Renal Professor Hints Assessment 11
1/12/11
Calculating fractional excretion of sodium, potassium; Assessing clearance ratios; Calculation of Plasma
anion gap and urinary anion gap.
𝐺𝐹𝑅 =

[𝑈𝑟𝑖𝑛𝑒𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 ] 𝑥 𝑈𝑟𝑖𝑛𝑒 𝐹𝑙𝑜𝑤 𝑅𝑎𝑡𝑒 (𝑚𝑙/𝑚𝑖𝑛)
[𝑃𝑙𝑎𝑠𝑚𝑎𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 ]
Inulin could also work (freely filtered), but creatinine is used more in the clinical setting since it estimates
being freely filtered (even though it is slightly secreted)
𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒𝑥 =
[𝑈𝑟𝑖𝑛𝑒𝑥 ] 𝑥 𝑈𝑟𝑖𝑛𝑒 𝐹𝑙𝑜𝑤 𝑅𝑎𝑡𝑒 (𝑚𝑙/𝑚𝑖𝑛)
[𝑃𝑙𝑎𝑠𝑚𝑎𝑥 ]
𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒 𝑅𝑎𝑡𝑖𝑜𝑥 =
𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒𝑥
𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 (𝑜𝑟 𝑖𝑛𝑢𝑙𝑖𝑛)
𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒 𝑅𝑎𝑡𝑖𝑜𝑥 =

If CR > 1.0 then secretion of x is occurring, if CR<1.0 it suggests that reabsorption is occurring. If CR is 0
it is either too large to be filtered, or it is completely reabsorbed (glucose, amino acids).
𝑅𝑒𝑛𝑎𝑙 𝑃𝑙𝑎𝑠𝑚𝑎 𝐹𝑙𝑜𝑤 =

𝐶𝑙𝑒𝑎𝑟𝑎𝑛𝑐𝑒𝑥
𝐺𝐹𝑅
[𝑈𝑟𝑖𝑛𝑒𝑃𝐴𝐻 ] 𝑥 𝑈𝑟𝑖𝑛𝑒 𝐹𝑙𝑜𝑤 𝑅𝑎𝑡𝑒 (𝑚𝑙/𝑚𝑖𝑛)
[𝑃𝑙𝑎𝑠𝑚𝑎𝑃𝐴𝐻 ]
𝐹𝑖𝑙𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝐹𝑟𝑎𝑐𝑡𝑖𝑜𝑛 = 𝐺𝐹𝑅/𝑅𝑃𝐹
FF usually equals 20%
𝑃𝑙𝑎𝑠𝑚𝑎 𝐴𝑛𝑖𝑜𝑛 𝐺𝑎𝑝 = 𝑁𝑎 – (𝐶𝑙 + 𝐻𝐶𝑂3)
𝑈𝑟𝑖𝑛𝑎𝑟𝑦 𝐴𝑛𝑖𝑜𝑛 𝐺𝑎𝑝 = (𝑁𝑎 + 𝐾)– 𝐶𝑙

Urinary Anion Gap
o Indirect estimate of NH4 in urine
o Clinical labs can’t measure NH4 easily in the urine, therefore labs measure the urinary anion gap
and estimate NH4 indirectly
o Sodium and potassium are the major urinary cations (we must consider potassium in urine, don’t
necessarily have to consider it with plasma anion gap since it has a small plasma concentration)
o Chloride is the major urinary anion
 Not bicarbonate
o Urinary anion gap is about 10 mEq/L normally
 Can vary widely depending on meal states, etc.
o This is useful when you are trying to evaluate normal anion gap metabolic acidosis (usually
hyperchloremic since it’s metabolic acidosis)
𝐹𝑖𝑙𝑡𝑒𝑟𝑒𝑑 𝑙𝑜𝑎𝑑 = 𝑃𝑙𝑎𝑠𝑚𝑎𝑥 × 𝐺𝐹𝑅
Essential information: Understand the directional changes that occur in the fluid spaces (total body water,
intracellular fluid volume, extracellular fluid volume and its components) during pathophysiologic settings
such as volume expansion volume deficiency, dehydration, etc.
2/3 TBW is ICF
Renal Professor Hints Assessment 11
1/12/11
1/3 TBW is ECF
¾ ECF is interstium
¼ ECF is plasma volume (NOTE: PLASMA Na tells you nothing about TBNa content or size of ECFV (since it also
reflects TBW)!, ECFV is controlled by TBNa)
Look at P.102
Volume Depletion
(isotonic)
Volume Loss
(H2O)
TBW
↓
↓
ECFV
↓
↓
ICFV
Unchanged
↓
Isotonic Volume
Expansion
↑
Depends on TBNa
and TBW relative
concentrations
Hypotonic
Volume
expansion
↑
Hypertonic
(salt
intake)Volume
Expansion
unchanged
↑
↑
↑ (movement
into ICFV)
↓ (movement
into ECFV)
Be able to evaluate an arterial blood gas with attendant electrolytes. Only simple acid-base disorders will be
included (i.e., No mixed acid-base disorders).





Henderson-Hasselbach Equation:
o H+=24 x [Acid (carbon dioxide) /Base (Bicarbonate)]
o At normal pH (7.4) the H+ is 40 nEq/L
o The only way you can change pH is to change this ratio
H+ is usually equal to 80 minus the last two digits of the pH (ex. pH of 7.4, 80 – 40 = 40)
Golden Rules
o Carbon dioxide and bicarbonate always change in the same direction in all of the four disorders
o Secondary mechanisms are always present in a simple disorder (if it is not a mixed disorder)
o These mechanisms never fully correct but always bring pH back towards normal
24× (𝐶𝑂2 )
𝐻+ =
Note: If pH=7.40 then (80-40=40nEq/L of H+), therefore 40=[24 x 40 (normal CO2) ]
𝐻𝐶𝑂3
/HCO3, this makes bicarb equal to 24 which is normal for a pH of 7.40 under normal circumstances (way
to check yourself)
In respiratory orders chloride changes opposite than bicarbonate (think—in respiratory acidosis we have
too much CO2too much H+bicarbonate goes down immediately due to buffering and more later due to
kidney regulation of bicarbonate)
Renal Professor Hints Assessment 11
1/12/11
Utilizing clinical information and measurements of plasma and urinary concentrations you should be able to
assess renal handling of sodium, water, and potassium. For example: in a given clinical setting, is the kidney
appropriately conserving these solutes and water (or alternatively is there evidence for inappropriate wasting
or conservation).
Sodium:
If you are volume depleted you will be trying to conserve sodium, if you have volume excess you will be giving off
sodium. If you see someone who has a huge loss of volume and they are giving off tons of sodium something does
not fit here.
Water:
Differences in DI and Primary Polydipsia
Condition
Central DI
Polyuria
Nephrogenic DI
+
Primary Polydipsia
+
low (<100)
+
Uosm
low (<100mOsm/kg H2O)
Posm
high*
high*
low
PNa
high*
high*
low
Uosm in response
to water deprivation
no change
(<300)
no change
(<300)
increase
(>500)
Uosm in response
to DDIVP
increase
little/no change
*- usually seen if there is decrease in access to water
low (<100)
little/no change
Potassium:
Decreased Secretion
(hyperkalemia)
Increased Secretion
(hypokalemia)
Increased movement into
cells (hypokalemia)
Renal failure
Diuretics (metabolic
alkalosis)
Insulin
Distal tubular dysfunction
Prolonged vomiting,
nasogastric suction
(metabolic alkalosis)
Epinephrine
Recall: Contraction
Alkalosis (decreased
volume increase
aldotherefore increase
H+ secretion by alpha
intercalated) Aldo also
increase K secretion –
Increased movements
into extracellular fluid
(hyperkalemia
>5.5meq/L)
Blocking insulin (blocks K
(via Na/K ATPase) into
ICF, but K channel
remains open and
therefore results in
increased ECF K )
Beta antagonists (blocks
into ICF, but K channel
remains open and
therefore results in
increased ECF K )
Renal Professor Hints Assessment 11
1/12/11
don’t forget this.
hypoaldosteronism
Measure urine chloride
(should be low in
vomiting—due to loss of
HCl)
Bartter’s syndrome,
Gitelman’s syndrome
(metabolic alkalosis)
Hyperaldosteronism (and
hyper renin) This is also
a hypertensive
hypokalemic disorder
(most of the others are
hypotensive)
Renal Tubular acidosis
(metabolic acidosis)
Cushings, Congenital
adrenal hyperplasia (all
working on the aldo
receptor (either aldo or its
precursors, ie.
DOC)increase K
secretion via principal
cells
Increased plasma K (not a
cause of hyperkalemia per
se but increases movement
of K intracellularly)
Alkalosis (exchange H
into ECF for K into cell)
Acidosis (exchange H into
cell for K into ECF)
Tx. Bicarbonate therefore
moves K into cells
Albuterol
Rapid cell proliferation
(think tumor—uses lots of
K)
Increased Posm shifts fluid
from ICF to ECF and K
exists with water (solvent
drag)
Cell lysis
EKG Findings with Potassium Disorders ( KNOW ABOUT THE U WAVE AND SPIKED T WAVE—NOT JUST
FOR ASSESSMENT).
Tx. Hypokalemia: Amiloride, Triamterene, sprinolactone, oral or i.V, replacement
Tx. Hyperkalemia: insulin, bicarbonate, albuterol
Note: changes in plasma sodium mainly determined by changes in total body water
Free Water:
- in hypotonic urine Cwater is positive as Uosm < Posm
Renal Professor Hints Assessment 11
1/12/11
- in isotonic there is no Cwater as Uosm = Posm
- in hypertonic urine Cwater is negative as Uosm > Posm
Estimation of TBW from sodium
- Water excess = 0.6 TBW x (1- [Na]observed/140)
- Water deficit= 0.6 TBW x ([Na]observed/140 -1)
Proximal tubular disorders: know clinical features of Fanconi syndrome, cystinuria, cystinosis, wilson’s ds,
primary renal phosphate wasting syndromes; know normal physiology of prox tubule
Defect
Clinical
Signs
Fanconi’s
Cystinuria
(AR)
Cystinosis
Wilson’s ds. (AR)
Dysfunctional proximal tubule
(most likely due to energy
producing machinery, ie.
Mitochondria, sodium gradient,
ATP pathways, etc.)
Defect in
cystine,
ornithine,
lysine,
arginine
transporter
(COLA)
Cystine stone
formation
Lysosomal storage
disorder
Defect in ATPB7
causes increased
copper in liver and
elsewhere, decreased
ceruloplasmin
Increased amino acids, glucose,
phosphate, bicarbonate, uric acid
in urine
Presents as a hyperchloremic
hypokalemic (since bicarbonate
is gone) metabolic acidosis
Damages kidney,
thyroid, cornea, and
retina, growth
retardation
RTA in kidneys
(defect in
bicarbonate
excretion), causes
nephrocalcinosis also
Kayser Fleischer
rings, basal ganglia
tremor,
parkinsonism, etc.
Causes
Wilson’s ds, Lowes,
Galactosemia, Tyrosinemia,
Hereditary fructose intolerance,
Mitochondrial disorders,GSD’s
Acquired: Heavy metals, drugs,
chemicals, cancer,
hyperparathyroidism (phosphate
depletion)
Normal function of PT:
OMO-defect in
phosphatonin (FGF23)
Bone, dental ds., low
calcitriol levels (should
be elevated with low
phosphate)
Tx. With phosphate and
calcitriol
Calcium and PTH are
normal while ALP is
elevated
Can be seen in both
cystinuria and
cystinosis
Hypophasphatemic Rickets, RTA
II (Since bicarbonate is lost)
Cystinosis* (common)
ADHR-defect in FGF23
Cystine stones
Muscle cramps, dehydration,
polyuria, polydipsia, fatigue,
failure to thrive, and rickets.
Increased ALP
Associations
Primary Renal
Phosphate Wasting
Syndromes
XLH-defect in PHEX
Cystine crystals on slit
lamp exam
Common cause of
Fanconi’s
Impaired transport of
cystine from lysosome
into cytoplasm
Note: Tx. Of this does
not correct Fanconi’s
RTA,
nephrocalcinosis
Renal Professor Hints Assessment 11
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


1/12/11
Reabsorbs glucose, amino acids, bicarbonate, phosphate
Reabsorbs 50% of filtered sodium chloride and water
Secretes many compounds, final pathway in synthesis of hormones (ex. Calcitriol)
THINK: BULK REABSORPTION
Distal tubular disorders: know normal physiology; know clinical features of Bartter syn, Gitelman
syndrome, Liddle syn, nephrogenic diabetes insipidus, renal tubular acidosis
Defect
Bartter’s (AR)
Na/K/2Cl pump (NKCC2) and
ROMK (potassium back
transporter) Think: Loop
Diuretic
Gitelmans
Thiazide sensitive
transporter in
distal convoluted
tubule
Liddle Syndrome
Gain of function of
epithelial sodium
channel (opposite of
what Amiloride
/Triamterene do)
NDI
Mut. In AQP2 or
anything
downstream
Type I: impaired
ammonia secretion in
collecting duct
(hypokalemic)
Can also be mut. in chloride
channel or barrtin channel (this
is associated with sensineural
hearing loss)
Clinical
Signs
Hypochloremic metabolic
alkalosis
Think: It’s acidosis since
there is such a huge loss of
volumeincrease
RAASincrease K and H
secretionbicarb goes up in
serum and chloride goes down
Hypochloremic metabolic
alkalosis
Dehydration, salt craving,
hypercalciuria (neonatal has
nephrocalcinosis but adult form
doesn’t), hypokalemia,
hyperaldosteronism, elevated
PGE2
Hyperplasia of Juxtaglomerular
apparatus
Tx. Potassium and magnesium
supplements
Hypochloremic
metabolic
alkalosis
Similar to
Bartter’s but has
hypomagnesemia
and
hypermagnesuria
Less symptomatic
since less sodium
is conserved via
DCT than in the
thick ascending
limb ( think a loop
vs. a thiazide)
Hypertension,
hypokalemic
metabolic alkalosis
RTA
Type II: Can’t reabsorb
bicarbonate in the PT
Inability to
concentrate urine in
the face of high
plasma osmolarity
Type IV: deficiency of
aldosterone
(hyperkalemic)
Hyperchloremic
Metabolic Acidosis
Urine pH in Type I
may be 6-7.0, whereas
in Type IV and II it is
<5.5 Think: Type II is
giving off bicarb in
urine (can’t reabsorb it).
Remember, RTA is a
normal anion gap
acidosis (always check
anion gap in metabolic
acidosis)
Fractional excretion of
bicarbonate (urine
bicarb/plasma bicarb all
over urine
creatinine/plasma
creatinine –just and
indicator for absorption
or secretion) is >1015% in proximal RTA,
<5% in distal RTA, <510% in hyperkalemic
RTA
Positive urinary anion
gap in Type I and
hyperkalemic RTA,
negative during acidosis
Renal Professor Hints Assessment 11
1/12/11
due to diarrhea
U-B CO2 is low in
Types I and IV but
normal in Type II
Characteristics of RTA Types
Finding
Plasma K+
Type II
(bicarb loss)
Low
Type I (can’t
secrete H)
Low
Type IV
(aldo def.)
High
Urine pH
< 5.5
>5.5
Variable
Urine Anion
Gap
U-B PCO2
Positive
Positive
Positive
Normal
Low
Low
FE HCO3-
> 15%
< 5%
<5-10%
Associated
Findings
Fanconi
syndrome
Increased
UCa2+
Renal
insuff. in
some
TTKG: (Kurine/Kplasma)/(Uosm/Posm), ratio of concentrations of potassium divided by total
concentrations—basically uses the serum osmolarity as a baseline to let us know if potassium is
being appropriately secreted or reabsorbed relative to total osmolarity. If TTKG<2.0 in the face
of hypokalemia then it is appropriate. If TTKG>8.0 in the face of hyperkalemia then it is
appropriate. Tells us that the mineralocorticoids are working correctly.
Pitfalls: Can’t be used well when sodium is less than 20 mEq/L or urine osmolarity is
<300mOsm/kg
Question: Patient presents wtih cardiac arrhythmias and a spiked T wave on EKG. The TTKG
is 4.3 is this appropriate?
Renal Professor Hints Assessment 11
1/12/11
Answer: No, the spiked T wave along with the cardiac arrhythmia points toward hyperkalemia.
We would expect a TTKG > 8.0 in hyperkalemia (getting rid of potassium) if everything was
working correctly. There perhaps could be an issue with a mineralocorticoid binding, receptors,
etc.
She said to know these two slides in class. Below are the sites that certain diuretics work on.
• Acetazolamide:
carbonic anhydrase
• Furosemide,
bumetanide, ethacrynic
+
+
-
acid: Na -K -2Cl
cotransporter
• Thiazides: Na-Cl
cotransporter
Renal Professor Hints Assessment 11
1/12/11
In general, be familiar with normal ranges of electrolytes.
NORMAL LAB VALUES
CHEMISTRIES
Na+
Cl+
K
HCO3
BUN
Cr
HEMATOLOGY
Hgb
WBC
Hct
Glc
Plt
Sodium
135 – 145 mEq/L
WBC
4.5 – 11.0 x 103 / L
Potassium
3.5 – 5.1 mEq/L
RBC
Chloride
98 – 106 mEq/L
Hemoglobin
3.8 – 5.7 x 106 / L
13.5 – 17.0 g/dL
Bicarbonate
22 – 29 mEq/L
Hematocrit
39 – 50%
BUN
7 – 18 mg/dL
MCV
80 – 96 mcm3
Creatinine
0.6 – 1.2 mg/dL
MCH
27 – 33 pg/cell
Glucose
70 – 115 mg/dL
MCHC
32 – 36% hgb / cell
Calcium
8.4 – 10.2 mg/dL
Platelets
Phosphate
2.7 – 4.5 mg/dL
RDW
150 – 400 x 103 / L
11.0 – 16.0%
Magnesium
1.3 – 2.1 mg/dL
Segs (Neuts)
35 – 73%
Anion gap
7 – 16 mEq/L
Lymphocytes
15 – 52%
Osmolality
NH3
275 – 295 mOsm/kg
10-35mMol/L
Monocytes
4 – 13%
Eosinophils
1 – 3%
Protein
6.0 – 8.0 mg/dL
Basophils
0 – 1%
Albumin
3.5 – 5.5 g/dL
Reticulocyte count
0.5-1.5%
Total bilirubin
0.2 – 1.0 mg/dL
URINALYSIS
Dir. bilirubin
0.0 – 0.2 mg/dL
Color
<yellow>
Lipase
10 – 140 U/dL
Turbidity
<clear>
Amylase
25 – 125 U/dL
Specific Gravity
1.003 – 1.035
SGOT/AST
7 – 40 U/L
pH
4.5 – 8.0
SGPT/ALT
7 – 40 U/L
Ketones
<negative>
GGT
9 – 50 U/L
Protein
<negative>
AlkPhos
38 – 126 U/L
Blood
<negative>
Uric Acid
2.0 – 6.9 mg/dL
Glucose
<negative>
LDH
120 – 240 U/L
Nitrite
<negative>
Free T4
0.71 – 1.85 ng/dL
Leukocyte Esterase
<negative>
0.32 – 5.00 IU/mL
20-60 mg/dl
Osmolality
50 – 1400 mOsm/kg
Sodium
40 – 220 mEq/day
2.3-3.5 g/dL
Potassium
25 – 125 mEq/day
pH
7.35 – 7.45
COAGULATION
PaCO2
35 – 45 mmHg
PT
12.3 – 14.2 sec
PaO2
80 – 100 mmHg
PTT
25 – 34 sec
HCO3-
21 – 27 mEq/L
Bleeding Time
2 – 7 min
O2 Saturation
95 – 98%
Thrombin Time
6.3 – 11.1 sec
Base Excess
 2 mEq/L
Fibrinogen
200 – 400 mg/dL
TSH
Ceruloplasmin
Globulin
ARTERIAL BLOOD GASES
Iron
TIBC
Ferritin
31-184 mcg/dL
235-434 mcg/dL
10-320 ng/mL
Folate
B12
7-24
ng/mL
200-1000 pg/mL
Renal Professor Hints Assessment 11
1/12/11
Hey Everybody:
I know we are all feeling a little elated and pressured all at the same time but I just wanted to send a quick
note about the renal pathophysiology review. Not many people attended the review yesterday and I had
assumed it would be the standard review of past questions too but it was not. It was actually a review but
only lasted about 30-40 minutes.
Dr. Wall stated the following:
Know high yield topics from the module pages 102-108
Know the lecture on renal syndromes pages 446-463 (I believe this was covered in the last review very
well too).
Know urine analysis results and interpretation.
1. He covered briefly TBW and total body Na+.
2. He also covered simple acid base: metabolic, acute and compensated respiratory
acidosis/alkalosis, plasma Anion Gap.
3. There will be at least one GFR question know how creatinine clearance relates to muscle mass
and indications.
4. He covered UA routine findings and indications 3+. protein. RBC and red cell casts: inflammatory
versus not, acute versus chronic.
5. He mentioned again renal syndromes lecture (pp 446-463, problems 21-24).
6. Know Urine anion gap and its implications ( if high e.g. 10 indicates kidneys have a problem)
think RTA.
7. He also said to know where in the kidneys the different diuretics work, loops, hydrochlorothiazide,
etc.
8. Know the common glomerular diseases.
There will be basically 1 question per contact hour and but he did comment that Renal Syndromes and
Urine analysis are probably OVER represented.