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Acute renal failure (arf)
- 1. CHAIRPERSON – DR. SANJEEV KUMAR SPEAKER - DR. ASHISH KUMAR
- 2. DEFINITION AKI 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 Acute Renal Failure should now be restricted to patients who have AKI and “need renal replacement therapy”.
- 3. ‘ACUTE KIDNEY INJURY’ Abrupt reduction [<48 hrs] in kidney function, defined as an absolute increase in S creatinine of ≥0.3 mg/dL A percentage increase in S creatinine of ≥ 50% [1.5 fold from baseline] or a reduction in urine output-- documented oliguria of < 0.5 ml/kg/hr, for more than six hours.
- 6. Hilton, R. BMJ 2006;333:786-790 CAUSES OF ACUTE KIDNEY INJURY AKI
- 7. Pre-renal causes of AKI – Volume depletion • Renal losses (diuretics, polyuria) • GI losses (vomiting, diarrhea) • Cutaneous losses (burns, Stevens-Johnson syndrome) • Hemorrhage • Pancreatitis – Decreased cardiac output • Heart failure • Pulmonary embolus • Acute myocardial infarction • Severe valvular heart disease
- 8. Post-renal causes of AKI – Ureteric obstruction • Stone disease, • Tumor, • Fibrosis, • Ligation during pelvic surgery – Bladder neck obstruction • Benign prostatic hypertrophy [BPH] • Cancer of the prostate • Neurogenic bladder • Drugs(Tricyclic antidepressants, ganglion blockers, • Bladder tumor, • Stone disease, hemorrhage/clot) – Urethral obstruction (strictures, tumor)
- 9. Renal Causes of AKI • Large Vascular • Small vascular and Glomerular • Interstitial nephritis • Acute tubular necrosis
- 10. Renal Causes of AKI • Large Vascular • Renovasc disease + ACEI • Renal artery thrombosis/dissection • Cholersterol emboli (recent Cardiac cath/aortic surgery) • Renal vein Thrombosis (hypercoagulable, Nephrotic)
- 11. • Acute Glomerulonephritis (GN) / Small vascular • Anti–glomerular basement membrane (GBM) disease (Goodpasture syndrome) • Anti–neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis, microscopic polyangiitis) • Immune complex GN (lupus, postinfectious, cryoglobulinemia, primary membranoproliferative glomerulonephritis) • IgA nephropathy • HUS/TTP • Malignant hypertension
- 12. • Tubular • Ischemic • Toxic – Heme pigment (rhabdomyolysis, intravascular hemolysis) – Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, methotrexate) – Drugs (aminoglycosides, lithium, amphotericin B, pentamidine, cisplatin, ifosfamide, radiocontrast agents)
- 13. • Interstitial • Drugs (penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides) • Infection (pyelonephritis, viral nephritis) • Systemic disease (Sjogren syndrome, sarcoid, lupus, lymphoma, leukemia )
- 14. Pre-renal AKI • History -- blood or volume loss -- cardiac failure, arrhythmia, (cardiogenic shock) -- sepsis • Physical exam – focus on volume status – Vital signs – current and preceding the development of AKI – Neck veins, lungs, heart, mucous membranes and edema
- 15. Pre-renal AKI • There is no intrinsic kidney damage in pre-renal AKI; rising BUN and creat occur because the kidneys are inadequately perfused. • Therefore, normal renal physiologic responses occur, manifested in urine electrolytes that reflect intact renal tubular function.
- 16. Pre-renal AKI • Intact renal tubular function in the setting of impaired renal perfusion results in avid tubular reabsorption of sodium. • Therefore, low urine Na (<20 mEq/L) and low fractional excretion of Na (<1%) and of urea (<35%) in pre-renal ARF.
- 18. Pre-renal AKI • Laboratory studies – BUN:creatinine ratio – elevated in pre-renal; >20:1 – Urine sediment: hyaline and fine granular casts – Urine Specific gravity: high – Urine dipstick: negative (no blood or protein) – Urinary to plasma creatinine ratio: high – Urinary Na: low – FENa: low
- 19. • Sustained prerenal azotemia is the main factor that predisposes patients to ischemia- induced acute tubular necrosis (ATN) • Prerenal azotemia and ischemic tubular necrosis represent a continuum. Azotemia progresses to necrosis when blood flow is sufficiently compromised to result in the death of tubular cells. • Most cases of ischemic AKI are reversible if the underlying cause is corrected.
- 20. Renal or Intrinsic AKI • In all types of intrinsic AKI, BUN:creat ratio preserved (10-20:1) • The history, P/E, and especially urine analysis will help to differentiate
- 21. Renal or Intrinsic ARF – Vascular Type • Large vessels – must be bilateral – Renal vein thrombosis – Renal artery stenosis • Small vessels – Vasculitis – Atheroembolic – Malignant hypertension – Thrombotic microangiopathies (HUS/TTP)
- 22. Renal or Intrinsic AKI – Glomerular • History – systemic or primary kidney • P/E – BP (usually hypertensive) -- edema • BUN:creatinine ratio: preserved • Urine analysis : + protein, blood RBCs,+ • Often require kidney biopsy RBC Casts
- 23. Renal or Intrinsic AKI – Interstitial • History – exposure to medications usually 7- 14 days earlier -- penicillins, cephalosporins, dilantin • P/E – maculopapular erythematous skin rash -- 1/3 have fever, arthralgias • BUN:creatinine ratio: 10-20:1 • Urine analysis: + protein, blood WBCs, WBC casts, eosinophils
- 24. Renal or Intrinsic ATN – Acute Tubular Necrosis • The most common type of hospital-acquired ARF • May be 1) ischemic or 2) nephrotoxic in etiology • Most common ATN is ischemic, most often due to a prolonged pre-renal state (prolonged reduced renal perfusion)
- 26. Renal or Intrinsic ATN – Acute Tubular Necrosis • History – prolonged pre-renal state -- exposure to nephrotoxin aminoglycoside antibiotics ethylene glycol pigments (myoglobin, hemoglobin) • P/E – assess volume status (to exclude pre- renal AKI)
- 27. Renal or Intrinsic ATN – Acute Tubular Necrosis • BUN:creatinine ratio: preserved (10-20:1) • Urine analysis : negative protein, blood -- granular casts (dirty brown casts) -- renal tubular epithelial cells • Urine chemistries – Urinary Na: high (>40 meq/L) FENa: high (>2%) Urinary to plasma creatinine ratio: low
- 28. Contrast-Induced AKI Prevalence • Less than 1% in patients with normal renal function • Increases significantly with renal insufficiency Risk factors • Renal insufficiency • Diabetes mellitus • Multiple myeloma • High osmolar (ionic) contrast media • Contrast medium volume
- 29. Contrast-induced AKI Clinical Characteristics • Onset - 24 to 48 hrs after exposure • Duration - 5 to 7 days • Non-oliguric (majority) • Dialysis - rarely needed • Urinary sediment - variable • FENa: Low
- 30. Contrast-induced AKI Prophylatic Strategies • Use I.V. contrast only when necessary • Hydration • Minimize contrast volume • Low-osmolar (nonionic) contrast media
- 31. Post-Renal AKI • Elevated pressure in urinary conduits results in renal parenchymal destruction if unrelieved • important to rule out quickly: – potential for recovery of renal function is often inversely related to the duration of the obstruction
- 32. Post-Renal AKI • History – symptoms (frequency, hesitancy, etc) -- carcinoma, DM, stones, medications • P/E – distended bladder, prostatic enlargement, pelvic masses , lymph nodes • Laboratory studies-- elevated BUN:creat ratio -- unremarkable urine sediment -- variable urine chemistries • Renal ultrasound – hydronephrosis • Treatment is to relieve the obstruction – Bladder catheterization – Nephrostomy tubes
- 33. AKI: URINE VOLUME • Anuria (< 100 ml/24h) – Acute bilateral arterial or venous occlusion – Bilateral cortical necrosis – Acute necrotizing glomerulonephritis – Obstruction (complete) – ATN (very rare) • Oliguria (100-500 ml/24h) – Pre-renal azotemia – ATN • Non-Oliguria (> 500 ml/24h) – ATN – Obstruction (partial)
- 34. INVESTIGATIONS Biochemistry Blood urea, creatinine, electrolytes, Blood gas analysis. Urine osmolality/sodium/creatinine
- 35. 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.
- 36. There is abrupt drop in GFR but the S.Cr. does not start going up for 24 or 36 hours after the acute insult . 40 80 0 GFR (mL/min) 0 7 14 21 28 4 Days 2 0 6 Serum Creatinine (mg/dL) Relationship between GFR and serum creatinine in AKI
- 37. 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.
- 38. 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.
- 39. Fractional Excretion of Na • Since urinary indices depend on urine sodium concentration, they should be interpreted cautiously if the patient has received diuretic Spot urine Na may be affected (raised) by diuretic use and baseline impaired kidney function (CKD where maximum urine Na reabsorption is impaired) Fractional excretion of Na accounts for this by including creatinine: FxExNa = urine [Na] ÷ plasma [Na] X 100 urine creatinine ÷ plasma creatinine
- 40. RENAL INDICES • Renal Failure Index (RFI) RFI = urine [Na] urine creatinine /serum creatinine
- 41. URINE AND SERUM LABORATORY VALUES Prenal Renal BUN/Cr >20 <20 FeNa <1% >1% RFI <1% >1% UNa (mEq/L) <20 > 40 Specific gravity high low Pre-renal
- 42. URINE ANALYSIS • Dipstick for blood, protein – Suggests a renal inflammatory process • Microscopy may show cells, casts, crystals
- 43. RBCs in Urine Present in glomerulonephritis , vasculitis , HUS TTP scleroderma crisis
- 44. URINARY CASTS Hyaline –prerenal ARF Granular –ATN (muddy brown) Red blood cell casts –glomerulonephritis,vasculitis malignant hypertension WBC casts- AIN, pyelonephritis ,leukemic or lymphomatous infiltrates
- 45. Red Blood Cell Cast • Two examples of red blood cell casts, typical of glomerular bleeding.
- 46. White Blood Cell Cast
- 47. Pigmented Granular Casts • Pigmented granular (“muddy brown”) casts are characteristic of acute tubular necrosis
- 48. Crystals • Urate crystals – acute urate nephropathy • Oxalate crystals –ethylene glycol ingestion /acyclovir/ indinavir • Eosinophiluria > 5 % of WBC s AIN ,atherothrombotic disease
- 49. 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
- 50. 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
- 51. Immunology... • ANCA • p-ANCA - Anti PR3 antibodies • c-ANCA - Anti MPO antibodies – Associated with systemic vasculitis - Wegener’s granulomatosis; Microscopic polyangiitis. • AntiGBM antibodies – Present in Goodpasture’s disease
- 52. Serology • Hepatitis B and C, HIV serology
- 53. Radiology • Renal ultrasonography : For renal size, symmetry, evidence of obstruction • Pyelography : localization • MRA/ Doppler US : arterial /venous obstruction
- 54. NEW MARKER • Cystatin C –protein Produced by nucleated cells Filtered and completely reabsorbed Changes in serum levels occur sooner
- 55. NOVEL BIOMARKERS • 1. IL- 18 • 2.KIM-1 • 3.Gro α/KC • 4.NGAL-neutrophil gelatinase associated lipocalin • 5.NHE-3 -Sodium–hydrogen antiporter 3
- 56. Complications
- 57. Complications
- 58. Complications
- 59. Other Complications Hyperuricemia Infection- pneumonia, sepsis Git- nausea, vomiting, malnutrition, git bleeding CNS- asterixis, mental changes, seizures Uremic syndrome
- 60. AKI: PREVENTION Recognize patients at risk (postoperative states, cardiac surgery, septic shock) Prevent progression from prerenal to renal Preserve renal perfusion(isovolemia, cardiac output, normal blood pressure) Avoid nephrotoxins (aminoglycosides, NSAIDS, amphotericin)
- 61. GENERAL PROTOCOL FOR MANAGEMENT OF AKI • Treat the underlying disease • Strictly monitor intake and output (weight, urine output, insensible losses, IVF) • Monitor serum electrolytes • Adjust medication dosages according to GFR • Avoid highly nephrotoxic drugs • Attempt to convert oliguric to non-oliguric renal failure (furosemide)
- 62. FLUID THERAPY If patient is fluid overloaded • fluid restriction (insensible losses) • attempt furosemide 1-2 mg/kg • Renal replacement therapy If patient is dehydrated: • restore intravascular volume first • then treat as euvolemic If patient is euvolemic: • restrict to insensible losses (30-35 ml/100kcal/24 hours) + other losses (urine, chest tubes, etc)
- 63. SODIUM • Most patients have dilutional hyponatremia which should be treated with fluid restriction • Severe hyponatremia (Na< 125 mEq/L) : dialysis or hemofiltration
- 64. POTASSIUM • Oliguric renal failure is often complicated by hyperkalemia, increasing the risk of cardiac arrhythmias • Treatment of hyperkalemia: – sodium bicarbonate (1-2 mEq/kg) – insulin + hypertonic dextrose – sodium polystyrene : 1 gm/kg . (Hypernatremia and hypertension are potential complications) – dialysis
- 65. MANAGEMENT OF AKI Metabolic acidosis – soda bicarb ., if < 15 meq Hyperphosphatemia – PO4 binders –sevalamer Hypocalcemia –calcium carbonate Nutrition –restriction of dietary protein < 0.8 g/kg /d calories – 25-30 kcal /kg/d enteral nutrition preferred
- 66. Criteria for Initiation of RRT Anuria Oliguria Pulmonary edema Hyperkalemia >6.5mmol/L Severe acidemia <7.2 Uremic encephalopathy Uremic pericarditis
- 67. Thank you