NEPHROLOGY FOR STEP 3

exhaustedcrumMechanics

Oct 24, 2013 (4 years and 2 months ago)

102 views

NEPHROLOGY FOR STEP 3

By James K. Rustad, M.D.

Copyright © 2009 All
Rights Reserved.

Outline


Renal Failure (Post
-
Renal, Pre
-
renal and Intra
-
renal)


Glomerulonephritis


Nephrotic

syndrome


Acid
-
Base Disturbances


Imbalances of Sodium

Post
-
Renal


Distended bladder on
exam.


Large volume
diuresis

after passing urinary
catheter.


Bilateral
hydronephrosis

on
ultrasound.


Post
-
void residual >
200 ml is suspicious.



Black arrow = renal capsule

Black arrowhead = sinus fat

White arrow = dilated calyx

White arrowhead = renal cortex

Hydronephrosis


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


Lower tract: Foley cath.


Upper tract:
Ureteral

stent or
percutaneous

nephrostomy
.


Pre
-
renal


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).


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! Pre
-
renal usually improves with IVF

Pre
-
renal vs. Renal

Pre
-
renal

Renal

BUN/
Creatinine

>20:1

<20:1

Urine sodium

< 10




FE乡

㰠1

㸠1

Intra
-
Renal


Acute Tubular Necrosis
(ATN)


Caused by
hypoperfusion

to the
point of tubular cell
death or from toxic
injuries.


Muddy Brown Casts


ATN (continued)


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.


Begins at least 5 days
after treatment.

Contrast Nephropathy

Aminoglycoside

Toxicity

Rhabdomyolysis

leading to ARF


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


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


EKG

most urgent step.


Severe muscle necrosis
leads to
Hyperkalemia
.


Look for
peaked T
waves.

Treat with
immediate IV calcium
gluconate
, insulin,
glucose.


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


The Pentad:


Acute Renal Failure


Fever


Rash


Arthralgia


Peripheral blood
eosinophilia


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


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)


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



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


URI 7
-
10 days before
presentation


“Cola or tea” colored
urine


Periorbital

edema/HTN


ASO titer, Low serum
complement


Treat infection/HTN




Clinical Scenario


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


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


G
ood Pasture Syndrome


Hemoptysis

+
Hematuria


Proteinuria

+ Renal
Failure


Anti
-
G
BM antibody!


Tx
:
Plasmapheresis

+
Prednisone +
Cyclophosphamide


Lupus Nephritis


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


N
ot enough albumin (
Hypoalbuminemia
)


E
dema


P
roteinuria

> 3.5 gm/24 hours


H
yperlipidemia

Nephrotic

Syndrome


Renal causes: Minimal Change Disease,
Membranous Nephropathy, FSGS


Systemic: SLE, Diabetes,
Amyloidosis

Minimal Change Disease


Electron Microscopy Normal vs. MCD


Normal Kidney


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


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


When all or at least
more than 80% of the
glomeruli

seen in the
biopsy is affected.


Only certain
proportion of the
glomeruli

seen in the
biopsy involved.

DIFFUSE

FOCAL

Kidney Biopsy Review


When the entire globe
of the
glomerulus

is
affected .


Only a segment of
glomerulus

involved.

GLOBAL

SEGMENTAL

Focal Segmental
Glomerular

Sclerosis


Most common cause of
Nephrotic

syndrome in
black patients, obese
patients, IVDA, heroin
abuse, HIV.


Acid
-
Base Disturbances

Normal pH


7.4 = 40
nmol
/L


24 X 40/24


H + = 24 X PCO2
(respiratory)/HCO3
-

(metabolic)


pH < 7.4 is
acidotic


Anion Gap


(Na+)


(
Cl
-

+HCO3
-
)


MUDPILES


Methanol


Uremia


DKA


Paraldehyde/Propylene
glycol


INH/Iron


Lactic acidosis


Ethylene
glycol


Salicylates



“My name is MUD!”

Normal anion gap (8
-
12
mEq
/L)


Diarrhea


Glue sniffing


Renal tubular acidosis


Hyperchloremia


Metabolic Acidosis: Compensation


For every 1
mEq

HCO3
-

down, there is
1.3 mmHg PCO2
down


Increased ventilation,
blow off CO2


Metabolic Alkalosis


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


Adaptation: 0.7 mm Hg
of PCO2 up for every
1mEq/L up of HCO3
-


Decrease ventilation!

Respiratory Acidosis


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)


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


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


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


Serum Na+ > 145


Causes: Diabetes
insipidus
, dehydration.



Diabetes
insipidus


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


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


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


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


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


Central Pontine
Myelinolysis

or
Osmotic
Demyelination

Syndrome (flaccid
paralysis,
dysarthria
,
dysphagia
).


Thank you for your attention!