Introduction

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2. Introduction Objectives: The importance of ruling out reversible aetiology of kidney injury. Investigations and management of AKI Understanding HIV Related acute kidney injury. 2011/03/07 Dr M.M.Mahlangu 2

3. Biography Mr J.T is a 42yr old male patient: Stays in Soshanguve, with his wife and 2 children. Is a non-smoker and non-alcoholic. Self-employed by selling vegetables and fruits. 2011/03/07 Dr M.M.Mahlangu 3

4. Case presentation (summary) Has Retroviral disease (RVD) diagnosed 6/12 ago, had a baseline CD4 of 59 cells/L and now is 267 cells/L on Regimen 1A (3TC 150mg bid. + D4T 20mg bid + EFV 600mg nocte) Previously treated for PTB (6mont) from May- October/2010, diagnosed on CXR and positive AFB sputum 2011/03/07 Dr M.M.Mahlangu 4

5. Case presentation (summary) Presented on the 06/11/10 with features suggestive of acute kidney injury stage III according to AKIN in renal failure (acute kidney injury network) Aetiology: Prerenal: acute enteritis and sepsis Intrinsic: acute interstitial nephritis (acute pyelonephritis and Bactrim induced) Risk factor: RVD 2011/03/07 Dr M.M.Mahlangu 5

6. Case presentation (summary) Complication: Severe anaemia, which is multifactorial (HIV, RENAL FAILURE, DIC, DRUGS) Uremic Encephalopathy stage I Peripheral Neuropathy multifactorial (HIV, RENAL FAILURE, DRUGS) Biochemically had hypercalcaemia, hyperphosphataemia and hyperkalaemia 2011/03/07 Dr M.M.Mahlangu 6

7. Case presentation He presented with a 2/52 history of enteritis with watery stools, no dysentery and no previous history of chronic diarrhoea and no reports of malaena stools. Develop generalised body pains and weakness and of fatigue x 1 week Had bilateral flank sharp pains, worse on initiation of micturition, followed by BOM, and Dysuria with frequency and nocturia.. 2011/03/07 Dr M.M.Mahlangu 7

8. Case presentation Urinary output was 300ml or more per day, Urine was dark and smelly. Disorientated Peripheral neuropathy and purities. History of SOB at rest x 2-5days, no history of coughing. On 02/11/10, he presented to casualty and was discharged on supportive therapy and high doses of Bactrim. 2011/03/07 Dr M.M.Mahlangu 8

9. Case presentation Past Med History: above Allergies: NIL Drug History: No over counter medication/Herbal Intoxication 2011/03/07 Dr M.M.Mahlangu 9

10. Summary of symptoms Mr J.T is RVD Reactive on HAART Presenting with following problems: Acute kidney injury with: Acute Enteritis Urinary tract infection (acute pyelonephritis) Peripheral neuropathy 2011/03/07 Dr M.M.Mahlangu 10

11. Case presentation On Examination, he looked disoriented to self and place with poor cooperation and confused. BP: 109/80 mm Hg (supine) and 90/50 (erect), indicative of Orthostatic hypotension Mild Pyrexia with TEMP of 38.5 Tachycardia with pulse of 110 bpm, regular and low volume On peripheral signs had moderate to severe pallor, and no peripheral oedema, nor lymphadenopathy. 2011/03/07 Dr M.M.Mahlangu 11

12. Case presentation CNS: Had asterixis No meningeal irritation No focal deficit RESP: Symmetrical chest movement, with tachypnoea of RR=24br/min GAEB, no pulmonary oedema CVS: AP Beat 5Th ICS normal position, no Friction Rub S1 was loud d/t tachycardia No features of infective endocarditis 2011/03/07 Dr M.M.Mahlangu 12

13. Case presentation Abdomen: Soft and tender both lumbar area with renal angle tenderness. No organomegaly On PR: NIL 2011/03/07 Dr M.M.Mahlangu 13

14. Case presentation Urinalysis: Leukocyte=3+ Blood= 2+ Protein=Trace Suggestive of (AIN/UTI) Skin: No petechial rash/ nor uremic frosts. 2011/03/07 Dr M.M.Mahlangu 14

15. Differential diagnosis Mr J.T is a 41yr male PT with acute kidney injury in renal failure due to the following aetiology: Severe acute enteritis with volume depletion (infectious) Sepsis with vasoconstriction. Acute pyelonephritis and bactrim induced acute interstitial nephritis 2011/03/07 Dr M.M.Mahlangu 15

16. Differential diagnosis Other Differential Aetiology: Haemolytic Uremic syndrome (common in children, present with Nephritic Sx) HIVICK with crescentic RPGN (HTN; OLIGURIA; Fluid overload) TTP (not all pentad features) Salmonella Typhoid with AKI Acute meningitis with sepsis and AKI 2011/03/07 Dr M.M.Mahlangu 16

17. Investigation ABG: Moderate-severe metabolic acidosis with respiratory compensation (PH=7.108; Pco2=1.83kpa; Po2=10.00kpa; HCO3=4.1; BE= -24.00) ii. CXR: Normal No features of Globular heart (pericarditis) 2011/03/07 Dr M.M.Mahlangu 17

18. Investigation 2011/03/07 Dr M.M.Mahlangu 18

19. Investigations iii. 24 HR Creatinine Clearance done on 15/11/10: Volume collection: 2400ml Cr Clearance: 23 ml/min Du- Protein: 2.54g/24hr (secondary to AIN with proteinuria, no clinical and Laboratory features of Nephrotic syndrome) Urine urea was 55mmol/l and urine Cr was 391 iv. FE Urea was >50%, which indicates Acute Tubular Necrosis. 2011/03/07 Dr M.M.Mahlangu 19

20. Investigation 2011/03/07 Dr M.M.Mahlangu 20

21. Investigation Peripheral smear: mild red cell fragments and schistocytes. Anaemia could be microcytic hypochromic, because of D4T he might have had macrocytosis LDH= 680(H) v. Blood and urine culture: E. Coli was cultured Susceptibility: resistant to ciprobay and susceptible to meropenem. Stool culture and tests were negative 2011/03/07 Dr M.M.Mahlangu 21

22. Investigation vi. Clotting Profile: INR:1.53(H); D-Dimers: 2.53(H); Fibrinogen: -0.1g/l(L). This shows DIC d/t sepsis. vii. CD4 Count: Absolute CD4 is 267 X 10_6 presently and baseline CD4 was 59 X 10_9 (May/2010) This shows compliance and good response. 2011/03/07 Dr M.M.Mahlangu 22

23. Investigation viii. Liver function test: Total protein: 56g/l(L) ALP: 90 Albumin : 16g/l(L) ALT: 34 AST:64 ix. Kidney sonar: Both RT and Left have no Hydronephrosis, size is 10.7 X 5cm and 12.0 X 5cm respectively. No cortico-medullary tuft and no scarring. 2011/03/07 Dr M.M.Mahlangu 23

24. Investigation x. Lumbar puncture in an immunocompromised patient with confusion was indicated and came back Negative. xi. Hepatitis B/C; Syphilitic studies; malaria and Widal test for typhoid were all negative 2011/03/07 Dr M.M.Mahlangu 24

25. Management Acute management: Fluid Rehydration: Maintained on CVP line, measurement was 3cm H2O. Maintained on 0.9% N/S running at 200ml/hr. Correction of hyperkalaemia: Salbutamol Nebs 10ml of calcium gluconate iv stat 50ml of 50% Dextrose iv 10 unit of actrapid iv 2011/03/07 Dr M.M.Mahlangu 25

26. Management Correction of Metabolic acidosis Gave 100ml of 8.5% NaHCO3 and maintained 100ml in 900ml of 5% Dextrose. Transfused the patient with 3 units of Blood. Because of Uremic encephalopathy and a very high urea >90 mmol/l, we initiated a 96 hr (4 days), continuous peritoneal dialysis in our renal unit (we used a 1.5% dialysate) 2011/03/07 Dr M.M.Mahlangu 26

27. Management Intravenous antibiotics: We started with IV ciprobay and flagyl prior to culture results. On the 4th day in Hospital started on meropenem for 7 days. Supportive Treatment: Thiamine 100mg/day Tegretol 200mg/day for neuropathy (few days) Stopped Bactrim and started on Dapsone. 2011/03/07 Dr M.M.Mahlangu 27

28. Management Adjustment of HAART relative to eGFR: Reduced 3TC to 150mg/day Reduced D4T to 20mg/day Continued with EFV of 600mg/day Long term management: He was discharged and follows up at MOPD for his renal Injury, and has improved He also attends our HIV Specialised Clinic, where his HAART was adjusted based on eGFR 1-2 monthly visit. 2011/03/07 Dr M.M.Mahlangu 28

29. Discussion This case shows that AKI in HIV patients can be managed, but what is important are: Take a proper renal History Do a proper examination Exclude: pre-renal; post-renal and exacerbating agents. If the cause of AKI is unknown, do a renal biopsy (e.g. HIVICK) Management will be directed on the cause of renal injury 2011/03/07 Dr M.M.Mahlangu 29

30. Approach to Acute Kidney Injury AKI denotes the loss of kidney function over hrs to days resulting in accumulation of nitrogenous waste and distribution of volume, electrolyte and acid-base homeostasis. Classification of AKI is based on rise in serum creatinine and/or urine output. Stage I: S Creat >150-200% or <0.5ml/kg/6hr Stage II: S Creat >200-300% or <0.5ml/kg/12hr Stage III: S Creat >300% or <0.3ml/kg/24hr 2011/03/07 Dr M.M.Mahlangu 30

31. Approach to Acute Kidney Injury The approach is to delineate whether the AKI is Pre-renal that accounts for 50-80% of cases, Intrinsic accounting for 10-30% and post-renal that accounts for 5-10%. Always remember that there can be an overlap. The incidence of AKI in HIV patients is expected to be high due to opportunistic infections and drug toxicity. Risk factors for AKI is low CD4 count 2011/03/07 Dr M.M.Mahlangu 31

32. Approach to Acute Kidney Injury A retrospective study from 2002 - 2007 was released by UCT recently where 58% of HIV patients with AKI in renal failure had ATN and had recovery of 82%, received acute dialysis and factors that determined survival was: Higher CD4 count Lower Pre-dialysis serum Creatinine (<1230 umol/L) Longer Hospitalisation 2011/03/07 Dr M.M.Mahlangu 32

33. Approach to Acute Kidney Injury In another study in USA showed AKI was 4.6X more in HIV patients. Our respected Nephrologist Prof Naicker from Wits University stated �Aggressive and appropriate management in HIV AKI is potentially reversible�. Forms of Acute kidney Injury: 2011/03/07 Dr M.M.Mahlangu 33

34. Approach to Acute Kidney Injury Acute Tubular Necrosis: Tubular cell destruction d/t O2 deprivation and exposure to toxins Common Aetiology to ATN: Severely low Blood pressure Vasoconstriction d/t sepsis Severe dehydration d/t diarrhoea HIV patients are prone to both diarrhoea and sepsis. 2011/03/07 Dr M.M.Mahlangu 34

35. Approach to Acute Kidney Injury 2) Acute interstitial nephritis: Mostly d/t severe allergic RXN to Meds. Infection like Pyelonephritis Common drugs: Penicillins; NSAIDs; Quinolones 3) Crystalluria: Number of drugs are insoluble and form crystals like Indinavir and atazanavir Other rare drugs include acyclovir and sulphonamides. 2011/03/07 Dr M.M.Mahlangu 35

36. Approach to Acute Kidney Injury 4) Acute Glomerulonephritis: Glomerular inflames, leading to hematuria, HTN, water retention and swelling. Aetiology: Infections/Cancers/Immune systemic RXN Ig A nephropathy Post-infectious Gn (Strep/staph) Parasitic and fungal Crescentic Glomerulonephritis. 2011/03/07 Dr M.M.Mahlangu 36

37. Approach to Acute Kidney Injury 5) Infections and neoplasm associated with AKI: A nephrology survey in Africa showed that Malaria and diarrhoeal pathogens are most common causes of AKI. Sepsis and infection lead to dehydration and vasoconstriction Hepatitis B can cause either nephritic and /or nephrotic syndrome leading to AKI 2011/03/07 Dr M.M.Mahlangu 37

38. Approach to Acute Kidney Injury 6)Thrombotic Micro-angiopathy: Thrombocytic thrombocytopenic purpura presenting with thrombocytopenia, micro-angiopathic haemolytic anaemia, fever, neurologic and renal abnormality Another type is Haemolytic Uraemic syndrome presenting with micro-angiopathic anemia, thrombocytopenia, fever and severe AKI. 2011/03/07 Dr M.M.Mahlangu 38

39. Evaluation of AKI in HIV patients Questions which need to be answered on history and EXMN? Is there volume depletion? Could there be urinary obstruction? Has the patient been exposed to major nephrotoxins? Does the patient have pre-existing condition? Is there need for serological test and renal biopsy? 2011/03/07 Dr M.M.Mahlangu 39

40. Evaluation of AKI in HIV patients Urinary pattern and frequency: Hematuria, dysuria, and pyuria Urgency, frequency, dribbling, and incontinence, especially in elderly Volume status: Dizziness or orthostatic instability may point toward volume depletion Weight gain and swelling may point to fluid overload. 2011/03/07 Dr M.M.Mahlangu 40

41. Evaluation of AKI in HIV patients Medication: Over-counter medication or Herbal products NSAIDs, ACEI, Aminoglycosides, AMB Pre-existing conditions: Diabetes mellitus, Hypertension, liver cirrhosis, polycystic kidney disease Other potential Aetiology: Connective tissue disease Vasculitides Haematological malignancy 2011/03/07 Dr M.M.Mahlangu 41

42. Evaluation of AKI in HIV patients On EXMN check the Blood pressure both in supine and erect position. Cardiac EXMN: Location and character of Apex beat S3 gallop (volume overload) S4 gallop (pressure overload) Pericardial rub RESP EXMN: Kussmaul Respiration d/t acidosis and check for pulmonary oedema in fluid overload. 2011/03/07 Dr M.M.Mahlangu 42

43. Evaluation of AKI in HIV patients Genito-urinary EXMN: Do PV and PR Skin: Uremic frosts and Petechial rash in vasculitis and uremic syndrome. CNS: Higher centre assessment. 2011/03/07 Dr M.M.Mahlangu 43

44. Evaluation of AKI in HIV patient Urinalysis: Pre-renal: FE UREA< 35%, no blood or protein ATN: Protein (1), Blood (1), FE UREA>50% GN: Protein (2/3), Blood (2+), FE UREA<35% AIN: Protein (1+), Blood (1+), FE UREA>50% FE UREA is more sensitive of 85%, specificity of 92 % and positive predictive value of 98%. 2011/03/07 Dr M.M.Mahlangu 44

45. Evaluation of AKI in HIV patients II. CBC and coagulation profile: May provide information about underlying disease. III. Radiological evaluation: Assist in urinary tract obstruction Renal artery stenosis Renal size, for CKD which can be normal in HIV patients. 2011/03/07 Dr M.M.Mahlangu 45

46. Evaluation of AKI in HIV patients IV. Indication for Biopsy: AKI, diagnosis not clear. Nephrotic syndrome Nephritic syndrome of unclear aetiology RPGN V. Indications for dialysis: Volume overload refractory to diuretics Hyperkalaemia refractory to medical treatment 2011/03/07 Dr M.M.Mahlangu 46

47. Evaluation of AKI in HIV patients Metabolic acidosis refractory to medical TX Uremic syndrome Serositis Seizure and confusion Bleeding 2011/03/07 Dr M.M.Mahlangu 47

48. References Journal of international society of nephrology www.aidsmap.com www.kidney-international.org 2011/03/07 Dr M.M.Mahlangu 48

49. THANX AND GOD BLESS !! 2011/03/07 Dr M.M.Mahlangu 49