Transcript Nephrology for Step 3

NEPHROLOGY FOR STEP 3
By James K. Rustad, M.D.
Copyright © 2009 All Rights Reserved.
Outline
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Renal Failure (Post-Renal, Pre-renal and Intrarenal)
Glomerulonephritis
Nephrotic syndrome
Acid-Base Disturbances
Imbalances of Sodium
Post-Renal
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Distended bladder on
exam.
Large volume diuresis
after passing urinary
catheter.
Bilateral
hydronephrosis on
ultrasound.
Post-void residual >
200 ml is suspicious.
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Black arrow = renal capsule
Black arrowhead = sinus fat
White arrow = dilated calyx
White arrowhead = renal cortex
Hydronephrosis
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Large hypoechoic area
(black on U/S = no
echoes) in center of
kidney. Dilation extends
into the parenchyma. The
normal hyperechoic area
in the center of the
kidney (hilum) is
replaced by a large
hydronephrotic renal
pelvis. This kidney has
hydronephrosis due to
obstruction of upper
ureter.
Treatment of Obstruction
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Lower tract: Foley cath.
Upper tract: Ureteral
stent or percutaneous
nephrostomy.
Pre-renal
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Hypotension.
Hypovolemia
(decreased renal
perfusion).
CHF: pump doesn’t work,
can’t perfuse kidney.
Constrictive pericarditis:
heart cannot fill, can’t
perfuse kidney.
GI Bleed (digested
blood is source of urea).
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Excess diuresis.
Dehydrated patient
may have high BUN
(azotemia) due to lack
of fluid volume to
excrete waste products.
Nothing wrong with
kidney itself – will try to
absorb sodium to
maintain volume.
Treat the underlying cause! Prerenal usually improves with IVF
Pre-renal vs. Renal
Pre-renal
Renal
BUN/Creatinine
>20:1
<20:1
Urine sodium
< 10
20
FENa
<1
>1
Intra-Renal
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Acute Tubular Necrosis
(ATN)
Caused by
hypoperfusion to the
point of tubular cell
death or from toxic
injuries.
Muddy Brown Casts
ATN (continued)
Contrast Nephropathy
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Typically begins
immediately after study.
Renal function recovers
after 3-5 days.
Prevent: Hydration, ½
NS 75 cc/hr 8-12 hr
before and after study.
Acetylcysteine 600 mg
BID for 2 days if
diabetes, CHF, CRI.
Aminoglycoside Toxicity
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Begins at least 5 days
after treatment.
Rhabdomyolysis leading to ARF
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Labs: CPK elevated, Urine
dipstick (urinalysis best
initial test) shows blood
but no RBC on microscopy.
Urine myoglobin most
accurate.
Tx: IVF, IV sodium
bicarbonate to alkalinize
urine to solubilize
myoglobin.
Mannitol and diuresis
decrease contact time of
myoglobin with tubule.
Clinical Situation
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Patient is brought to the
emergency room after a
seizure leading to
prolonged immobility on
sidewalk. Next step?
A) Urinalysis
B) Urine Myoglobin
C) EKG
D) CPK
E) Phosphate level
F) Creatinine
Acute Rhabdomyolysis
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EKG most urgent step.
Severe muscle necrosis
leads to Hyperkalemia.
Look for peaked T
waves. Treat with
immediate IV calcium
gluconate, insulin,
glucose.
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Order Potassium level
(cellular destruction).
Order Calcium level
(hypocalcemia):
damaged muscle may
bind increased calcium.
Hyperphosphatemia
may lead to calcium
binding with phosphate.
Order chemistries to
detect decreased serum
bicarb.
Acute Interstitial Nephritis
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The Pentad:
Acute Renal Failure
Fever
Rash
Arthralgia
Peripheral blood
eosinophilia
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Urine: WBC casts,
eosinophil positive
(Wright Stain)
Causes: Penicillin, Sulfonamide,
Rifampin, Allopurinol, Indinavir,
5-aminosalicylates, Proton Pump
inhibitors.
If NSAID induced: Fever, rash,
eosinophilia, eosinophiluria
usually absent.
Treatment: Stop medication!
Prednisone may be prescribed.
Glomerulonephritis
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RBC Casts, Dysmorphic RBC
Hematuria, proteinuria, HTN
Causes:
IgA Nephropathy
Post-streptococcal GN
Wegener’s granulomatosis
Goodpasture Syndrome
Endocarditis
Lupus Nephritis
IgA Nephropathy (Berger’s Disease)
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History of URI 1-2 days before presentation + Painless
recurrent hematuria
Recurrent hematuria following exertion
Serum IgA increased in 50% of patients
Normal complement
Renal Biopsy to confirm
Treatment: ACE inhibitor and ARB
Consider adding Fish Oil
Prednisone if tx-refractory or nephrotic
syndrome/markedly proliferative disease.
IgA Nephropathy Biopsy: Mesangial
Hypercellularity
IgA Nephropathy Immunofluorescence
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IgA mesangial deposits =
characteristic and defining
feature of the disease
Deposits are exclusive of
IgA in only ~26% of
cases; usually
accompanied by IgG
(~37%) or IgM (~13%),
and the three Igs may be
present in ~25% of cases.
However, IgA must be
dominant or codominant
Post-streptococcal GN
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URI 7-10 days before
presentation
“Cola or tea” colored
urine
Periorbital
edema/HTN
ASO titer, Low serum
complement
Treat infection/HTN
Clinical Scenario
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Patient with sinusitis,
rhinorrhea, bloody
nasal discharge and
cough, shortness of
breath, hemoptysis.
Hematuria, Proteinuria
and Renal Failure.
+ for c-ANCA
Most likely diagnosis?
Wegener’s granulomatosis
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Confirm with biopsy of
nasopharyngeal lesion if
possible.
Alternative: renal biopsy
(crescentic necrotizing
GN). Focal or diffuse
necrotizing
extracapillary GN is
histological hallmark of
ANCA-associated
Vasculitis.
Tx: Corticosteroid and
Cyclophosphamide
Good Pasture Syndrome
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Hemoptysis +
Hematuria
Proteinuria + Renal
Failure
Anti-GBM antibody!
Tx: Plasmapheresis +
Prednisone +
Cyclophosphamide
Lupus Nephritis
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Type I: Minimal
Mesangial
Type II: Mesangial
Proliferative
Type III: Focal
Proliferative
Type IV: Diffuse
Proliferative
Type V: Membranous
Type VI: Advance
Sclerosis
Nephrotic Syndrome
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Not enough albumin (Hypoalbuminemia)
Edema
Proteinuria > 3.5 gm/24 hours
Hyperlipidemia
Nephrotic Syndrome
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Renal causes: Minimal Change Disease,
Membranous Nephropathy, FSGS
Systemic: SLE, Diabetes, Amyloidosis
Minimal Change Disease
Electron Microscopy Normal vs. MCD
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Normal Kidney
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MCD: The individual foot processes
can no longer be made out- they
have all just “melted” together into
a single thin layer. Barrier in
filtration process can no longer
keep protein from being filtered out
of the blood and into urine.
Membranous Nephropathy
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Most common cause of
Nephrotic syndrome in
adults.
Causes: idiopathic,
carcinoma, Hep B, Hep
C, SLE, Drugs:
Penicillamine,
Captopril, Gold
Treatment: Prednisone
Kidney Biopsy Review
DIFFUSE
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When all or at least
more than 80% of the
glomeruli seen in the
biopsy is affected.
FOCAL
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Only certain
proportion of the
glomeruli seen in the
biopsy involved.
Kidney Biopsy Review
GLOBAL
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When the entire globe
of the glomerulus is
affected .
SEGMENTAL
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Only a segment of
glomerulus involved.
Focal Segmental Glomerular Sclerosis
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Most common cause of
Nephrotic syndrome in
black patients, obese
patients, IVDA, heroin
abuse, HIV.
Acid-Base Disturbances
Normal pH
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7.4 = 40 nmol/L
24 X 40/24
H + = 24 X PCO2
(respiratory)/HCO3(metabolic)
pH < 7.4 is acidotic
Anion Gap
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(Na+) – (Cl- +HCO3-)
MUDPILES
Methanol
Uremia
DKA
Paraldehyde/Propylene
glycol
INH/Iron
Lactic acidosis
Ethylene glycol
Salicylates
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“My name is MUD!”
Normal anion gap (8-12 mEq/L)
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Diarrhea
Glue sniffing
Renal tubular acidosis
Hyperchloremia
Metabolic Acidosis: Compensation
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For every 1 mEq
HCO3- down, there is
1.3 mmHg PCO2
down
Increased ventilation,
blow off CO2
Metabolic Alkalosis
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Vomiting (urine
chloride < 20)
Diuretic use (except
carbonic anhydrase
inhibitors): Ucl>20
Antacids/milk-alkali syndrome
Hyperaldosteronism
Bicarbonate addition
Loss of H+ from GI tract or
kidney
Loss of Chloride from GI tract
or kidney
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Adaptation: 0.7 mm Hg
of PCO2 up for every
1mEq/L up of HCO3Decrease ventilation!
Respiratory Acidosis
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Primary disturbance?
PCO2 Up
Acute causes:
Airway obstruction
Status asthmaticus
Alveolar defects
(pulmonary edema,
pneumonia)
CNS depression,
neuromuscular impairment
Ventilatory restriction (flail
chest with rib fractures)
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Chronic causes: COPD,
abnormal chest wall
mechanics.
Compensation: Acute (for
any PCO2 up go 1-3
mEq/L up in HCO3-)
Chronic: For any 1 mm Hg
up in PCO2 go up 0.4
mEq/L in HCO3-)
Respiratory Alkalosis
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Primary disturbance?
PCO2 down
Cause:
High altitude residence
Pregnancy, Pulmonary
disorder, CNS disease,
Aspirin intoxification
Hepatic failure, Sepsis
Anxiety
Hyperventilation
High Carbon Dioxide
Respiratory Acidosis
Metabolic Alkalosis
CO2
High
High (compensation)
pH
<7.4
>7.4
Low Carbon Dioxide
Respiratory Alkalosis
Metabolic acidosis
CO2
Low
Low (compensatory)
pH
>7.4
<7.4
High Bicarbonate
Metabolic Alkalosis
Respiratory acidosis
Bicarb
High
High (compensation)
pH
>7.4
<7.4
Low Bicarbonate
Metabolic acidosis
Respiratory alkalosis
Bicarb
Low
Low (compensation)
pH
<7.4
>7.4
Clinical Scenario: Aspirin Overdose
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Causes two different
primary disturbances:
Respiratory Alkalosis
and Metabolic Acidosis
Look for co-existing
tinnitus, hypoglycemia,
vomiting, history of
“swallowing several
pills.”
Alkalinize urine with
Bicarbonate: speeds
excretion.
Imbalances of Sodium
Hypernatremia
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Serum Na+ > 145
Causes: Diabetes
insipidus, dehydration.
Diabetes insipidus
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Lab: Urine osmolality
less than serum.
How do you
differentiate between
central and
nephrogenic DI?
Vasopressin challenge:
Uosm increases in
central, minimal
change in nephrogenic.
Central vs. Nephrogenic DI
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Central: Decreased
production of vasopressin
(trauma, neurosurgery,
idiopathic). Treatment:
intranasal DDAVP.
Nephrogenic: renal tubules
unresponsive to vasopressin
(Lithium, Demeclocycline,
hypokalemia,
hypercalcemia). Treat the
cause, thiazide or
amiloride.
Clinical Scenario
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78 year old male from nursing home with altered
mental status, serum sodium 160. BUN/Cr high and
Uosm very high >800. Started DSW: after 10
hours the patient developed a seizure. What
happened?
Rapid correction of hypernatremia. In
hypernatremic patient: slow correction 0.5 mEq/L
per hour by free water or D5W (no more than 12
mEq/L over first 24 hours). Check serum sodium
every 2 hours!
Hyponatremia
Hypovolemia
Isovolemia
Hypervolemia
Diarrhea
Vomiting
Diuretics
SIADH
Hypothyroidism
Cortisol insufficiency
Polydipsia
Beer Potomania
CHF
Nephrotic syndrome
Cirrhosis
Hyponatremia
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In True hyponatremia: Serum Osmolality should be
low.
Hyponatremia with normal plasma osmolality:
Pseudohyponatremia due to hyperlipidemia or
hyperproteinemia.
Hyponatremia with elevated plasma osmolality:
mannitol or hyperglycemia. For every 100 above 100
mg/dl of glucose > correct serum Na+ 1.6. Example: Plasma
glucose 400 and Serum Na+ 130 > corrected will be 134.8
Treatment of Hyponatremia
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Asymptomatic: increase serum sodium 0.5 mEq/L
per hour (10-12 mEq/L per day).
Hypovolemia: Use Normal saline.
Hypervolemia, SIADH: FLUID RESTRICTION!
Symptomatic: Hypertonic saline, 1-2 mEq/L per
hour first 3-4 hr then 0.5-1 mEq/L per hour. No
more than 10-12 mEq/L per day in first 24 hours.
Rapid Correction of Hyponatremia
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Central Pontine
Myelinolysis or
Osmotic Demyelination
Syndrome (flaccid
paralysis, dysarthria,
dysphagia).
Thank you for your attention!