Transcript Acute Renal Failure - University of North Texas

Acute Renal Failure
A. Symptoms
1.Polyuria, Oliguria or Anuria hematuria
2.Dysuria
3.Uremia
a.Definition: symptomatic azotemia
b.Acidosis (± tachypnea)
c.Mental Status changes
d.Hypervolemia / Hypertension
e.Hyperkalemia
f. Pericarditis
1. Duration <3 months
2. Oliguria <400 ml urine/24 hours
3. Absolute increase Scr by 0.5 or 1.0 mg/dl or
relative increase 25%
4. Cockcroft – Gault Equation
(140-age) x wt(kg)
-----------------------Serum Cr x 72
B. Etiologies
1. Location of Lesion
a. Prerenal - ~70% of cases
b. Intrinsic - ~25% of cases
c. Post-renal (obstructive) - <5% of cases
d. FeNa= urine Na x serum Cr
------------------------------X 100
serum Na x urine Cr
Urine Na
FeNa
response IVF
BUN/Scr
Prerenal
<10
<1%
good
>20
Renal (ATN)
>10
>1%
poor
nl
Pre-renal azotemia
1.
Decreased effective arterial volume
-
CHF,,Cirrhosis,,Nephrotic syndrome,,Sepsis
Renal Artery Stenosis (atherosclerosis,
fibromuscular dysplasia)
Cardiopulmonary bypass (>3 hours)
-
Intravascular volume depletion
–
–
–
–
–
GI loss…Vomiting..diarrhea…etc
Renal loss diuretc..osmotic diuresis..etc
Cutaneous loss hyperthermia..burns
Hemorrhage
Third space pancreatitis..severe
hypoalbuminemia..cappillary leak
II.Parenchymal Damage
•
Nephritis (inflammation): glomerular vs.
interstitial
•
Tubular Injury: most common cause of ARF
Nephrotic Syndrome (total protein losses)
III. Obstruction of Outflow (~5%) Urinary Tract
Infection (UTI) with Pyelonephritis
a. Urinary Calculus disease (renal stones)
b. Crystal Deposition
c. Bladder tumors with extensive invasion
d. Prostatic Enlargement: BPH vs. Carcinoma
e. Unilateral obstruction with only one
functioning kidney
Vascular hypertension
Atherosclerotic (atheroembolism) - cholesterol
emboli, 5-10% of hospitalized ARF Trauma
b. Vasculitides
c. Post-operative - aortic aneurysm repair, aortic
cross-clamping
d. Vasoconstricting Agents - NSAIDs,
vasopressors
1.
a.
1. Drug Induced
a. ACE Inhibitors
b. Radiocontrast Dye Interstitial Nephritis
c.
d.
e.
f.
- sulfonamides, NSAIDS, other
antibiotics
Amphotericin
Cis-Platinum
Aminoglycosides
Non-steroidal anti-inflammatory drugs
(NSAIDs)
Pathophysiology
Ischemia is the underlying problem in ARF
leads to depletion of cellular ATP and release
of calcium
b. Reactive oxygen species produced leading to
further cell death
c. Calcium release leads to phospholipase
activation
d. Neutrophils may mediate reperfusion injury
(ICAM-1 is involved)
e. Many nephrotoxins are renal vasocontrictors
1.
2.
a.
C. Initial Evaluation
1. Consider possible etiologies and direct
evaluation
2. Medications should always be suspected
3. Standard Blood Testing
a. Electrolyte/renal panel, Ca2+, Phosphate,
Mg2+, Albumin
b. Complete Blood Count
c. Foley catheter to rule out bladder
obstruction
1. Urine for electrolytes, dipstick and
a.
b.
c.
d.
e.
microscopic analysis
Osmolality, creatinine, Na+, K+, ClUrine spot protein to creatinine ratio
(normal is <0.2)
Pigment: Hemoglobin (myoglobin)
Cells, Casts, Crystals, Organisms
Consider Urine culture
1.
2.
3.
4.
a.
b.
Renal/Pelvic Sono - stones, hydronephrosis,
mass
Consider Abdominal radiograph if ultrasound is
not done to rule out stones
ESR, ASO titer, ANA, C3/C4 Anti-GBM Abs
Renal Biopsy in rapidly progressing disease
ANCA and Anti-GBM diseases - consider
cyclophosphamide + glucocorticoids
Idiopathic rapidly progressive glomerulonephritis
often ANCA positive (other inflammatory
diseases such as bacterial endocarditis can
given ANCA+)
Pathology Summary
1. Glomerular Involvement
a. Diffuse: all glomeruli in a section are diseased
b. Focal: some glomeruli in a section are diseased
c. Segmental: parts of individual glomerulus
affected
2.Focal Glomerulonephritis:
a. Some glomeruli are dead( necrosis, collapse,
sclerosis
b.Acute or chronic inflamation is often seen
3.Crescent Glomerulonephritis (very poor
4.
Focal and Segmental Glomerulosclerosis: portions
of many glomeruli are destroyed
5.
a.
b.
Minimal Change Glomerulonephritis
Glomeruli appear okay, but function is poor
Electron microscopic evidence of basement
membrane disease
Response to glucocorticoids is usually very good
c.
6. IgA Deposition
a.IgA nephropathy
b.Deposition of IgA immune complexes
c.Differential includes Systemic Lupus (SLE) and
Henoch-Schonlein Purpura (HSP)
7. Proliferative Glomerulonephritis
a. Increase in mesangeal cell number
b. Usually follows insults (eg. PostStreptococcal)
c. May be seen in collagen vascular disease,
SLE
8. Collapsing Glomerulonephritis
a. Major form seen in HIV nephropathy
b. Usually late stage
c. Rapid progression to renal failure (weeksmonths)
d. No effective therapy to date
9.Tubular Necrosis
a.Tubular cells die and slough off basement
membrane
b.The dead tubular cells form casts which
can occlude lumen
c.Glomular basement membrane may also
be damaged
E. Management
Renal Diet
a. Low phosphate, potassium, sodium, and
protein
b. High calcium and vitamin D
c. Various multivitamin formulas available for
renal patients, eg. Nephrovit®
d. Low protein diet may slow progression
slightly in chronic renal disease
e. Phosphate and Calcium
f. Dangerous if product of Calcium and
Phosphage > ~70 (mg/dl) (will lead to
precipitation)
If product is close to 70, then phosphate
should be lowered with aluminum
compounds
b. These compounds should be given with
meals to bind the phosphate directly
c. If product is <60, then calcium should be
given 500-1000mg po tid with meals
d. If calcium is low but phosphate normal, then
calcium should be given before meals
e. Consider using 1,25 dihyroxyvitamin D
supplements
a.
1. Acidosis
Renal tublar acidosis (RTA) is common in
early renal failure
Oral bicitra (citrate replaces bicarbonate)
may be used
Bicitra is contraindicated in edematous
states due to high sodium content
2. Hyperuricemia
Check uric acid levels
Uric acid deposition in renal tubules may
worsen progression of renal failure
Allopurinol may be given (100-200mg po
qd) to attempt normalization of uric acid
3. Hypertension
a. ACE inhibitors generally contraindicated in
moderate to severe renal failure
b. Calcium blockers such as nifedipine
c. Labetolol is also very effective but patient
should have LV EF>50% and no
bronchospasm
d. Consider Hydralazine for afterload reduction
e. Pure alpha-adrenergic blocking agents may
be effective, but tachyphylaxis may occur
f. Diuretic improve hypertension/ volume
overload
4. Volume overload
a. Attempt to maximize cardiac output and
improve intravascular volume
b. Diuretics often worsen renal failure but may
be necessary to prevent pulmonary edema
c. In general, potassium sparing diuretics
should be avoided (high risk hyperkalemia)
e. Dopamine or mannitol can be tried, but are
usually not effective
f. Albumin infusions are probably not helpful,
but may help diuresis in low albumin states
g. Dialysis may be required particularly in
severe volume overload situations
5. Protein Load
Reducing protein load is thought to reduce
azotemia
b. Appears to slow progression of CRF
c. Patients with moderate renal disease - some
decrease in progression on low protein diet
d. Patients with severe renal disease show no
benefit on low protein diet
a.
6. Hospital inpatients with ARF ~50% mortality
rate
7. Newer Agents
a. Atrial natriuretic factor (ANF)= dilators +
diuretic
b. ANF (Auriculin®) ? efficacy in oliguric ARF
c. ANF may increase renal dysfunction in
diabetics receiving radiocontrast
d. Brain derived natriuretic factor (BDNF) may
be effective some patients
e. Other vasodilators (eg. calcium channel
blockers) are not effective
f. Investigation renal growth/regeneration
factors
8. Dialysis Indications
1. Serum abnormalities unresponsive to medical
therapy
a. Severe Acidosis
b. Severe Hyperkalemia
II Uremia
a. Mental status changes (usually delirium)
b. Nausea and vomiting
c. Pericarditis (pericardial friction rub)
III Volume Overload
•
Hemofiltration or hemodialysis can be used
to allow recovery of kidney after ARF
a. Average duration of need for these
therapies was 9 days in ARF
b. After this time, kidneys regain function and
increase urine output
c. Native kidneys may continue with minimal
function for 6-12 months of hemodialysis
d. After that, native kidneys usually shut down
permanently
Kidney Transplantation
Excellent (and improving) results with
cadaveric grafts.
Living Related Donor kidneys superior to CRT
1. New kidney usually placed in
extraperitoneally in the pelvis
2. Cyclosporin ,Prednisone, OKT3,
mycophenolic acid, FK506
immunosuppression
Combined Kidney Pancreas transplant in
Diabetic ESRD patients