clinical pharmacy in nephrology
DESCRIPTION
CLINICAL PHARMACY IN NEPHROLOGY. ACUTE RENAL FAILURE. Background. Common in Hospitalized patients Associated with high Morbidity and Mortality Often Multifactorial Identifiable risk factors. Acute Renal Failure. Sudden decrease in function (hours-days) Often multifactorial - PowerPoint PPT PresentationTRANSCRIPT
CLINICAL PHARMACY IN NEPHROLOGY
ACUTE RENAL FAILURE
Background
• Common in Hospitalized patients• Associated with high Morbidity and
Mortality• Often Multifactorial• Identifiable risk factors.
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