ACUTE RENAL FAILURE Background Common in Hospitalized patients Associated with high Morbidity and Mortality Often Multifactorial Identifiable risk factors.

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