Acute kidney injury defnition, causes,
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Acute kidney injury defnition, causes,
- 1. ACUTE KIDNEY INJURY – DEFNITION, CAUSES, INVESTIGATIONS, MANAGEMENT DR. SUBODH KUMAR MAHTO PGIMER,DR.RML HOSPITAL. NEW Delhi
- 2. Definition ARF is a sudden and usually reversible decrease in the glomerular filtration rate (GFR) occurring over a period of hours to days . The term “Acute Kidney Injury” now replaces the term ARF; the term ARF should now be restricted to patients who have AKI and “need renal replacement therapy”.
- 3. What is AKI AKI is defined as - Increase in Serum Cr by 0.3 mg/dl within 48 hours OR Increase in Serum Cr to 1.5 times of baseline, which is known or presumed to have occurred within the prior 7 days OR Urine volume <0.5 ml/kg/h for 6 hours.
- 4. Natural history of AKI
- 5. Acute kidney injury classification
- 7. RIFLE CRITERIA 1] RIFLE criteria define three grades of severity and two outcome classes. The most severe classification met by either criterion should be used 2] It describes acute kidney injury as an abrupt (within 48 hours) reduction in kidney function and separates renal dysfunction into categories in terms of the degree of renal insult 3] The degree of renal dysfunction, according to the RIFLE criteria, is determined by the worst value of either urine output or an assessment of the glomerular filtration rate (GFR)
- 8. AKIN criteria 1. Increase the sensitivity of the RIFLE criteria by recommending that a smaller change in serum creatinine (≥26.2 µmol/L) be used as a threshold to define the presence of AKI and identify patients with Stage 1 AKI (analogous to RIFLE-Risk) 2. A time constraint of 48 h for the diagnosis of AKI was proposed. 3. Any patients receiving renal replacement therapy (RRT) were to now be classified as Stage 3 AKI (RIFLE-Failure)
- 11. ETIOLOGY
- 12. PRE RENAL AKI •Pre renal AKI is the most common(55 %) form of AKI •Represents a physiologic response to mild to moderate renal hypo perfusion. • Prerenal AKI is rapidly reversible upon restoration of renal blood flow and glomerular ultrafiltration pressure.
- 13. More severe hypoperfusion may lead to ischemic injury of renal parenchyma and intrinsic renal AKI. Thus, prerenal AKI and intrinsic renal AKI due to ischemia are part of a spectrum of manifestations of renal hypoperfusion.
- 14. Generalized or localized reduction in RBF Haemorrhage Volume depletion ( vomiting, diarrhoea, inappropriate diuresis, burns) Cardiogenic shock Distributive shock (sepsis, anaphylaxis) Cardiac failure Hepatic cirrhosis Nephrotic syndrome NSAIDs ACEI / ARBs AAA RAS /occlusion Reduced GFR PRE-RENAL (Hemodynamic) AKI PRERENAL AKI
- 15. Hypovolemia leads to glomerular hypoperfusion, but filtration rate are preserved during mild hypoperfusion through several compensatory mechanisms. During states of more severe hypoperfusion, these compensatory responses are overwhelmed and GFR falls, leading to prerenal AKI. • Prerenal AKI can complicate any disease that induces : hypovolemia, low cardiac output, Systemic vasodilatation, or selective renal vasoconstriction.
- 16. NSAIDS- they reduce afferent renal vasodilation ACEIs and ARBs- limit renal efferent vasoconstriction
- 18. PRE RENAL AKI- [NUTSHELL] Decreased RBF and GFR Increased Na and H2O reabsorption Oliguria High Uosm (>500), low UNa ( FeNa <1%) Elevated BUN / S.Cr. Ratio Bland urinary sediments
- 19. Renal / Intrinsic AKI TubularGlomerular VascularInterstitial ATN Ischemia (50%) Toxins (30%) Ac. Interstitial nephritis Drug induced - NSAIDs, antibiotics Infiltrative - lymphoma Granulomatous- sarcoidosis, tuberculosis Infection related - post-infective, pyelonephritis Vascular occlusions - Renal artery occlusion - Renal vein thrombosis - Cholesterol emboli Ac.GN –post-infectious, – SLE, –ANCA associated, –anti-GBM disease –Henoch-Schönlein purpura –Cryoglobulinaemia, –Thrombotic microangiopathy •TTP •HUS 5% 85% 8 -12% < 2%
- 21. GLOMERULAR AKI 1] AKI from glomerular damage occurs in severe cases of acute glomerulonephritis (GN). 2] Acute GN can be due to a primary renal disease such as idiopathic rapidly progressive GN or 3] As part of a systemic disease such as systemic lupus erythematosus, bacterial endocarditis, or Wegener’s granulomatosis.
- 23. TUBULAR AKI Acute tubular necrosis (ATN) is the term used to designate AKI resulting from damage to the tubules. The two major causes of ATN are: Ischemic – resulting from severe or protracted decrease in renal perfusion. Nephrotoxic – resulting from a variety of exogenous compounds (e.g. aminoglycosides, amphotericin B, cis- platinum, radiocontrast media) and endogenous compounds (e.g. hemoglobin in hemolysis, myoglobin in rhabdomyolysis) that are toxic or potentially toxic to the kidney.
- 25. INTERSTITIAL AKI AKI from interstitial damage can result from acute interstitial nephritis due to – • an allergic reaction to a variety medications (commonly antibiotics such as penicillins, cephalosporins, sulfonamides) or • an infection (bacterial illnesses such as leptospirosis, legionella, rarely pyelonephritis and viral illnesses such as Hanta virus.
- 26. VASCULAR AKI AKI from vascular damage occurs because injury to intrarenal vessels due to decreases renal perfusion and diminishes GFR. Causes of vascular injury include – malignant hypertension, atheroembolic disease, preeclampsia/eclampsia, hemolyticuremic syndrome (HUS) Thrombotic thrombocytopenia
- 29. Symptoms • Polyuria • Oliguria/anuria • Hematuria • Dysuria • Azotemia –Mental status changes
- 30. • Acidosis ( respiratory rate) • Hypervolemia/hypertension • Hyperkalemia • Pericarditis
- 31. Pre renal azotemi a Post renal azotemia Acute tubular necrosis Acute glomerul onephrit is Acute interstiti al nephritis Serum BUN:Cr ratio >20:1 >20:1 <20:1 >20:1 <20:1 UNa (mEq/L) <20 Variable >20 <20 Variable FE Na % <1 Variable >1 <1 <1;>1 Urine osmolality (mosm/kg) >500 <400 250-300 Variable Variable
- 32. Urinary Index Schrier: J Clin Invest 114(1):5, 2004 Prerenal Laboratory test azotemia ATN Urine osmolality (mOsm/kg) >500 <400 Urine sodium level (mEq/L) <20 >40 Urine/plasma creatinine ratio >40 <20 Fractional excretion of sodium (%) <1 >2 Fractional excretion of urea (%) <35 >35 Urinary sediment Normal; Renal tubular occasional hyaline epithelial cells; or fine granular granular and casts muddy brown casts
- 33. Urinary Sediments Brenner and Rector: The Kidney, 8th edition Sediment Differential diagnosis Normal or few Pre renal azotemia Red blood cells Arterial thrombosis or embolism White blood cells Pre glomerular vasculitis HUS or TTP Scleroderma crisis Post renal azotemia Granular casts ATN (muddy brown) Glomerulonephritis or vasculitis Interstitial nephritis Red blood cell casts Glomerulonephritis or vasculitis Malignant hypertension Rarely interstitial nephritis
- 34. • White blood cell casts Acute interstitial nephritis or exudative glomerulonephritis Severe pyelonephritis Marked leukemic or lymphomatous infiltration • Eosinophiluria (>5%) Allergic interstitial nephritis (antibiotics > NSAIDs) Atheroembolic disease • Crystalluria Acute urate nephropathy Calcium oxalate (ethylene glycol toxicity) Acyclovir Indinavir Sulfonamides Radiocontrast agents
- 35. Ultrasonography in AKI Comprehensive Clinical Nephrology, Johnson 3rd edition Observation Clue to diagnosis of Shrunken kidneys Chronic kidney disease Normal size kidneys Echogenic Acute GN Normal Echo Prerenal Acute renal artery occlusion Enlarged kidneys Malignancy, renal vein thrombosis, diabetic nephropathy, HIV, amyloidosis, polycystic kidney. Hydronephrosis Obstructive nephropathy
- 36. Biomarkers • BUN and creatinine are functional biomarkers. • Kidney injury molecule-1(KIM-1): abundantly expressed in proxmial tubular cells injured by ischemia, detected shortly after injury in urine. • Neutrophil gelatinase associated lipocalcin (NGAL): upregulated after inflammation and injury, detected in plasma and urine.
- 37. Biomarkers • Cystatin C – Functional marker in blood – Tubular marker in urine • Others – IL-18 – L-FABP – Netrin-1 – Vimentin – Alanine aminopeptidase – Alkaline phosphatase – Gamma glutamyl transpeptidase
- 38. MANAGEMENT
- 39. Pre renal azotemia • Optimize renal perfusion. • Replace fluids • Excessive chloride – hyperchloremic meatabolic acidosis. • Inotropic drugs in cardio renal syndrome. • Preload and after load reducing drugs • Anti arrhythmic drugs.
- 40. • HEPATORENAL SYNDROME: - assess intravascular volume status. - albumin may prevent AKI - orthotopic liver transplantation - terlipressin, octreotide, norepinephrine with iv albumin. • INTRINSIC AKI : - AGN respond to immunosuppressive agents - scleroderma induced AKI – ACE inhibitors - rhabdomyolysis – 10 l of fluid, alkaline fluids • POST RENAL AKI:
- 41. Ischemia and nephrotoxin associated AKI • Volume resuscitation and vasopressors. • Eliminate nephrotoxic agents. • Renal replacement therapy. • Nephrotoxin specific • Volume overload • Hyponatremia • Hyperkalemia
- 42. • Hyperphosphatemia • Hypocalcaemia • Hypermagnesimia • Hyperuricemia • Metabolic acidosis. • Nutrition • Drug dosing
- 44. KDIGO RECOMMENDATIONS • Protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI • Total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI. • Administer 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis , 1.0–1.5 g/kg/d in patients with AKI on RRT and up to a maximum of 1.7 g/kg/d in patients on CRRT and in hypercatabolic patients.
- 45. Contd • Nutrition preferentially via the enteral route in patients with AKI. • Insulin therapy targeting plasma glucose 110– 149mg/dl • No diuretics to prevent AKI, except in the management of volume overload. • No low-dose dopamine to prevent or treat AKI. • No fenoldopam • No atrial natriuretic peptide (ANP) or IGF-1
- 46. Contd… • Aminoglycosides if no alternatives • Normal kidney function in steady state,single dose daily rather than multiple-dose daily treatment regimens. • Aminoglycoside drug levels monitoring when treatment with multiple daily dosing is used for more than 24 hours or single- daily dosing is used for more than 48 hours. • Topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, • Systemic mycoses or parasitic infections use azole antifungal agents and/or the echinocandins .
- 47. Contrast-induced AKI • Who develop changes in kidney function after administration of intravascular contrast media • screen for pre-existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium. • Consider alternative imaging methods in patients at increased risk for CI-AKI. • Use the lowest possible dose of contrast medium in patients at risk for CI-AKI.
- 48. Contd… • Iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media • I.v. volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions • Oral NAC, together with i.v. isotonic crystalloids • No fenoldopam • No intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI.
- 49. Dialysis • Volume overload, hyperkalemia, acidosis resistant to medications. • Severe uremia ( asterixis, pericardial rub or effusion, encephalopathy,uremic bleeding) • Time to initiate dialysis? • BUN > 100 mg/dl without signs of recovery of kidney function.
- 50. COMPLICATIONS
- 51. • UREMIA: Mental changes and bleeding complications • VOLUMEIC STATUS: both hyper and hypovolemia seen • HYPONATREMIA: excess hypotonic solutions, seizures • HYPERKALEMIA: hemolysis,rhabdomyolysis muscle weakness, arrhythmias • INFECTIONS • CARDIAC COMPLICATIONS: arrhythmias, pericarditis.
- 52. • ACIDOSIS • HYPERPHOSPHATEMIA AND HYPOCALCEMIA: catabolic state, metastatic deposition, vitamin D parathyroid axis, paresthesia, muscle cramps, seizures carpopedal spasms, prolonged QT. • BLEEDING decreased erthyropoiesis and platelet dysfunction • MALNUTRITION hypercatabolic state.
- 53. Outcome and prognosis • Pre renal azotemia better prognosis. • Can recover even after dialysis requiring AKI. • Temporary dialysis high risk of progressive CKD and 10% develop ESRD. • Premature death likely in AKI.