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CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
CME: Acute Renal failure
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  • This slide depicts the inverse relationship between P Cr and GFR (measured by inulin clearance) in a large number of subjects with varying degrees of renal function. The hyperbolic relationship between P Cr and GFR complicates the use of absolute increments in P Cr (e.g., > 0.5 or 1.0 mg/dl) as yardsticks for defining acute renal failure.
  • One of the things to bear in mind when we are talking about acute renal failure is that our marker for acute renal failure is generally the serum creatinine concentration, but this is a relatively poor marker of renal function. Certainly, there are issues related to the correlation between creatinine and level of GFR related to protein mass so that a creatinine of 1 does not represent the same level of GFR in a cachectic 70-year-old as in a highly muscular 25-year-old, but in addition the change in serum creatinine that occurs lags behind the change in GFR that is seen with acute renal failure. Here you see the abrupt drop in GFR in a patient with acute renal failure, but the serum creatinine lags behind so that it may not start going up for 24 or 36 hours after the acute insult and certainly when we see a patient with aggressively rising serum creatinine, that does not mean that the renal function is continuing to deteriorate. The GFR may be close to 0 and be maintained at that level close to 0 during that period of time. The creatinine has not come back into a steady state at this new very low GFR.
  • Transcript

    • 1. Dr S. Karthikeyan, Prof P. Vijayaraghavan’s Unit Stanley Medical College
    • 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. Acute kidney injury classification -ADQI
    • 4. RIFLE criteria
    • 5. Serum Creatinine as a marker for AKI and GFR
      • Normal S.Creatinine is 0.6-1.2mg/dl and is the most commonly used parameter to assess renal function.
      • Unfortunately the correlation between S.Creatinine concentration and GFR may be confounded by several factors.
    • 6. Serum Creatinine (mg/dl) GFR (ml/min per 1.73m 2 ) 1.0 0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0 40 60 80 100 120 140 160 180 20 0
    • 7.
      • There is abrupt drop in GFR but the S.Cr. does not start going up for 24 or 36 hours after the acute insult .
      Relationship between GFR and serum creatinine in ARF 40 80 0 GFR (mL/min) 0 7 14 21 28 4 Days 2 0 6 Serum Creatinine (mg/dL)
    • 8. Creatinine is not an ideal marker
      • 1. Creatinine excretion is dependent on renal factors independent of function:
        • Certain medications such as cimetidine and trimethoprim interfere with proximal tubular creatinine secretion and may cause rise in S. creatinine without fall in GFR.
    • 9.
      • 2. S.Creatinine is dependent on nonrenal factors independent of renal function
        • S.Creatinine is dependent on muscle mass, infection, volume of distribution, age, gender, race, body habitus, diet, presence of amputations.
        • Eg. S. Creatinine of 1.2mg/dl in a 40kg elderly signifies severe reduction of GFR while the same value in a 100kg represents a normal renal function
      • 3. Creatinine production and excretion must be in a steady state before creatinine may be used in any formula for the estimation of GFR.
    • 10. NEW MARKER
      • Cystatin C –protein
      • Produced by nucleated cells
      • Filtered and completely reabsorbed
      • Changes in serum levels occur sooner
    • 11. NOVEL BIOMARKERS
      • 1. IL- 18
      • 2.KIM-1
      • 3.Gro α /KC
      • 4.NGAL-neutrophil gelatinase associated lipocalin
      • 5.NHE-3
    • 12. Spectrum of AKI
      • Prerenal : renal hypoperfusion
      • Renal (Intrinsic) :
        • Glomerular
        • Tubular
        • Vascular
        • Interstitial
      • Post renal: obstruction
      Injury
    • 13. PRE-RENAL ( Hemodynamic ) AKI PRERENAL AKI 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
    • 14. Pre renal AKI characteristics:
        • Decreased RBF and GFR
        • Increased Na and H 2 O reabsorption
        • Oliguria
        • High U osm (>500) , low U Na ( FeNa <1%)
        • Elevated BUN / S.Cr. Ratio
        • Bland urinary sediments
    • 15. 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%
    • 16. ATN
      • CAUSES:
      • 1.Ischemia
      • 2.Infection with or without sepsis
      • 3.Toxins –exogenous- radiocontrast,ampho-B
      • aminoglycosides
      • -endogenous-rhabdomyolysis,
      • hemolysis
    • 17. ATN cont….
      • Common sites –
        • S3 segment of the proximal tubule
        • Thick ascending limb (more glycolytic machinery
        • for ATP synthesis)
      • Medullary blood flow -- 10% to 15% of
      • total RBF
      • Relative hypoxia in the outer medulla ;
    • 18.
      • PaO2
      • 50 mm of Hg
      • PaO2
      • 20 mm of Hg
      10 mm of Hg PaO2
    • 19.  
    • 20. Phases of ATN
      • Initiation : - hours to days
      • GFR declines
      • Extension :-
      • continuing ischemic injury and inflammation
      • GFR low
      • Maintenance:-
      • 1-2 weeks
      • GFR stabilises
      • uremic complications may arise
      • Recovery :-
      • GFR rises
    • 21. ATN characteristics:
        • Decreased GFR, Oliguria
        • Decreased Na reabsorption
        • Low U osm (< 350), High U Na (FeNa >1%)
        • Elevated BUN / S.Cr.
        • Urinary sediments- Muddy pigmented granular casts
    • 22.
      • 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
    • 23. Complications
      • METABOLIC:
      • hyperkalemia, hyponatremia,
      • hypocalcemia, hyperphosphatemia,
      • hyperuricemia, metabolic acidosis
      • CVS:
      • pericarditis/effusion , hypertension ,MI,
      • arrhythmias, pulmonary edema
      • GIT:
      • nausea, vomiting, malnutrition ,GI hemorrhage
      • CNS:
      • asterixis ,mental changes ,seizures
      • INFECTIONS:
      • pneumonia ,sepsis
    • 24. Approach to a patient with AKI
      • Differentiate acute or chronic renal failure
      • Distinguishing between acute and chronic renal
      • failure is important, as the approach to these
      • patients differs greatly.
    • 25.
      • Factors that suggest chronicity :
        • Long duration of symptoms,
        • Absence of acute illness, anaemia,
        • hyperphosphatemia, and hypocalcaemia,
        • Previous Serum creatinine measurements
        • Small kidneys on ultrasound (except for in -Diabetes, PCKD, Urinary Tract Obstruction)
    • 26.
      • Exclude obstruction
      • Urological evaluation
        • Renal stones,
        • Symptoms of bladder outflow obstruction- Prostate
        • enlargement
        • Prolapsed uterus
        • A palpable bladder.
    • 27.
      • CONTD ...
        • X-ray KUB
        • Renal ultrasonography – detect dilatation of the renal
        • pelvis and calyces
        • CT Scan
    • 28.
      • Evidence of renal parenchymal disease
      • (other than ATN)
        • History and examination (systemic features)
        • Urine dipstick
        • Urine microscopy (red cells, red cell casts,
        • eosinophils, proteinuria)
    • 29.
      • Signs of major “ vascular occlusion”
        • Loin pain
        • Macroscopic haematuria
        • Anuria
        • Renal asymmetry
    • 30. DD of Azotemia
      • Acute rise in S. Creatinine
      • Medications that block tubular creatinine secretion
        • Trimethoprim
        • Cimetidine
      • Substances that interfere with creatinine assay
      • Cefoxitin
      • Flucytosine
    • 31. Contd…
      • Acute elevation of BUN
        • Protein loading
        • Catabolic state - severe sepsis
        • GI bleeding
        • Corticosteroid therapy
        • Antibiotics -Tetracycline
    • 32.
      • Assess the volume status of the patient:
        • Pulse,
        • JVP,
        • postural blood pressure,
        • daily weights,
        • fluid balance/fluid challenge
    • 33. INVESTIGATIONS Biochemistry
      • Blood urea,
      • creatinine,
      • electrolytes,
      • Blood gas analysis.
      • Urine osmolality/sodium
    • 34.  
    • 35.
      • Sr.Creatine kinase, myoglobin in urine
        • Markedly elevated CK and myoglobinuria suggests rhabdomyolysis
      • Serum immunoglobulins, serum protein electrophoresis, Bence Jones proteinuria
        • Monoclonal band on serum protein electrophoresis, and Bence Jones proteinuria suggest multiple myeloma
    • 36.
      • Urine analysis:
        • Dipstick for blood, protein - Suggests a renal inflammatory process
        • Microscopy for cells, casts, crystals
    • 37. RBC s
      • Present in
      • glomerulonephritis ,
      • vasculitis ,
      • HUS TTP
      • scleroderma crisis
    • 38. Casts:
      • Hyaline –prerenal ARF
      • Granular –ATN (muddy brown )
      • Red blood cell casts –glomerulonephritis,vasculitis
      • malignant hypertension
      • WBC casts- AIN, pyelonephritis ,leukemic or
      • lymphomatous infiltrates
    • 39. Crystals
      • Urate crystals – acute urate nephropathy
      • Oxalate crystals –ethylene glycol ingestion /acyclovir/
      • indinavir
      • Eosinophiluria  > 5 % of WBC s
      • AIN ,atherothrombotic disease
    • 40. 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
      • Coagulation studies
        • Disseminated intravascular coagulation associated with sepsis
    • 41. 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
    • 42. 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
    • 43. 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
    • 44. Management principles in ARF
      • Identify and correct pre-renal and post-renal factors
      • Optimise cardiac output and RBF :
      • Stop/adjust the dose of nephrotoxic drugs (ACEI, ARBs,
      • NSAIDs)
    • 45. Management principles...
      • Accurately monitor fluid balance and daily body
      • weight
      • Identify and treat acute complications
        • Hyperkalaemia,hypertension
        • Acidosis,
        • Pulmonary oedema
    • 46. Management of complications
      • Volume overload –salt restriction < 1 – 1.5 g/d
      • water restriction -< 1 litre /d
      • diuretics
      • Hyponatremia –restriction of oral & intravenous fluids
      • Hyperkalemia – K binding resins ,glucose + insulin
      • Ca gluconate ,soda bicarb.
      • Metabolic acidosis – soda bicarb ., if < 15 meq
      • Hyperphosphatemia – PO4 binders –sevalamer
    • 47. Contd….
      • Hypocalcemia –calcium carbonate
      • Nutrition –restriction of dietary protein < 0.8 g/kg /d
      • calories – 25-30 kcal / d
      • enteral nutrition preferred
    • 48. Contd …
      • Identify and aggressively treat infection;
        • Minimise indwelling lines
      • Identify and treat bleeding tendency :
        • Prophylaxis - proton pump inhibitor or H2 antagonist,
        • transfuse if required
    • 49. Absolute indication for dialysis
      • Evidence of uremia ;
      • Intractable volume overload
      • Hyperkalemia
      • Severe metabolic acidosis refractory to medical
      • measures
    • 50. Thank you Thank you

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