Nephrology & Urology
Archer Online USMLE Reviews
www.ArcherReview.com
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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 NSAID’s 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, NSAID’s, cyclosporine and
CKD are risk factors
 ARB’s 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
 Dipstick test detects (-)
charge
 Does not detect light chains
 Function of urine
concentration
 Total Protein : creatinine
ratio estimates 24 hour urine
collection
 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 *****

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 NSAID’s, ACE inhibitors. ARB’s 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 RBC’s, 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: Sjogren’s 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 Crohn’s 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 other’s safety as well.
 Patients with symptoms suggestive of a berry aneurysm
( severe headache, focal neurological deficits)

Q
 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
 Cushing’s 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 t-
waves 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 man’s K was 9.6
Next Step  IV CALCIUM CHLORIDE (
CALCIUM GLUCONATE AN
ALTERNATIVE)

 30 y/o woman evaluated in the emergency department for a 2-
day 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
 65 y/o man with CAD  and then
cardiogenic shock. Ph 7.26. PCo2 40 HCO3-
10 Na+ 136 Cl- 110 Albumin 2.0
1. What's the Anion Gap?
2. Corrected Anion Gap ? {gap + 2.5(measured
albumin)}
3. Delta Anion Gap?
4. Delta Hco3-? ( 24 – bicarb)
5. Delta Gap?
6. Adequately Compensated or mixed ?
7. 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. Sam’s
wife tells you that she had an argument in the evening about 5 hrs ago over
Sam’s 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 tubulo-
interstitial 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 aldosteronismCushing’s syndrome,
11 or 17 hydroxylase deficiency, Licorice / carbenoxolone,
Liddle’s syndrome, Steroids
 Normotensive causes: Bartter’s syndrome ( thiazide), Gitelman’s
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