Download 28. Acute renal failure

28. Acute renal failure
Causes
 Prerenal: decreased effective arterial volume (hypovolemia, CHF, sepsis), ACE-I, NSAIDs
 Acute tubular necrosis (ATN): progression of prerenal state, drugs (aminoglycosides, ampho,
cisplatin), myo- or hemoglobinuria, multiple myeloma. Sediment: muddy brown granular casts
 Contrast-induced acute renal failure: peaks in 3-5 days, resolves in 7-10 days
 If high-risk: pre- and post- hydration and N-acetylcysteine 600 mg po bid on day prior to and day of
contrast with iv hydration
 Acute interstitial nephritis (AIN): drugs (antibiotics, NSAIDs) or infection; sediment: WBC casts,
WBCs, RBCs; may be associated with fever, rash, eosinophilia, and eosinophiluria
 Vascular: RAS (+ ACE-I), thrombosis, hypertensive crisis, scleroderma, cholesterol emboli,
HUS/TTP, preeclampsia
 Acute glomerulonephritis: sediment may show dysmorphic RBCs and RBC casts
 Post-renal: obstruction (malignancy, BPH, bilateral stones), neurogenic bladder, anticholinergics
Workup
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Degree of and type of workup varies depending on history
Examine urine sediment
Determine if patient is oliguric/anuric (output <400 mL/24 hrs)
Fractional excretion of sodium (FENa); refer to formulae section
 <1% suggests prerenal, contrast, or pigment nephropathy
 >1% suggests ATN
 Diuretics may elevate FENa even if patient is prerenal
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Glomerular diseases
1. Anti-GBM disease (e.g.
Goodpasture’s)
2. ANCA-associated
 Wegener’s
 Polyarteritis nodosa
3. Immune-complex associated
 SLE
 MPGN
 Cryoglobulinemia
 Etc.
Urine eosinophils (if AIN suspected)
SPEP, urine for protein electrophoresis and Bence-Jones protein
Glomerular disease suspected: ANCA, ANA, anti-GBM, ASLO, cryocrit
C3, C4 to differentiate low-complement immune complex disease (endocarditis, SLE, MPGN,
PSGN, cryoglobulinemia, visceral abscess) from normal complement immune complex disease (IgA
nephropathy/HSP, fibrillary GN); complement levels can also be low in setting of cholesterol emboli
 Ultrasound useful in evaluating for hydronephrosis and determining chronicity of renal disease
 Biopsy may be needed if cause remains unclear
Management
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Optimize hemodynamic factors (fluids if hypovolemic, pressors if hypotensive, etc.)
Avoid nephrotoxins (e.g. contrast, nephrotoxic drugs)
Watch for and correct electrolyte (hyperkalemia, hyperphosphatemia) and acid/base disturbances
Check medication dosing frequently and adjust for renal function
Consider dialysis if refractory to medical management
Specific treatments:
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AIN: stop offending agent, consider steroids
Scleroderma renal crisis: ACE-I
HUS/TTP: plasma exchange
Glomerulonephritis: steroids, immunosuppressive drugs may be needed; discuss with renal fellow early
if suspected
 Postrenal: remove obstruction
Ishir Bhan, M.D.
MGH Medical Housestaff Manual
79
29. Dialysis
Emergent indications
 Acidosis (refractory to medical management)
 Electrolyte imbalances (refractory to medical management), generally hyperkalemia, and hypercalcemia (Ca
>18), tumor lysis syndrome (in settings of very high uric acid)
 Intoxications. Lithium, salicylates, theophylline, alcohols
 Overload (volume)
 Uremia (with complications, e.g. pericarditis)
Hemodialysis (HD)
 Principle. Blood flows along one side of a semipermeable membrane, dialysate along the other. Fluid
removal occurs via pressure gradient. Solute removal occurs via concentration gradient, and in a manner
inversely proportional to molecular size (effective at removing potassium, urea, creatinine but not very
effective for removing PO4).
 Access. Double-lumen central catheter (tunneled or temporary), AV fistula, or AV graft
 Contraindications. Hemodynamic instability (see CVVH), arrhythmias, bleeding
 Complications. Hypotension (from ultrafiltration, medication, temperature of dialysate, bleeding, infection,
arrhythmia, ischemia), arrhythmias, HIT, access complications
Continuous veno-venous hemofiltration (CVVH)
 Indications. Patients who are hemodynamically unstable and who are not likely to tolerate the large fluid
shifts associated with HD
 Principle. Blood flows along one side of a highly permeable membrane and fluids and solutes pass by
convection. Filtrate is discarded and fluid with plasma-like solute concentrations is infused. Fluid balance is
precisely controlled by adjustment of the quantity of replacement fluid infused.
 Anticoagulation by citrate v. heparin and bicarbonate. Citrate achieves regional anticoagulation by calcium
chelation (metabolized in liver); contraindication is liver failure. Need to watch calcium levels and citrate
toxicity (suggested by rising total calcium, falling ionized calcium, rising anion gap).
 Complications. Hypotension, hypophosphatemia, hypocalcemia, access complications
Peritoneal dialysis
 Principle. Gravity assisted infusion into peritoneum; control H2O and Na balance by adjusting the glucose
concentration in the fluid; very long dwell times pull out less fluid as the glucose equilibrates
 Access. Catheter placed by transplant surgery generally.
 Contraindications. Recent abdominal surgery, infection, ileus
 Orders: PD fluid: 1.5%, or 2.5 %, or 4.25% dextrose (higher dextrose removes more fluid)
 Typical prescription. Volume 2 L, dwell time 6 hours, dextrose 1.5% for a total of 4 exchanges in 24 hour
period. Prescription written generally by peritoneal dialysis nurse (PD unit 617-720-1317). PD nurse on call
24/7 for any issues.
 Complications
 Infection: fairly common. Can occur at exit site, tunnel, and/or peritoneum. Catheter removal may be
necessary especially if fungal infection. Diagnose by finding >100 WBC with >50% PMN in fluid. 5060% infections are GPC, 15-20% GNR, remainder are fungal or no identifiable organism. Can treat with
either intravenous or peritoneal antibiotics.
 Hyperglycemia: exacerbated by inflammation, long dwell time, and higher dextrose concentrations.
Treat by adding insulin sc
 Clots: add heparin in first few infusions (but involve renal)
Ishir Bhan, M.D.
MGH Medical Housestaff Manual
80
30. Acid-base
General considerations
 Determine if patient is alkalemic (pH>7.44) or
acidemic (pH<7.36)
 Determine if process is metabolic or respiratory
 Acidemia
Respiratory acidosis
acute, pH 0.08 for 10 mm Hg pCO2
chronic, pH 0.03 for 10 mm Hg pCO2
 Alkalemia
Respiratory alkalosis
chronic, pH 0.02 for 10 mm Hg pCO2
 pCO2 >40  respiratory acidosis
 HCO3 <24  metabolic acidosis
 pCO2 <40  respiratory alkalosis
 HCO3 >24  metabolic alkalosis
Metabolic acidosis
 Check the anion gap: Na – (Cl + HCO3). Normal is ~7 to 13
 in hypoalbuminemia, “expected” AG lower by 2.5 for every 1 g/dL reduction in albumin.
 The diagnostic utility of a high AG is greatest when the AG is above 25 mEq/L
 If AG elevated, look for causes of AG acidosis: ketones, lactate, renal failure, methanol, ethylene
glycol, ethanol, paraldehyde, salicylates
 Calculate ( anion gap/ HCO3), i.e. ratio of ∆AG (measured AG  expected AG) to ∆HCO3 (24 
HCO3).
 If / = 1, suggests pure gap met acidosis (i.e. lactic acidosis)
 If / <1, suggests mixed gap/non-gap metabolic acidosis
 If / >1, suggests underlying metabolic alkalosis in addition to the metabolic acidosis
 If AG not elevated, check urine anion gap [Na + K – Cl].
 In normal subjects, urine AG is positive or near 0
 Positive urine AG suggests renal etiology, e.g. renal tubular acidosis type I or IV.
 Negative urine AG, suggests diarrhea, recent saline administration, recently resolved respiratory alkalosis,
RTA II, acetazolamide; rarely: ureteral diversions and pancreatic fistulas
Metabolic alkalosis
 Check urine Cl (avoid measuring while diuretics are active)
 UCl < 20 suggests saline-responsive metabolic alkalosis: prior diuretic use, volume depletion,
vomiting, NGT drainage, villous adenoma, resolved respiratory acidosis
 UCl > 20 and euvolemia suggests saline-resistant metabolic alkalosis:
 if hypertensive: hyperaldosteronism, Cushing’s syndrome, licorice ingestion, Liddle’s
 if normotensive: extreme hypokalemia, exogenous alkali, Bartter’s, Gitelman’s
Respiratory acidosis
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CNS depression, especially from medications
Airway disease: COPD, asthma, upper airway abnormalities
Neuromuscular disease
Parenchymal lung disease: pneumonia, pulmonary edema, restrictive lung disease
Thoracic cage abnormalities: pneumothorax, kyphoscoliosis
MGH Medical Housestaff Manual
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30. Acid-base
Respiratory alkalosis
 Any cause of hypoxia causing increased respiratory drive (e.g. pneumonia, pulmonary embolism,
pulmonary edema)
 Pain, anxiety
 Salicylates
 Pregnancy/progesterone
 Sepsis
 Liver failure
 Primary CNS disorder
Ishir Bhan, M.D.
MGH Medical Housestaff Manual
82
31. Sodium disorders
Hypernatremia
Na stores depleted
H2O depleted >Na
UNa >20
H2O stores depleted
Na stores relatively normal
UNa <10
Renal loss
Osmotic diuresis
Extrarenal loss
Perspiration
Diarrhea
Volume replacement with normal saline, free
H2O replacement with hypotonic saline
Na excess
Na >H2O
UNa variable
Renal loss
Central DI
Nephrogenic DI
UNa >20
Extrarenal loss
Insensible losses
Hypertonic HD
NaHCO3 treatment
Free H2O replacement
Diuretics + H2O
Hyponatremia
Remember to correct for hyperglycemia. (Hyperlipidemia and paraproteinemia are no longer a problem with Na
measurement at MGH given newer lab technique due to electrode.)
Extracellular volume deficit
UNa >20
Renal loss
Osmotic diuresis
Diuretics
Mineralocort
deficiency
Na-losing
nephropathy
UNa <10
Extrarenal loss
Vomiting
Diarrhea
Third spacing
Isotonic saline
Mineralocorticoid prn
Extracellular volume normal
(mild excess)
UNa >20
SIADH
Glucocorticoid deficiency
Thyroid dysfunction
Reset osmostat
Free H2O restriction
Treat underlying condition
Extracellular volume excess
UNa >20
Normal circ volume
Renal failure
UNa <10
Low circ volume
CHF
Cirrhosis
Nephrotic synd.
Sodium + H2O restriction
May need diuretic
Treat underlying condition
If hyponatremia is severe, hypertonic saline may be needed.
Caution when correcting hyponatremia too rapidly because of possible pontine osmotic demyelination.
In asymptomatic patients, recommended average correction of 0.5 mEq/L per hour.
Reshma Kewalramani, M.D.
MGH Medical Housestaff Manual
83
32. Potassium disorders
Hyperkalemia
Pseudohyperkalemia
Hemolysis
Plts >1,000,000
WBC >200,000
Familial pseudohyperkalemia
Tourniquet-related
Sample drawn upstream from
iv solution containing K
Redistribution
Acidosis
Hypertonic states
Digoxin overdose
Hyperkalemic periodic
paralysis
Beta blocker
Impaired K excretion
Renal failure
Aldosterone insufficiency
Low GFR (10-20% of nl)
Usually in assoc with
endogenous or exogenous
potassium load
Other (drugs)
K sparing diuretics
ACE inhibitors
Normal GFR
Aldosterone
insufficiency
Addison’s
Hyporenin-hypolado
Aldosterone
unresponsiveness
SLE
Amyloid
Obstructive uropathy
Renal transplant
Hypokalemia
Spurious
WBC >100,000 (if left
at room temperature,
WBC may take up K)
TTKG 
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Redistribution
Insulin
Alkalemia
Beta2 agonist
Theophylline toxicity
Familial hypokalemic
periodic paralysis
urine K  plasma K 
urine Osm plasma Osm
Extrarenal loss
(low TTKG)
Diarrhea
Laxative abuse
Villous adenoma
Sweat losses
Inadequate intake
Metabolic acidosis
Type 1 RTA
Type 2 RTA
Carbonic anhydrase
inhibitors
Uretero-sigmoidostomy
Renal loss (high TTKG)
Metabolic alkalosis
Vomiting
Nasogastric suction
Diuretics
Increased
mineralocorticoid
Bartter’s
During hypokalemia, the expected TTKG is <2. A higher value suggests K+
secretion is inappropriately stimulated.
During hyperkalemia, the expected TTKG is >10. A lower value suggests
that that K+ secretion is inappropriately suppressed (e.g., in
hypoaldosteronism).
MGH Medical Housestaff Manual
No specific disorder
Magnesium depletion
Cisplatin
Recovery from ARF
Post-op diuresis
Reshma Kewalramani, M.D.
84
33. Hyperkalemia treatment
EKG changes in hyperkalemia
 Patterns best seen in leads V4-5
 Correct diagnosis can usually be made when K > 6.7.
K
> 5.5
> 6.5
>7
>8
> 10
> 12-14
EKG changes
peaking in T waves
QRS widening
P wave amplitude decreases, duration of P wave increases, prolongation of PR interval
P wave disappears, auricular standstill
ventricular rhythm may become irregular and may simulate atrial fibrillation
asystole or ventricular fibrillation
General considerations
 Interpatient variability in effects of hyperkalemia, time course of hyperkalemia (e.g., end stage renal disease
vs. acute tissue break down)
 K > 7, EKG changes, changes in muscle strength generally warrant immediate treatment
Therapy
Dose
Onset of
effect
Duration
of effect
Comments
Calcium
10 mL (1 amp) of 10% calcium
gluconate or calcium chloride
solution infused over 2-3 min
1-3 min
30-60 min
Stabilizes cardiac membrane
Caution in patients taking
digoxin as hypercalcemia
can induce digitalis toxicity
Sodium
bicarbonate
1 mEq/kg iv bolus (1 amp of
sodium bicarb ~45 mEq)
5-10 min
1-2 hours
K lowering most prominent
in metabolic acidosis
Insulin and
glucose
10 U iv plus D50 1-2 amps (note
more than 1 amp may be needed to
prevent hypoglycemia)
30 min
4-6 hours
Enhances Na-K-ATPase
pump in skeletal muscle
Causes 0.5-1.5 mEq/L fall in
K
Albuterol,
nebulized
10-20 mg nebulized over 15 min
15 min
15-90 min
Drives potassium into cells
by increasing Na-K-ATPase
activity
Lowers K by 0.5-1
Kayexalate (Na
15-50 g po or pr, plus sorbitol
1-2 hours
4-6 hours
Binds K in gut and releases
Na
polystyrene sulfonate)
Diuresis
Furosemide 40-80 mg iv
Dialysis
Consider dialysis when
conservative measures fail,
if hyperkalemia is severe, or
if ongoing hyperkalemia a
likely issue
Andrew Yee, M.D.
MGH Medical Housestaff Manual
85