Nephrology & Urology

Archer Online USMLE Reviews

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Archer Slides are intended for use with Archer USMLE step 3
video lectures. Hence, most slides are very brief summaries of
the concepts which will be addressed in a detailed way with
focus on High-yield concepts in the Video lectures.
These slides are only SAMPLES

Renal Failure

Acute Vs. Chronic

Acute : Pre-Renal, Renal, Post renal, Glomerular,
tubular, intersititial
Indicators : BUN/CREA, FeNA, Urine Spgravity,
serum Sodium, serum osmolality, urine output.
Chronic stages elective hemodialysis Stage V,
Emergent hemodialysis indications
Acute tubular necrosis : toxic, pigment induced,
Ischemic
Evaluating renal function : urinalysis - ? Protein, ?rbc , ?
Wbc, ? Casts , ? Crystals, ? Bacteria, ? Nitrite, ?
Cytology , ? Leucoesterase,
- Creatinine clearance, Renal ultrasound, Renal biopsy

RENAL BIOPSY

Indications:
Nephrotic syndrome
Glomerular disease
Unexplained renal failure
Contraindications: single kidney, bleeding,
severe hypertension. obesity and uncooperative
patient

DEFINITION OF ARF

PCr > 0.5mg/dL if baseline < 3.0mg/dL

PCr > 1.0 mg/dL if baseline > 3.0 mg/dL

Urine Output :
TOTAL ANURIA
0 cc
ANURIA
< 100 cc
OLIGURIA
100-400 cc
NON OLIGURIA
400-1000cc
POLYURIA
> 1000cc

CAUSES OF NONOLIGURIC PRE

RENAL ARF

Diuretics
Osmotic diuresis
Hypercalcemia
Protein malnourished
Post obstructive diuresis
Diabetes Insipidus

NSAID ARF

Form of pre renal

Occurs in states where RBF decreased and thus
prostaglandin dependent
Nonselective and selective NSAIDs inhibit
compensatory afferent arteriolar vasodilation
Volume contraction, CHF, cirrhosis, CKD,
vascular disease and elderly increases risk.
COX-2 inhibitors have similar effect
Allergic interstitial nephritis can also occur

ACE INHIBITOR ARF

Rapidly reversible ARF

Increase SCr > 0.5Mg/dL if < 2.0 mg/dL or increase SCr
> 1.0 mg/dL if > 2.0 mg/dL
Bilateral renal artery stenosis, unilateral stenosis in
solitary kidney, small vessel disease and decreased RBF:
CHF, cirrhosis, decreased ECF
Inhibition of A-II efferent arteriole vasoconstriction
leads to decrease PGC and GFR
Age, diuretics, diabetes, NSAIDs, cyclosporine and
CKD are risk factors
ARBs pose similar risk

POST RENAL ARF

Caused by anatomic obstruction of urine flow

Accounts for 5-10% of ARF
Patients are often asymptomatic and thus should always
be considered
Ultrasound useful, but can have 10-20% false negatives
Patients are often oligo-anuric, but any pattern of urine
output may occur
Intraureteric obstruction, Extraureteric obstruction,
Urethral obstruction

INTRARENAL ARF

Renal parenchymal diseases

Glomerular
Vascular
Tubular
Interstitial
Acute tubular necrosis most common

Glomerular syndromes
Nephrotic Vs Nephritic Syndromes
NEPHROTIC SYNDROME
Urinary albumin > 3.0 3.5
gm/24 hours
Hypoalbimunemia
Edema
Hyperlipidemia
Lipiduria
FSGN ( HIV), MGN( SLE, hepb,
Cancer solid tumors ), Minimal
( children), MPGN ( HepC)
FSGN Rx High dose steroids,
cyclosporine
MGN Methylprednisolone pulse,
cyclosporin
Others : DM, Malignancy,
vasulitis, amyloidosis

Nephritic Syndrome

Hematuria/ RBC Casts

Oliguria
Hypertension
Decreased GFR
Proteinuria +/ Focal glomerulonephritis

IgA nephropathy
Focal SLE ( Type III )

Diffuse glomerulonephritis

Post infectious
Diffuse SLE ( Type IV )

IgA nephropathy : most common

presentation asymptomatic
microhematuria with mild
proteinuria

RAPIDLY PROGRESSIVE
GLOMERULONEPHRITIS

Characterized by > 50% decrease in GFR over days to weeks

Characterized pathologically by crescent formation and clinically
by progression to ESRD in untreated patients within weeks
Related to the degree of crescent formation
Present with active urine sediment, hypertension and oliguric
ARF
Nephrologic emergency
Classification of RPGN:
Type 1: Anti GBM
Type 2: Immune complex
Type 3: Pauci-immune ( p-ANCA )
Early evaluation and biopsy

Proteinuria - Microalbuminuria

Normal: 150 mg/day

Albumin
30 mg
Plasma proteins 60 mg
Tubular protein 60 mg

Microalbuminuria

Albumin excretion rate > 15

ugm/min = 30 mg/day
Predictor of early diabetic
nephropathy and CVD
Urine albumin: urine
creatinine < 0.03
Positive in exercise, fever,
stress, CHF
Repeat urinalysis in 3-6
months if u think its
transient proteinuria
ACE Inhibitor *****

Dipstick test detects (-)

charge
Does not detect light chains
Function of urine
concentration
Total Protein : creatinine
ratio estimates 24 hour urine
collection

ATN
Ischemic (50%)
Toxic:
EXOGENOUS TOXIN ATN :
-Antibiotics, Radiocontrast, Non steroidals,
Anesthetics, Chemotherapeutics, Heavy metals/
solvents
ENDOGENOUS TOXIN ATN :
Pigment Nephropathy Myoglobin, Hemoglobin
Crystal Nephropathy Uric acid , Calcium,
Oxalate

RADIOCONTRAST ATN

Risk factors: CRF especially diabetic, CHF, elderly and multiple

myeloma
ATN begins abruptly and SCr peaks in 3-5 days
Usually reversible, but some have prolonged renal damage
Usually nonoliguric, but oliguria can be seen and FE Na
decreased
Prevention : Consider non contrast study if high risk
D/C NSAIDs, ACE inhibitors. ARBs etc
Ensure optimal volume status and RBF
0.9% saline @ 1cc/kg/hr for 6 hours prior
D5W + 3 amps NaHCO3 @ 3.5 cc/kg/hr for 1 hour and
then 1 cc/kg/hour for 6 hours after
N-acetylcysteine 600mg bid pre and day of study
Minimize amount of contrast and consider iso-osmolar agent -

nonionic and/or isosmolar contrast are less

nephrotoxic

ATHEROEMBOLIC ARF

Results from cholesterol emboli to small renal

arteries and arterioles
Livedo reticularis A clue!!!
Aortic surgery, trauma, angiography, fibrinolytic
therapy or spontaneously
Eosinophilia, eosinophiluria, leukocytosis and
complement activation
Retinal, peripheral and abdominal vessels

MYOGLOBINURIC ARF

Rhabdomyolysis: trauma,alcohol, cocaine, seizures,

hypokalemia, hypophosphatemia
ECF volume depletion
Heme (+) urine without RBCs, hyperkalemia,
hyperuricemia, hyperphosphatemia and hypocalcemia
Decreased FE Na
ECF volume repletion, ?mannitol, and ?alkaline diuresis
Hypercalcemia during recovery

ACUTE INTERSTITIAL
NEPHRITIS

Fever, rash, eosinophila, eosinophiluria and

active urine sediment
Occurs 10-15 days after exposure to usually new
medication
NSAID induced associated with nephrotic
syndrome
? Renal biopsy
Rx: Stop the agent and ?steroids

CRYSTAL INDUCED ARF

Uric acid
Calcium oxalate
Methotrexate
Sulfonamides
Acyclovir
Indinavir

DIAGNOSTIC MANAGEMENT
ARF

History / Chart review

Physical exam
Urinalysis
Urine indices
Radiologic studies
Miscellaneous studies

NON DIALYTIC MANAGEMENT

ARF

Preventive measures
Fluid balance
Acid base balance
Electrolyte balance
Nutritional balance
Drug management
Management of uremia

INDICATIONS FOR Emergency

DIALYSIS
REFRACTORY

Hyperkalemia
Acidemia
Hypoxemia/ volume overload
Uremia - manifestations
? Prophylactic when BUN > 60-100 mg/dL

Chronic Tubulo-Interstitial Diseases

Chronic issues :
Toxins: Analgesics, Heavy metals, Chinese herbs, Lithium,
Cyclosporine, Radiation, Cisplatin
Hematologic diseases: Myeloma
Immunologic: Sjogrens syndrome, Transplant rejection
Infection: Bacterial pyelonephritis, Tuberculosis, Sarcoid
Anatomic: Obstruction, Reflux
Metabolic disorders: Gout, Oxalosis, Hypercalcemia,
Hypokalemia, Cystinosis
Hereditary: ADPKD, MCD
Vascular : Nephrosclerosis, Ischemic nephropathy,
Atheroembolic disease

Acute cases : check urine eosinophil count, peripheral eosinophilia

Oxalate Nephropathy

Precipitation of calcium oxalate can cause

interstitial and intratubular crystals leading to
inflammation and fibrosis
Primary hyperoxaluria leads to ESRD
Ethylene glycol, methoxyflurane, excessive
intake ascorbic acid
Increase intestinal absorption: Ileal bypass, short
bowel syndrome and Crohns disease

Chronic Urate Nephropathy

Related to deposition of sodium urate in the

medullary interstitium
Secondary inflammation and interstitial fibrosis
and CRF
Hypertension, bland urinalysis and hyperuricenia
Associated with tophaceous gout or an increase
in uric acid out of proportion to degree of CRF

Analgesic Nephropathy

NSAID induced interstitial nephritis ( associated

with nephrotic syndrome proteinuria)
NSAID induced vasomotor renal insufficiency

Hepatorenal Syndrome

The diagnosis of HRS iS of exclusion and depends mainly on serum creatinine level, as no specific tests establish the
diagnosis of HRS.
Serum creatinine level is a poor marker of renal function in patients with cirrhosis. But no other reliable noninvasive
markers exist for monitoring renal function in these patients.
Diagnosis of HRS depends on the presence of a reduced GFR in the absence of other causes of renal failure in patients
with chronic liver disease.

Major criteria (All major criteria are required to diagnose HRS.)

Low GFR, indicated by a serum creatinine level higher than 1.5 mg/dL or 24-hour creatinine clearance
lower than 40 mL/min
Absence of shock, ongoing bacterial infection and fluid losses, and current treatment with nephrotoxic
medications
No sustained improvement in renal function (decrease in serum creatinine to <1.5 mg/dL or increase in
creatinine clearance to >40 mL/min) after diuretic withdrawal and expansion of plasma volume with 1.5 L
of plasma expander
Proteinuria less than 500 mg/d and no ultrasonographic evidence of obstructive uropathy or intrinsic
parenchymal disease
Additional criteria (Additional criteria are not necessary for the diagnosis but provide supportive evidence.)
Urine volume less than 500 mL/d
Urine sodium level less than 10 mEq/L
Urine osmolality greater than plasma osmolality , Urine red blood cell count of less than 50 per high-power
field & Serum sodium concentration greater than 130 mEq/L
Urinary indices are not considered major criteria because a subset of patients with HRS may have high urine
sodium levels and low urine osmolality (similar to acute tubular necrosis [ATN]), while other patients with
cirrhosis and ATN may have low urine sodium levels and high urine osmolality.

Case Studies

) A 25 y/o male comes to your office with complaints of dark red colored urine and
pain in the legs that started this morning. He has been working out at the local gym
excessively for the past three days. He does consume alcohol on weekends but reports
having involved in a binge drinking episode that included 10 beers yesterday. On
physical examination, he weighs 70kg and he has some tenderness in his calf muscles
which he attributes to the excessive squats he performed yesterday. Urine dipstick
reveals large blood. If this patient develops acute renal failure , the most likely
mechanism would be:
A) Interstitial nephritis due to pigment
B) Glomerulonephritis
C) Acute Tubular necrosis due to pigment deposition
D) Acute Tubular Necrosis due to Ischemia
E) Alcohol related direct toxic injury
1b) Lab studies revealed normal electrolytes and normal creatinine but a CPK of
50,000. His Urine output has been at 70 ml/hr for the past 6 hours. Your first step in
the management to prevent development of patient's Acute Renal Faliure :
A) Intravenos Fluids
B) Furosemide
C) Calcium Gluconate
D) No treatment because serum creatinine is normal
D) Sodium Bicarbonate

Case Study

A 7-year-old boy is brought to the emergency department by his mother

because of "tea-colored urine" for the last several days. He has also had some
nausea and vomiting, and his eyes appear swollen when he wakes up in the
morning. The eye swelling tends to resolve over the course of the day. He is
generally very healthy and there is no family history of any chronic diseases.
His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is
96/min, and respiratory rate is 16/min. Physical examination is unremarkable.
A urinalysis shows red cell casts. At this time the most appropriate study to
confirm your diagnosis is
A. antinuclear antibody
B. antistreptolysin O antibody
C. renal biopsy
D. renal ultrasound
E. urine culture

Case
studies
contd
1c) The above patient has been adequately treated but his repeat CPK after 2
days is still elevated at 48,000. He complains of increasing pain in his left leg
and some tingling and pricking sensations. On examination his left leg was
mildly swollen and there was pain on passive stretching of the leg muscles.
Dorsalis pedis and posterior tibial pulses are intact. The most likely diagnosis
at this time:
A) Deep Vein Thrombosis
B) Cellulitis
C) Compartment Syndrome
D) Edema due to renal failure
E) Congestive Heart Failure
1d) The immediate course of treatment in this condition would be :
A) Anticoagulation with Heparin
B) Antibiotics
C) Emergency Fasciotomy
D) Loop diuretics
E) Elevation of the leg

Case Study 2

Q1) A 12 y/o boy is brought to you by his mother for skin rash and complaints of intermittent
abdominal pain, joint pains for past 2 days. He did have an upper respiratory infection about 2 days
ago. On physical exam, his vitals are normal. Abdomen is benign with out any tenderness or
rigidity. However, you notice patchy purple discolorations on his extremities and the back. Lab
studies are obtained that revealed

WBC: 6.6 , HGB: 15.3 , MCV: 88 , Platelets: 290,000 ( normal 180k to 400k)
BUN: 11 , Creatinine : 0.6 ( normal) , Anti streptolysin O titer : negative
Streptozyme : negative ,Urine dipstick : normal without any blood
Urinalysis : normal/ no rbcs/ no protein

The mother is very anxious and asks about the long term prognosis of her son. Your response :
A) Reassure the mother that boys disorder is self limiting and does not require any follow up
B) Tell her the boy needs to be admitted and treated vigorously to prevent renal failure
C) Tell her that renal failure develops 100% of such cases and hence needs very cautious follow up
D) Tell her that 50% of such cases progress to end stage renal disease.
E) Tell her that the boy requires follow up monthly urinalysis for at least 3 months in order to make
sure there is no heamaturia/ renal dysfunction.
If the boy presented with Renal failure in the above case, the most likely underlying pathology
would be :
A) IgA mediated vasculitis
B) Post streptococcal glomerulonephritis
C) Anti GBM disease
D) Acute tubular necrosis
E) Interstitial Nephritis.

ADPKD

Autosomal Dominant Polycystic Kidney Disease

Clinical features
Associations
Prognosis
Screening for Berry Aneurysms:
MRA of head recommended screening test to detect berry
aneurysms
Screen only if
family history of subarachnoid hemorrhage ( Family hx of a
ruptured berry aneurysm) not just a family history of berry
aneurysm.
Patients with with high risk jobs (pilots/ bus-drivers) - an
event during such a job is a risk to others safety as well.
Patients with symptoms suggestive of a berry aneurysm
( severe headache, focal neurological deficits)

A 46 y/o woman who is a school bus driver by occupation presents to your office for
regular follow up. She has a history of ADPKD. Her blood pressure is well controlled
at 120/70 on enalapril. She has no other problems. She denies any headache. There is no
family history of intracranial or subarachnoid hemorrhage. However, she is concerned
that her head might explode because her sister who also has ADPKD was recently
diagnosed of having a berry aneurysm. She wants to be screened for berry aneurysm as
soon as possible. Her physical examination is benign and does not reveal any focal
neurological deficits. Which of the following suggests the necessity for screening in her
case?
A. Family history of berry aneurysm
B. Polycystic kidneys
C. School bus driving
D. Cysts in the liver
E. No screening necessary in her case

Copy right: Archer

Ans. C

High risk jobs ( pilot, bus driver etc) is one of the

indications to screen for berry aneurysm in
asymptomatic ADPKD patients.
Family hx of berry aneurysm alone does not warrant
screening for berry aneurysm in asymptomatic
ADPKD patients. Asymptomatic ADPKD patients
must be screened if there is a family history of
Ruptured berry aneurysm ( history of SAH in the
family etc)
E. is not the answer because this patient is a school bus
driver by occupation and needs to be screened

UTIs

CASE STUDY

A 76 YO DEBILITATED MALE, In extended care facility ,

develops every 6 months mild fever, frequency of micturation
with urinary incontinence. USUALLY E.COLI count is
>100,000.
What is the appropriate treatment?
A. CYSTOSCOPY and IVP
B. Continuous low dose antibiotics
C. Catheterize and irrigate the Bladder daily
D. Treat only the acute episode of infection
E. No need of treatment as this is colonization

Symptomatic complicated UTI should be

treated. Number of UTI are less than 2 in 6
mos- no need for continuous Abx.
His Symptoms are associated with UTI and are
not persistent. So just treat the acute episode
REMEMBER THE INDICATIONS FOR
TREATING ASYMPTOMATIC
BACTERIURIA.

Recurrent UTIs

DEFINED AS 2 OR MORE EPISODES IN

PAST 6 MONTHS OR 3 OR MORE
EPISODES IN PAST ONE YEAR.
Use Bactrim DS post sexual activity for women
with hx of recurrent UTIs related to sexual
activity.
Use daily bactrim for people withj no relation to
sex activity.

OTHER ISSUES

Evaluating painless hematuria elderly

Painful hematuria
Treating asymptomatic bacteriuria
Pyelonephritis pyonephric abscess
When to admit and when to order imaging
studies in pyelonephritis?

Hematuria
Painless

( Asymptomatic) Hematuria
Painful Hematuria
Gross Hematuria
Microscopic Hematuria

Hematuria

Not every red urine needs to be a Hematuria

A reddish discoloration of urine can occur with out a
positive dipstick or urine microscopy .

Causes of Red urine but negative dipstick test

Ingestion of red pigmented foods ( eg: beets, berries, rhubarbs, paprika)

Drugs like Rifampin or Phenazopyridine derivatives
( remember these drugs only cause reddish urine but NOT a positive dipstick)
Diseases such as Porphyria

Causes of a Positive Dipstick but no true Hematuria: Here

Dipstick stains positive for blood but no RBCs in the urine:

Myoglobinuria ( Rhabdomyolysis, vigorous exercise)

Hemoglobinuria ( Intravascular hemolysis)

Hematuria

Screening test for hematuria is urine dipstick.

Dipstick :
Dipstick is highly sensitive but not specific. False negatives
are very rare but false positives are common.
Dipstick detects blood" but it does not say whether this
"blood" is an RBC or a Pigment.
Pigments such as myoglobin ( as in rhabdomyolysis) or
Hemoglobin ( as in hemoglobinuria, Black water fever) can
stain as "Blood" on dipstick but there are no RBCs on
urine microscopy.
So, a dipstick positivity should be confirmed always with
urine microscopy before calling it a hematuria.

Hematuria

Painful vs. Painless Hematuria

The distinction is important so that you can consider the
relevant differential diagnosis and choose appropriate
investigations.
Painful hematuria is often associated with urolithiasis ( renal
calculi) or inflammation/ infection of the bladder ( Cystitis).
Painless or Asymptomatic hematuria is often seen with
tumors of the urinary tract, bladder cancer,
glomerulonephritis and benign prostatic hypertrophy.
A hematuria accompanied by a classic flank pain should
raise a suspicion of renal calculus and the next investigation
in such a scenario should be a Non-Contrast CT scan.
Approach to painless hematuria depends on the risk profile
of the patient ( i.e; risk of having a renal/ urological disease)

Gross Hematuria

Grossly Reddish or Tea colored urine, dipstick positive for blood and
urine microscopy shows RBCs.

Any patient with gross hematuria should always be referred for

urological evaluation unless this is secondary to an infection.

If a woman has gross hematuria but the urine dipstick also reveals leucoesterase
or nitrite or if the woman has symptoms of UTI ( dysuria etc) or if the cultures
are growing bacteria, this can be treated as UTI ( cystitis) with antibiotics with out
referring for further evaluation. A repeat urinalysis should be obtained after
resolution of the infection. Even in this setting of infection, if there are risk
factors for urological malignancy the patient should still be referred for further
evaluation ( since hematuria from cancer can also be intermittent).

Runner's hematuria or March hematuria is another benign condition that presents

as gross hematuria after a severe physical activity. In such cases, patients may be
observed for resolution. However, if the hematuria is persistent or if the patient
has any risk factors for having a urological malignancy, must be referred to a
urologist

Microscopic Hematuria

Microscopic hematuria is defined as three or more red blood

cells per high-power field on microscopic evaluation of
urinary sediment from two of three properly collected
urinalysis specimens. ( >3rbc/hpf on 2 or more occassions).
Always confirm on repeat testing. Repeat urinalyses to
establish whether significant hematuria is present must
be done within 3 to 6 months of the initial test.
Look for glomerular origin of hematuria If urinalysis
reveals Red cell casts/ dysmorphic RBCs or Renal function is
compromised/ new onset HTN, combined with mild
proteinuria consider glomerulonephritis or renal
parenchymal disease in such cases, next step is referral to a
nephrologist and renal biopsy.

Microscopic Hematuria
Rule out benign causes first.
Some benign causes of Microhematuria :
A) Exercise
B) Sexual activity
C) Menstruation
D) UTI
If UTI is present ( symptoms and dipstick for leucoesterase are clues
that point towards infection) - treat it with antibiotics and repeat
urinalysis after the infection has cleared.
E) Benign Prostatic Hypertrophy
F) Prostatitis
Recurrent painless Hematuria consider IgA nephropathy
Other clues
1. Consider strongly CA.Bladder in the elderly and in smokers
2. R/O benign causes like BPH ( Ask for symptoms of BPH)
3. R/O Prostate Ca in the elderly and in those with family history
DO NOT NEGLECT POSSIBILITY OF BLADDER CA IN Patients
WITH HEMATURIA

Microscopic Hematuria

Symptomatic Microhematuria : If the microhematuria is associated

with classic flank pain next step is Non Contrast CT scan to
rule out renal calculus. In pregnant women do ultrasound to
avoid radiation.
Asymptomatic MicroHematuria : Patients without the
classic flank pain of urolithiasis should be evaluated
extensively. Once benign causes such as infection and the
kidney ( glomerular) origin are ruled out, further approach
should be defined based on the patient's risk profile.

For patients with low risk of urological disease, a less extensive work-up
may be appropriate ( First do upper tract imaging and if this is negative,
add urine cytology+cystoscopy).
If the patient is a high risk of having a urological malignancy, extensive
work-up is needed ( see the risk factors below) --> Upper tract imaging
+ cystoscopy+ urine cytology all are needed. Urine cytology should be
obtained in all patients with asymptomatic hematuria since it is an easy
and non invasive step. Sensitivity of urine cytology is only 48% but
remember that if it is positive it is highly specific for urological cancer (
94% specificity)

Painless Hematuria
Risk Factors for Significant Disease in Patients with Microscopic
Hematuria :
Smoking history
Occupational exposure to chemicals or dyes (benzenes or aromatic
amines)
History of gross hematuria
Age >40 years
History of urologic disorder or disease
History of irritative voiding symptoms
History of urinary tract infection
Analgesic abuse
History of pelvic irradiation

Previous use of Cyclophosphamide ( increases the risk of bladder cancer

where as ongoing use often causes hemorrhagic cystitis as a adverse
effect)
These high-risk patients require aggressive work up with CT Urogram +
Cystoscopy + Urine Cytology!

What Imaging Studies?

What imaging studies should be done as initial step in evaluating
Asymptomatic Hematuria?

For both high risk and low risk patients, upper tract imaging must be
performed as an initial step.
For upper tract imaging, CT urography ( i.e; non-contrast CT followed by
contrast CT imaging from kidney to bladder) is best recommended initial
test now to evaluate asymptomatic hematuria. CT urography is less affected
by overlying bowel gas and is more sensitive for detecting small tumors and
calculi than the IVP.
IVP used to be the best preferred test for upper tract imaging in hematuria
evaluation but now CT urogram is becoming the preferred method. IVP and
ultrasound are good to image the urinary tract but they do not completely
assess the renal parenchyma. If you order an IVP, you may eventually need
to order a CT urogram again to image the parenchyma better - so, in order
to avoid ordering multiple studies, CT urogram is recommended as the best
initial test.

Upper tract imaging preferred modality is Helical CT or CT Urogram ( If

you do not find CT Urogram in the choices or if you want to reduce radiation
exposure such as in pregnant women, you can choose IVP+renal
ultrasound for upper tract imaging remember IVP is more invasive and we
are not using now. So, where available, CT urogram is first choice for imaging
the upper tract. But if IVP is used it must be combined with renal ultrasound
because IVP only images the tract but does not look at the kidney itself).
In patients with high risk of bladder ca, Helical CT followed by urine cytology
and cystoscopy must all be performed.
In patients with low risk for bladder ca, you may choose step-wise approach.
First step then is upper tract imaging. Then urine cytology or cystoscopy.

Bladder Ca

Most common histology is Transitional Cell ca

Routine screening in all patients for bladder ca with
either urinalysis or cytology is not recommended
Screening for bladder cancer in high risk individuals (
those exposed to dyes/ leather, smokers) is
controversial no clear recommendations.
High risk History : Smoking history, Occupational
exposure to dyes, rubber, or leather, previous
exposure to Cyclophosphamide

Bladder Ca

Do not routinely screen but however, if you find

Hematuria ( even microscopic) on routine
urinalysis that was done for another purpose
do not neglect this finding. ABNORMAL LAB
always need to be addressed pursue further
w/u for this hematuria ( BPH, Ca.Bladder,
ca.prostate, cystitis, r/o glomerulonephritis)

Remember Micro-HEMATURIA is the most

common manifestation of bladder cancer.

Clinical Symps/ Signs

Hematuria
Urinary frequency or dysuria
Flank or suprapubic pain
Constitutional symptoms, such as weight loss
Weight loss
Adenopathy
Palpable suprapubic mass
Organomegaly
BLADDER CA CAN BE TOTALLY
ASYMPTOMATIC

IMPORTANT
Refer all patients ( especially those at
high risk) presenting with unexplained
hematuria for cystoscopy, even if their
hematuria is intermittent, and regardless
of the findings on history and physical
exam.

Bladder Ca - Diagnosis

Freshly voided urine sample for cytology

Imaging of the urinary tract
Cystoscopy and exam under anesthesia with
biopsies
Additional diagnostic evaluations, based on
findings from the cystoscopy and pathologic
evaluation of the tumor, to assess the upper
urinary tract or to look for metastatic disease
lfts, ivp, cxr, ct scan of abd/pelvis, bone scan.

Bladder Ca - Rx

Surgical resection for non invasive bladder ca.

Radical Cystectomy Rx of choice for muscle-invasive
bladder ca.
Adjuvant Intravesical therapy with BCG/ mitomycin-c
for Cis, T1 tumors, tumor > 5cm size.
Adjuvant chemotherapy on case-by case basis
gemcitabine+cisplatin or methotrexate
Local side effects of BCG include: Cystitis (90% of
patients) , Hematuria (30%) , Contracted bladder ,
Ureteral obstruction, Inflammation (prostatitis,
epididymitis, epididymoorchitis)
Systemic side effects of BCG, which should resolve in
48 hours, include: Flu-like symptoms , Arthralgias ,
Rash

Bladder Ca

Post radical cystectomy requires urinary

diversion
External diversions include conduits, usually
composed of a section of bowel (ileum or
colon).
Internal conduits include those that require a
stoma to empty the reservoir (Kock pouch and
Indiana pouch) and orthotopic replacements
(e.g., Le Bag, Mainz pouch,

Complications Urinary diversion

Watch for the following after urinary diversion:

Bleeding , Infection , Hernias , Necrosis , Reflux,

Incontinence , Obstruction of conduit, upper tract, or
intestines and Recurrent cancer

Monitor for bacteremia, treat patients with Proteus or

Pseudomonas sp., and observe patients with other
organisms if they are asymptomatic.
Monitor closely:

Vitamin B12 levels , Acid/base status , Electrolyte levels and

Bone mineralization

Painful Hematuria
UTI/ Cystitis/ Pyelonephritis
Renal Calculi
IMAGING CHOICES:
Computed tomography ( NON CONTRAST) is the
best imaging modality for the evaluation of urinary
stones, renal and perirenal infections, and associated
complications
Ultrasound : Excellent for detection and
characterization of renal cysts (Limitations in detection
of small solid lesions (<3 cm)) Also, used for stones
eval in pregnancy.

Prostate Disorders
Benign

Prostate Hypertrophy
Prostatitis Acute & Chronic
Carcinoma of Prostate
Chemoprophylaxis of Prostate cancer
Utility of PSA ( see Oncology)

Electrolytes

Hypernatremia

Hypernatremia

Defined as serum sodium > 145 meq/L

Hospital acquired in >80% of patients
Requires defect in renal concentrating ability and
defect in thirst mechanism
Normal patients do not become hypernatremic
Hypernatremia occurs in very young and very
old with a defect in thirst
Isovolemic, Hypovolemic & Hypervolemic

Isovolemic Hypernatremia : Usually hemodynaically

stable unless serum sodium > 170 meq/L
Causes:
Hypodipsia
Increases insensible losses
Nephrogenic diabetes insipidus congenital,
acquired CRF, Hypokalemia, Hypercalcemia, Sickle cell
disease Amyloidosis, Obstruction, Alcohol, Lithium,
Demeclocycline, Glyburide, Amphotericin

Essential hypernatremia
Central Diabetes Insipidus : Granulomas, Histiocytosis,
Infections, CVA, Postpartum necrosis, Pregnancy, Head
traumaPost hypophysectomy, Suprasellar masses, Intrasellar
masses

Polyuria

? Water or solute diuresis

Water diuresis i.e. diabetes insipidus vs
polydipsia ( Uosm < 150 mOsm )
Solute diuresis i.e. electrolyte vs non electrolyte (
Uosm 300 - 400 mOsm )
Diagnostics: Urinalysis, urine osmolality, and
urine electrolytes

Hypovolemic Hypernatremia Causes

Renal causes
Loop diuretics
Osmotic diuresis
Gastrointestinal causes
Vomiting / nasogastric drainage
Diarrhea / cathartics
Water loss into cells
Exercise / seizures
Cuteaneous causes
Burns / excessive sweating

Hypervolemic Hypernatremia
Causes :
Hypertonic sodium solutions
Hypertonic feedings
Ingestion of sea water
Hypertonic dialysis
Primary aldosteronism
Cushings syndrome

Signs and Symptoms Hypernatremia

Depend on rate, degree and duration

Depressed sensorium
Irritability
Focal neurologic deficits / seizures
Muscle spasms
Nausea/vomiting
Thirst / fever
Volume depletion / hyperglycemia

Therapy of Hypernatremia

Hemodynamic or osmolal problem?

Acute or chronic problem?
Prior losses and present losses?
Rate of correction?
Acute: 1-1.5 meq/L/hour reduction
Chronic: 0.5 meq/L/hour reduction or 50% within first 24hours
- WHICH FLUID ?

Isovolemic
water: PO or intravenous
Water deficit = 0.6 (BWKg) x (Pna/140 -1)
Hypovolemic unstable pt????
Correct volume problem i.e. normal saline
Correct osmolal problem
Hypervolemic
Salt removal with loop diuretics and free water

CASE STUDY

Hypercalcemia
Etiology
Clinical features : bones, moans, stones, groans
Investigations: Ca, Phos, EKG, PTH, Urinary calcium excretion ( R/o familial
hypocalciuric hypercalcemia)
Management:
Criteria for surgery in primary hyperparathyroidism
Sestamibi scan only if surgery is planned/indicated
Hypercalcemic crisis management ivf + lasix after volume repletion only
Indications for corticosteroids : are useful for treating hypercalcemia caused
by vitamin D toxicity, certain malignancies (eg, multiple myeloma, lymphoma),
sarcoidosis, and other granulomatous diseases
Cinacalcet (Sensipar) -- Directly lowers parathyroid hormone (PTH) levels by
increasing sensitivity of calcium sensing receptor on chief cell of parathyroid
gland to extracellular calcium. Also results in concomitant serum calcium
decrease Indicated for hypercalcemia with parathyroid carcinoma.
Do not lower Calcium too much Serum calcium reduction may cause lowered
seizure threshold, paresthesia, myalgia, cramping, and tetany;

Criteria for Surgery Primary

hyperparathyroidism

Serum total calcium level >12 mg per dL (3 mmol per L) at any time
Hyperparathyroid crisis (discrete episode of life-threatening
hypercalcemia)
Marked hypercalciuria (urinary calcium excretion more than 400 mg
per day)
Nephrolithiasis
Impaired renal function
Osteitis fibrosa cystica
Reduced cortical bone density (measure with dual x-ray
absorptiometry or similar technique)

Bone mass more than two standard deviations below age-matched controls (Z
score less than 2)

Classic neuromuscular symptoms

Proximal muscle weakness and atrophy, hyperreflexia, and gait
disturbance
Age younger than 50

Hypercalcemia Breast Cancer

Management:
Principal Rx : Bisphosphonates for moderate to severe
hypercalcemia ( Aridia, Zolendronic acid) ( and also
prevent osteoporosis) ( esply pts on Aromatase
inhibitors are even prone to osteoporosis)

Manage hypercalcemic crises as in all other cases ( IV

Fluids and only after complete hydration, then
furosemide)

Hyponatremia

Classify Hypotonic, Isotonic and Hypertonic

Classify hypovolemic or euvolemic
Hypovolemic Hyponatremia Diarrhea, Vomiting,
early excess diuresis
Euvolemic Hyponatremia SIADH
Isotonic Hyponatremia Pseudohyponatremia (
Hyperglycemia, Hypertriglyceridemia, does not occur
with uremia)
Rx Correct volume and then osmolal problem
Volume problem Isotonic saline always !!!!!!!!!!
Asymptomatic fluid restriction
CNS symptoms 3% Saline

Hyperkalemia

Several causes : Medication interaction is a

common one ( ACEI+Spironolactone+beta
blocker, HEPARIN), renal failure, Addisons
disease, Rhabdomyolysis, Metabolic acidosis,
Hyperglycemic states.

Effects : arrhythmias, Can lead to tall tented twaves on EKG

Ekg- Hyperkalemia
The following changes may be seen in
hyperkalaemia
small or absent P waves
atrial fibrillation
wide QRS
shortened or absent ST segment
wide, tall and tented T waves
ventricular fibrillation

58 year old man on

haemodialysis presents with
profound weakness after a
weekend fishing trip.

The mans K was 9.6

Next Step IV CALCIUM CHLORIDE (
CALCIUM GLUCONATE AN
ALTERNATIVE)

30 y/o woman evaluated in the emergency department for a 2day history of muscle weakness. An electrocardiogram taken in
the emergency department is shown.
Which of the following is the best immediate treatment
option?
( A ) Hemodialysis
( B ) 50% glucose, 50 mL, intravenously
( C ) Calcium gluconate, 10 mL
( D ) Sodium polystyrene sulfonate (Kayexalate), 50 g, in
sorbitol, rectally
( E ) Peritoneal dialysis

Hyperkalemia - Treatment
MNEMONIC CBIGKDrop
Check the EKG If EKG changes, calcium
gluconate IV
B BICARBONATE/ Beta agonists
I INSULIN
G DEXTROSE
K KAYEXALATE If total body potassium is
an issue
D Hemodialysis for refractory Hyperkalemia

HYPOKALEMIA - EKG
The following changes may be seen in
hypokalaemia.
small or absent T waves
prominent U waves
first or second degree AV block
slight depression of the ST segment

Acid Base Disorders

Formulas, Case studies and
Management

Acid Base Disorders

Metabolic Alkalosis
Respiratory Alkalosis
Metabolic Acidosis
Respiratory Acidosis
Mixed Disorders

Acid Base Disorders

Common clinical problems

Associated with life threatening conditions
Often misdiagnosed
Demands an understanding of physiology and
pathophysiology
pH is a major determinant of enzymatic reactions
Acedemia denatures the enzymes, decreases
threshold for ventricular fibrillation and increases
respiratory drive. Alkalemia suppresses respiratory
drive, can cause myocardial ischemia, coronary
vasospasm etc

Acid Base Disorders

- CARBONIC ACID - BICARBONATE
SYSTEM : H + HCO3 H2CO3 H2O +
CO2
- HENDERSON-HASSELBACH
EQUATION : pH = pKa + log HCO3 / H2CO3
- PLASMA ACIDITY : determined by :
Balance between concentration of plasma
bicarbonate and pCO2
Measured as pH or H ion concentration

Acid Base Disorders

1. Factors affecting plasma Bicarbonate :
Rate of H ion input
Rate of H ion excretion via kidneys
Rate of H ion or bicarbonate loss via GI tract
Availability of non bicarbonate buffers
Volume of distribution of bicarbonate
2. Factors affecting pCO2
Rate of CO2 excretion via alveolar ventilation
Rate of CO2 production

ACIDEMIA-ALKALEMIA

Refers to plasma acidity

Acidemia: pH < 7.36
Alkalemia: pH > 7.44

Metabolic Disorder:
- Acid-base disorder caused by primary
change in plasma bicarbonate
- Plasma bicarbonate = 24-28 meq/L
Respiratory Disorder
- Acid-base disorder caused by primary
change in pCO2
pCO2 = 36 - 44 mmHg

Compensatory Mechanisms :

Appropriate proportional physiologic

responses which tend to restore pH
toward, but not to normal
Terms over and under
compensation should be avoided

INSTEAD USE MIXED

DISORDER!!!

Metabolic Acidosis
Calculate Anion Gap : Na - (Cl + HCO3) - Normal 3 - 10
meq/L
Given entirely by Unmeasured anions are related to (-) charge
on albumin One gram albumin = 2.5 meq/L anion
i.e. Albumin of 4 gm/L, baseline anion gap would be 10
meq/L which is Normal. Correct Gap for Albumin!!! If
albumin is 2gm%, the baseline anion gap should be 5 in
which case 10 should be assumed as increased Anion gap.

Delta Gap : Delta AG / Delta HCO3:

1:1 = Anion gap acidosis
>1 = Anion gap acidosis plus metabolic alkalosis
< 1 = Increased Anion gap acidosis plus normal
anion gap acidosis
Classify Metabolic Acidosis
Increased Gap
- Normal Anion gap

Calculate Compensation
Compensation Metabolic Acidosis
Occurs in 12-24 hours and limit PCO2 10 mmHg
:
Expected pCO2 = 1.5x HCO3 + 8 +/- 2
pCO2 = last 2 digits pH
pCO2 = HCO3 + 15
If measured Pco2 is less than expected pco2 as
calculated by this equation suspect a primary
respiratory alkalosis. If it is more than expected
suspect primary respiratory acidosis. This is how
you diagnose mixed disorders!!!

Example

1.
2.
3.
4.

5.
6.
7.

65 y/o man with CAD and then

cardiogenic shock. Ph 7.26. PCo2 40 HCO310 Na+ 136 Cl- 110 Albumin 2.0
What's the Anion Gap?
Corrected Anion Gap ? {gap + 2.5(measured
albumin)}
Delta Anion Gap?
Delta Hco3-? ( 24 bicarb)
Delta Gap?
Adequately Compensated or mixed ?
Name the disorder ?

Normal Anion-Gap Metabolic Acidosis

Gastrointestinal Loss of Bicarbonate

Diarrhea

Urinary diversion

Small bowel, pancreatic, or bile drainage ( fistulas, surgical

drains )

Cholestiramine

Renal Loss of Bicarbonate ( or Bicarbonate equivalent )

Renal tubular acidosis

Recovery phase of Ketoacidosis

Renal Insufficiency

Acidifying Substances- HCl, NH4Cl, Arginine HCl, Lysine HCl,

Sulfur
To differentiate calculate Urinary Anion Gap = Urine (Na + k)
(cl-). Normal is from +10 to -10. If UAG > +10 Renal loss.
If UAG < -10 or more negative GI Causes ( neGUTive)

Increased Anion Gap Acidosis

Ketoacidosis - diabetic, alcoholic, starvation

Lactic acidosis
Uremia
Toxins - Ethylene glycol, methanol, salicylate,
paraldehyde
Osmolar Gap = Measured Osmolarity
Calculated Osmolarity
Calculated Serumosm = 2(Na) + Glucose/18
+BUN/2.8 ( + ethylalcohol/4.5)

Plasma Level v. Osmolality

Ethanol 4.6
Methanol 3.2
Ethylene glycol 6.2
Isopropanol 6.1
For example, a blood ethanol level of 100mg/dL
would increase plasma osmolality 100/4.6 or 22
mOsm/L

Case Study

Sam is a 35 y/o alcoholic who is brought to the ER in a comatose state. Sams

wife tells you that she had an argument in the evening about 5 hrs ago over
Sams alcohol habits. Sam apparently got mad over the discussion, drove his
car and returned an hour ago in a very intoxicated state. Wife called the EMS
and rushed him to the ER. On examination Sam is disoriented and
hallucinating , Pulse 120 Tm 99, RR 26 BP 126/76. The rest of the physical
exam is normal except for stuporos state and alcohol smell. Lab studies
revealed Na 130 k 3.4 cl- 95 Hco3 16, Glucose 90 Creatinine 1.6 BUN 45.
Blood Ethylalcohol level was 180. Serum osmolarity was 360mg%. ABGs
revealed 7.28, Pco2 28, Po2 76 Sao2 93. The next best step in management ?

A) Endotracheal intubation in view of severe acidosis

B) Hemodialysis because this is an acute renal failure causing acidosis
C) Fomepizole because of suspicion of ethylene glycol intoxication
D) Supportive treatment for now because this is an ethylalcohol induced
lactic acidosis
E) Bicarbonate drip to reverse the acidosis because this is renal tubular
acidosis

Ethylene Glycol Poisoning

Envelope shaped crystals

Treatment : Consider Antidote (

Fomepizole or Ethanol ) if Level >
20mg% or if you suspect ethylene
glycol intake with 2 or more a)
arterial ph < 7.3, Hco3 <20, osmolar
gap>10, calcium oxalate crystals in
urine.
Antidote blocks Alcohol
dehydrogenase and prevents the
Glycolic acid formation. In case of
methanol, toxic meatbolite is formic
acid

Ethylene glycol found in

antifreeze and de-icer
Toxicity results at doses >1.0
ml/kg

Ethylene glycol causes CNS

depression , converts to
Glycolic Acid (metabolite)
effects Metabolic

Acidosis &Renal Failure

Oxalic acid (metabolite)

effects Calcium oxalate

crystal deposition

C/F: Confusion, Ataxia,

Slurred speech
,Hallucination, Tetany
Seizures (Hypocalcemia)
Hypertension
Tachycardia

Increased Osmolal Gap

Ethanol
Methanol
Ethylene Glycol
Formaldehyde
Paraldehyde
Lactic Acidosis
ESRD
Ketoacidosis

Mannitol
Isopropyl alcohol
Hyperlipidemia
Hyperproteinemia
Diethyl ether

Isopropanol Ingestion

Present with CNS depression, hypotension,

arrhytmias and gastritis
Acetest reaction positive
Increased osmolal gap
No metabolic acidosis
Anion gap normal

Renal Tubular Acidosis

Type 1 ( distal)
Type 2 (proximal)
Type 4 (hyporeninemic hypoaldosteronism)

Type I RTA (Distal)

Causes: autoimmune diseases, hyperglobinemia

states and hereditary
Present with normal anion gap acidosis, urine pH
>5.5, hypokalemia, hypercalciuria,
nephrocalcinosis and stones
Treatment: alkali i.e. K citrate

Type II RTA (Proximal)

Isolated defect or associated with generalized proximal

dysfunction i.e. Fanconi syndrome
Failure to reclaim filtered bicarbonate
Increase FEHCO3
Urine pH > 5.5, but may be < 5.5 once HCO3 < 16
meq/L
Causes:

Multiple myeloma
Acetozolamide
Ifosfamide
Lead, cadmium, copper

Type 4 RTA

Hypoaldosteronism or aldosterone resistance

Causes: diabetes mellitus, HIV and tubulointerstitial disease
Present with hyperkalemia, normal anion gap
acidosis and normal urine pH

Metabolic Alkalosis
Calculate compensation
PCO2= ( 0.7 x HCO3 ) + 21 . If measured Pco2
is more than this then there is concomitant
respiratory acidosis. If less than this then
concomitant respiratory akalosis.
Delta Gap to r/o mixed disorder metabolic
acidosis + metabolic alkalosis if delta gap >1

Causes of Metabolic Alkalosis

Saline responsive : ECF depleted ( contraction alkalosis ), Urine
chloride < 10 meq/L, do not go by urine sodium in assessing
volume status
Gastrointestinal Loss eg : Surreptious vomiting, NG tube
suctions,Villous adenoma, Chloride diarrhea, Diuretics (late),Post
hypercapnea
Saline resistant : Saline Resistant Metabolic Alkalosis , Increased
mineralocorticoid effect,Urine Cl > 20 meq/L
Hypertensive causes:Primary aldosteronismCushings syndrome,
11 or 17 hydroxylase deficiency, Licorice / carbenoxolone,
Liddles syndrome, Steroids
Normotensive causes: Bartters syndrome ( thiazide), Gitelmans
syndrome ( like loop diuretic), Diuretics (present), Severe
potassium depletion, Severe magnesium depletion

Metabolic Alkalosis - Treatment

Saline responsive
Normal saline to volume replete
KCl

Saline resistant

Inhibit or remove excess mineralocorticoid effect

Miscellaneous
Acetazolamide, HCl, NH4Cl
Hemodialysis

Case Study

A 26 year old woman presents to the ER with generalized weakness associated with
perioral numbness. She is moderately built and looks slightly depressed. On
physical exam, she has mild pallor. She denies use of any medications. BP 120/88
mmHg and physical exam is normal. Lab data: Cr 1.2mg/dL, BUN 15mg/dLNa
136 , K 2.8 , Cl 88 , HCO3 38. Urine Na 45 meq/L, Urine K 35 meq/L, Urine Cl
8 meq/L, Urine specific gravity 1.010, Urine pH 7

The most likely diagnosis is :

A)
Laxative Abuse
B)
Surreptious vomiting
C)
Licorice abuse
D)
Malabsorption Syndrome
E)
Hyporeninemic Hypoaldosteronism
Treatment :
A)
IV normal saline
B)
Spronolactone
C)
Amiloride
D)
Psychiatry consult
E)
Reassurance because this is self limiting