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SMOKESCREEN

SMOKESCREEN. DR EM Klaus 31 st May 2010 Department Internal Medicine Division Nephrology Consultant : Prof B van Rensburgh. Case Presentation:. 14y Female Secondary School Student Nigeria Father recent immigrant to RSA

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SMOKESCREEN

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  1. SMOKESCREEN DR EM Klaus 31st May 2010 Department Internal Medicine Division Nephrology Consultant : Prof B van Rensburgh

  2. Case Presentation: • 14y Female • Secondary School Student • Nigeria • Father recent immigrant to RSA • Referral from Nephrologists in Rumuigbo, Port Harcourt, Nigeria for renal biopsy

  3. Referral History: • Illness started end March 2010: • Fever • Progressive facial, leg swelling • Oliguria • No antecedent history: • No skin sepsis, no sore throat • No arthralgia, skin rash or mouth ulcers

  4. Referral History: • 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

  5. Referral History: • Abdominal: • Minimal Ascites • No organomegaly • Sideroom: Urinalysis • 3+ proteinuria • Numerous RBC, leukocytes and epithelial cells • Granular casts

  6. Referral History: • Lab: • 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

  7. Referral History: ?

  8. Referral History: • Lab: • Peripheral Blood smear = P. falciparum malaria

  9. Referral History: • Management: • Hospitalized 2 – 21 April 2010 • Rx: • Quinine IVI • Rocephin & Ciprofloxacin IVI • Renal function not improved. Diagnosed as acute GN • Fluid restrict • Furosemide IVI • Single Dialysis • Prednisolone & Azathioprine

  10. History: • Medication on arrival Universitas: • Proguanil 50mg BID PO • Prednisone 30mg BID PO • Azathioprine 50mg BID PO • Lasix 100mg BID PO daily • ASA 75mg OD PO • Norvasc 10mg OD PO • Simvastatin 20mg OD PO

  11. Examination: 4th May 2010 • Mass=54kg; L=155cm BMI=22,5 kg/m² • Apyrexial BP=130/80 P=78 • General: • 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

  12. Examination: 4th May 2010 • Side room: • Urine Dipstix: 3+ prot; 4+blood; 3+ Leucocytes; • Urinalysis: WBC casts; Granular casts • Na=125 K=3.5 C02=17 • BUN=64.8Creat=894 • CRP=6.2 • Alb=12 Chol=8,6 • Urine Prot: Creat = 0.22mg/mg

  13. 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

  14. Special Investigations: • Urine (5th May) = Burkholderia Cepacia • Sensitive to Ciprofloxacin, Bactrim • Sputa MCS = Negative • 24 hr Urine (6th May) = • Volume = 566ml • Creat Clearance = 8,7 ml/min • Prot = 0,31g/24 hr

  15. Special Investigations: • 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

  16. Renal Biopsy: 13th May • Immuno Florescence: • Granular positivity with IgA, IgG, IgM, C1q, C3 and C4 • Light Microscopy: • All 9 glomeruli had extracapillary proliferation with formation of fibrocellular cresents compatible with CLASS IV LUPUS NEPHRITIS. • Activity score 18/24 • Chronicity 4/12.

  17. Problem Statement: 14 y Female • Class IV Lupus Nephritis • Complication: • Nephrotic Syndrome • Renal Failure • UTI

  18. Malaria- Associated Renal Disease

  19. Malaria: • Protozoan • Genus Plasmodium • Acquired: • Sting of infected Anopheles mosquito • Blood transfusions (Prevalence amongst blood donors in a teaching hospital in Nigeria 32%) • Infected vector introduced in aircraft (“aircraft malaria”)

  20. Malaria: • Protozoan • Genus Plasmodium • Falciparum RBC any age • Malariae Aging RBC • Vivax Young RBC • Ovale Young RBC

  21. Malaria: Reported malaria cases (annual), By Country, Total, 2003 Source: WHO and UNICEF. World Malaria Report 2005.

  22. Malaria immune status: • NB in assessing suspected severe malaria • Individuals might have partial immunity (i.e. grown up in areas with malaria transmission throughout the year) • 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). • In patients without malaria immunity diagnosis established if parasitaemia present.

  23. Life Cycle:

  24. Pathogenesis: • Antigen-monocyte interaction • ↑ expression intracellular adhesion molecule-1 and CD 14 • InteractionTh1 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

  25. Pathogenesis:Plasmodium falciparum • Infection induces changes RBC that cause them to : • Adhere to each other and to the endothelium. • Changes in RBC deformability • Sequestered in the microcirculation • Maturation of the parasite occurs prior to haemolysis and infection of new red blood cells. • Blockage of the microcirculation → organ dysfunction and failure

  26. Pathogenesis: Microvascular sequestration of P. falciparum in the human brain. (Photo by Kamolrat Silamut, Wellcome Mahidol University Oxford Tropical Medicine Programme)

  27. One or more of the following clinical or laboratory features Clinical manifestations 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.) Impaired consciousness Multiple convulsions Respiratory distress (acidotic breathing) Pulmonary oedema (radiological) Circulatory collapse Abnormal bleeding Jaundice Hemoglobinuria Laboratory test Hyperparasitemia Acidosis Hyperlactatemia Renal impairment Hypoglycemia Severe anemia WHO criteria for severe malaria: 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).

  28. Classic presentation of severe malaria is: • Discoloured urine due to haemoglobinuria from severe intravascular haemolysis: ‘blackwater fever’

  29. Classic presentation of severe malaria is:

  30. Acute Renal Failure: • Fluid, electrolyte disturbance and Renal Failure • common esp P falciparum • Mortality: 15 – 45% • Untreated mortality: > 70%

  31. Acute Renal Failure Treatment: • Common complication of severe malaria (non-immune adults and children) • Treatment: • 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

  32. 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 • Hemofiltration • 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

  33. Glomerulonephritis • Acute Transient GN • Chronic GN

  34. Acute Transient GN: • P.ovale, P. vivax, • P.falciparum • Acute nephritic / nephrotic syndrome • Microscopic hematuria, mild proteinuria • Low C3 and C4 • Circulating immune complexes • Mesangial proliferation • Fine granular deposits of IgM and C3

  35. Chronic GN: • P. malariae (P. vivax) • Clinical: • Nonspecific, quartan malaria • Heavy proteinuria, nephrotic syndrome • Hypertension (late finding) • Lab: • Complement normal • Cholesterol normal (nutritional deficiency)

  36. P. falciparum Infects all RBC Severe Malaria Th1 response P. malariae Senescent RBC Indolent infection Th2 response Prolonged parasitemia, increased humoral and cell-mediated response Chronic GN:

  37. Prognosis of Chronic GN : • Despite successful treatment of malaria: ESKD in 3 -5 years • Unmodified by steroids, immunosuppressive agents • Progression: • Genetics • Malnutrition • EBV • Autoimmunity

  38. References: • Nicholas Day, Arjen M. Dondorp, The Management of Patients with Severe Malaria. Am. J. Trop. Med. Hyg., 77(Suppl 6), 2007, pp. 29–35 • WHO Guidelines for the Treatment of Malaria. “WHO severe falciparum malaria” Trans R Soc Trop Med Hyg 2000; 94 (Suppl. 1): 1–90). • Gary Maartens Severe malaria. CME June 2008 Vol.26 No.6 • Johnson , Feehaly. Comprehensive Nephrology -3rd edition Disclosure Statement: No conflict of interest to be declared with this presentation

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