Clinical pharmacy in Nephrology

1. CLINICAL PHARMACY IN
NEPHROLOGY
ACUTE RENAL FAILURE

2. Background
• Common in Hospitalized patients
• Associated with high Morbidity and
Mortality
• Often Multifactorial
• Identifiable risk factors.

5. Sponsored
Medical Lecture Notes – All Subjects
USMLE Exam (America) – Practice

6. 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

8. 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

9. Acute Renal Failure
Diagnosis (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

10. Acute Renal Failure
Diagnosis (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

12. 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

16. 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

17. 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.

19. 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.

20. 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 .

22. 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

23. 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)

24. 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.)

25. 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)

26. 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

27. Prevention
What works?
• Maintenance of euvolemia
• Avoidance of nephrotoxins when possible
– NSAIDs, aminoglycoside, Amphotericin, IV
contrast
• BP control--avoidance of excessive hypo-
or hypertension

28. Prevention
What doesn’t work?
• Empiric use of:
– Diuretics (i.e., Furosemide, Mannitol)
– Dopamine (or Dopamine agonists such as
Fenoldopam)
– Calcium-channel blockers

29. Acute Renal Failure
Treatment
• Water and sodium restriction
• Protein restriction
• Potassium and phosphate restriction
• Adjust medication dosages
• Avoidance of further insults
– BP support
– Nephrotoxins

30. 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

32. Dialysis Indications
• Refractory hyperkalemia
• Metabolic acidosis
• Volume overload
• Mental status changes