Nephrology Small Group Questions Flashcards
JD has slowly progressive chronic kidney disease (CKD). The results of 24 hr urine collections in 2008 and 2012 are given below. JD was on a similar diet and fluid intake on both occasions.
2008 2012
body weight (kg) 70 70 serum creatinine (mg/dl) 1.0 2.0 urine flow rate (ml/min) 1.0 0.8 urine creatinine (mg/dl) 100 125
What is the creatinine clearance (GFR) in 2008?
100 mL/min
Cx = (Ux x V) / Px
What does an increase in serum creatinine from 1 mg/dL to 2 mg/dL imply?
Serum creatinine doubled so GFR has decreased by approx 50% due to a loss of functioning nephrons
How is the amount of creatinine produced and excreted calculated?
for creatinine, production = urinary excretion
What determines the amt of creatine a person produces?
muscle mass (differs w/ gender and age)
What determines the amt of creatine in a person’s plasma?
muscle mass and GFR
JD has slowly progressive chronic kidney disease (CKD). The results of 24 hr urine collections in 2008 and 2012 are given below. JD was on a similar diet and fluid intake on both occasions.
2008 2012
body weight (kg) 70 70 serum creatinine (mg/dl) 1.0 2.0 urine flow rate (ml/min) 1.0 0.8 urine creatinine (mg/dl) 100 125
What is the filtered load of creatinine in 2008? In 2012?
FL = GFR x Px
2008: 1 x 100 = 1 mg/min
2012: 2 x 50 = 1 mg/min
Why does creatinine provide a good estimate of GFR?
it is not reabs and only partially secreted (<10%)
*aka the entire filtered load gets excreted
If there has been no change in _______ then a change in serum creatinine conc is due to a change in GFR
muscle mass
How is GFR estimated without 24 hr urine collections? What is a limitation of using this to est GFR?
(140 - age) / Serum Creatinine
(x 0.85 if the pt is female)
limitation: only valid in steady state conditions such as CKD. Invalid in acute kidney injury with abrupt changes in GFR (un-steady state conditions)
Describe the stages of kidney disease (1-5)
1: damage with normal or elev GFR (>90)
2: damage with mildly dec GFR (60-89)
3: moderate dec in GFR (30-59)
4: severe dec GFR (15-29)
5: kidney failure (<15 or dialysis)
What is GFR in which you start to see physical abnormalities?
60 mL/min/1.73m2
Healthy people with 1 kidney or polycystic kidney disease are considered to be stage ___ of CKD
1
An inc in serum creatinine always implies kidney disease.
F: a male body builder can have a SCr of 1.3 with stage 1 disease while a 50 year old woman can have a SCr of 1.3 with stage 3
MUSLCE MASS determines SCr for each indiv
*they have different GFRs –> diff stages of CKD
What effect does urine flow rate have on GFR?
No effect. A change in UFR is simply a reflection of the amt of water which is reabs NOT the amt of water that is filtered at the glomerulus.
T or F: GFR changes with the urine flow rate
F: GFR remains constant at different flow rates
What effect does an inc urine flow rate have on creatinine clearance?
No effect. As flow rate inc the conc of creatinine in the final urine is decreased (bc less water has been reabs) but the amount in the urine is not changed.
What is a clearance ratio? What information does it provide?
= Cx / Clearance of creatinine
It tells you the renal handling of a substance. The closer to 1 the ratio its, the substance is handled more like creatinine (no reabs and little secretion)
What does a low clearance ratio (<1) indicate?
the substance is highly reabs
What does a high clearance ratio (<1) indicate?
the substance is highly secreted
What happens to the urine flow rate and fractional excretion of Na after a hemorrhage?
Both will decrease. Na and H2O to be retained due to hypovolemic state (renin, sympathetic activ, etc)
–> inc osmolarity of urine due to dec H2O excretion
renal blood flow decreases but GFR remains normal (autoreg mech)
T or F: in a mild to moderate hypovolemic state, GFR will decrease.
F: auto-regulatory mechanisms keeps it at normal levels
T or F: in a mild to moderate qhypovolemic state, RPF will decrease.
T
What happens to the clearence of urea in a mild to moderate hypovolemic state?
it will decrease bc urea follows water (in hypovolemia, water reabs increases therefore urea reabs will inc too)
What needs to be checked when a pt is started on a drug that is excreted by the kidneys?
GFR (which assesses renal function). Need to adjust the dosing of the drug to reflect kidney function
(dec GFR/clearance = dec dosage)
A 58 year old female was admitted with moderately severe congestive heart failure. Physical examination revealed bibasilar rales, cardiac enlargement, neck vein distention, hepatomegaly, and 3+ pitting pretibial edema. The serum sodium concentration was 121 meq/l; BUN was 30 mg/dl and hematocrit 33%.
What does the information presented above tell you about total body exchangeable sodium?
nothing can be determined from looking at the serum Na conc in isolation
–> the pitting edema, cardiac enlargement, JVD, and hepatomegaly indicate inc ECFV which requires an inc in exchangeable Na.
A 58 year old female was admitted with moderately severe congestive heart failure. Physical examination revealed bibasilar rales, cardiac enlargement, neck vein distention, hepatomegaly, and 3+ pitting pretibial edema. The serum sodium concentration was 121 meq/l; BUN was 30 mg/dl and hematocrit 33%.
How do you account for the low serum sodium concentration? How is this corrected?
H2O retention that is disproportionate to the retention of Na
corrected by restricting water and salt intake and diuretic therapy
What are the mechanisms leading to the development of edema and other signs of expanded ECFV in association with hyponatremia in a patient with congestive heart failure?
CHF causes dec cardiac output/dec BP. The body senses this as an decrease in ECFV. Therefore the body signals for an inc in Na and H2O reabsorption (activation of renin-aldosterone, sympathetic activation, ADH release) to inc ECFV. WIthout correcting the heart problem, the ECFV will continue to expand.
How does ADH release affect urine osmolarity
ADH release inc Uosm
*H2O is reabs
T or F: In hypervolemia hyponatremia TB sodium is decreased
it is inc but TBW is increased more
SrNa = TB Na / TBW
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
Which of the above data are most helpful in selecting the proper therapy?
change in BW and signs of volume depletion
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
What is the most likely explanation for the disparity in BUN and serum creatinine concentration?
Urea travels with water. Therefore if more water is being reabs, urea will also be reabs and the BUN will increase. This does not happen with creatinine
Why is volume depletion often assc with an increase in BUN?
In volume depletion,water is being conserved. Urea travels with water. Therefore if more water is being reabs, urea will also be reabs and the BUN will increase.
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
If fluid is to be administered intravenously, how much and what type should be given? Assume that the serum sodium concentration prior to the onset of vomiting was 145 meq/l.
Math is wrong?
Prior to volume depletion:
BW= 140 pounds (63.6 kg)
TBW = 38.2 liters.
TBosm = 38.2 x 145 meq/l = 5539 meq.
After volume depletion:
BW = 140 - 5.9 =
TBW = 38.2-5.9 = 32.3 liters.
TBosm = 32.3 x 132 meq/l = 4264 meq.
Subtracting this quantity from 5539 meq reveals the total cation deficit to be 1275 meq. This is equivalent to the total body sodium deficit.
The sodium deficit can be corrected by administration of 0.9% sodium chloride intravenously over a period of 3-4 days, as determined by frequent assessment of the patient’s status by physical examination. Additional fluid administration as 0.45% sodium chloride or 5% dextrose will be necessary to replace “insensible” and continuing urinary loss of water.
A 53 year old male was admitted to the hospital after having been seen in the Nephrology Clinic with a history of persistent hyponatremia. He denied any history of shortness of breath but admitted to a 30-pack year history of cigarette smoking. The patient was thin and appeared chronically ill. Examination of the chest revealed scattered expiratory rhonchi but no cardiac enlargement. There was no hepatomegaly or ankle edema. Skin turgor was normal.
What does the physical examination tell you about the possible cause of the hyponatremia?
no physical signs of ECFV excess (no cardiac enlargement, no hepatomegaly, and no edema)
No signs of volume depetion
hyponatremia with normal volume suggests a problem in water handeling, especially if renal function is normal.
BP: 145/95 mmHg. Serum sodium: 118 meq/l potassium: 4.1 meq/l chloride: 85 meq/l bicarbonate: 25 meq/l BUN: 5 mg/dl creatinine: 0.8 mg/dl glucose: 109 mg/dl Urine osmolality: 317 mosm/kg H20 urine sodium: 88 meq/l
Which laboratory values are most helpful in assessment of the possible mechanism(s) in the development of hyponatremia?
Plasma osmolarity is too low ( SIADH
SIADH can be Dx bc…
- normal renal function (~SCr)
- no physical findings that suggest hypovolemia
- slightly elevated BP
*SIADH = inappropriate ADH secretion
What is the etiology of SIADH?
malignant tumors (esp bronchogenic carcinoma) infectious diseases Endocrinologic abnormalities (adrenal, pituitary, and thyroid probs)
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
If you are volume depleted, what happens to urine sodium?
it should be absent (bc your body is trying to conserve it)
What is the etiology of SIADH?
malignant tumors (esp bronchogenic carcinoma) infectious diseases indocrinologic abnormalities (adrenal, pituitary, and thyroid probs)
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
What is the most frequent cause of hypernatremia in the elderly,immobilized, or demented individuals?
inadequate fluid intake
*esp people
If the pt is inadequate fluid intake, will inc ADH restore the ECFV?
no, be there is no water present for the ADH to move
An 81 year old male with previously known dementia was admitted to hospital because of disorientation, confusion, and increasing unresponsiveness. One month earlier he had fallen at home and fractured his left hip, requiring orthopedic surgical treatment. At that time:
BW: 70 kg
Serum sodium:140 meq/l
Following this he was no longer ambulatory at home and his wife stated that it was difficult to get him to eat or drink more than small quantities of fluid. On admission to the hospital he was described as being thin and debilitated, with no edema.
BP: 120/76 mmHg
Serum sodium: 173 meq/l
Assuming no change in total body exchangeable sodium, what was the deficit in total body water on admission? What was the effect on extracellular and intracellular fluid volume?
use eq: Sr Na = TBna / TBW
t = 0:
TBW = (70)(0.6) = 42 L
ECF: (42)(1/3) = 14 L
ICF: (42)(2/3) = 28 L
TBNa = (42)(140) = 5880 meq
t = +1 month:
TBW = 173/5880 = 34 L
ECF = (34)(1/3) = 11.3 L
ICF = (34)(2/3) = 22.6 L
Tota water loss = 42 - 34 = 8 L
Both ICF and ECF dec by 19%
T or F: when hypernatermia is due to water deficit only, the percentage change in the ECF and ICF are equal
T
What is the treatment for a pt with severe hypernatremia due to water deficit only?
IV 5% dextrose given slowly (should not exceed 0.5 to 1 meq/hr)
When is an infusion of sodium containing soln indicated?
when there is a combined water and sodium deficit
when the pt is hemodynamically unstable
What is osmotic diuresis?
increase in the solute load of the tubule obligates water to be excreted
What is the osmolarity of isotonic urine?
300 mOsm
