6.19.07 nephrology board review shah

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:– Hgb: 11.5g/dl– HCT: 32– PLT: 84,000/uL– WBC: 5400/uL– Serum BUN: 20mg/dl– Serum Cr: 1.2mg/dl– Serum Na:114meq/dl– Serum K: 4.1meq/L

– Serum Cl: 80meq/L– Serum HC03: 28meq/K– Serum total protein: 6.9g/dl– Serum Alb: 2.5g/dl– Cholesterol 186mg/dl– Serum Osm:241 mosmol/kg H20– Urine Osm: 200mosmol/kg H20– Spot Urine Na: 10meq/L


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


A) Nonosmotic stimulation of ADH

B) Hepatorenal syndrome

C) Low-Na diet

D) Reset osmostat

E) Pseudohyponatremia



• 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.


• 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 HyponatremiaHypotonic Hyponatremia

HypovolemicHyponatremia

Euvolemic Hyponatremia HypervolemicHyponatremia

Una> 20FeNa> 1%

Una< 10FeNa< 1%

Renal Losses

Extra-renal Losses

Uosm>100 Uosm<100 Uosm var.

SIADHAdrenal InsufHypothyroid

1 polydipsiaLow Solute

Resetosmostat

Una<10FeNa<1%

Una> 20FeNa> 1%

CHFCirrohsisNephrosis

Renal Failure

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


Which of the following therapies is most appropriate at this time?

A) Hypertonic salineB) FurosemideC) MorphineD) Normal SalineE) VancomycinF) Fluid restriction


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


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.


What is the diagnosis?

A) AIN caused by drugsB) Rhabdomyolysis with ATNC) ATN 2/2 radiocontrast exposureD) Renal arterial dissection with prerenal

azotemiaE) Cholesterol emobolization


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


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.


What is the diagnosis?

A) Acute cystitisB) Genitourinary TBC) NephrolithiasisD) Transitional cell ca of the bladderE) Vesicoureteral reflux disease


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.


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


What disease process best explains the acid-base disorder?

A) Proximal RTAB) Salicylate toxicityC) ETOH-induced lactic acidosisD) Ethylene glycol toxicity

ProfessorProfessorFuller’s Fuller’s 5 Rules5 Rules

For For Acid-BaseAcid-Base

Adapted from K.Lee presentation 9/2005

“Rules of Five” -- #1

Identify the Disorder

pH < 7.40 = Acidemia

pH > 7.44 = Alkalemia



Find the Primary DisturbanceAcidosis

HCO3 < 24 = MetabolicpCO2 > 44 = Respiratory

AlkalosisHCO3 > 24 = MetabolicpCO2 < 40 = Respiratory


“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



ALWAYS Calculate the Anion GapAG > 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




Low Anion Gap (if AG<7): think excess cations- Paraproteinemias (Multiple Myeloma)- Hypermagnesemia / Hypercalcemia- Lithium Intoxications




*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



Check for Compensation

1. METABOLIC ACIDOSISHCO3 +15 = pCO2Each fall in HCO3 by 10 mEq/L, the pCO2 should fall 12 mmHgWinter’s: (HCO3)(1.5) + 8 +/- 2= pCO2

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




1. RESPIRATORY ACIDOSISACUTE: Each rise in pCO2 by 10 mmHg, HCO3 should rise 1mEq/LCHRONIC: Each incr pCO2 by 10 mmHg, HCO3 should rise 4mEq/L

2. RESPIRATORY ALKALOSISACUTE: Each fall in pCO2 by 10 mmHg, HCO3 should fall 2 mEq/LCHRONIC: Each fall in pCO2 by 10mmHg, HCO3 should fall 5 mEq/L




1. Compensation NEVER completely normalizes pH from original disorder

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



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



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/oHCO3 > 28 = pre-existing met alkalosisHCO3 < 24 = pre-existing non-gap acidosis


MNEMONIC for GAP ACIDOSIS“M-U-D-P-I-L-E-S”

M – MethanolU – UremiaD – DKA or starvation ketoacidosisP – Propylene Glycol (additive in IV benzo’s)

*paraldehyde: rarely seen -- previous use for EtOH detoxI – Ingestions (Cocaine / MDMA or Ecstasy)

*INH: rare, unless seizure present // Iron toxicity rareL - LactateE – EtOH ketoacidosis / Ethylene GlycolS - Salicylates


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 / HypoaldosteronismA – Acetazolamide / AldactoneM – Miscellaneous

toluene (glue sniffing), CaCl, MgSO4

euvolemic DKA


Urine Anion Gap (for NG acidosis)

Urine anion gap aka urine net chargeUrine 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, (+) UAGAdapted 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.


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


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=PCO2rule#5: Delta gap is NA (only in AG acidosis)Thus, nongap metabolic acidosis with appropriate

respiratory compensation. AG is LOW….hmmm…



What disease process best explains the acid-base disorder?

A) Proximal RTAB) Salicylate toxicity- gap acidosisC) ETOH-induced lactic acidosis- gap acidosisD) 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: (-) ketonesmeasured Osm: 310



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



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 ACIDOSISEtOH ketoacidosis / Ethylene Glycol (no ketones)Salicylates (should see resp alkalosis)



Which of the following is the most appropriate treatment?

1. observation & repeat lytes / ABG in 1 hr2. NaHCO3 100 mEq IVP3. D5W w/ 150 mEq NaHCO3/L over 3 hrs4. Hemodialysis5. Fomepizole or EtOH gtt + Hemodialysis


Lowering the Threshold

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

1. Methanol2. Isopropyl Alcohol3. Ethylene Glycol4. Cyanide



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

Methanol->Formaldehyde + formic acid

Isopropyl Alcoholosmolal gap (ketosis) w/o gap acidosis

Ethylene GlycolGlycolic acid+ Ca ox crystalPositive Osmolar gap

Cyanide– lactic acidosis

Calcium Oxalate Crystals

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


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.


What is the most probable dx?

A) Rhabdo caused by atorvastatinB) Indinavir nephrolithiasisC) Indinavir tubulointerstitial renal

disease and atrophyD) HIV-associated nephropathyE) 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 < 5.3Glucosuria / Myeloma

IV >15 usually Low Urine K+

< 5.3 DM & HIV


COMPLEMENT LEVELS

DISEASE C3 C4Post-inf GN Low Low / norm.MPGN Low Low / norm.SLE Low LowCryos Low LowSBE Low / norm. LowChol Emboli Low NormalParaprotein Normal NormalANCA Normal Normal


6.19.07 nephrology board review shah

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