acute renal failure
DESCRIPTION
ACUTE RENAL FAILURE. Background. Common in Hospitalized patients Associated with high Morbidity and Mortality Often Multifactorial Identifiable risk factors. Renal biopsy. Renal biopsy on hospital day 2 demonstrating massive oxalosis. Acute dialysis. Acute Renal Failure. - PowerPoint PPT PresentationTRANSCRIPT
ACUTE RENAL FAILURE
Background
• Common in Hospitalized patients
• Associated with high Morbidity and Mortality
• Often Multifactorial
• Identifiable risk factors.
Renal biopsy
Renal biopsy on hospital day 2 demonstrating massive oxalosis
Acute dialysis
Acute Renal Failure
• Sudden decrease in function (hours-days)
• Often multifactorial
• Pre-renal and intrinsic renal causes 70%
• oliguric UOP < 400 ml
• Non-oliguric (up to 65%)
• Associated with high mortality and morbidity
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, GIB, Catabolic state, hypovolemia
– BUN/Cr helpful in classifying cause of ARF• ratio> 20:1 suggests prerenal cause• ratio 10-15:1 suggests intrinsic renal cause
Acute Renal FailureDiagnosis (cont’d)
• Urinalysis– Unremarkable in pre and post renal causes– Differentiates ATN vs. AIN. vs. AGN
• Muddy brown casts in ATN
• WBC casts in AIN
– Hansel stain for Eosinophils
Acute Renal FailureDiagnosis (cont’d)
• Urinary Indices;– FE Na = (U/P) Na X (P/U)CrX 100
• FENa < 1% C/W Pre-renal state– May be low in selected intrinsic cause
» Contrast nephropathy
» Acute GN
» Myoglobin induced ATN
• FENa> 1% C/W intrinsic cause of ARF
Prerenal Azotemia• Nearly as common as ATN (think of as early
part of the disease spectrum)• Diagnose by history and physical exam
– N/V, Diarrhea, Diuretic use,...
• low FENa (<1%)
• high BUN/creat ratio, normal urinary sediment
• Treat by correction of predisposing factors
Acute Renal Failure Etiologies
• Acute Tubular Necrosis– Most common cause of intrinsic cause of ARF– Often multifactorial– Non-oliguria carries better prognosis– Ischemic ATN:
• Hypotension, sepsis, prolonged pre-renal state
– Nephrotoxic ATN:• Contrast, Antibiotics, Heme proteins
Acute Tubular Necrosis (ATN) -- 2
• 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.
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: CRF, Hypovolemia.
Rhabdomyolytic ARF• Diagnose with serum CPK (usu. > 10,000),
urine dipstick (+) for blood, without RBCs on microscopy, pigmented granular casts
• Common after trauma (“crush injuries”), seizures, burns, limb ischemia occasionally after IABP or cardiopulmonary bypass
• Treatment is largely supportive care.• Alkalinization of urine .
Acute Glomerulonephritis• Rare in the hospitalized patient
• Most common types: acute post-infectious GN, “crescentic” RPGN
• 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
Acute Glomerulonephritis (2)
• If diagnosis is post-infectious, disease is usually self-limited, and supportive care is usually all that is necessary.
• For RPGN, may need immunosuppressive therapy with steroids ± Cytoxan, plasmapheresis (if assoc. with anti-GBM)
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.)
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)
Acute Renal Failure Etiologies
• Post-Renal– Bladder outlet obstruction
• BPH, intrapelvic pathology
– Crystalluria• Acyclovir, Indanivir, Uric Acid
– Papillary tip necrosis• DM with pyelonephritis• Analgesic abuse• Sickle cell disease
Prevention
What works?
• Maintenance of euvolemia
• Avoidance of nephrotoxins when possible– NSAIDs, aminoglycoside, Amphotericin, IV
contrast
• BP control--avoidance of excessive hypo- or hypertension
Prevention
What doesn’t work?
• Empiric use of:– Diuretics (i.e., Furosemide, Mannitol)– Dopamine (or Dopamine agonists such as
Fenoldopam)– Calcium-channel blockers
Acute Renal Failure Treatment
• Water and sodium restriction• Protein restriction• Potassium and phosphate restriction• Adjust medication dosages• Avoidance of further insults
– BP support– Nephrotoxins
Hyperkalemia
• Highly Arrhythmogenic– Usually with progressive EKG changes
• Peaked T waves ---> Widened QRS--> Sinus wave
– K> 5.5 meq/L needs evaluation/intervention– Usually in setting of Decrease GFR but:
• medication also a common cause– ACEI
– NSAIDS
– Septra, Heparin
Dialysis Indications
• Refractory hyperkalemia
• Metabolic acidosis
• Volume overload
• Mental status changes