Acute Renal Failure

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Slide 1 : Acute Renal failure (Acute Kidney Injury) Anil K. Saxena, MD; FRCP (Dublin) Renal Physician, Nephrology Division, Al- Rahba Hospital - Johns Hopkins Medicine, Abu Dhabi, UAE Renal autoregulation, Definitions, Pathogenesis, Diagnosis & General Principles of Management
Slide 2 : 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.
Slide 3 : RENAL BLOOD FLOW “Effective Circulating Volume” Normal RBF/RPF Intrarenal Autoregulation GFR, FF Renal Perfusion Pressure Cardiac out put Mean Arterial Pressure
Slide 4 : 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
Slide 5 : 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 - .18 - .22)
Slide 6 : Renal autoregulation F = ?P R F = Flow ?P = Pressure Changes R = Resistance RBF = Renal blood flow Raff = Afferent arteriolar resistance RAP = Renal arterial pressure Reff = Efferent arteriolar resistance
Slide 7 : Renal blood flow (RBF) Major sites of renal vascular resistance -Glomerular afferent (Raff ) and efferent (Reff) arterioles Changes in Raff and Reff affect RBF.
Slide 8 : 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
Slide 9 : Intrarenal Mechanisms for Autoregulation Figure - shows normal conditions normal renal perfusion pressure and a normal GFR. RBF Reff / Raff ratio =N N Engl J Med 357;8 August 23, 2007
Slide 10 : RBF Afferent Arteriole PGC GFR. Efferent Arteriole PGE Ang II Figure: shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction. Intrarenal Mechanisms for Autoregulation under decreased Perfusion Pressure MAP Reff / Raff ratio = N Engl J Med 357;8 August 23, 2007
Slide 11 : Reff / Raff ratio Figure: Loss of vasodilatory PGs increases afferent resistance causing drop in the glomerular capillary pressure below normal values and the fall in GFR RBF PGC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE NSAID T Reduced perfusion pressure with a NSAID. N Engl J Med 357;8 August 23, 2007
Slide 12 : Reduced perfusion pressure with an ACEI or ARB. PGC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE ACEI /ARB T Figure: Loss of angiotensin II action reduces efferent resistance; this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease. Reff / Raff ratio RBF N Engl J Med 357;8 August 23, 2007
Slide 13 : 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
Slide 14 : Renal autoregulation failure Failure to decrease arteriolar resistance Structural changes in renal arterioles and small arteries Old age, Atherosclerosis Chronic HTN, Malignant or accelerated HTN CKD Reduction in vasodilatory prostaglandins NSAIDs Cyclooxygenase-2 inhibitors N Engl J Med 357;8 August 23, 2007
Slide 15 : Renal autoregulation failure Afferent glomerular arteriolar vasoconstriction Sepsis Hypercalcemia Hepatorenal syndrome Cyclosporine or tacrolimus Radiocontrast agents Failure to increase efferent arteriolar resistance ACEI Angiotensin-receptor blockers Renal - artery stenosis N Engl J Med 357;8 August 23, 2007
Slide 16 : ARF - definition An abrupt fall in GFR over a period of minutes to days with rapid & sustained rise in nitrogenous waste products in blood. (Rate of production of metabolic waste exceeds the rate of renal excretion)
Slide 17 : Definitions … Well over 30 definitions used in published studies (Ranging from subtle increases in S. Cr. levels – requirement of dialysis) Multiple aetiologies Different outcomes Classification according to severity and outcome - elusive
Slide 18 :
Slide 19 :
Slide 20 :
Slide 21 : Clinical markers of ARF Reduced GFR Raised S.Creatinine
Slide 22 : Relationship between GFR and serum creatinine in ARF
Slide 23 : 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.
Slide 24 : Figure: The abrupt drop in GFR but the S.Cr. does not start going up for 24 or 36 hours after the acute insult .
Slide 25 : Acute Kidney Injury Network (AKIN- 2005) Continuum of the renal injury STAGE I RISK (R) STAGE II INJURY (I) STAGE V ESRD (E) STAGE III FAILURE (F) STAGE IV LOSS (L) Severity Outcome
Slide 26 : – RIFLE criteria/staging system
Slide 27 : D/D of Azotemia Acute rise in S. Creatinine Medications that block tubular creatinine secretion Trimethoprim Cimetidine Substances that interfere with creatinine assay Cefoxitin Flucytosine
Slide 28 : D/D of Azotemia Acute elevation of BUN Protein loading Catabolic state - severe sepsis GI bleeding Corticosteroid therapy Antibiotics -Tetracycline
Slide 29 : Definitions…. Azotemia - silent Uremia - symptomatic Oliguria - < 400 mL/24 h Anuria - < 100 mL/24 h Nonoliguric ARF - > 400 ml / 24 h
Slide 30 : D/D of Azotemia Acute rise in S. Creatinine Medications that block tubular creatinine secretion Trimethoprim Cimetidine Substances that interfere with creatinine assay Cefoxitin Flucytosine
Slide 31 : D/D of Azotemia Acute elevation of BUN Protein loading Catabolic state - severe sepsis GI bleeding Corticosteroid therapy Antibiotics -Tetracycline
Slide 32 : ARF: Life threatening consequences Volume overload Hyperkalaemia Uremia: Pericarditis Encephalopathy Platelet dysfunction Metabolic acidosis
Slide 33 : Epidemiology INCIDENCE 1-5% of all patients 7-23 % in the ICU Crit Care Med 16 (11): 1106-1109, 1998
Slide 34 : ARF- Community vs. Hospital Acquired Obialo, C. I. et al. Arch Intern Med 2000;160:1309-1313.
Slide 35 : Epidemiology MORTALITY 20-70% Overall 79% for patients requiring RRT (ICU) Nephrol Dial Transplant. 1994:9 S179-S182
Slide 36 : Epidemiology MORTALITY ARF Outcome ~ Severity of Underlying Disease Significant Mortality difference - Ischemic -30% vs. Nephrotoxic- 10%
Slide 37 : MORTALITY ARF is an independent predictor of a poor renal outcome Vascular/ cardiac surgery – ARF increases mortality Cardiac surgery patients Matched illness severity / comorbidities 63% mortality dialysis 4.3 % mortality intact renal function Am J Med 1998; 104 (4) 343-348
Slide 38 : Predictors of mortality Multisystem failure Mechanical ventilation Hypoalbuminemia Hyperbilirubinemia Severe Lactic acidosis Dialysis requirement
Slide 39 : Spectrum of AKI Prerenal : renal hypoperfusion Renal (Intrinsic) : Glomerular Tubular Vascular Interstitial Post renal: obstruction injury
Slide 40 : Spectrum …. Hemodynamic AKI (˜30%) Parenchymal AKI (65%) Acute tubular necrosis (55%) Acute glomerulonephritis (˜5%) Vasculopathy (3%) Acute interstitial nephritis (˜2%) Obstruction (˜5%)
Slide 41 : PRE-RENAL (Hemodynamic) AKI PRERENAL AKI
Slide 42 : Prerenal AKI Renal hypoperfusion 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
Slide 43 : Renal / Intrinsic AKI Tubular Glomerular Vascular Interstitial 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% N Engl J Med 1996;334 (22):1448-60
Slide 44 : ATN Sepsis - 48% Hemodynamic (excluding sepsis) - 32% Toxic – 20% NSAIDS Radiocontrast media ACEI Antibiotics (Gentamicin, Amphotericin) Crit care Med 1996; 24(2) 192-198
Slide 45 : PaO2 50 mm of Hg PaO2 20 mm of Hg 10 mm of Hg PaO2
Slide 46 : ATN Medullary blood flow constitutes about 10% to 15% of total RBF Relative hypoxia in the outer medulla predisposes to ischemic injury in S3 segment of the proximal tubule Thick ascending limb (more glycolytic machinery for ATP synthesis)
Slide 47 :
Slide 48 : Pathophysiology of ATN: Tubular Epithelial Cell Injury and Repair
Slide 49 :
Slide 50 : ATN Renal Tubular obstruction, Tubular back leak Decreased GFR, Oliguria Decreased Na reabsorption Low Uosm (< 350), High UNa (FeNa <1%) Elevated BUN / S.Cr. Urinary sediments- Muddy pigmented granular casts
Slide 51 : Principal POST-RENAL causes of AKI Intra-luminal Stone, Blood clots, Papillary necrosis Pelvic malignancies Prolapsed uterus Retroperitoneal fibrosis Intrinsic Intra-mural Urethral stricture, BPH, Carcinoma prostate, Bladder tumour, Radiation fibrosis Extrinsic Post-renal Urinary outflow tract obstruction
Slide 52 : 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;786-790
Slide 53 : Distinguishing between acute and chronic renal failure is important, as – The approach to these patients differs greatly. This may, save a great deal of unnecessary investigation.
Slide 54 : Factors that suggest chronicity include – Long duration of symptoms, Nocturia, Absence of acute illness, anaemia, hyperphosphatemia, and hypocalcaemia,
Slide 55 : Has obstruction been excluded? Complete anuria Palpable bladder Renal ultrasound Hilton et al, BMJ 2006;333;786-790
Slide 56 : Careful urological evaluation P/H Renal stones, H/O Symptoms of bladder outflow obstruction- Prostate enlargement Prolapsed uterus A palpable bladder. Catheterization
Slide 57 : Complete anuria suggests renal tract obstruction X-ray KUB Renal ultrasonography – detect dilatation of the renal pelvis and calyces, CT Scan
Slide 58 : Is the patient euvolaemic? Pulse, JVP/CVP, postural blood pressure, daily weights, fluid balance Disproportional increase in urea /creatinine ratio Urinary sodium concentration (unless on diuretics) Fluid challenge
Slide 59 :
Slide 60 : Does evidence of renal parenchymal disease exist (other than ATN)? History and examination (systemic features) Urine dipstick and microscopy (red cells, red cell casts, eosinophils, proteinuria)
Slide 61 : Has a major vascular occlusion occurred? Atherosclerotic vascular disease Renal asymmetry Loin pain Macroscopic haematuria Complete anuria
Slide 62 : What investigations are most useful in ARF? Urinalysis: Dipstick for blood, protein, or both - Suggests a renal inflammatory process Microscopy for cells, casts, crystals - Red cell casts diagnostic in glomerulonephritis Hilton et al, BMJ 2006;333;786-790
Slide 63 : RBCs Dysmorphic red blood cells suggest glomerular injury.
Slide 64 : Red blood cell cast Marker of glomerular injury Granular cast
Slide 65 : Pigmented granular (“muddy brown”) casts Marker of acute tubular necrosis
Slide 66 : May- Grünwald - Giemsa staining Marker of acute interstitial nephritis.
Slide 67 : Biochemistry Serial blood urea, creatinine, electrolytes, Blood gas analysis, serum bicarbonate – Important metabolic consequences of ARF include hyperkalaemia, metabolic acidosis, hypocalcaemia, hyperphosphataemia
Slide 68 : 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
Slide 69 : 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
Slide 70 : Haem…. Coagulation studies Disseminated intravascular coagulation associated with sepsis
Slide 71 : 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;786-790
Slide 72 : Immunology ANCA 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
Slide 73 :
Slide 74 : serology Hepatitis B and C, HIV serology– Important implications for infection control within dialysis area Radiology Renal ultrasonography For renal size, symmetry, evidence of obstruction
Slide 75 :
Slide 76 :
Slide 77 : 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)
Slide 78 : Avoid Aminoglycosides 33 % of nephrotoxicity “therapeutic levels” Amphotericin hydration, Liposomal formulation Radiocontrast media - Hydration N-acetyl cysteine
Slide 79 : Management principles.. Accurately monitor fluid balance and daily body weight Identify and treat acute complications Hyperkalaemia, Acidosis, Pulmonary oedema
Slide 80 : Optimise nutritional support Maintaining calories enhances patient survival Maintaining protein intake MAY enhance recovery & outcome protein intakes of > 1.2- 1.4 g/kg/ day can dramatically increase urea production WITHOUT evidence of outcome benefit
Slide 81 : 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
Slide 82 : Initiate dialysis before uraemic complications set in.
Slide 83 : Radiocontrast induced nephropathy (RCIN) Less than 1% in patients with normal renal function Increases significantly with renal insufficiency Dialysis - rarely needed
Slide 84 : Risk Factors Patient Related Elderly Dehydration Underlying CKD Diabetes mellitus Urgent procedure Multiple myeloma CHF ( LVEF < 40%) Hypertension Low hematocrit Intra-aortic balloon pump
Slide 85 : Contrast properties High osmolar contrast Ionic contrast High viscosity Large volume
Slide 86 : Clinical Characteristics Onset - 24 to 48 hrs after exposure Duration - 5 to 7 days Non-oliguric (majority) Urinary sediment – May contain the “muddy-brown” pigmented casts and renal tubular cells typical of ATN or may be quite bland. Low fractional excretion of Na
Slide 87 : Mechanism Hemodynamic- reduce RBF Direct tubulotoxicity Cytokine release Osmolar injury Tubular obstruction
Slide 88 : Patients who are administered contrast media through an arterial vessel, are at the risk of developing Atheroembolic (cholesterol) AKI
Slide 89 : Prophylactic Strategies Use I.V. contrast only when necessary Hydration with normal saline (1-1.5 mL/Kg/ h) 6 -12 h before and after the procedure. Use Low/ iso osmolar (nonionic) contrast media Minimize contrast volume N-acetylcysteine - 600-1200 mg BID for two doses before and 2 doses after the procedure
Slide 90 : Conclusions. ARF is common worldwide Occurs in all clinical & community settings It carries a high morbidity and mortality risks. Involves high cost of management.
Slide 91 : Conclusions.. The most common cause of in-hospital ARF is ATN that results from multiple acute insults e.g. sepsis, Hypotension, and use of nephrotoxic drugs or Radiocontrast media
Slide 92 : Conclusions ARF is increasingly common, particularly among hospital inpatients, elderly people, and critically ill patients. It carries a high mortality
Slide 93 : Conclusions.. Patients at risk are - elderly people; patients with diabetes, hypertension, or vascular disease; and those with pre -existing renal impairment
Slide 94 : Conclusions.. ARF is often preventable. Rapid recognition of incipient ARF and early treatment of established ARF may prevent irreversible loss of nephrons.
Slide 95 : 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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