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Internal Medicine Board Review > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Which lab findings suggest that hematuria is caused by GN?

A

The presence of hematuria associated with red cell casts, dysmorphic red cells, or proteinuria suggest GN as a cause.

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2
Q

What are the causes of BUN:Cr ratio of >20?

A

BUN:Cr ratio >20 is caused by prerenal azotemia or increased protein breakdown.

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3
Q

What is the definition of oliguria? Anuria?

A

Oliguria is defined as urine output <0.5ml/kg/hour for at least 6 hours. Anuria is <50ml/day of urine output.

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4
Q

What is the underlying cause of prerenal kidney injury?

A

Prerenal kidney injury is due to underperfusion of the kidneys, either from true loss of volume or decreased effective arterial blood volume.

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5
Q

What causes do you consider in a patient with hypertension and hypokalemia?

A

Renal artery stenosis or fibromuscular dysplasia should be considered in a patient with hypertension and hypokalemia.

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6
Q

With postrenal AKI, how does the amount of urine produced relate to the degree of obstruction?

A

In patients with postrenal AKI, the amount of urine produced does not correlate to the degree of obstruction as some patients will have a postobstructive diuresis and in some patients with obstruction the chronic damage to the tubules impairs their ability to reabsorb water and solutes.

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7
Q

Drug-induced ATN is usually due to which 2 major nephrotoxins?

A

IV contrast, amphotericin, and aminoglycosides are major drug causes of ATN.

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8
Q

What are some manifestations of cholesterol emboli?

A

Clinical features of atheroembolic disease include livedo reticularis, eosinophilia, low complement levels, and a step-wise increase in creatinine.

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9
Q

What are Hollenhorst plaques?

A

Hollenhorst plaques are cholesterol emboli to the retinal arterioles. They appears as orange-white dots interrupting the circulation.

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10
Q

Characterize the clinical presentation of acute interstitial nephritis.

A

Acute interstitial nephritis is usually a drug hypersensitivity reaction leading to fever, eosinophilia and rash.

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11
Q

The biopsy picture of AIN due to NSAIDs resembles which glomerulonephropathy?

A

The biopsy picture of AIN due to NSAIDs resembles minimal change disease.

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12
Q

What is the definition of nephrotic range proteinuria?

A

Nephrotic range proteinuria is defined as >3.5 gm/day of proteinuria.

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13
Q

What are the systemic complications of nephrotic syndrome?

A

The complications of nephrotic syndrome include hypoalbuminemia, hypogammaglobulinemia, and hypercoagulability (due to loss of anti-thrombin III).

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14
Q

What are the complement levels in patients with PIGN?

A

Complement levels are low in patients with PIGN, and they remain low for 6-8 weeks.

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15
Q

Poststreptococcal GN can occur after streptococcal infection at which sites?

A

Poststreptococcal GN can follow streptococcal infection of the throat or skin.

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16
Q

Symptoms of GN due to streptococcal infection start how long after the initial infection?

A

Symptoms of PIGN start 1-6 weeks after infection. This contrasts to IgA nephropathy which begins concurrent with the pharyngitis (synpharyngitic).

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17
Q

What infections are associated with development of IC-mediated MPGN?

A

Hepatitis C and hepatitis B are associated with immune-complex mediated MPGN.

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18
Q

When does the GN due to IgA nephropathy present, relative to an inciting viral illness?

A

Glomerulonephritis due to IgA nephropathy presents concurrent with the viral illness.

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19
Q

What are the findings on renal biopsy in patients with IgA nephropathy?

A

Renal biopsy in IgA nephropathy shows deposition of IgA and complement in the mesangium and glomerular capillaries on immunofluorescence staining.

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20
Q

In addition to anti-GBM antibodies, which other feature defines Goodpasture syndrome?

A

In addition to anti-GBM antibodies, patients with Goodpasture syndrome also have pulmonary involvement often presenting with hemoptysis.

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21
Q

How are anti-GBM diseases diagnosed?

A

Anti-GBM antibodies in the serum establish a diagnosis of anti-GBM disease. Renal biopsy can also establish the diagnosis by revealing anti-GBM IgG deposited in a linear fashion along the glomerular basement membrane.

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22
Q

RPGN has which hallmark finding on renl biopsy?

A

The hallmark biopsy finding in RPGN is crescents from collapsing glomerulonephritis.

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23
Q

What are the 3 categories of RPGN, based on underlying mechanisms?

A

The 3 categories of RPGN include:

  1. Anti-GBM antibodies
  2. Immune complex deposition (IgA deposits, ANA, cryoglobulins, or antibodies against an infectious agent)
  3. No evidence of immune deposits (“pauci-immune”)
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24
Q

What is the empiric treatment for RPGN?

A

RPGN should be treated with high dose methylprednisolone followed by prednisone + cyclophosphamide +/- plasmapheresis (if pulmonary hemorrhage).

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25
What drugs and diseases are associated with minimal change disease?
Most MCD is idiopathic, but it may also be associated with drugs (NSAIDs, lithium) and lymphomas.
26
“Maltese crosses” under polarized light are seen in the urine sediment of patients with what process?
“Maltese crosses” under polarized light microscopy represent oval fat bodies and are seen in nephrotic syndrome.
27
FSGS is found in what patient groups?
FSGS is the most common cause of nephrotic syndrome in African Americans. It is also associated with HIV, heroin use, obesity, sickle cell disease, and chronic vesicoureteral reflux.
28
Solid tumors are associated with which glomerular disease?
Solid tumors are associated with membranous nephropathy.
29
Which RTA is associated with diabetic nephropathy?
Diabetes is associated with type 4 RTA.
30
What is the classic finding seen on renal biopsy in a patient with diabetic nephropathy?
Renal biopsy in diabetic nephropathy shows expansion of the mesangium, thickening of the GBM, and sclerosis of the gloeruli (termed the Kimmelstiel-Wilson lesion).
31
What is the definition of microalbuminuria?
Microalbuminuria is low-grade proteinuria in the range of 30-300mg/dl.
32
When are glucocorticoids not used to treat nephrotic syndrome?
Glucocorticoids are useful in treatment of all types of nephrotic syndrome except those caused by diabetes and amyloidosis.
33
What is the definition of chronic kidney disease and what are its stages?
``` Chronic kidney disease is defined as either: 1. kidney damage >3 months, with or without decreased GFR, with either pathological abnormalities or markers of kidney damage or 2. GFR<60 for >3 months with or without kidney damage. Stages of CKD: Stage 1: GFR >90 but with microalbuminuria present Stage 2: GFR 60-89 Stage 3a: GFR 45-59 Stage 3b: GFR 30-44 Stage 4: GFR 15-29 Stage 5: GFR <15 or on dialysis ```
34
What is the effect of hyperphosphatemia in patients with CKD?
Hyperphosphatemia is associated with increased risk of death and heart disease, even in patients without CKD - but especially in those with stage 3-5 CKD.
35
Which bone disorders can be caused by CKD?
Patients with CKD can have 3 types of bone disease. 1. Osteitis fibrosa cystica due to secondary hyperparathyroidism (high bone turnover disease). 2. Adynamic bone disease dues to oversuppression of PTH release (low bone turnover disease) often caused by overtreated of #1. 3. Osteomalacia, a low bone turnover disease associated with unmineralized bone.
36
Which phosphate binders should be used in the hypercalcemic patient?
Non-calcium-based phosphate binders should be used in the hypercalcemic patient to prevent suppression of PTH and development of adynamic bone disease.
37
How is adynamic bone disease different from secondary hyperparathyroidism?
In adynamic bone disease the PTH is suppressed by hypercalcemia. In secondary hyperparathyroidism the hyperphosphatemia and normal/low calcium drive icnreased PTH release.
38
What are the signs/symptoms of uremia?
Signs and symptoms of uremia include anorexia, nausea/vomiting, pericardial and pleural effusions, hemorrhagic pericarditis, platelet dysfunction and bleeding, pruritis, sensory neuropathies, and CNS dysfunction.
39
How is normochromic-normocytic anemia in CKD treated?
Normochromic-normocytic anemia in CKD is treated with erythropoiesis stimulating agents if the Hgb is <10.
40
What is the risk of gadolinium use in the patient with CKD?
Use of gadolinium in CKD can cause nephrogenic systemic sclerosis, a devastating and irreversible condition.
41
When is dialysis initiated in a CKD patient?
Dialysis is initiated in a CKD patient when they have a GFR<15 and develop symptoms of uremia.
42
What is the most common cause of death in the dialysis patient?
The most common cause of death in a dialysis patient is cardiovascular disease. The second leading cause of death is infection.
43
What organisms are associated with peritonitis in the patient on CAPD?
Peritonitis in a CAPD patient is most commonly due to Gram-positive skin organisms (S. epidermidis and S. aureus) followed by Gram-negative organisms.
44
Which immunomodulators are used in kidney transplant patients?
Following renal transplant most patients are treated with triple immunosuppression with 1. a calcineurin inhibitor, 2. mycophenolate mofetil, and 3. a corticosteroid.
45
What is the most common presenting symptom of polycystic kidney disease?
Most patients with PCKD present in their 20s with microscopic hematuria.
46
When is a renal cyst considered benign?
Renal cysts are considered benign when they appear simple on U/S and the patient is asymptomatic. Simple cysts have well-defined margins, dense (compressed) surrounding tissues and no solid component.
47
Which antiretroviral drug causes renal stones?
The HIV drug indinavir can cause renal stones.
48
Name the common causes of calcium stones.
Calcium phosphate stones are more common in those with primary hyperparathyroidism, taking acetazolamide, and with distal (Type 1) RTA. High urinary oxalate excretion causing calcium oxalate stones is seen in those taking large amounts of vitamin C, steatorrhea, and those with uricosuria (because uric acid crystals can act as a nidus for stone formation.
49
Which bacteria cause staghorn calculi?
Struvite stones are seen with UTIs with urease producing bacteria such as Proteus and Klebsiella.
50
Name one of the most important general recommendations for patients with kidney stones, regardless of the type of stones.
Renal stone producers should drink enough fluids to promote 2L/day of urine output regardless of the type of stone.
51
What effect does respiratory rate have on pH?
Respiratory rate affects pCO2 and thus can rapidly affect acid-base levels. Renal changes to compensate for changes in pH occur much more slowly.
52
What is the calculation used to determine the serum osmolality? The osmolal gap?
Osm = 2[Na] + glucose/18 + BUN/2.8. Osmolal gap = measures osm - calculated osm.
53
Which poisonings cause and increased OG and normal AG?
Isopropyl alcohol, acetone, and ethanol all cause an elevated osmolal gap with normal anion gap.
54
Which poisonings cause both an increased AG and OG?
Methanol, ethylene glycol, and propylene glycol all elevate both the osmolal gap and the anion gap.
55
What are the causes of HAGMA?
Four common causes of HAGMA include: ketosis, uremia, lactic acidosis, and toxins.
56
Which abnormality is sometimes noted in the urine of patients who have ingested ethylene glycol?
Calcium oxalate crystals are often seen in the urine of patients with ethylene glycol ingestion.
57
What are the potential PE findings in a patient who has ingested methanol?
Patients with methanol ingestion may have visual changes, often described as walking through a snowstorm.
58
What is the treatment for methanol and ethylene glycol ingestions?
The standard treatment of both methanol and ethylene glycol toxicity are fomepizole and dialysis.
59
What are the 2 main causes of NAGMA?
The two main causes of NAGMA are GI losses of bicarbonate and RTA.
60
Which cause of NAGMA also causes hyperkalemia?
A patient with NAGMA and hyperkalemia most likely has type 4 RTA (hyperaldosteronism).
61
What are the most important regulators of ADH secretion from the posterior pituitary?
The two most important regulators of ADH secretion are 1. osmoreceptors in the hypothalamus, and 2. volume receptors in the left atrium and blood vessels.
62
Name 2 causes of hyperosmolar hyponatremia.
Hyperglycemia and mannitol are two common causes of hyperosmolar hyponatremia.
63
For each 100mg/dl increase in glucose over 100, how should you correct the serum sodium lab result?
For each 100mg/dl rise in glucose the sodium concentration decreases by 1.6mEq/L.
64
What are the causes of low-volume hypoosmolar hyponatremia?
Low-volume hypoosmolar hyponatremia is caused by diuretics, GI losses, 3rd spacing of fluids, and primary adrenal insufficiency (Addison disease).
65
What are the causes of high-volume hypoosmolar hyponatremia?
High-volume hypoosmolar hyponatremia is caused by CHF, cirrhosis, and nephrotic syndrome, or acute or chronic renal failure.
66
What drugs cause SIADH?
The most common drugs associated with SIADH are NSAIDs, SSRIs, carbamazepine, psychotropic drugs.
67
Which endocrinopathies must be ruled out in all patients with hyponatremia?
Hypothyroidism and glucocorticoid deficiency need to be ruled out in all patients with hyponatremia.
68
What is the suggested rate of correction for severe hyponatremia?
The goal of correction of hyponatremia is 4-6mEq/L over the first 24 hours and should not exceed 9mEq/L over 24 hours.
69
When is osmotic demyelination syndrome most likely to occur?
Osmotic demyelination syndrome is most likely to occur in a patient with chronic, sever hyponatremia (Na<115 for >2 days) whose sodium is corrected rapidly (>10mEq/L over 24 hours).
70
What is the usual cause of hypernatremia?
Hypernatremia always represents a water deficits. It usually occurs when a patient has decreased access to water or if the thirst mechanism is defective.
71
What is the usual serum sodium in a patient with DI who has access to water?
The DI patient with access to water usually has a normal to borderline high sodium.
72
Which tubule is the most permeable to water?
The proximal tubule is most permeable to water which follows Na and Cl absorption.
73
Which tubule sets up the osmotic gradient for the thin, descending limb of the loop?
The active transport of solutes into the interstitium by the thick, ascending limb of the loop of Henle sets up the osmotic gradient in the interstitium.
74
Where do loop diuretics exert their effect?
Loop diuretics cause diuresis by preventing Na reabsortion in the thick ascending segment of the loop of Henle.
75
Which diuretics are less effective in patients with poor kidney function?
Thiazides are less effective in patients with poor kidney function because they have to be secretes into the filtrate to be effective.
76
Which 2 hormones exert their effects in the distal tubules?
Aldosterone and ADH exert their effects in the distal tubules.
77
What is the serum potassium level in distal Type 4 RTA?
Serum potassium is elevated in type 4 RTA.
78
Which RTA can cause renal stones?
Type 1 RTA is associated with renal stones due to hypercalciuria.
79
Multiple myeloma is associated with which RTA?
Multiple myeloma is associated with type 2 RTA.
80
Diabetic nephropathy causes which RTA?
Diabetic nephropathy causes type 4 RTA.
81
Which potassium derangement can be seen in Cushing syndrome?
Hypokalemia is seen in Cushing syndrome.
82
Addison disease causes which type of potassium derangement?
Addison disease is associated with hyperkalemia.
83
Discuss the effects of NSAIDs on serum potassium.
NSAIDs typically decrease renin, so they make the potassium go up - but generally only if the patient has pre-existing renal issues.
84
How does acid-base status affect potassium levels?
Alkalosis, beta-agonists, and insulin increase potassium uptake into cells leading to hypokalemia. Acidosis, alpha-agonists, and beta-blockers decrease potassium uptake into cells leading to hyperkalemia.
85
What EKG changes are seen with hyperkalemia?
The sequence of ECG changes in hyperkalemia are peaked T waves and short QT interval, progressive lengthening of PR and QRS intervals, loss of P waves + QRS widening into sine wave, then ventricular fibrillation or cardiac standstill.
86
What is special about the treatment of hyperkalemia in patients taking digoxin?
In patients taking digoxin IV calcium gluconate should not be given as it may enhance the effect of digoxin.
87
When hypokalemia occurs with HTN and alkalosis, what is the probable cause?
Hypertension and hypokalemia should make you think about primary or secondary hyperaldosteronism.
88
What are the differences between Bartter and Gitelman syndromes?
Bartter syndrome resembles a patient taking a loop diuretic leading to hypokalemia, hypomagnesemia, and normal urine calcium excretion. Gitelman syndrome resembles a patient taking a thiazide diuretic with hypokalemia, hypomagnesemia, and low urinary calcium excretion.
89
What are the most common causes of asymptomatic hypercalcemia?
The most common causes of asymptomatic hypercalcemia are thiazide diuretic use and primary hyperparathyroidism.
90
What is the effect of hypomagnesemia on serum calcium levels? What is the effect of hypermagnesemia on serum calcium levels?
Both hypo- and hypermagnesemia are associated with hypocalcemia. Hypercalcemia can cause hypomagnesemia.
91
Hypomagnesemia causes what other electrolytes abnormality?
Hypomagnesemia can cause hypokalemia in addition to hypocalcemia.
92
What is refeeding hypophosphatemia?
Refeeding of malnourished patients can cause severe hypophosphatemia by redistribution of phosphate into cells.
93
Newly diagnosed hypertension in which age groups suggests that the cause might be secondary?
Newly diagnosed HTN in those <30yo and those >55yo should prompt consideration of secondary HTN
94
Review the 4 types of diuretics.
1. Loop diuretics 2. Thiazide diuretics 3. Carbonic anhydrase inhibitors 4. Aldosterone antagonists/K-sparing diuretics
95
Which diuretic is especially important to give to patients with systolic dysfunction and low ejection fraction?
Aldosterone antagonists are preferred in systolic HF because of evidence of improved patient outcomes.
96
ACEIs/ARBs are absolutely contraindicated in which patients? Renin inhibitors?
ACEIs/ARBs are absolutely contraindicated in pregnant patients. Renin inhibitors are teratogenic and thus contraindicated in pregnant patients.
97
Why are beta-blockers not recommended as 1st line drugs for monotherapy?
JNC8 does not recommend beta-blockers as first line antihypertensives due to higher rate of cardiovascular death, MI, or stroke compared to ARBs.
98
What are the two 1st line antihypertensive agents in the African American population?
Thiazides and CCBs are considered 1st line agents in African Americans.
99
What are the JNC8 blood pressure goals in adults and elderly patients?
JNC8 BP goal is <140/90 in adults and <150/90 in the elderly.
100
What is the goal for BP reduction in patients who present with hypertensive crisis?
The treatment goal for BP reduction in hypertensive crisis is a steady decrease of diastolic BP to 100-105mmHg within 2-6 hours.
101
What is the main cause of renovascular HTN in men >50 years old?
Atherosclerosis is the main cause of renovascular HTN in men >50 years old.
102
What is the main cause of renovascular HTN in women <40 years old?
The main cause of renovascular HTN in women <40 years old is fibromuscular dysplasia.
103
What does the combination of a continuous abdominal bruit (+/- low potassium) imply in a hypertensive patient?
The presence of a continuous abdominal bruit +/- low potassium in a hypertensive patient suggest renovascular HTN.
104
How do you confirm the diagnosis of primary hyperaldosteronism?
Screen for primary hyperaldosteronism with a plasma aldosterone:renin ratio (ARR). To confirm the diagnosis check for suppressed aldosterone after IV saline infusion or 3 day salt load. If aldosterone does not suppress, the patient has primary hyperaldosteronism.
105
How do you screen for pheochromocytoma?
Screen for pheochromocytoma with plasma-free metanephrines or urinary fractionated metanephrines.
106
What are the 4 categories of HTN in pregnancy?
1. Chronic HTN: preexisting or before 20th week of gestation 2. Preeclampsia: HTN + proteinuria after 20th week 3. Gestational HTN: after 20th week but with no proteinuria 4. Chronic HTN with superimposed preeclampsia: worsening HTN + new-onset proteinuria after the 20th week in a woman with preexisting controlled, chronic HTN
107
What is the definition of eclampsia?
Eclampsia is defined as grand mal seizures in a woman with preeclampsia or gestational HTN.
108
What are the defining features of preeclampsia?
HTN with proteinuria after 20th week OR HTN without proteinuria in a woman with any of the following features: thrombocytopenia, LFT abnormalities, pulmonary edema, cerebral or visula symptoms.

Internal Medicine Board Review (13 decks)

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