Nephrology Board Review

Sidharth Shah, MD.

June 2007
Make sure you know….

 Hyponatremia
 Hypernatremia (H20 deficit)
 ETOH ketoacidosis
 RF 2/2 atheroembolic disease
(cholesterol emboli)
 Obstructive uropathy
 Indinavir --> crystal nephropathy
 Stage 2 HTN
Question 1
 42 yo male brings in his 10yr old son
as he’s concerned that the child is
happy all the time and appears to be
“like a puppet”. What syndrome does
the child likely have?
 Nephrology MKSAP: Q87
 64 yo male admitted with a 5 day history of lethargy and
mild confusion. He is known to have alcoholic cirrhosis,
nonbleeding esophageal varicies, & ascites. There is no
history of recent ETOH consumption, melena, or
hematemesis. No co abdominal pain & has not fallen. He’s
on a 2gm Na diet and takes a MVI qday.

 Exam:
– VS: BP 110/70, HR 87bpm, Temp 36. Icteric sclerae, and
spider angiomata present. No JVD. Lungs are clear, with
decreased breath sounds as both bases. Cardiac:
HRRR. No gallop, rub. Abdomen is protruberent but not
tender, with a shifting dullness. Liver is not palpable.
Extremities show 1+ ankle edema. Asterixis is present,
but the patient has not focal neurologic signs.
Nephrology MKSAP: Q87
 Labs: – Serum Cl: 80meq/L
– Hgb: 11.5g/dl – Serum HC03: 28meq/K
– HCT: 32 – Serum total protein: 6.9g/dl
– PLT: 84,000/uL – Serum Alb: 2.5g/dl
– WBC: 5400/uL – Cholesterol 186mg/dl
– Serum BUN: 20mg/dl – Serum Osm:241 mosmol/kg H20
– Serum Cr: 1.2mg/dl – Urine Osm: 200mosmol/kg H20
– Serum Na:114meq/dl – Spot Urine Na: 10meq/L
– Serum K: 4.1meq/L
Nephrology MKSAP: Q87

What is the cause of this patient’s hyponatremia?

A) Nonosmotic stimulation of ADH

B) Hepatorenal syndrome

C) Low-Na diet

D) Reset osmostat

E) Pseudohyponatremia
Nephrology MKSAP: Q87

What is the cause of this patient’s hyponatremia?

• Nonosmotic stimulation of ADH

• Hepatorenal syndrome: Hyponatremia can be seen in

HRS, but does not cause it.

• Low-Na diet: Never associated with hyponatremia

• Reset osmostat: Would have appropriate dilute urine

• Pseudohyponatremia: Occurs in high serum levels of

protein or lipids.
Hyponatremia Workup

 1) Measure plasma osmolality

– Hypertonic hypo Na: excess of another

effective osmole (glc, mannitol)
 Each 100mg/dl increase in glc >100mg/dl leads
to a decrease of [Na] by 2.4meq/L

– Isotonic hypo Na: lab artifact from

hyperlipidemia or hyperproteinemia
 Hypotonic Hyponatremia
Hypotonic Hyponatremia

ypovolemic Euvolemic Hyponatremia Hypervolemic

yponatremia Hyponatremia

Uosm>100 Uosm<100 Uosm var.

Una> 20 Una< 10 Una<10 Una> 20
FeNa> 1% FeNa< 1% FeNa<1% FeNa> 1%

Renal Extra-renal
Losses Losses
SIADH 1 polydipsia Reset
Adrenal Insuf Low Solute osmostat
Hypothyroid
CHF Renal Failure
Cirrohsis
Nephrosis
Harrison’s: VIII-29
 36 yo male undergoes knee surgery to repair torn
ligaments. Postop, he is prescribed APAP for pain.
One day later he reports worsening pain. Exam
reveals BP 120/75, HR 80/min, RR 14/min and temp
98.6F. He has severe pain at the knee but no
redness or signs of infection.
 Lytes:
– Na: 128meq/L K: 4.0meq/L
– Cl: 95mg/dl Bicarb: 25mg/dl
– BUN: 12mg/dl Cr 1.0mg/dl
Harrison’s: VIII-29
 Which of the following therapies is
most appropriate at this time?
A) Hypertonic saline
B) Furosemide
C) Morphine
D) Normal Saline
E) Vancomycin
F) Fluid restriction
Harrison’s: VIII-29
 36 yo male undergoes knee surgery to repair torn
ligaments. Postop, he is prescribed APAP for pain.
One day later he reports worsening pain. Exam
reveals BP 120/75, HR 80/min, RR 14/min and temp
98.6F. He has severe pain at the knee but no
redness or signs of infection.
 Lytes:
– Na: 128meq/L K: 4.0meq/L
– Cl: 95mg/dl Bicarb: 25mg/dl
– BUN: 12mg/dl Cr 1.0mg/dl
Harrison’s VIII-21
 33yo male is brought for medical
attention after completing a marathon.
Upon finishing, he was disoriented and
light-headed. His normal weight is
60kg. Exam reveals a body temp of
38.3, BP 85/60mmHg and HR 125/min.
Neck veins are flat, skin turgor is poor.
Serum Na is 175meq/L. What is the
free H20 deficit?
Harrison’s VIII-21
 Free H20 deficit:

[Na]- 140 x (total body water)=

140
175-140 x (60kg)(0.5)=
140
0.25 x 30= 7.5L

Desired change in Na: 175meq-140meq= 35meq

35meq x __1hr__ = 70hrs

0.5meq
Harrison’s: VIII-50
 72 yo male develops ARF after cardiac
cath. Exam is notable for diminished
peripheral pulses, livedo reticularis,
epigastric tenderness, and confusion.
Labs show BUN 131, Cr 5.2, & Phos 9.5.
UA: 10-15 WBC, 5-10 RBC, and 1
hyaline cast/HPF.
Harrison’s: VIII-50
 What is the diagnosis?

A) AIN caused by drugs

B) Rhabdomyolysis with ATN
C) ATN 2/2 radiocontrast exposure
D) Renal arterial dissection with prerenal
azotemia
E) Cholesterol emobolization
Harrison’s: VIII-50
 72 yo male develops ARF after cardiac
cath. Exam is notable for diminished
peripheral pulses, livedo reticularis,
epigastric tenderness, and confusion.
Labs show BUN 131, Cr 5.2, & Phos 9.5.
UA: 10-15 WBC, 5-10 RBC, and 1
hyaline cast/HPF.
Cholesterol Atheroembolic
Renal Disease

 Pathophysiology:
– Showers of cholesterol emboli what can cause
“stepwise progression” of renal failure

 Characterized by:
– Pyuria
– Progressive RF (nonoliguric)
– Hypocomplementemia
– Eosinophiluria
– Associated organ dysfunction
 Harrison’s: VIII-9
 In the ED, a male patient presents with right flank pain
without radiation during micturition and intermittent polyuria
with other periods of decreased urine output. Denies having
dysuria, hematuria, and fever. Denies any PMHx, and ROS
is negative.
 Exam shows VSS, and normal abdominal exam except for
mild costophrenic angle tenderness on the right. Rectal
exam shows no tenderness, and there is a normal prostate
examination. No edema is note to the lower extremities. UA
is bland without pyuria, bacteria, or casts. Serum BUN/Cr
50/2.0mg/dl. Renal U/S shows bilateral hydronephrosis.
Harrison’s: VIII-9
 What is the diagnosis?

A) Acute cystitis
B) Genitourinary TB
C) Nephrolithiasis
D) Transitional cell ca of the bladder
E) Vesicoureteral reflux disease
 Harrison’s: VIII-9
 In the ED, a male patient presents with right flank pain without
radiation during micturition and intermittent polyuria with other
periods of decreased urine output. No dysuria, hematuria, and fever
reported. Denies any PMHx, and ROS is negative.
 Exam shows VSS, and normal abdominal exam except for mild CVA
tenderness on the right. Rectal exam shows no tenderness, and there
is a normal prostate examination. No edema is note to the lower
extremities. UA is bland without pyuria, bacteria, or casts. Serum
BUN/Cr 50/2.0mg/dl. Renal U/S shows bilateral hydronephrosis.
 Obstructive Uropathy
 Pathophysiology:
– Azotemia= obstruction of outflow tracts of two normal kidneys or
one in the presence of bilateral renal disease.
– Anuria= complete obstruction
– Oliguria, frequency, polyuria, nocturia= partial obstruction
 Labs:
– High BUN/Cr= decreased tubular flow and increased tubular
reabsorption of urea
– Urine indices and [Na] are not reliable
– Associated with Type IV RTA (hyperkalemia)
 Remember:
– Polyuria may happen as a physiologic respone OR
– Postobstructive diuresis 2/2 Na & H20 retention and abnormal renal
tubular handling of Na & H20
MKSAP Nephrology: Q23
 63 yo factory worker presents with
upper & lower extremity & diffuse
muscle weakness over the past 2 wks.
For the past 6 mos, he has had low
back pain that was sufficiently severe
to cause him to miss work several
occasions. Buffered salicylate tx
relieved the pain somewhat.
MKSAP Nephrology: Q23
 Labs:
– Hgb: 8g/dl K 2.6meq/L
– HCT 24% Na 135meq/L
– PLT 106K/ul Cl 117meq/L
– BUN 10mg/dl Bicarb 15meq/L
– Cr 1.0mg/dl Glc 88mg/dl
– Osm 277mosmol/L Cal 11mg/dl

– ABG: 7.30/31 (pCO2)

– UA: neg for albumin; +sulfosalicylic acid

MKSAP Nephrology: Q23
 What disease process best explains
the acid-base disorder?

A) Proximal RTA
B) Salicylate toxicity
C) ETOH-induced lactic acidosis
D) Ethylene glycol toxicity
 Professor
Fuller’s
5 Rules
For
Acid-Base

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #1
 Identify the Disorder

pH < 7.40 = Acidemia

pH > 7.44 = Alkalemia

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #2
 Find the Primary Disturbance
Acidosis
HCO3 < 24 = Metabolic
pCO2 > 44 = Respiratory
Alkalosis
HCO3 > 24 = Metabolic
pCO2 < 40 = Respiratory

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #3
Why We Don’t Spark!

 ALWAYS Calculate the Anion Gap

LAW OF ELECTRONEUTRALITY REIGNS SUPREME

AG = (Unmeasured Cations) + Na + K = (Unmeasured Anions) + Cl + HCO3

*note: K usually omitted b/c only small magnitude of changes in serum*

AG = Na – Cl – HCO3 = UA – UC
normal = 10 (+/-2) UC: Ca++, Mg++
UA: albumin, PO4-, sulfates, other

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #3
 ALWAYS Calculate the Anion Gap
AG > 20 : highly significant
*think about Osmolal Gap*

Osmolal Gap: calc{Osm} – meas{Osm} </= 10

 measured Osm: what the lab detects from your blood sample
 calculated Osm: 2(Na) + BUN/2.8 + Gluc/18 + EtOH/4.6

*Rapid detection by Serum Alcohol Screen obviates need for

ethylene glycol, methanol, or isopropyl alcohol corrections

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #3
 ALWAYS Calculate the Anion Gap

Low Anion Gap (if AG<7): think excess cations

- Paraproteinemias (Multiple Myeloma)
- Hypermagnesemia / Hypercalcemia
- Lithium Intoxications

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #3
 ALWAYS Calculate the Anion Gap

*Remember to correct for low albumin state:

For each drop in albumin by 1mg/dl (from 4mg/dl),

add 2.5 to your calculated Anion Gap

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #4
 Check for Compensation

1. METABOLIC ACIDOSIS
HCO3 +15 = pCO2
Each fall in HCO3 by 10 mEq/L, the pCO2 should fall 12 mmHg
Winter’s: (HCO3)(1.5) + 8 +/- 2= pCO2

2. METABOLIC ALKALOSIS
Each rise in HCO3 by 10 mEq/L, the pCO2 should rise 6 mmHg

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #4
 Check for Compensation

1. RESPIRATORY ACIDOSIS
ACUTE: Each rise in pCO2 by 10 mmHg, HCO3 should rise 1mEq/L
CHRONIC: Each incr pCO2 by 10 mmHg, HCO3 should rise 4mEq/L

2. RESPIRATORY ALKALOSIS
ACUTE: Each fall in pCO2 by 10 mmHg, HCO3 should fall 2 mEq/L
CHRONIC: Each fall in pCO2 by 10mmHg, HCO3 should fall 5 mEq/L

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #4
 Check for Compensation

1. Compensation NEVER completely

normalizes pH from original disorder
2. If pH is normal…
mixed acid-base disorder must be
present

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #5
 Calculate the Delta Gap (or 1:1)

Each 1 point rise in AG above normal AG (=10)

should be accompanied by a 1 mEq/L decrease in HCO3

If HCO3 is > than predicted by 1:1, metabolic alkalosis also present

If HCO3 is < than predicted by 1:1, non-gap acidosis also present

Adapted from K.Lee presentation 9/2005

 “Rules of Five” -- #5
 Calculate the Delta Gap (or 1:1) : method #2

Δ Gap = current AG – normal AG

= current AG - 12

Δ Gap + current HCO3 = HCO3 before d/o

HCO3 > 28 = pre-existing met alkalosis
HCO3 < 24 = pre-existing non-gap acidosis

Adapted from K.Lee presentation 9/2005

MNEMONIC for GAP ACIDOSIS
“M-U-D-P-I-L-E-S”
M – Methanol
U – Uremia
D – DKA or starvation ketoacidosis
P – Propylene Glycol (additive in IV benzo’s)
*paraldehyde: rarely seen -- previous use for EtOH detox
I – Ingestions (Cocaine / MDMA or Ecstasy)
*INH: rare, unless seizure present // Iron toxicity rare
L - Lactate
E – EtOH ketoacidosis / Ethylene Glycol
S - Salicylates

Adapted from K.Lee presentation 9/2005

MNEMONIC for NON-GAP ACIDOSIS
“D-U-R-H-A-M”
D – Diarrhea (also fistula or kayexalate)
U – Ureteral Diversion (ileal conduit)
R - RTA (renal tubular acidoses)
H – Hyperalimentation / Hypoaldosteronism
A – Acetazolamide / Aldactone
M – Miscellaneous
toluene (glue sniffing), CaCl, MgSO4
euvolemic DKA

Adapted from K.Lee presentation 9/2005

 Urine Anion Gap (for NG acidosis)
 Urine anion gap aka urine net charge
Urine Na + Urine K – Urine Cl = UAG
– normal value mildly + or zero
– can’t use if urine pH >6.5
– hyperchloremic metabolic acidosis from a
non-renal source, NH4+ production is
appropriately increased >> Urine Cl  and
leads to (-) UAG
– Type I & IV RTA & renal failure, (+) UAG
Adapted from K.Lee presentation 9/2005
MKSAP Nephrology: Q23: Revisited

 63 yo factory worker presents with

upper & lower extremity & diffuse
muscle weakness over the past 2
wks. For the past 6 mos, he has had
low back pain that was sufficiently
severe to cause him to miss work
several occasions. Buffered salicylate
tx relieved the pain somewhat.
MKSAP Nephrology: Q23: Revisited
 Labs:
– Hgb: 8g/dl K 2.6meq/L
– HCT 24% Na 135meq/L
– PLT 106K/ul Cl 117meq/L
– BUN 10mg/dl Bicarb 15meq/L
– Cr 1.0mg/dl Glc 88mg/dl
– Osm 277mosmol/L Cal 11mg/dl

– ABG: 7.30/31 (pCO2)

– UA: neg for albumin; +sulfosalicylic acid

MKSAP Nephrology: Q23: Revisited

135 117 10 Gluc 88

2.6 15 1.0 ABG: 7.30 / 30 /
U/A: (-) alb / +SSA

rule#1: acidemic / rule#2: metabolic / rule#3: AG = 3 (low)

rule#4: compensation - Yes- Bicarb+15=PCO2
rule#5: Delta gap is NA (only in AG acidosis)
Thus, nongap metabolic acidosis with appropriate
respiratory compensation. AG is LOW….hmmm…

Adapted from K.Lee presentation 9/2005

MKSAP Nephrology: Q23: Revisited
 What disease process best explains the
acid-base disorder?

A) Proximal RTA
B) Salicylate toxicity- gap acidosis
C) ETOH-induced lactic acidosis- gap acidosis
D) Ethylene glycol toxicity- gap acidosis
A little more fun….
30 y/o M w seizure d/o previously well-controlled on
phenytoin. After a night of “partying”,
he has another seizure. In the ED…

140 100 12 Gluc 80 EtOH 100

4.8 12 1.0 ABG: 7.25 / 28 / 100
U/A: (-) ketones
measured Osm: 310

Adapted from K.Lee presentation 9/2005

 A little more fun….

140 100 12 Gluc 80 EtOH 100

4.8 12 1.0 ABG: 7.25 / 28 / 100
U/A: (-) ketones / meas Osm: 310

rule#1: acidemic / rule#2: metabolic / rule#3: AG = 28

rule#4: compensation - yes, roughly fits acute
rule#5: (28-12) + 12 = 28 (prior met. alkalosis)
osmolal gap = 0 = 2(140) + 12/2.8 + 80/1.8 + 100/4.6

Adapted from K.Lee presentation 9/2005

 A little more fun….
Methanol (EtOH screen showed just EtOH)
Uremia (BUN/Cr wnl)
DKA (gluc 100 & negative urine ketones)
Propylene glycol (unless his friends are pharmacists)
Ingestions (UDS later returned negative)
LACTIC ACIDOSIS
EtOH ketoacidosis / Ethylene Glycol (no ketones)
Salicylates (should see resp alkalosis)

Adapted from K.Lee presentation 9/2005

 A little more fun….

Which of the following is the most appropriate

treatment?
1. observation & repeat lytes / ABG in 1 hr
2. NaHCO3 100 mEq IVP
3. D5W w/ 150 mEq NaHCO3/L over 3 hrs
4. Hemodialysis
5. Fomepizole or EtOH gtt + Hemodialysis

Adapted from K.Lee presentation 9/2005

 A little more fun….

Which of the following is the most appropriate

treatment?
1. observation & repeat lytes / ABG in 1 hr
2. NaHCO3 100 mEq IVP
3. D5W w/ 150 mEq NaHCO3/L over 3 hrs
4. Hemodialysis
5. Fomepizole or EtOH gtt + Hemodialysis

Adapted from K.Lee presentation 9/2005

 Lowering the Threshold
What if his EtOH level = 0 (osmolal gap now 22)
and urine with +rbc’s +rectangular crystals?

1. Methanol
2. Isopropyl Alcohol
3. Ethylene Glycol
4. Cyanide

Adapted from K.Lee presentation 9/2005

 A little more fun….
What if his EtOH level = 0 (osmolal gap now 22)
and urine with +rbc’s +rectangular crystals?

 Methanol
Calcium Oxalate Crystals
->Formaldehyde + formic acid
 Isopropyl Alcohol
osmolal gap (ketosis)
w/o gap acidosis
 Ethylene Glycol
Glycolic acid+ Ca ox crystal
Positive Osmolar gap
 Cyanide
– lactic acidosis

Adapted from K.Lee presentation 9/2005 Fluoresce under Wood’s Lamp

MKSAP Nephrology: Q46
 43 yo woman presents with back pain and is
evaluated for renal insufficiency. Infection
with HIV was dx 2 yrs ago, and the patient
began taking active antiretroviral tx with
zidovudine, lamivudine, & indinavir 1 yr later
because of decreasing CD4 count &
development of oral candidiasis. Six mos
ago, she developed fasting hyperglycemia
and hypercholesterolemia and was treated
with rosiglitazone and atorvastatin.
MKSAP Nephrology: Q46
 Exam: BP 130/85, HRRR, RR is 18/min, temp is 37.8, no orthostatic
changes. No JVD or HJR. The cardiac, pulmonary, & abdominal
examinations are normal, but 2+ LE edema is noted.

 Labs:
– BUN 22mg/dl K 6.0meq/L
– Na 141meq/L Cr 3.2 mg/dl
– Cl 101meq/L Cal 7.2mg/dl
– Bicarb 19meq/L PO4 9.0mg/dl
– Uric acid 9.0mg/dl Cholesterol 177mg/dl

 FBS and AIC elevated. HCT 31%, MCV elevated. WBC 3300/ul, PLT
normal.

 UA: protein TR, 2+hematuria, No ketones, no glucose. Muddy brown casts

and tubular epithelial cells seen. No crystals or erythrocytes.
MKSAP Nephrology: Q46
 What is the most probable dx?

A) Rhabdo caused by atorvastatin

B) Indinavir nephrolithiasis
C) Indinavir tubulointerstitial renal
disease and atrophy
D) HIV-associated nephropathy
E) Diabetic nephropathy
MKSAP Nephrology: Q46
 Exam: BP 130/85, HRRR, RR is 18/min, temp is 37.8, no orthostatic
changes. No JVD or HJR. The cardiac, pulmonary, & abdominal
examinations are normal, but 2+ LE edema is noted.

 Labs:
– BUN 22mg/dl K 6.0meq/L
– Na 141meq/L Cr 3.2 mg/dl
– Cl 101meq/L Cal 7.2mg/dl
– Bicarb 19meq/L PO4 9.0mg/dl
– Uric acid 9.0mg/dl Cholesterol 177mg/dl

 FBS and AIC elevated. HCT 31%, MCV elevated. WBC 3300/ul, PLT
normal.

 UA: protein TR, 2+hematuria, No ketones, no glucose. Muddy brown

casts and tubular epithelial cells seen. No crystals or erythrocytes.
 Renal Tubular Acidosis

TYPE K+ HCO3 Urine pH Features

I  <15 > 5.3 Stones / Sjogrens

II avg 15 < 5.3 Glucosuria / Myeloma

IV  >15 usually Low Urine K+

< 5.3 DM & HIV

Adapted from K.Lee presentation 9/2005

 COMPLEMENT LEVELS

DISEASE C3 C4
Post-inf GN Low Low / norm.
MPGN Low Low / norm.
SLE Low Low
Cryos Low Low
SBE Low / norm. Low
Chol Emboli Low Normal
Paraprotein Normal Normal
ANCA Normal Normal
Adapted from K.Lee presentation 9/2005