Nephrology Flashcards

1
Q

What is the normal protein in urine per 24 hour?

A

<300 mg

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2
Q

A diabetic patient is evaluated with a UA that shows no protein. Microalbuminuria is detected (level between 30 and 300 mg per 24 hours).

What is the next best step in the management of this patient?

a. Enalapril
b. Kidney biopsy
c. Hydralazine
d. Renal consultation
e. Low-protein diet
f. Repeat UA annually and treat when trace protein is detected.

A

A. An ACE inhibitor or angiotensin receptor blocker (eg. losartan, valsartan) is the best initial therapy for any degree of proteinuria in a diabetic patient.

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3
Q

A woman is admitted to the hospital with trauma and dark urine. The dipstick is markedly positive for blood.

What is the best initial test to confirm the etiology?

a. Microscopic examination of the urine
b. Cystoscopy
c. Renal ultrasound
d. Renal/bladder CT scan
e. Abdominal x-ray
f. Intravenous pyelogram

A

A. Hemoglobin and myoglobin make the dipstick positive for blood, but no red cells are seen on microscopic examination of the urine. Abdominal x-ray detects small bowel obstruction (ileus) but is very poor at detecting stones or cancer. Renal CT is the most accurate test for stones, but would not be done until the etiology of the positive dipstick has been confirmed as blood.

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4
Q

Urinary casts shows dysmorphic red cells, what is the most likely diagnosis?

A

Glomerulonephritis

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5
Q

Urinary casts shows white cells, what is the most likely diagnosis?

A

Pyelonephritis

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6
Q

Urinary casts shows eosinophil, what is the most likely diagnosis?

A

Acute (allergic) interstitial nephritis

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7
Q

Urinary casts shows hyaline, what is the most likely diagnosis?

A

Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitates or concentrations into a cast

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8
Q

Urinary casts shows broad, waxy, what is the most likely diagnosis?

A

chronic renal disease

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9
Q

Urinary casts shows granular “muddy-brown”, what is the most likely diagnosis?

A

Acute tubular necrosis; they are collections of dead tubular cells

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10
Q

What is the cause of prerenal azotemia?

A

decreased perfusion

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11
Q

What is the cause of postrenal azotemia?

A

obstruction

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12
Q

What is the cause of intrinsic renal disease?

A

ischemia and toxins

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13
Q

A 20-year-old African American man comes for a screening test for sickle cell. He is found to be heterozygous (trait or AS) for sickle cell.

What is the best advice for him?

a. Nothing needed until he has a painful crisis
b. Avoid dehydration
c. Hydroxyurea
d. Folic acid supplementation
e. Pneumococcal vaccination

A

B. The only significant manifestation of sickle cell trait is a defect in renal concentrating ability or isosthenuria. These patients will continue to produce inappropriately dilute, high-volume urine despite dehydration. Hydroxyurea is used to prevent painful crises when they occur more than 4 times a year. Painful crises rarely occur in sickle cell trait. They do not have hemolysis, so there is no need for additional folic acid supplementation. Splenic function is abnormal only in those who are homozygous, so pneumococcal vaccination is not routinely indicated.

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14
Q

It is an injury to the kidneys from ischemia and/or toxins resulting in sloughing off of tubular cells into the urine. Sodium and water reabsorptive mechanisms are lost with tubular cells. Proteinuria is not significant since protein, not tubules, spills into the urine when glomeruli are damaged.

A

Acute Tubular Necrosis (ATN)

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15
Q

A patient comes with fever and acute, left lower quadrant abdominal pain. Blood cultures on admission grow. E. Coli and Candida albicans. She is started on vancomycin, metronidazole and gentamicin, and amphotericin. She has a CT scan that identifies diverticulitis. After 36 hours, her creatinine rises dramatically.

Which of the following is most likely the cause of renal insufficiency?

a. Vancomycin
b. Gentamicin
c. Contrast media
d. Metronidazole
e. Amphotericin

A

C. Radiographic contrast media has a very rapid onset of injury. Creatinine rises the next day. Vancomycin, gentamicin, and amphotericin are all potentially nephrotoxic, but they would not cause renal failure with just 2 or 3 doses. They need 5 to 10 days to result in nephrotoxicity. Metronidazole is hepatically excreted and does not cause renal failure.

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16
Q

A 74-year-old blind man is admitted with obstructive uropathy and chest pain. He has a history of hypertension and diabetes. His creatinine drops from 10 mg/dL to 1.2 mg/dL 3 days after catheter placement. The stress test shows reversible ischemia.

What is the most appropriate management?

a. Coronary artery calcium score on CT scan
b. One to two liters of normal saline hydration prior and during angiography.
c. N-acetylcysteine prior to angiography
d. Mannitol during angiography
e. Furosemide during angiography
f. Intravenoous sodium bicarbonate before and during angiography

A

B. Saline hydration has the most proven benefit at preventing contrast-induced nephrotoxicity. Mannitol and furosemide may or may not prevent nephrotoxicity. There is minimal data to support their use.

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17
Q

A patient with mild renal insufficiency undergoes angiography and develops a 2 mg/dL rise in creatinine from ATN despite the use of saline hydration before and after the procedure.

What do you expect to find on laboratory testing?

a. Urine sodium 8 (low), FENa > 1%, urine specific gravity 1.035 (high)
b. Urine sodium 58 (high), FENa >1%, urine specific gravity 1.005 (low)
c. Urine sodium 5 (very low), FENa <1%, urine specific gravity 1.040 (very high)
d. Urine sodium 45 (high), FENa > 1% urine specific gravity 1.005 (low)

A

C. Although contrast-induced renal failure is a form of ATN, the urinary lab values are an exception from the other forms of ATN. Contrast causes spasm of the afferent arteriole that leads to renal tubular dysfunction. There is tremendous reabsorption of sodium and water, leading the specific gravity of the urine to become very high. This results in profoundly low urine sodium. The usual finding in ATN from nephrotoxins would be UNa above 20, FENa greater than 1%, but a low specific gravity. Specific gravity correlates with urine osmolality.

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18
Q

A patient with extremely severe myeloma with a plasmacytoma is admitted for a combination chemotherapy. Two days later, the creatinine rises.

What is the most likely cause?

a. Cisplatin
b. Hyperuricemia
c. Bence-Jones proteinuria
d. Hypercalcemia
e. Hyperoxaluria

A

B. Two days after chemotherapy, the creatinine rises in a person with a hematologic malignancy. This is most likely from tumor lysis syndrome leading to hyperuricemia. Cisplatin, as with most drug toxicities, would not produce a rise in creatinine for 5 to 10 days. Bence-Jonces protein and hypercalcemia both cause renal insufficiency, but it would not happen as a result of treatment. Treatment for myeloma would end up decreasing both the calcium and Bence-Jonce protein levels because they are produced from the leukemic cells. Cancer cells do not release oxalate.

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19
Q

What should be given prior to chemotherapy to prevent renal failure from tumor lysis syndrome?

A

Allopurinol, Hydration, Rasburicase

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20
Q

A patient who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalysis shows an abnormality.

What did she take?

a. Aspirin
b. Acetaminophen
c. Ethylene glycol
d. Ibuprofen
e. Opiates
f. Methanol

A

C. Ethylene glycol is associated with acute kidney injury based on oxalic acid and oxalate precipitating within the kidney tubules causing ATN. Aspirin is renal toxic but does not lower calcium levels and has no abnormality on urinalysis. Acetaminophen is hepatotoxic. Ibuprofen and all NSAIDs are renal toxic by constricting the afferent arteriole, causing allergic interstitial nephritis and papillary necrosis. They have no impact on calcium levels and the only time they would be found in the urine is in the case of papillary necrosis. Papillary necrosis causes sudden flank pain and fever. Methanol causes inflammation of the retina and has no renal toxicity. Opiates by injection are associated with focal-segmental glomerulonephritis, not AKI.

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21
Q

A man comes to the emergency department after a triatlon, followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and the urine is dark. Intravenous fluids are started.

What is the next best step in the management of this patient?

a. CPK level
b. EKG
c. Potassium replacement
d. Urine dipstick
e. Urine myoglobin

A

B. EKG is done to detect life-threatening hyperkalemia. Your question may have “potassium level” as the answer. CPK level, urine dipstick for blood and myoglobin should all be done, but the EKG will see if he is about to die of a fatal arrhythmia from hyperkalemia. Potassium replacement in a person with rhabdomyolysis would be fatal.

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22
Q

What are the indication of dialysis?

A

Fluid

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23
Q

This is renal failure developing secondary to liver disease. Patient usually has severe liver disease (cirrhosis), new-onset renal failure with no other explanation, very low urine sodium (less than 10-15 mEq/dL), FENa below 1%, Elevated BUN:creatinine ratio (greater than 20:1).

A

Hepatorenal Syndrome

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24
Q

What are your treatment options for hepatorenal syndrome?

A

Midodrine
Octreotide
Albumin

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25
Q

This is a form acute renal failure that damages the tubules occurring on an idiosyncratic (idiopathic) basis. Antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders.

A

Acute (Allergic) Interstitial Nephritis

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26
Q

Patient presents with fever, rash, arthralgias, eosinophilia and eosinophiluria, what is the most likely diagnosis?

A

Acute (Allergic) Interstitial Nephritis

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27
Q

This is the most accurate test for Acute (Allergic) Interstitial Nephritis.

A

Hansel or Wright stain

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28
Q

When creatinine continues to rise after stopping the offending drug in Acute (Allergic) Interstitial Nephritis, what should you give?

A

Glucocorticoids (prednisone, hydrocortisone, methylprednisolone)

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29
Q

This is a sloughing off of the renal papillae. It is caused by toxins such as NSAIDs, or sudden vascular insufficiency leading to death of the cells in the papillae and their dropping off the internal structure of the kidney.

A

Papillary Necrosis

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30
Q

This is the best initial test for Papillary Necrosis

A

Urinalysis that shows red and white cells and may show necrotic kidney tissue

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31
Q

What is the most accurate test for Papillary Necrosis?

A

CT Scan that shows the abnormal internal structure of the kidney from the loss of papillae

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32
Q

What are the characteristics of Tubular disease?

A
Acute
Toxins
None nephrotic
No biopsy needed
No steroids
Never add immunosuppressive agents
33
Q

How would you treat tubular diseases?

A

Correct hypoperfusion

Removing the toxin

34
Q

What are the characteristics of Glomerular disease?

A
Chronic
Not from toxins/drugs
All potentially nephrotic
Biopsy sample
Steroids often
35
Q

This type of glomerulonephritis presents with lung and kidney involvement, but there is no upper respiratory tract involvement. There is no skin, joint, GI, eye, or neurological involvement.

A

Goodpasteur Syndrome

36
Q

This is the best initial test for Goodpasteur Syndrome

A

Antiglomerular basement membrane antibodies

37
Q

What is the most accurate test for Goodpasteur Syndrome?

A

Lung or Kidney Biopsy

38
Q

How would you treat Goodpasteur Syndrome?

A

Plasmapheresis and Steroids

39
Q

It is the most common cause of acute glomerulonephritis

A

IgA Nephropathy (Berger Disease)

40
Q

The most accurate test for IgA nephropathy.

A

Kidney Biopsy

41
Q

How would you treat severe proteinura in glomerulonephritis.

A

ACE inhibitors and steroids

42
Q

This is the most common organism leading to postinfectious glomerulonephritis (PIGN).

A

Streptococcus

43
Q

This follows throat infection or skin infection (impetigo) by 1 to 3 weeks and presents with dark (coca-colored) urine, edema that is often periorbital, hypertension, and oliguria.

A

Postinfectious Glomerulonephritis

44
Q

How would you confirm PSGN from group A beta hemolytic streptococci (pyogenes)?

A

Antistreptolysin O (ASO) titers and anti-DNase antibody titers

45
Q

Complement levels are high/low in PSGN

A

low

46
Q

This is a congenital defect of collagen that results in glomerular disease combined with sensorineural hearing loss and visual disturbance from loss of the collagen fibers that hold the lens of the eye in place

A

Alport Syndrome

47
Q

This is a systemic vasculitis of small and medium-sized arteries that most commonly affects the kidney. Virtually every organ in the body can be affected, but it tends to spare the lung. Although it is of unknown etiology, it can be associated with hepatitis B.

A

Polyarteritis Nodosa

48
Q

What organ does PAN spares?

A

Lung

49
Q

This is the best initial test to screen PAN

A

Angiography of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset hypertension and characteristic symptoms

50
Q

This is the most accurate test for PAN

A

Biopsy

51
Q

These are the standard of care for Polyarteritis Nodosa.

A

Prednisone and Cyclophosphamide

52
Q

This is the most accurate test for Lupus Nephritis.

A

Biopsy

53
Q

How would you treat severe Lupus Nephritis

A

Glucocorticoids combined with either Cyclophosphamide or Mycophenolate

54
Q

This is the most accurate test for Amyloidosis.

A

Biopsy

55
Q

What would you see in the biopsy of Amyloidosis.

A

green birefringence with Congo red staining

56
Q

Treatment for Amyloidosis

A

Melphalan and Prednisone

57
Q

This occurs when proteinuria is so massive that the liver can no longer increase the production of albumin to compensate for urinary losses. Maasive proteinuria leads to edema, hyperlipidemia, and thrombosis.

A

Nephrotic Syndrome

58
Q

These are two most common causes of nephrotic syndrome

A

Diabetes and Hypertension

59
Q

This is the best initial test for Nephrotic Syndrome

A

Urinalysis

60
Q

This is the most accurate test to determine the cause of nephrotic syndrome.

A

Renal biopsy

61
Q

What is the best initial therapy for nephrotic syndrome?

A

Glucocorticoids

62
Q

This are agents used to control proteinuria in nephrotic syndrome.

A

ACE inhibitors or ARBs

63
Q

Define Uremia.

A
Presence of:
Metabolic acidosis
Encephalopathy
Hyperkalemia
Pericarditis
64
Q

These are the most common cause of ESRD.

A

diabetes and hypertension

65
Q

TTP/HUS is associated with HIV, cancer, and drugs such as cyclosporine, ticlopidine, and clopidogrel

A

TTP

66
Q

A low ADAMTS 13 level supports the diagnosis of _____

A

TTP

67
Q

How would you treat TTP?

A

Plasmapheresis

68
Q

What is the most common cause of death from PCKD?

a. Intracerebral hemorrhage
b. Stones
c. Infection
d. Malignancy
e. Renal failure

A

E. Renal failure occurs in PCKD from recurrent episodes of pyelonephritis and nephrolithiasis causing progressive scarring and loss of renal function. PCKD does not have malignant potential. Only 10% to 15% of affected people have cerebral aneurysms, most of which do not rupture. Connective tissue is weak throughout the body.

69
Q

This electrolyte imbalance occurs when there is loss of free water (e.g. sweating, burns, fever, pneumonia, diarrhea, and diuretics)

A

Hypernatremia

70
Q

This leads to high-volume water loss from insufficient or ineffective antidiuretic hormone (ADH). Any CNS disorder (stroke, tumor, trauma, hypoxia, infection) can damage the production of ADH in the hypothalamus or storage in the posterior pituitary.

A

Diabetes Insipidus

71
Q

It is a loss of ADH effect on the collecting duct of the kidney. This is caused by lithium or demeclocycline, chronic kidney disease, hypokalemia, or hypercalcemia. They make ADH ineffective at the tubule.

A

Nephrogenic DI

72
Q

This is the best initial test for Diabetes Insipidus.

A

Water Deprivation Test

73
Q

Polyuria and Nocturia

a. Central DI only
b. Nephrogenic DI only
c. A & B
d. none of the above

A

C

74
Q

Urine osmolality and Sodium

a. Low in Central DI
b. Low in Nephrogenic DI
c. High in Central DI
d. High in Nephrogenic DI
e. A & B
f. C & D
g. A & C
h. B & D

A

E

75
Q

Positive water deprivation

a. Central DI only
b. Nephrogenic DI only
c. A & B
d. none of the above

A

C

76
Q

Response to ADH

a. Central DI only
b. Nephrogenic DI only
c. A & B
d. none of the above

A

A

77
Q

ADH level

a. Low in Central DI
b. Low in Nephrogenic DI
c. High in Central DI
d. High in Nephrogenic DI
e. A & B
f. C & D
g. A & C
h. B & D
i. A & D
g. B & C

A

I

78
Q

What is your treatment goal for Central DI?

A

Replace ADH (vasopressin also known as DDAVP)

79
Q

What is your treatment goal for Nephrogenic DI?

A

Correct plasma and calcium
Stop lithium or demeclocycline
Give hydrochlorothiazide or NSAIDs for those having NDI despite these interventions