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Acute Renal failure (Acute Kidney Injury) DR. BHUMIKA SAMBYAL
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To function properly kidneys require:
Normal renal blood flow Functioning glomeruli and tubules Clear urinary outflow tract for drainage and elimination of formed urine from the body.
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Renal Autoregulation Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR) despite large changes in the systemic blood pressure
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Renal autoregulation RBF - blood perfusing the kidneys each minute (1200 ml/min) Renal Plasma Flow (RPF) - plasma flowing to kidneys each minute (670 ml/min or 55-60% of RBF) GFR - amount of plasma filtered each minute by the glomeruli. (Normal GFR -125 ml /min for men and 100 ml/min for women) Filtration Fraction (FF) - the ratio of GFR to RPF (Normal )
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Renal blood flow (RBF) Major sites of renal vascular resistance -Glomerular afferent (Raff ) and efferent (Reff) arterioles Changes in Raff and Reff affect RBF.
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Intrarenal autoregulation
Vasoconstrictors Renin Angiotensin II Endothelin ADH Vasodilators PGs Kinins NO ANP RBF GFR Figure : RBF / GFR is maintained by a balance between vasodilators and vasoconstrictors of Afferent and Efferent arterioles
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Intrarenal Mechanisms for Autoregulation
Afferent Arteriole PGC GFR. Glomerulus Efferent Arteriole Tubule RBF Reff / Raff ratio =N N Engl J Med 357;8 August 23, 2007 Figure - shows normal conditions normal renal perfusion pressure and a normal GFR.
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Intrarenal Mechanisms for Autoregulation under decreased Perfusion Pressure
MAP Afferent Arteriole RBF PGC Efferent Arteriole Ang II PGE Reff / Raff ratio = Panel B shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction. GFR. N Engl J Med 357;8 August 23, 2007 Figure: shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction.
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Renal autoregulation failure
Renal autoregulation breaks down as MAP falls below 80 mm Hg, Further adjustments in intra-renal hemodynamics are unable to maintain RBF and GFR Hallmark of ARF After age 30, RBF/ GFR decreases progressively with age; at 80 years it is nearly half of that at 20 years
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Acute renal failure (ARF) or acute kidney injury (AKI)
Deterioration of renal function over a period of hours to days, resulting in the failure of the kidney to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis ARF Rapid deterioration of renal function (increase of creatinine of >0.5 mg/dl in <72hrs.) “azotemia” (accumulation of nitrogenous wastes) elevated BUN and Creatinine levels decreased urine output (usually but not always) Oliguria: <400 ml urine output in 24 hours Anuria: <100 ml urine output in 24 hours
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The ARF Paradigm 1. Pre-renal 2. Intrinsic Renal 3. Post-renal
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RIFLE CLASSIFICATION CATEGORY RISK GFR&S.CREATININE CRITERIA
URINE OUTPUT RISK GFR decrease >25% or creatinine up 1.5 times baseline <0.5 ml/kg/hr for 6 hrs INJURY GFR decrease>50% or Creatinine up 2 times baseline <0.5 ml/kg/hr for 12 hrs FAILURE GFR decrease>75% or Creatinine up 3 times baseline or Creatinine>4 mg/dl or Acute rise0.5 mg/dl <0.3 ml/kg/hr for 24 hrs Or anuria for 12 hrs END STAGE End stage kidney disease(>3 months)
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Pre-renal ARF Renal Perfusion
2. Intrinsic Renal 3. Post-renal Pre-renal ARF Renal Perfusion Volume Depletion Arterial Volume Renal Vasoconstricn Renal losses: diuretics, osmotic diuresis, etc Extra-renal losses: vomiting, diarrhea, skin Cardiogenic (CHF, ACS, arrhythmias, shock) Septic shock Hepatorenal syndrome Adrenal insufficiency Radiocontrast Prostaglandin inhibition Calcinurin inhibitors ACE inhibitors Amphotericin B When autoregulatory mechanisms are maximized, any small renal insult will subsequently precipitate acute renal failure.
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PRE-RENAL (Hemodynamic) AKI
Generalized or localized reduction in RBF Hypovolaemia Haemorrhage Volume depletion ( vomiting, diarrhoea, inappropriate diuresis, burns) Hypotension Cardiogenicshock Distributive shock (sepsis, anaphylaxis) Oedema states Cardiac failure Hepatic cirrhosis Nephrotic syndrome Renal Hypoperfusion NSAIDs ACEI / ARBs AAA RAS /occlusion Hepatorenal syndrome Reduced GFR PRERENAL AKI
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Ac. Interstitial nephritis
Renal / Intrinsic AKI Glomerular Tubular Interstitial Vascular Ac. Interstitial nephritis Drug induced - NSAIDs, antibiotics Infiltrative -lymphoma Granulomatous- sarcoidosis, tuberculosis Infection related - post-infective, pyelonephritis Ac.GN post-infectious, SLE, ANCA associated, anti-GBM disease Henoch-Schönlein purpura Cryoglobulinaemia, Thrombotic microangiopathy TTP HUS ATN Ischemia (50%) Toxins (30%) Vascular occlusions - Renal artery occlusion - Renal vein thrombosis - Cholesterol emboli 85% < 2% 5% 8 -12% N Engl J Med 1996;334 (22):
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Retroperitoneal fibrosis
Post-renal Urinary outflow tract obstruction Intrinsic Extrinsic Intra-luminal Stone, Blood clots, Papillary necrosis Intra-mural Urethral stricture, BPH, Carcinoma prostate, Bladder tumour, Radiation fibrosis Pelvic malignancies Prolapsed uterus Retroperitoneal fibrosis Principal POST-RENAL causes of AKI
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ACUTE RENAL FAILURE Acute renal failure (ARF) has four well-defined stages/phases: onset, oliguric or anuric, diuretic, and convalescent. Treatment depends on stage and severity of renal compromise.
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Phases of ARF: Onset – initial phase of insult or injury
Oliguric – less than 400cc/24 hr - for older (600 – 700 cc/24 hr) - lasts 8-14 days or 1-2 weeks -↓K+, ↑Na, ↑Mg Diuretic – Lasts 10 days - diuresis of 3-5L/day - ↑BUN & Creatinine level - dangers: hyponatremia, hypotension, shock Recovery – lasts from 6-12 months - avoid nephrotoxic drugs
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Relationship between GFR and serum creatinine in ARF
S.Cr. poor marker of renal function. Poor correlation between S.Cr. and level of GFR related to muscle mass. S.Cr. of 1.0 does not represent the same level of GFR in a cachectic 70-year-old as in a highly muscular 25-year-old.
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How do we diagnose it?
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History & Physical Will Guide DDx
Primer on Kidney Diseases 3rd Ed. pg 248.
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Acute Renal Failure Diagnosis
Blood urea nitrogen and serum creatinine CBC, peripheral smear, and serology Urinalysis Urine electrolytes U/S kidneys Serology: ANA,ANCA, Anti DNA, HBV, HCV, Anti GBM, cryoglobulin, CK, urinary Myoglobulin
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Acute Renal Failure Diagnosis
Urinalysis Unremarkable in pre and post renal causes Differentiates ATN vs. AIN. vs. AGN Muddy brown casts in ATN WBC casts in AIN RBC casts in AGN Hansel stain for Eosinophils
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Acute Renal Failure Diagnosis
Laboratory Evaluation: Scr, More reliable marker of GFR Falsely elevated with Septra, Cimetidine small change reflects large change in GFR BUN, generally follows Scr increase Elevation may be independent of GFR Steroids, Catabolic state, hypovolemia BUN/Cr helpful in classifying cause of ARF ratio> 20:1 suggests prerenal cause
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The Value of Urinalysis
Pre-renal Intrinsic renal Glomerular ATN AIN Post-renal High specific gravity, normal or hyaline casts Proteinuria, hematuria, RBC casts Low specific gravity, muddy brown casts, tubular epithelial cells Mild proteinuria, hematuria, WBC, WBC casts, eosinophils Normal or hematuria, WBC, occasional granular casts
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Normal or hyaline casts Tubular cells & “muddy brown” granular casts
Pre-renal vs. ATN Favours Pre-renal Favours ATN Creatinine:Urea ratio UNa Uosm FENa U specific gravity Urinalysis > 20:1 < 20 > 500 mO/kg < 1 % > 1.018 Normal or hyaline casts <10-15:1 > 40 ~ isotonic > 2 % < 1.010 Tubular cells & “muddy brown” granular casts
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Acute Tubular Necrosis
Most common cause of intrinsic cause of ARF Often multifactorial Ischemic ATN: Hypotension, sepsis, prolonged pre-renal state Nephrotoxic ATN: Iodinated contrast Rhabdomyolysis Hemoglobinuria Cast nephropathy(myeloma &Tamm horsfall prteins) Antibiotics-Aminoglycosides,Amphotricin B,I/V acyclovir Other drugs-Cisplatin,ethylene glycol/methanol Tumor lysis syndrome
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Acute Tubular Necrosis
Diagnose by history, FENa (>2%) sediment with coarse granular casts, RTE cells Treatment is supportive care. Maintenance of euvolemia (with judicious use of diuretics, IVF, as necessary) Avoidance of hypotension Avoidance of nephrotoxic medications (including NSAIDs and ACE-I) when possible Dialysis, if necessary 80% will recover, if initial insult can be reversed
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Contrast nephropathy 12-24 hours post exposure, peaks in 3-5 days
Non-oliguric, FE Na <1% !! RX/Prevention: 1/2 NS 1 cc/kg/hr 12 hours pre/post Mucomyst 600 BID pre/post (4 doses) Risk Factors: CKD, Hypovolemia ,DM,CHF
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Acute Glomerulonephritis
Rare in the hospitalized patient Diagnose by history, hematuria, RBC casts, proteinuria (usually non-nephrotic range), low serum complement in post-infectious GN), RPGN often associated with anti-GBM or ANCA Usually will need to perform renal biopsy
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Atheroembolic ARF Associated with emboli of fragments of atherosclerotic plaque from aorta and other large arteries Diagnose by history, physical findings (evidence of other embolic phenomena--CVA, ischemic digits, “blue toe” syndrome, etc), low serum C3 and C4, peripheral eosinophilia, eosinophiluria, rarely WBC casts Commonly occur after intravascular procedures or cannulation (cardiac cath, CABG, AAA repair, etc.)
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Acute Interstitial Nephritis
Usually drug induced methicillin, rifampin, NSAIDS Develops 3-7 days after exposure Fever, Rash , and eosinophilia common U/A reveals WBC, WBC casts, + Hansel stain Often resolves spontaneously Steroids may be beneficial ( if Scr>2.5 mg/dl)
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How do we assess a patient with AKI?
Is this acute or chronic renal failure? History and examination Previous Serum creatinine measurements Small kidneys on ultrasound (except for in -Diabetes, PCKD, Urinary Tract Obstruction) Hilton et al, BMJ 2006;333;
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Distinguishing ARF from CRF
Helpful clues… Previous creatinine values Hb – anemia suggests chronic problem Renal ultrasound – small, echogenic kidneys suggest a chronic problem X-rays – renal osteodystrophy suggests chronic problem Renal biopsy Exceptions to the “small kidneys = CRF” rule: early DM, amyloid, HIV nephropathy, PCKD
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RBCs Dysmorphic red blood cells suggest glomerular injury.
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Red blood cell cast Granular cast Marker of glomerular injury
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Pigmented granular (“muddy brown”) casts
Marker of acute tubular necrosis
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May- Grünwald - Giemsa staining
Marker of acute interstitial nephritis.
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Biochemistry Serial blood urea, creatinine, electrolytes, Blood gas analysis, serum bicarbonate – Important metabolic consequences of ARF include hyperkalaemia, metabolic acidosis, hypocalcaemia, hyperphosphataemia
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Biochem…. Creatine kinase, myoglobinuria –
Markedly elevated CK and myoglobinuria suggests rhabdomyolysis Serum immunoglobulins, serum protein electrophoresis, Bence Jones proteinuria – Immune paresis, monoclonal band on serum protein electrophoresis, and Bence Jones proteinuria suggest multiple myeloma
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Haematology Full blood count, blood film:
Eosinophilia may be present in acute interstitial nephritis, cholesterol embolization, or vasculitis (CSS) Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy –TTP, HUS
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Haem…. Coagulation studies
Disseminated intravascular coagulation associated with sepsis
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Immunology Antinuclear antibody (ANA) , Anti-double stranded (ds) antibody - ANA positive in SLE and other autoimmune disorders;DNA antibodies anti-ds DNA antibodies more specific for SLE C3 & C4 complement concentrations- Low in SLE, acute post infectious glomerulonephritis, Cryoglobulinemia ASO and anti-DNAse B titres High after streptococcal infection Hilton et al, BMJ 2006;333;
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Immunology ANCA AntiGBM antibodies p-ANCA - Anti PR3 antibodies
c-ANCA - Anti MPO antibodies Associated with systemic vasculitis - Wegener’s granulomatosis; CSS, Microscopic polyangiitis. AntiGBM antibodies Present in Goodpasture’s disease
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serology Hepatitis B and C, HIV serology– Radiology
Important implications for infection control within dialysis area Radiology Renal ultrasonography For renal size, symmetry, evidence of obstruction
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Management principles in ARF
Identify and correct pre-renal and post-renal factors Optimise cardiac output and RBF- Review drugs: Stop ACEI, ARBs, NSAIDs Adjust doses / monitor drug concentrations (where appropriate)
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Avoid Aminoglycosides Amphotericin Radiocontrast media -
33 % of nephrotoxicity “therapeutic levels” Amphotericin hydration, Liposomal formulation Radiocontrast media - Hydration N-acetyl cysteine
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Management principles..
Accurately monitor fluid balance and daily body weight Identify and treat acute complications Hyperkalaemia, Acidosis, Pulmonary oedema
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Optimise nutritional support
Maintaining calories enhances patient survival Maintaining protein intake MAY enhance recovery & outcome protein intakes of > g/kg/ day can dramatically increase urea production WITHOUT evidence of outcome benefit
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Management principles…
Identify and aggressively treat infection; Minimise indwelling lines Remove bladder catheter if anuric. Identify and treat bleeding tendency: Prophylaxis - proton pump inhibitor or H2 antagonist, avoid aspirin transfuse if required
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Initiate dialysis before uraemic complications set in.
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Radiocontrast induced nephropathy (RCIN)
Less than 1% in patients with normal renal function Increases significantly with renal insufficiency Dialysis - rarely needed
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Prophylactic Strategies
Use I.V. contrast only when necessary Hydration with normal saline (1-1.5 mL/Kg/ h) h before and after the procedure. Use Low/ iso osmolar (nonionic) contrast media Minimize contrast volume N-acetylcysteine mg BID for two doses before and 2 doses after the procedure
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Indications for Dialysis (dialyzable drug intoxication)
HYPERKALEMIA not amenable to medical therapy ACIDOSIS not amenable to medical therapy UREMIA resulting in pericarditis, neuropathy or encephalopathy Critical VOLUME OVERLOAD not responsive to diuresis (dialyzable drug intoxication)
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Conclusions. ARF is common worldwide
Occurs in all clinical & community settings It carries a high morbidity and mortality risks. Involves high cost of management.
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Conclusions.. ARF is often preventable.
Rapid recognition of incipient ARF and early treatment of established ARF may prevent irreversible loss of nephrons.
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Conclusions.. No drug treatment has been shown to limit the progression of, or speed up recovery from, ARF. Advice from a nephrologist should be sought for all cases of ARF.
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THANK YOU
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