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Acute Renal Failure Hai Ho, M.D.
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What is acute renal failure?
Impairment of kidney function leading to retention of substances normally excreted by the kidney Hours and days
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Epidemiology Overall mortality rate: 40-50%
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Kidney anatomy & physiology
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Kidney anatomy & physiology
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Compartmentalize causes?
Prenal Renal or intrinsic Postrenal
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Pathophysiology of prerenal failure?
Hypoperfusion to the kidney
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Common causes of prerenal failure?
Hypovolumia Bleeding Burn Dehydration from GI loss Hypervolumia Congestive heart failure Third-spacing – cirrhosis, acute pancreatitis Peripheral vasodilation Septic shock Acute glomerulonephritis. Most common type in children is following a streptococcal infection but rare in adults, with poorer prognosis in adults.
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Common cause of intrinsic renal failure?
Acute tubular necrosis – most common cause of acute renal failure in hospitalized patients Glomerulonephritis – rare, common in children after streptococcal infection
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What is acute tubular necrosis?
Disorder resulting from damage of renal tubule cells
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What cause acute tubular necrosis?
Prerenal azotemia Ischemia > 30 minutes Most common in hospitalized patients Rhabdomyolysis Contrast dye Drugs Aminoglycosides Amphotericin NSAID ACE-inhibitor
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Common cause of postrenal failure?
Ureteric obstruction – tumors, stones Bladder outflow obstruction (prostatism)
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Clinical presentations of acute renal failure?
Asymptomatic Decreased or no urine output Hypervolumia Pulmonary edema – tachycardia, tachapnea Peripheral edema Uremia – lethargy, nausea, anorexia Arrhythmia – hyperkalemia, acidosis
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Diagnostic tests Renal function – GFR Plasma creatinine
May not rise initially due to compensatory hypertrophy and hyperfiltration, therefore not detect actively declining GFR Interesting in the trend rather than absolute value Affect by muscle mass Creatinine clearance Stable renal function Cockcroft-Gault equation Creatinine: rising=acute, progressing, stable=chronic, decrease=improving
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Cockcroft-Gault equation
(140-age) x lean body weight (kg) PCr (mg/dL) x 72 Women – multiple by 0.85
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Diagnostic tests Renal function – GFR BUN:Cr Plasma creatinine
May not rise initially due to compensatory hypertrophy and hyperfiltration, therefore not detect actively declining GFR Interesting in the trend rather than absolute value Creatinine clearance Stable renal function Cockcroft-Gault equation BUN:Cr 15:1 to 20:1 – prerenal, due to increased BUN absorption 10:1 – cirrhosis or other hypoprotein state Creatinine: rising=acute, progressing, stable=chronic, decrease=improving
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Diagnostic tests Renal function – GFR Fractional excretion of sodium
Plasma creatinine May not rise initially due to compensatory hypertrophy and hyperfiltration, therefore not detect actively declining GFR Interesting in the trend rather than absolute value Creatinine clearance Stable renal function Cockcroft-Gault equation Fractional excretion of sodium Creatinine: rising=acute, progressing, stable=chronic, decrease=improving
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Fractional excretion of sodium
UNa x PCr FENa = x 100 PNa x UCr Interpretation <1% – prerenal, glomerulonephritis, obstruction >2% – ATN 1-2% - either prerenal or ATN Not accurate before diuretics or IVF <1% in glomerulonephritis, vasculitis, acute urinary obstruction too
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Diagnostic tests Urinalysis Dipstick – hematuria and proteinuria
Microscopic examination RBC cast – glomerulonephritis
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RBC cast Damaged glomerular basement membrane
Although the red blood cells may enter the urinary stream via disrupted tubular elements, their most common means of entry is through a damaged glomerular basement membrane. The presence of these casts indicates a glomerular injury. In some cases the erythrocytes are destroyed. The typical sign for these erythrocytes casts is a red brown mass. Other renal diseases that may or may not cause direct damage to or destroy the glomerulus and which give rise to blood cell casts and hematuria. The more common of these include acute pyelonephritis and renal infarction
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RBC cast
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Diagnostic tests Urinalysis Dipstick – hematuria and proteinuria
Microscopic examination RBC cast – glomerulonephritis WBC cast – acute pyelonephritis
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WBC cast They consist of mucoprotein casts with incorporated leukocytes. With chronical renal inflammation, especially with pyelonephritis, the leukocytes enter the urinary stream through two major pathways, transglomerular or transtubular
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Diagnostic tests Urinalysis Dipstick – hematuria and proteinuria
Microscopic examination RBC cast – glomerulonephritis WBC cast – infection such as pyelonephritis Granular cast – protein aggregate or degenerative cellular casts as in acute tubular necrosis
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Granular cast
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Granular cast
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Diagnostic tests Urinalysis Renal ultrasound
Dipstick – hematuria and proteinuria Microscopic examination RBC cast – glomerulonephritis WBC cast – infection such as pyelonephritis Granular cast – protein aggregate or degenerative cellular casts as in acute tubular necrosis Positive blood on dipstick but negative RBC on microscopic exam - rhadomyolysis Renal ultrasound
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Renal ultrasound? Obstruction – hydronephrosis
Chronic disease – atrophic kidney
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Renal biopsy Selective cases such as glomerulonephritis, vasculitis, nephrotic syndrome
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Treatment? Treat the underlying cause Prerenal – increase perfusion
Intrinsic – if possible, remove the culprit Postrenal – relieve the obstruction
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General management Hyperkalemia – low K diet, lasix, insulin/glucose, NaHCO3, Kayexalate, Ca gluconate Fluid retention and overload – diuresis, fluid restriction Diet – low protein, high carbohydrates Acetylcysteine with 0.45% NS with contrast study – reduce nephropathy Dialysis Diuretics might have harmful effect – not to use to increase urine output
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References Acute tubular necrosis. Acute renal failure
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