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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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