malignant malaria
  • Usually oliguric
  • Catabolic State
  • Cholestatic Jaundice
  • Rarely hepatocellular
  • Lasts a few days to several weeks
malaria associated acute renal failure1
MALARIA ASSOCIATED ACUTE RENAL FAILURE
  • Occurs 4 - 7 days from onset of fever
  • Early onset hyperkalemia
  • Hyperuricemia common
  • High urinary uric acid-creatinine ratio
  • Oliguria lasts a few days to several weeks
histopathology of marf
HISTOPATHOLOGY OF MARF
  • Distal tubules, Necrosis, Degeneration
  • Proximal tubules
    • Cloudy swelling and Vacuolisation
    • Hemoglobin in lumen
    • Hemosiderin in Lumen
  • Oedematous interstitium
  • Tubular degeneration
  • Regeneration of epithelial cells
  • Dilatation of tubules
  • Features of acute tubular necrosis
glomerulonephritis in falciparum malaria
GLOMERULONEPHRITIS IN FALCIPARUM MALARIA
  • Manifestations include:
    • Mild proteinuria
    • Hematuria
    • Casts
  • Non-progressive,and reversible
  • ARF and Hypertension rare
  • Resolves in 4 – 6 weeks after antimalarials
  • Nephrotic syndrome is rare
histopathology of glomerulonephritis
HISTOPATHOLOGY OF GLOMERULONEPHRITIS
  • Mild mononuclear cell infiltration
  • Prominent mesangial proliferation
  • Increased mesangial matrix
  • Normal glomerular capillaries
  • Immune complex mediated
immunofluorescence of glomerular lesions
IMMUNOFLUORESCENCE OF GLOMERULAR LESIONS
  • Fine granular deposits of IgM and C3
    • Capillary walls
    • Mesangium
  • Malarial antigens
    • Glomerular endothelium
    • Medullary capillaries
electron microscopy of glomerulonephritis
ELECTRON MICROSCOPY OF GLOMERULONEPHRITIS
  • Electron dense deposits
  • Granular, Fibrillar, and Amorphous material
  • Situated in
    • Subendothelial,
    • Mesangial,
    • Paramesangial regions
pathogenesis of marf
PATHOGENESIS OF MARF
  • Hypovolemia
    • Release of Kinins, Kallikreins, Histamine
    • Increased capillary permeability
    • Insensible fluid loss
    • Renin Angiotensin System stimulation
    • Increased catecholamine secretion
    • Hyperviscosity
      • Decreased RBC deformability
      • Elevated fibrinogen
  • Causes renal ischemia and MARF
pathogenesis of marf1
PATHOGENESIS OF MARF
  • INTRAVASCULAR COAGULATION
  • Fibrin degradation products
  • Prolonged pro-thrombin time
  • Thrombocytopenia
  • Decreased platelet life span
    • Platelet agglutination
    • Splenic pooling
  • Alteration in coagulation factors
  • Low grade regional intra-vascular coagulation
    • Stasis and Inflammation
  • Hemolysis and MARF
pathogenesis of marf2
PATHOGENESIS OF MARF
  • Fever
  • Cholestatic Jaundice
    • Obstructive Jaundice and ARF
    • Tubulotoxicity of Bile acids
    • Severe oliguria in association with Jaundice
  • Rhabdomyolysis. Rare
    • Myoadenyl deaminase deficiency MAD
cytokines in marf
CYTOKINES IN MARF
  • Serum soluble CD14
    • Marker of inflammatory response
    • Elevated in complicated Malaria
  • TNFalfa.
    • Associated with tissue damage
    • Stimulates expression of adhesion molecules
      • ELAM 1 and ICAM-1
      • Facilitates thrombospondin secretion
  • IL-1, IL-6, IL-8
    • Acute phase reactions
    • Expression of adhesion molecules
    • Release of vasoactive mediators
    • Plasma leakage from intravascular compartments
cytokines in marf1
CYTOKINES IN MARF
  • GPI. Glycosilphosphatidylinositol
    • Elevated in MARF
    • Glycolipid substances
    • Acts like an endotoxin
    • Can induce TNF and IL-1
    • Cause hypoglycemia and pyrexia
humoral factors in marf
HUMORAL FACTORS IN MARF
  • Elevated catecholamines
  • Increased plasma renin activity
  • SIADHS
  • Inflammatory mediators
    • Kinins, Prosaglandins,
    • Histamine, Serotinin
    • Nitric Oxide, Endothelin,
    • Complement, Superoxidase
electrolyte imbalance in marf
ELECTROLYTE IMBALANCEIN MARF
  • Hyponatremia
    • 67% in heavy parasitemia
    • Dilutional
    • Water retention in renal failure
    • Resetting of osmoreceptors
    • SIADH due to fever
      • Delayed response to water load
      • Caution with IV fluids
      • Pulmonary edema a hazard
electrolyte imbalance in marf1
ELECTROLYTE IMBALANCEIN MARF
  • Hypernatremia. Rare
    • Pure water depletion
    • Cerebral edema
      • Blunted thirst
      • Inadequate provision of water
  • Hypokalemia in uncomplicated malaria
  • Hyperkalemia
  • Hypocalcemia with severe infection
  • Hypophosphatemia wih severe infection
treatment of marf
TREATMENT OF MARF
  • Antimalarial therapy essential
  • Quinine.
    • Normal doses in MARF for first 24 to 48 hours
    • Thereafter reduce dose to 10 mg/kg 12 hourly
    • Or 24 hourly for 7
  • Artemesin derivatives. Potent
    • Inhibit adherence properties
    • Reduce parasite count remarkably
  • Exchange transfusion
treatment of marf1
TREATMENT OF MARF
  • Dialysis in hypercatabolic states
  • Hemodialysis or Hemofiltraion
  • Peritoneal dialysis less preferable
    • Impaired peritoneal microcirculation
    • Parasitised erythocytes
    • Vasoconstriction
    • Reduced solute transport
    • Improved efficiency as parasitemia declines
    • Continuous PD beneficial
multiorgan failure in marf
MULTIORGAN FAILURE IN MARF
  • Cerebral malaria
  • Hemodynamic shock
  • Respiratory distress
  • MARF
  • Hematological disorders
  • Digestive disorders
  • Often fatal
marf at knh
MARF AT KNH
  • Were et al
  • 47 Patients with ARF
  • 21 (45%) with medical causes
  • 9 (19%) developed MARF
  • Overall mortality 40.4%
  • MARF mortality 33.3%
  • Cholestatic Jaundice in 4 patients
  • All patients with MARF were oliguric
marf at knh1
MARF AT KNH
  • Onset phase 2.9 days
  • Oliguria lasted 9.8 days
  • 5 patients not dialysed. 2 died
  • 4 patients had PD. 1 died
  • Mean duration of PD 11 days
  • Continuous PD. 8 cycles daily
  • All had heavy parasitemia. No BWF
marf in vietnam tang et al
MARF IN VIETNAM (TANG ET AL)
  • 64 (MARF) vs 66 (Severe Malaria only)
  • Clinically and biochemically, ATN
  • Associated cholestatic jaundice, & liver dys
  • Fatality associated with
    • Anuria, Short duration of illness
    • Hyperparasitemia, Multisystem involvement
  • Recovery unrelated to parasitemia
marf in vietnam tang et al1
MARF IN VIETNAM (TANG ET AL)
  • Recovery unrelated to hemoglobinuria
  • Oliguria 4 days (0-19)
  • Normal biochemistry 17 days (11-23)
  • Treated by PD
  • Mortality decreased from 75% to 26%
  • Good condition initially
  • Complications develop rapidly
  • Treat as ATN with circulatory shock
  • Early diagnosis and dialysis mandatory
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