NEPHROLOGY

ARF
Increase in BUN and Creatinine
In a short period of time from hours to days

urine sodium is
40-220
mEq/L/24 hours.
normal 24-hour urine osmolality is, on average, 500-800 mOsm/kg of
water. Random urine osmolality should average 300-900 mOsm/kg of
water.

BUN:Creatinine Ratio
FeNA

Prerrenal

Postrenal

Intrarenal

20:1

20:1 at the beginning

then 10:1

10: 1

Fe-Na > 2-3%

More than 1%
low; less 350/high;
more than 40

Less tan 1%

Urine Osmolality/Urine
Na

High(more tan 500)/Low

less tan 20

Less tan 350/ Urinary

Na+ >40

Urine specific Gravity

High(more tan 1.010

variable

Causes:

Not effective Arterial

Volume (Shock,
Hypovolemia, 3rd
Space) Low albumin
states

Decrease in Outflow of
urine (BILATERAL)

Tubular (ATN or AIN) or

Glomerular

Dx; Hydronephrosis on
CT or usg and/or 50ml
postvoid residual

Muddy Brown casts in

urinary sediment (ATN)

Other relevant
comments

Renal artery stenosis

A cause of Prerrenal Azotemia
High PA, but decrease renal perfusin
NO ACEI, NSAIDS, contrast, calcineurin inhibitors
because they cause vasoconstriction
ACEI
At the beginning cause decrease in GFR, due to vasodilatation (by blocking
Angiotensin vasoconstrictive effect) in the efferent arteriole, usually significant in
elderly, and people with underlying renal disease
Long term beneficial because decrease intraglomerular pressure, reducing
proteinuria (specially in DM)

Hepatorrenal Sd
Prerenal AKI
Phisio: Intense vasoconstriction of afferent arteriole
Always exclude intrisic cause
DX: No improvement in AKI after 1.5 of colloid, like
albumin
Tx: correct underlying liver disease; Mildodrine (alpha
agonist), Octreotide)
BEST: LIVER TRANSPLANTATION

ATN (intrarenal AKI)

Etiology: Ischemic or Toxic (amynoglycoside,
amphotericin, cisplatin, sepsis)
3 phases:
1. Prodromal
2. Oliguric (less than 400ml/24h) or Anuric (less than 100ml /
24hrs)
3. Postoliguric- diuretic phase

Tx: Hidration/ support, no medical therapy reverses

AIN (intrarenal AKI)

Etiology:

Sulfa Drugs:
acetazolamide,
furosemide, thiazide,
sulfonilureas

1. Adverse effect of medications (penicilins, cephalosporins,

sulfa drugs, allopurinol, rifampin, quinolones)
Some of the same toxins could
cause direct injury to the kidney
2. Infections: leptospirosis, legionella, CMV, rickettsia
but the difference is the lack of
3. Autoinmune disorders
allergic response so there would
not be fever, rash, joint pain, also
4. Idiopatic

the onset would be delay (days to

weeks)

PE: fever, rash, joint pain

Lab: eosinophilia, eosinophiluria, increase IgE,
hematuria, proteinuria
DX: Initial-UA, most accurate for eosinophils in urineHansel stain or Wright stain
Single mos accurate: biopsy, usually not necesary

Rhabdomyolisis (intrarrenal)
In ER EKG and K levels
Initial test: UA- positive for blood
Confirmed: CPK- 10,000- 100,000 (nl less than 500)
Lab: Metabolic Acidosis, hyperphosphatemia,
hipocalcemia, hiperuricemia, hyperkalemia
Tx; Calcium Gluconate if EKG anormalities otherwise
just Hydration and manitol, alkalization of urine

Ethylene Glycol (antifreeze)

Metabolic Acidosis, elevated AG
AKI
Dx. UA- envelopes
Tx. Fomipizole

Contrast agents(intrarrenal)
RF after 12-24 hrs
Creatinine peak 3-5 days
BUN: creatinine ratio: 20:1 (like prerenal, because of
vasoconstriction)
Prevention:
Hidration
Bicarb
N-acetylciseine

Glomerular Disease
Nephritic Sd
(glomerulonephritis)

Nephrotic Sd

Findings

1.
2.
3.
4.
5.

1.
2.
3.
4.

Dx:

Serum marker(ANCA, ANA etc)

Most Accurate: BIOPSY extremely
important-guides therapy

Edema
Hematuria
Red cell casts
Hypertension
Proteinuria (less than
2g/24hrs)

Edema
Hyperlipiduria
Low serum albumin
Proteinuria (more than 3.5
gr/24hr)

Base on level of proteins in urine

Most accurate: Biopsy

causes of Glomerulonephitis
V:
Wegener
Vascular
granulomat
G:
osis V
Glomerula
r

Churgstrauss Sd
V

Goodpasture
Sd G

Organs
affected
and or PE

Kidney,
lungs,
Upper RT
also: skin,
eyes, joints,
GI,
Neuropathy

Lung, skin, Lung, Kidney

kidney,
neuropath
y, Gi,
Cardiac
History of
asthma,
atopic
disease

LAb

ESR,
leukocitocis,
anemia, RF is
+,
Complement
nl

eosinophils

IgA
Polyarteri
Nephropa tis
thy
nodosa V
(Berger)
G

Postinfe
ctious
GF G

TTP/SHU

Kidney,
common
in Asians
under
35yrs
history of
URI
hematuri
a within12 days

All organs
except
lung
Associate
d HVB

Strep
+other
infection
s ; Cola
Urine

SHU: Hemolytic
Anemia,
Uremia,
Thrombocytope
nia
TTP: SHU+
fever,
neurologic

Anemia,
ESR,
pANCA

Low
Complem
ent (C3)

Abnormal blood
smear, LDH,
reticulocyte,
haptoglobin,
decreased

Hemosiderin
IgA
laden
Compleme
macrophage in nt NL
sputum

TX

DX

Steroids
+Cyclofosfamide

Initial:
antiproten
ase-3
(cANCA)
Most
Accurate:
Biopsykidney,
lung,
nasal
septum

Initial:
antimielo
peroxida
se
(pANCA)
Most
accurate:
Biopsy
-granulo
mas and
eosinoph
ils

Plasmaph Difficult,
eresis/ste AEI, ARB,
roids
Steroids

Initial:
Antibasem
ent
membrane
antibody
kidney or
lung
Most
Accurate:
Biopsy

IgA on
kidney
Biopsy

Initial:
Angiogr
aphy:
beading
Most
Accurat
e:
Biopsy
(sural
nerve is
common
)

Steroids
Supporta
+Cyclofos tive
famide

Initial:
Mainly clinical
ASO
Most
Accute:
Biopsyhumps

Cryoglobulinemia V
HVB/HBC
NO GI
LAB: ESR, low complement, RF+
Confirmatory: test for cryoglobulins
Tx. Hep tx- interfern-ribavirin

SLE
LAB: dsDNA, complement
Biopsy: essential
Sclerosis: No therapy
Proliferative: Steroids +mycophenolate

RPGN
ANCA
Tx; steroids + cyclophosphamide

Amyloidosis
AL: Multiple Myeloma, protein from Ig light chain
AA: From cronic inflamationPE:

Dx: Biopsy- affected organ, aspirating abdominal pad, rectum sample

Tx: Control underlying, Melphalphan, Prednidsone can protein
production

Glomerular basement membrane loses

its - charge

Nephrotic Sd

Antithrombi
n III, protein
C protein S

Proteinuria
more than
3.5gr
perb24hrs
edema

Hiperlipidem
ia

Low serum
albumin

HIPERLIPIDURIA

HIPERCOAGULAB
LE STATE
Tx: Steroids, if dont wort add
cyclophosphamide,
mycophenolate or azathioprine
ACEI ARB to prevent in HTA,
DM

Base for Diagnosis- 24hr urine Most accurate:

or protein:creatine ration in a
Biopsy
single spot

Causes of Nephrotic Sd and Asociations

Focal Segmental
Glomerulosclerisis
(FSGS)
Membranous

Membranoproliferati
ve
Minimal Change
Disease (Nil Lesion)
Mesangial

Heroin, HIV
Most common cause

Cancer, Lymphoma, Infections (endocarditis,

HVB) SLE, NSAIDS

I: HVC, SLE, lymphoprolipherative

II: C3 nephritic Factor
A mix of nepritic/nephroticsd
Children, LM is NL, EM-fusion of foot processes
Hodgkin lymphoma

IF- IgM deposits in mesangium

Steroid resistant

Proteinuriacauses

Micro albuminuria: 30300mg/24hrs

Glomerular/tub
ular

Stressors
Fever
Exercises
CHF

Orthostatic
Dx: 24hr urine
sample
splitting

Casts

Hyaline

Red cell casts

Broad Waxy

Dehydration

Gromerulonephritis

Chronic renal failure

Granular (dirty
or muddy also)
ATN

Wbc
casts;Pyeloneph
ritis

Indications for Dyalisis

Fluid overload

Acidosis

Neuropathies

Pericarditis

Hyperkalemia

Encephalopath
y

Uremia sx
(vomiting,
nausea,
bleeding
diathesis)

Take into considerations that all the above are indications after proving

Fluid and
Electrolites

Hyponatremia (less than 135 mEQ on serum)

Serum osmolality NL: 275
295 mosm/kg

Sx: NEUROLOGIC
HYPONATREMIA

High

Pseudohyponatr
emia

Hyperglyce
mia

Hyperlipide
mia

Osmolalit
y
Correct hyponatremia;
for every 100mg/dl
beyond normal- 1.6
mEq/L increase
Hypervolemic
States
CHF, nephrotic
sd,
Cirrhosis, Renal
insuficiency

Euvolemic state
SIADH
Hypothyroidism,
Psychogenic
Polydipsia, ACEI,
endurance
exercises

Low
True
Hyponatremia
Hypovolemic States
Urine
Sodium
Less than 20
Dehydratin,
Vomiting,
Diarrheae,
Sweating

More than 20
ACEI, Renal
salt wasting,
Addison
disease,
Cerebral

SIAD
H

ETIOLOG
Y:

CNS diseases: Inf,

stroke, tumor,etc

Pulmonary diseases:
TB, PE, Pneumonia

Neoplastic: pancreas
lungs, duodenum,
thymus

Medications: SSRIs,
Haloperidol,
Thiazides,
carbamazepine,
tricyclic
antidepressant,
vincristine,
cyclophosphamide

Dx: Elevated
Urine
Osmolality
(>100) and
Urine Na in the
presence of
Hyponatremia.
Most Accurate:
ADH

Hypernatremi
aEtiology:
1. Insensible losses

Decrease in urine
volume after ADH

2. GI loss
3. Transcellular shif: Seizures,
rhabdomiolisis
4. Renal: Nephrogenic DI vs Central DI,
Idiopatic, Osmotic Diuresis
SX:

Tx:
Acute: Isotonic fluids IV,
not too fast!!!!
CEREBRAL EDEMA!!!!
Not >1mEq/2hr or
12mEq/day- If seizing
maximum 1mEq/1hr
CDI: Vassopressin
NDI: Diuretics or NSAIDS

Hypokalemia (<2.5-3 mEq/L)

EM always do
Presentation:

Mm weakness,
even
Rhabdomyolisis

ECG
Tx: Replace K
IV, Oral
Remember no
K in line close
to the heart,
and not to
quicky because
of fatal
arrythmias

Presentati
on:

Hyperkalemia
(>5meq/L)
Etiology:
Movement from the
cell to extracellular
space
Pseudo: hemolysis
during venipuncture
Acidosis
Insulin Insuficiency
Tissue breakdownrhabdon
Tumorlysissd

Decrease Excretion
Renal Failure
Hypoaldosteronism:
RTA IV, ACEI,
Heparin
Potassium sparing
Diuretics

Tx:
1. Ca Gluconate if ECG changes
2. Glucose +Insulin
3. Bicarbonate if acidosis
4. Resistant: Dialysis
5. Adyuvant: Cation exchange resib

Acid-Base
Disturbances

Steps when encounter disturbances in pH

Osis?
Alkalosis >7.45

Acidosis
<7.35
Respiratory
Metabolic

Metabolic

Respiratory

Compensation
Winters:
(M.Bicarb x
1.5) + 8 + 2

hypoventilati
on
Normal

Anion Gap: Na HCO3 +Cl (812)

Low

Elevated
Delta: Delta ratio to
figure out 3er
disturbance, if >24
Alkalosis if <24
acidosis

Follow algorithm in
next slides: Options
GI or RTA
Myeloma
Low Albumin
Lithium

Osmolar
Gap

Elevated
Methanol
Ethylene
Glycol

Urinary
Electrolites

Hiperventilati
on

Tx: respond to
isotonic fluid

Use of Urinary Anion Gap

Could be used to assess a nl AG metabolic acidocis
Formula: (Na+K) -Cl

_
Diarrhea

RTA type 1

RTA
Distal (Type 1)

Proximal (Type 2)

Etiology

Sporadic
Autoimmune: Sjogren,
LE
Drugs: Amphotericin,
lithium
Chronic hepatitis,
nephrocalcinosis

Presentation

Secondary
Hyperaldosteronism
+hypokalemia vs
nephrolithiasis/nephroca
lcinosis

Metabolic Acidosis+
hypokalemia + Bone
Lesions

Serum Potassium

Urine Ph

>5.4

<5.4

<5.4

Treatment

Oral Bicarbonate
K replacement

K replacement
Thiazides
High amounts of bicarb

Fludrocorsone

Fanconi Sd
Wilson disease
Myeloma
Acetazolamide
Vit D def
Autoinmune diseases

Basic Urine in
presence of acidemia

Type IV
(Hypoaldosteronism)
DM
Addison disease
Sickle cell
Renal Insuficiency

Hypercloremic metabolic
acidosis/nonAG,
Hyperkalemia, Renal
insufficiency
Na in Urine is
characteristic

Nephrolithiasis
Etiology
Calcium
Oxalate
(70%)
Calcium
phosphate
(10%)

Mg/aluminiu
m/phosphat
e (struvite)5-10%

Uric Acid
(5%)

Cysteine
(1%)

Urine pH
favor
growth

acid

Alkaline

Acid

acid

Crystals
Shape

envelopes

Coffin lids

Broken
glass

hexagonal

On Rx

radiopaque radiolucid

radiolucid

radiopaque

Allopurinol
(overprodu
cer)

Binder:
penicillami
ne,
captopril

Other
characteris
tic

Staghorn
shape;
related to
UTI

Add to tx

antibiotic

Tx:
Strain Urine
Parenteral analgesics
IV hydration
Calcium Channel Blockers
Stones less <5mm should
pass spontaneously
<2cm: lithotripsy

HTA

Tx: First try

Lifestyle
Modification, iffail
after 3-6
months mts

In DM or patients with
Renal diseases target:
<130/80

Px with >160/80
initial therapy with
2 medications

Common findings
in HTA

Malignant HTA:
encephalopathy or
nephropathy
w/papilledema

Hypertensive Emergency: acute

onset of severe hypertension in
association with severe and rapidly
worsening symptoms of end organ
damage Diastolic P: >120-130
Dx test: CT head to exclude
hemorrhage and ECG to exclude MI
Tx: infusion IV- Nitroprusside or
Labetalol
GOAL: reduce 25% BP within 1-2

Screen for
2dary HTA:

Disease

Feature

Renal Artery Stenosis

Upper Abdominal bruit

radiating laterally

Primary
Hyperaldosteronism

HTA + Hypokalemia

Pheochromocytoma

Episodic HT, headaches,

sweating, palpitations,
tachycardya

Cushing Disease

Ht, truncal obesity,

buffalo hump, menstrual
abnormalities, striae

Coarctation of the aorta

HT markedly greater in
Upper extremity
compared to lower
extremity

1. <25 yrs or >55

2. Key feature of history,
PE, or Lab abnormalities
consistent with a
particular form like
Hipokalemia +
Metabolic acidosis
3. Px remain hypertensive
despite increasing
dosages and numbers
of anti HTA