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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. Malarial infection Antimalarial drugs G-6-P-D Deficiency Quinine, Phosphates, Pyrimethamine. BLACKWATER FEVER.

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MALARIA ASSOCIATED RENAL FAILURE

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  1. MALARIA ASSOCIATED RENAL FAILURE Common in the tropics Plasmodium falciparum Renal tubules Acute intravascular hemolysis Heavy parasitic infection

  2. INTRAVASCULAR HEMOLYSIS • Malarial infection • Antimalarial drugs • G-6-P-D Deficiency • Quinine, Phosphates, Pyrimethamine

  3. BLACKWATER FEVER • Hemoglobinemia • Hemoglobinuria • Exclude drug causation • Scanty parasitemia • Re-infection in non-immune immigrants • Acute renal failure • Uncommon in Kenya

  4. RENAL HISTOPATHOLOGY OF BLACKWATER FEVER • Tubular Atrophy • Interstitial Lymphocyte infiltration • Focal fibrosis • Iron pigments in fibroblasts and tubules • Heme casts in tubular lumen

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. HISTOPATHOLOGY OF GLOMERULONEPHRITIS • Mild mononuclear cell infiltration • Prominent mesangial proliferation • Increased mesangial matrix • Normal glomerular capillaries • Immune complex mediated

  11. IMMUNOFLUORESCENCE OF GLOMERULAR LESIONS • Fine granular deposits of IgM and C3 • Capillary walls • Mesangium • Malarial antigens • Glomerular endothelium • Medullary capillaries

  12. ELECTRON MICROSCOPY OF GLOMERULONEPHRITIS • Electron dense deposits • Granular, Fibrillar, and Amorphous material • Situated in • Subendothelial, • Mesangial, • Paramesangial regions

  13. 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

  14. 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

  15. 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

  16. 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

  17. CYTOKINES IN MARF • GPI. Glycosilphosphatidylinositol • Elevated in MARF • Glycolipid substances • Acts like an endotoxin • Can induce TNF and IL-1 • Cause hypoglycemia and pyrexia

  18. HUMORAL FACTORS IN MARF • Elevated catecholamines • Increased plasma renin activity • SIADHS • Inflammatory mediators • Kinins, Prosaglandins, • Histamine, Serotinin • Nitric Oxide, Endothelin, • Complement, Superoxidase

  19. 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

  20. 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

  21. 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

  22. 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

  23. MULTIORGAN FAILURE IN MARF • Cerebral malaria • Hemodynamic shock • Respiratory distress • MARF • Hematological disorders • Digestive disorders • Often fatal

  24. 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

  25. 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

  26. 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

  27. 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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