Renal 2

Question 1

What are 6 common causes of nephrotic syndrome?

Answer 1

1. minimal change disease
2. focal segmental glomerulosclerosis
3. membranous nephropathy
4. membranoproliferative glomerulonephritis
5. diabetes mellitus
6. systemic amyloidosis

Question 2

What is the most common cause of nephrotic syndrome in:

a. children
b. Hispanics and African Americans
c. Caucasion adults

Answer 2

a. minimal change disease
b. focal segmental glomerulosclerosis
c. membranous nephropathy

Question 3

What is the cause of minimal change disease?

Answer 3

Usually idiopathic, but may be associated with Hodgkin lymphoma

Question 4

What is the cause of focal segmental glomerulosclerosis?

Answer 4

Usually idiopathic, but may be associated with:

HIV
heroin use

sickle cell disease

Question 5

How do minimal change disease and focal segmental glomerulosclerosis differ with regard to treatment?

Answer 5

Minimal change disease shows an excellent response to steroids, while focal segmental glomerulosclerosis shows poor response to steroids (and can progress to chronic renal failure).

Question 6

Why does minimal change disease show an excellent response to steroids?

Answer 6

The damage in minimal change disease is mediated by cytokines from T cells–steroids stop the production of cytokines.

Question 7

Normal glomeruli are observed on H&E stain, effacement of foot processes is seen on electron microscopy, and the immunofluorescence is negative (no immune deposits). What is the likely diagnosis?

Answer 7

minimal change disease

these are the classical histopathologic findings

Question 8

What are the classic histopathologic findings with minimal change disease?

Answer 8

1. normal glomeruli on H&E stain
2. effacement of foot process on EM
3. Negative IF, no immune deposits

Question 9

Minimal change disease is a cause of nephrotic syndrome. What type of protein loss is observed in this disease?

Answer 9

Selective protein loss: loss of albumin, but not immunoglobulin.

Question 10

Histopathology for a patient shows focal and segmental sclerosis of the glomeruli on H&E stain, effacement of foot processes on EM, and a negative IF (no immune complex deposits). With what risk factos is this disease associated?

Answer 10

This is focal segmental glomerulonephritis.

This disease is usually idiopathic, but it is associated with HIV infection, heroin use, and sickle cell disease.

Question 11

Which two causes of nephrotic syndrome are associated with immune complex deposition?

Answer 11

1. membranous nephropathy
2. membranoproliferative glomerulonephritis

Question 12

What is the cause of membranous nephropathy?

Answer 12

Usually idiopathic, but may be associated with:

Hep B or C

Solid tumors

SLE

Drugs (NSAIDS, penicillamine)

Question 13

What is the most common cause of death in SLE patients?

Answer 13

Renal failure

Question 14

What is the most common disorder SLE patients get within the kidney?

Answer 14

Diffuse nephritic glomerulonephritis, a nephritic syndrome

Question 15

A patient shows a thick glomerular basement membrane on H&E, has a positive IF (positive for immune complex deposition), and has a “spike and dome” appearance on EM. What is the likely diagnosis?

Answer 15

membranous nephropathy

Question 16

What is the functional unit of the glomerulus? What holds these units together?

Answer 16

The functional unit of the glomerulus is lobules, which are held together by mesangial cells.

Question 17

What is anuria?

Answer 17

A lack of urine production, defined in practice as the passage of <100mL of urine/day

Question 18

A 19 yo woman is brought to the ED b/c of a crush injury that occurred when a bookshelf fell on her abdomen and legs. Physical exam shows mutliple bruises on the lower abdomen and thighs. 2 days later, she develops generalized edema. Lab studies show a rise in creatinine from 1-4 mg/dL. She is aggressively hydrated, but remains oliguric. Why has her creatinine increased from 1-4 mg/dL?

Answer 18

This woman has suffered a crush injury, which can result in two prominent sequelae:

(1) hyperkalemia
(2) acute renal failure secondary to myoglobinuria.

The increased creatinine is a sign that she is experiencing renal failure secondary to myoglobinuria from the crush injury.

Question 19

What is the mechanism of action of furosemide?

Answer 19

Furosemide is a loop diuretic that inhibits the Na/K/2Cl“mega transporter” in the thick ascending loop of henle.

Due to this mechanism, furosemide can induce massive diuresis.

It is not a K+-sparing diuretic

Question 20

A 19 yo woman is brought to eh ED b/c of a crush injury that occurred when a bookshelf fell on her abdomen and legs. Physical exam shows mutliple bruises on the lower abdomen and thighs. 2 days later, she develops generalized edema. Lab studies show a rise in creatinine from 1-4 mg/dL. She is aggressively hydrated, but remains oliguric. Which of the following drugs is most likely contraindicated in this patient?

a. acetazolamide
b. furosemide
c. hydrochlorothiazide
d. mannitol
e. spironolactone

Answer 20

spirololactone

This woman has a cruch injury, and may develop hyperkalemia as the injured cells release K+ into the blood. Spirololactone is an aldosterone receptor inhibitor and therefore a K+-sparing diuretic. This will exaccerabte the hyperkalemia. Hyperkalemia can lead to arrythmia, which can be fatal

Question 21

What is the mechanism of actino of hydrochlorothiazide?

Answer 21

Hydrochlorothiazide inhibits resorption of NaCl in the early distal convoluted tubule.

Question 22

What is the pharmacological mechanism of action of mannitol in the kidney?

Answer 22

Mannitol is an osmotic diuetic.

It is contraindicated in anuria.

Question 23

What is the mechanism of action of acetazolamide?

Answer 23

Stimulated diuresis by inhibiting carbonic anhydrase in the proximal convoluted tubule and preventing the reabsorption of bicarbonate.

Due to its mechanism, this drug has the potential to cause metabolic acidosis.

Question 24

A 66 yo man is brought to the ED b/c of nausea, vomiting, and malaise. His records show he had an MI 4 weeks ago and recently completed treatment for a lower respiratory tract infection. Labs show a serum creatinine of 4.8 mg/dL. What is the cause of this man’s nausea, vomiting, and malaise?

Answer 24

Azotemia (increase in notrogenous waste products in the blood)

*The initial symptoms in acute renal failure are commonly due to the presence of azotemia.

Question 25

What is acute renal failure?

Answer 25

ARF is defined as a sudden decrease in renal function, resulting in an inability to maintain fluid and electrolyte balance and excrete nitrogenous wastes.

Question 26

What is the most common cause of acute renal failure?

Answer 26

Prerenal azotemia, which is due to renal hypoperfusion (decreased blood flow to the kidneys)

Question 27

What are 3 causes of decreased renal perfusion?

Answer 27

1. change in vascular resistance
2. decrease in intravascular volume (hypovolemia)
3. decreased cardiac output (e.g., cardiac failure, CHF)

Question 28

Prerenal azotemia, which occurs due to hypoperfusion of the kidney, can be due to changes in vascular resistance. Name four causes of a change in vascular resistance that lead to renal hypoperfusion.

Answer 28

1. sepsis
2. anaphylaxis
3. anesthesia
4. ACE inhibitors

Question 29

How do ACE inhibitors lead to renal hypoperfusion?

Answer 29

Angiotensin II (the product of ACE), leads to efferent renal arteriolar constriction out of proportion to its effect on the afferent arteriole. This leads to increased glomerular hydrostatic pressure, and increased GFR.

ACE inhibitors, therefore, disproportionately prevent the efferent renal arteriole from contricting as compared to the afferent. This leads to a decreased in the GFR and renal hypoperfusion.

Question 30

What is the normal range for serum creatinine?

Answer 30

0.8-1.4 mg/dL

Question 31

What is the typical presentation of acute interstitial nephritis?

Answer 31

Oliguria, fever, and rash that starts days to weeks aftger starting the offending drug.

Eosinophils are seen in the urine.

Question 32

How do you treat acute interstitial nephritis?

Answer 32

Treatment consists primarily of

supportive measures

removing the inciting drug

corticosteroids (e.g., prednisone)

Question 33

What drugs are known to cause acute interstitial nephritis?

Answer 33

NSAIDS

Antibiotics (penicillins, cephalosporins, sulfonamides)

diuretics (furosemide, thiazides)

phenytoin

allopurinol

cimetidine

proton pump inhibitors

Question 34

A 72 yo woman is brought to the ED b/c of periorbital edema, a maculopapular rash on her chest, and a fever (101). She has a hx of HTN, DM, and osteoarthritis. Labs show increased BUN and Cr. Urinalysis shows mild proteinuria and eosinophils. What is the likely diagnosis?

Answer 34

Acute Interstitial Nephritis.

classically presents with oliguria (increased BUN and Cr; edema), rash, and fever days to weeks after the inciting drug; eosinophils are seen in the urine.

Question 35

What is the normal range for serum K+, Na, Cl, and HCO3?

Answer 35

K+: 3.5-5 mEq/L

Na: 137-145 mEq/L

Cl: 98-110 mEq/L

HCO3: 22-26 mEq/L

Question 36

A 68 yo woman comes to the physician for a routine exam. She says that she occasionally has swelling of her ankles and cramping in her lower legs. Treatment with a diuretic is begun. What class of diuretic should be used in her case?

Answer 36

A K+-sparing diuretic; her K is low (normal is 3.5-5 mEq/L)

Potassium-sparing diuretics act on the principle cells of the cortical collecting duct, by either inhibiting the aldosterone receptor (spironolactone), or by inhibiting the Na+ channel on the lumenal membrane (amiloride, triemterene)

Question 37

What is the mechanism of action of spironolactone?

Answer 37

This acts by cometitively inhibiting the aldosterone receptor in the cortical collecting duct.

Question 38

What is the medial umbilical ligament?

Answer 38

The adult derivative of the distal portion of the umbilical artery

Question 39

What is the medial umbilical fold?

Answer 39

The fold of the parietal peritonem that covers the medial umbilical ligament, which is the adult derivative of the umbilical artery.

Question 40

What is the median umbilical ligament?

Answer 40

The urachus, which is the adult derviative of the allantoic duct. This passes from the upper end of the bladder to the umbilicus.

Question 41

What is the median umbilical fold?

Answer 41

The fold of the peritoneum that covers the median umbilical ligament, the adult derivative of the urachus.

Question 42

A 1 week old newborn is brought into the ED b/c of fluid draining from his umbilicus. Phys exam shows no abnormalities except clear fluid that is pooled around the umbilical stump. Labs of the fluid show a pH of 6.0, specific gravity of 1.020, 1-2 epithelial cells/hpf, and no leukocytes, RBCs, or hemoglobin. What is the fluid that is pooling around the umbilical stump? What patent embryonic structure is this fluid passing through?

Answer 42

The fluid is urine.

It’s passing through the median umbilical ligament, the adult derivative of the urachus. Failure of the urachus to close –> leaking of urine through the neonate’s umbilicus.

Question 43

A newborn has difficulty breathing. Phys. exam shows flattened facial features, low-set ears, and deformities of the feet. A chest X-ray shows pulmonary hypoplasia. The pregnancy was complicated by severe oligohydramnios. What is the patient’s condition? What is this condition a result of?

Answer 43

This patient has bilateral renal agenesis –> oligohydramnios –> Potter’s sequence.

Question 44

Renal agenesis is due to malformation of what embryonic structure?

Answer 44

The ureteric buds.

The ureteric buds form the ureters, renal pelvis, calyces, and collecting tubules. The collecting tubules induce the formation of metanephric vesicles, which differentiate into the tubular components of the nephron.

Question 45

What is renal agenesis?

Answer 45

Absent kidney formation, which may be unilateral or bilateral.

Question 46

What is the result of bilateral renal agenesis?

Answer 46

This leads to oligohydramnios, which leads to:

lung hypoplasia

flat face

low-set ears

developmental defects of the extremities

This is known as Potter’s sequence and is incompatible with life.