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Acte kidney injury-advances in diagnosis & management.
This document discusses advances in the diagnosis and management of acute kidney injury (AKI). It begins with objectives and outlines of topics including AKI definitions, classification systems, biomarkers for early detection, and management strategies. Novel biomarkers such as Kim-1, NGAL, and cystatin C allow detection of AKI earlier than serum creatinine. While renal replacement therapy is important for established AKI, prevention and treatment of underlying causes are priorities. Overall, awareness of AKI is increasing worldwide and standardized criteria along with new diagnostics and therapies can lead to better outcomes.
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Acte kidney injury-advances in diagnosis & management.
- 1. Dr.W.A.P.S.R Weerarathna. Registrarin Medicine-WD 10/02 ACUTE KIDNEY INJURY-ADVANCES IN DIAGNOSIS & MANAGEMENT
- 2. OBJECTIVES… Anatomy/Physiology of the kidneys Introduction- Acute Kidney Injury (AKI) AKI-new classification/staging systems Aetiology /mechanisms of AKI Predisposing factors of AKI in adults Novel markers of early detection of AKI Evaluation & management-Recent thoughts Summary References
- 3. IMPORTANT ANATOMY/PHYSIOLOGY 20-25 % of cardiac output! 10% of resting oxygen consumption Only 0.5% 0f human body mass! Normal size- 11.5 cm diameter Left kidney is 1.5 cm bigger than the right kidney By 40 years- 10.5 cm by 70 years-9.5 cm Size/e-GFR reduces with age!
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- 5. AKI complicates5-7% of acute care hospital admissions Up to 30% of ICU admissions! In hospital mortality exceeds 50% in ICU setup. In developing countries-diarrheal illnesses,infectious diseases like leptospirosis/malaria ect…. Small rises in S.Cr are associated with adverse patient outcomes including mortality. Mortality- 10% in uncomplicated AKI to 80% in those with MOF!
- 6. AKI-DEFINITION Acutekidney injury (AKI) has now replaced the term Acute renal failure to reflect the spectrum of illness severity & to facilitate standardized research. An universal definition and staging system has been proposed to allow earlier detection and management of AKI.
- 7. AKI Isa clinical syndrome characterized by a rapid deterioration of renal function over hours to days due to variety of causes resulting- Failure to excrete nitrogenous waste products Disturbance in fluid balance Abnormal electrolyte homeostasis Disturbance in acid-base balance
- 8. DETECTING AKI-NICE Detect AKI using (p)RIFLE, AKIN, KDIGO criteria: Serum creatinine rise ≥ 26 micromol/litre (0.3mg/dl)from baseline within 48 hours OR Serum creatinine rise by 50% or more in 7 days OR Urine output < 0.5ml/kg body weight/hour for 6 consecutive hours in adults
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- 10. RIFLE-2004 VS AKIN-2007CRITERIA Risk I njury Failure L oss of function End-Stage Renal disease
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- 14. CLASSIFICATION-PATHOPHYSIOLOGICAL 1.Pre renal azotemia/volume responsive AKI-(50-60%) 2. Intrinsic renal parenchymal disease- (20-30%) 3. Post renal obstruction- (5-15%)
- 16. AUTOREGULATION OF GFRUNDER DECREASED PERFUSION PRESSURE BY DRUGS
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- 19. AKI-OLIGURIC VS NONOLIGURIC Non- Oliguric: In hospital set-up, secondary Nephrotoxic agents. Non-oliguric has better prognosis than oliguric AKI.
- 20. AKI- ICU VSNON ICU Non-ICU AKI- the kidney is usually the only failed organ mortality rates of up to 10%. ICU AKI- is often associated with sepsis and with non-renal multi-organ system failure(MOF) mortality rates of over 50%
- 21. PREDISPOSING FACTORS FORAKI IN ADULTS • Chronic kidney disease (or history of) (STAGE 3-5/eGFR<60) • Diabetes • Heart failure (CCF/AHF) • Hypotension-SBP<100mmHg/drop of >40mmHg from the base line) • Sepsis • Hypovolaemia • Age 65 years or over • Use of drugs with nephrotoxic potential (for example, NSAIDs, ACEI) • Use of iodinated contrast agents within past week • Oliguria • Liver disease /jaundice • Limited access to fluids, e.g. via neurological impairment • Deteriorating early warning scores • Symptoms or history of urological obstruction
- 22. DIAGNOSTIC EVALUATION OFAKI STEP 1-History of the patient & Clinical exam STEP 2- Investigations Urinalysis/Haematological investigations/Radiology & imaging modalities STEP 3- Selected therapeutic trials STEP 4-Renal biopsy (in certain situations)
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- 24. PRE RENAL VSINTRINSIC RENAL
- 25. RADIOLOGY Renalultrasound /CT(useful for obstructive forms/post renal AKI & acute vs CKD) Doppler scans(to assess renal blood flow) Anterograde/retrograde Pyelography-in doughtful cases Nuclear imaging studies : DMSA: anatomy. DTPA and MAG3: renal function,urinary excretion and upper tract outflow ect… (MRI with Gd enhancement is better avoided to prevent NSF in ESRF)
- 26. HAEMATOLOGY FBC/CBC&PBF-for diagnostic clues BU/BUN & S.Cr-markers of glomerular filtration U&E’s/S.Ca/S.PO4 Coagulation profile ABG-anian gap –high in any cause of uraemia/low in MM CPK/Myoglobinuria/uric acid - rhabdomyalysis Immunological assays-compliments/ ANA/ANCA/AGBM/cryoglobulins-in GN & vasculitides Virological markers NOVEL BIOMARKERS-eairly & accurate diagnosis
- 27. NOVEL BIOMARKERS OFAKI-RATIONALE
- 28. IMPORTANT BIOMARKERS….RELEASED ASA RESULT OF KIDNEY INJURY!!!! Kidney injury molecule-1 (KIM-1) Neutrophil gelatinase associated lipocalin (NGAL) Cystatin –C Interleukin -18 Clusterin Osteopontin Cysteine rich protein (CYR 61) ect…
- 29. CYSTATIN-C Superiorto serum creatinine, as a surrogate marker of early and subtle changes of kidney function. Identifies kidney injury while creatinine levels remain in the normal range. Allows detection of AKI, 24-48 hours earlier than serum creatinine !
- 30. KIM-1 KIM-1is a type 1 trans-membrane glycoprotein Served as a marker of severity of AKI Can be used to predict adverse outcomes in hospitalized patients better than conventionally used severity markers.
- 31. NGAL Highlyup regulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 hours of cardiopulmonary bypass–associated AKI. Considered equivalent to troponin in acute coronary syndrome.
- 33. RENAL BIOPSY INDIGNOSIS OF AKI Considered when pre /post renal azotemia,ischaemic/nephrotoxic AKI are unlikely Suspicion of-GN/vasculitides /TIN/myeloma kidney/HUS&TTP Definitive diagnosis & prognostication of AKI Organ/life threatening bleeding may occur with coagulopathy/thrombocytopenia!
- 34. MANAGEMENT OF AKI-PRIORITIES Evaluate promptly to determine the cause Monitor the patient with S.cr/BU daily basis & UOP frequently Manage according to the cause and stage of AKI Evaluate patients at 3 months for resolution or worsening of preexisting CKD
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- 36. TREATMENT & PREVENTIONOF AKI Management of the specific cause Management of hypotension & shock-optimizing haemodynamics with fluid resuscitation & vasopressors Treatment if infection/concurrent sepsis Glycaemic control & nutritional support Elimination of nephrotoxic medication Use of diuretics Vasodilator therapy Growth factor intervention Role of erythropoitein RRT
- 37. HYPOTENTION /SHOCK-WHICH FLUID& HOW MUCH? KDIGO recommends using isotonic crystalloids(0.9% saline/Hartmann’s) rather than colloids (albumin or starches) . (increased risk of AKI with use of high molecular weight starches in severe sepsis-Lancet 2001; 357:911-6) Colloids- in some patients to avoid excessive fluid administration in patients requiring large volume resuscitation, or in specific patient subsets (e.g., a cirrhotic patient with spontaneous peritonitis, or in burns). Colloids- 4%Albumin is renoprotective and Hyperoncotic starch shows nephro- toxicity. There is no benefit of using colloids over crystalloids in managing AKI in terms of survival or need/duration of RRT.
- 38. VASOPRESSORS/INOTROPES Tothose who refractory to fluids to maintain renal perfusion Norepinephrine ,vasopressin Useful in septic shock/burns/liver failure Appropriate use of vasoactive agents can improve kidney perfusion in volume resuscitated patients with vasomotor shock. KDIGO recommends not to use low-dose dopamine to prevent or treat AKI/doesn’t provide any benefit in preventing or eairy treatment of AKI. (1A)
- 39. GLYCAEMIC CONTROL/NUTRITION Target glycaemic control Plasma glucose- 80-110 mg/dl Intense glycaemic control increases mortality & doesn’t delay RRT. Total calorie intake – 20-30 Kcal/Kg Protein intake – 0.8-1.0 g/Kg/day-non catabolic - 1.0-1.5 g/Kg/day-catabolic state
- 40. ROLE OF DIURETICS(FRUSEMIDE) No evidence to reduce incidence or severity of AKI Indicated only in volume over load states! Diuretics only converts oliguric to non oliguric renal faliure! It promotes eairly diuresis but no effects on survival! Increased the risk of AKI when given to contrast induced AKI.
- 41. ROLE OF VASODILATORTHERAPHY IN AKI Low dose dopamine –NO BENEFIT/NEGATIVE RESULTS UN VARIOUS STUDIES! Fenoldopen (pure dopamine type-1 receptor agonist/without systemic adrenergic stimulation)- NOT USEFUL! ANP-NOT USEFUL!
- 42. GROWTH FACTOR INTERVENTIONIN AKI • Recombinant human IGF-1 -peptide with renal vasodilatory/mitogenic and anabolic properties. • KDIGO Work Group recommends against its use in patients with AKI!
- 43. ROLE OF EPOIN PREVENTION OF AKI Recent animal studies suggest a potential clinical benefit of erythropoietin in AKI. • The renoprotective action of Epo may be related to pleomorphic properties including antiapoptotic and antioxidative effects, stimulation of cell proliferation, and stem-cell mobilization. • Although one recent RCT in the prevention of human AKI was negative, the usefulness of erythropoietin in human AKI should be further tested in RCTs. • NOT USEFUL IN PREVENTING AKI IN HUMAN
- 44. ROLE OF RRTIN AKI Established oligo-anuric AKI/do not respond to initial management HD/PD/CRRT(CVVH-continuous veno-venous haemofiltration/CVVD/CVVHD ect Indications or RRT- 1. Hyperkakaemia refractory to medication 2. Persisting anuria/oliguria despite adequate fluid resusitation 3. Fluid overload refractory to diuretics 4. Refractory metabolic acidosis 5. Uraemicsyndrome/ complications-encephalopathy/ pericarditis/vomiting 6. Poisoining-lithium/salicylates 7.Trends of S.Cr/BU levels-there is no definite level!
- 45. SUMMARY AKIis common & often preventable! Associated with increase in morbidity & mortality world wide. Many patients respond to simple measures if act accordingly. Novel staging systems, biomarkers, therapeutic modalities are implemented for better evaluation& management of patients with AKI. Timely RRT may improve the survival!
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