NEPHROLOGY Flashcards

1
Q

Represents a stage of CKD where the accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys leads to death unless the toxins are removed

A

end-stage renal disease

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2
Q

The pathophysiology of CKD involves two broad sets of mechanisms of damage:

A

(1) initiating mechanisms specific to the underlying etiology
(2) hyperfiltration and hypertrophy of the remaining viable nephrons

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3
Q

Most common inherited form of CKD

A

autosomal dominant polycystic kidney disease.

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4
Q

The normal annual mean decline in GFR with age from the peak GFR (~120 mL/min per 1.73 m2) attained during _________ is _________ , reaching a mean value of _________ at age 70

A

the third decade of life
~1 mL/min per year per 1.73 m2
70 mL/min per 1.73 m2

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5
Q

UACR above ________ in men and ________ in women serves as a marker not only for early detection of primary kidney disease, but for systemic microvascular disease as well

A

17 mg albumin/g creatinine

25 mg albumin/g creatinine

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6
Q

Serves as a well-studied screening marker for the presence of systemic microvascular disease and endothelial dysfunction

A

presence of albuminuria

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7
Q

T or F: The serum concentrations of urea and creatinine are readily measured complete surrogate markers for retained toxins in uremia

A

False. Accumulation of these two molecules themselves does not account for the many symptoms and signs that characterize the uremic syndrome in advanced renal failure

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8
Q

T or F: CKD is associated with increased systemic inflammation

A

True

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9
Q

The pathophysiology of the uremic syndrome can be divided into manifestations in three spheres of dysfunction:

A

(1) those consequent to the accumulation of toxins that normally undergo renal excretion;
(2) those consequent to the loss of other kidney functions,
(3) progressive systemic inflammation and its vascular and nutritional consequences

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10
Q

Hyponatremia is not commonly seen in CKD patients but, when present, often responds to

A

Water restriction

As long as water intake does not exceed the capacity for renal water clearance, the ECFV expansion will be isotonic and the patient will have a normal plasma sodium concentration

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11
Q

Medications that can inhibit renal potassium excretion and lead to hyperkalemia and must be cautiously used or avoided in CKD (2)

A

RAS inhibitors

Spironolactone and other potassium-sparing diuretics such as amiloride, eplerenone, and triamterene

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12
Q

Certain causes of CKD can be associated with earlier and more severe disruption of potassium-secretory mechanisms in the distal nephron, out of proportion to the decline in GFR. These include conditions associated with (2)

A
Hyporeninemic hypoaldosteronism (diabetes)
Renal diseases that preferentially affect the distal nephron (obstructive uropathy and sickle cell nephropathy)
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13
Q

Alkali supplementation may, in addition, attenuate the catabolic state and possibly slow CKD progression and is recommended when the serum bicarbonate concentration falls below

A

20–23 mmol/L

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14
Q

These changes that may lead to bone disease in CKD start to occur when the GFR falls below

A

60 mL/min

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15
Q

Hyperparathyroidism stimulates bone turnover and leads to

A

osteitis fibrosa cystica

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16
Q

Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and in advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so that they appear brown in color

A

osteitis fibrosa cystica

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17
Q

Brown tumor is also known as

A

osteitis fibrosa cystica

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18
Q

A devastating condition seen almost exclusively in patients with advanced CKD that is heralded by livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts

A

Calciphylaxis

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19
Q

The optimal management of secondary hyperparathyroidism and osteitis fibrosa in CKD is

A

prevention

Once the parathyroid gland mass is very large, it is difficult to control the disease

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20
Q

These are agents that are taken with meals and complex the dietary phosphate to limit its GI absorption

A

phosphate binders such as calcium acetate, calcium carbonate, sevelamer and lanthanum

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21
Q

Non-calcium-containing polymers that also function as phosphate binders; they do not predispose CKD patients to hypercalcemia and may attenuate calcium deposition in the vascular bed (2)

A

sevelamer and lanthanum

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22
Q

Enhance the sensitivity of the parathyroid cell to the suppressive effect of calcium, and produces a dose-dependent reduction in PTH and plasma calcium concentration in some patients

A

calcimimetic drugs such as cinacalcet

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23
Q

Current National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines recommend a target PTH level between

A

150 and 300 pg/mL

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24
Q

Very low PTH levels in CKD are associated with these conditions (3)

A

Adynamic bone disease
Fracture
Ectopic calcification

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25
Q

The leading cause of morbidity and mortality in patients at every stage of CKD

A

Cardiovascular disease

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26
Q

The CKD-related risk factors in the increased prevalence of cardiovascular disease are (6)

A
anemia
hyperphosphatemia
hyperparathyroidism
increased FGF-23
sleep apnea
generalized inflammation
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27
Q

The largest increment in cardiovascular mortality rate in dialysis patients is associated with (2)

A

congestive heart failure and sudden death

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28
Q

2 strongest risk factors for cardiovascular morbidity and mortality in patients with CKD that are thought to be related primarily, but not exclusively, to prolonged hypertension and ECFV overload

A

Left ventricular hypertrophy and dilated cardiomyopathy

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29
Q

The absence of hypertension in CKD may signify

A

poor left ventricular function

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30
Q

T or F, The use of exogenous erythropoiesis-stimulating agents do not have effect on the blood pressure

A

False. It can increase blood pressure and the requirement for antihypertensive drugs

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31
Q

The overarching goal of hypertension therapy in CKD is to

A

prevent the extrarenal complications of high blood pressure, such as cardiovascular disease and stroke

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32
Q

In CKD patients with diabetes or proteinuria >1 g per 24 h, blood pressure should be reduced to

A

<130/80 mmHg

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33
Q

First line of therapy in the management of hypertension in CKD

A

salt restriction

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34
Q

Antihypertensive drugs that appear to slow the rate of decline of kidney function in a manner that extends beyond reduction of systemic arterial pressure and that involves correction of the intraglomerular hyperfiltration and hypertension

A

ARBs and ACEi

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35
Q

Chest pain with respiratory accentuation, 2117 accompanied by a friction rub, is diagnostic of

A

pericarditis

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36
Q

T or F: In patients with uremic pericarditis/effusion, hemodialysis should be performed with heparin

A

False. Because of the propensity to hemorrhage in pericardial fluid.

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37
Q

Type of anemia in CKD

A

normochromic, normocytic

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38
Q

Anemia in CKD can be observed in what stage of CKD

A

Stage 3

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39
Q

Anemia in CKD is universal in what stage of CKD

A

Stage 4

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40
Q

The primary cause of anemia in CKD

A

insufficient production of EPO

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41
Q

Current practice in management of CKD is to target a hemoglobin concentration of

A

100–115 g/L

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42
Q

Coexistence of bleeding disorders and a propensity to thrombosis is unique in patients with

A

CKD

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43
Q

Subtle clinical manifestations of uremic neuromuscular disease usually become evident at what stage of CKD

A

Stage 3

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44
Q

Peripheral neuropathy usually becomes clinically evident after the patient reaches what stage of CKD

A

stage 4 CKD

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45
Q

Characterized by ill-defined sensations of sometimes debilitating discomfort in the legs and feet relieved by frequent leg movement

A

restless leg syndrome

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46
Q

T or F: Evidence of peripheral neuropathy without another cause is an indication for starting renal replacement therapy

A

True

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47
Q

A urine-like odor on the breath, derives from the break- down of urea to ammonia in saliva and is often associated with an unpleasant metallic taste

A

Uremic fetor

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48
Q

A class of drugs that result in glucose lowering, accompanied by striking reductions in kidney function decline and in cardiovascular events

A

SGLT-2 inhibitors

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49
Q

In advanced CKD, even on dialysis, patients may become more pigmented, and this is felt to reflect the deposition of retained pigmented metabolites called

A

urochromes

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50
Q

Although many of the cutaneous abnormalities in CKD improve with dialysis, this particular manifestation is often tenacious

A

pruritus

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51
Q

Pruritus in CKD may be caused by this electrolyte abnormality

A

hyperphosphatemia

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52
Q

A skin condition unique to CKD patients consists of progressive subcutaneous induration, especially on the arms and legs

A

nephrogenic fibrosing dermopathy

seen in patients exposed to gadolinium contrast of MRI

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53
Q

Stage of CKD that is contraindicated for exposure with gadolinium contrast

A

Stage 4-5

Stage 3 - precaution or minimize exposure

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54
Q

The most useful imaging study in evaluation of CKD

A

Renal utrasound

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55
Q

CKD causes with normal or increased kidney size on ultrasound (4)

A

DM nephropathy
Amyloidosis
HIV nephropathy
Polycystic kidney disease

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56
Q

_____________ that has reached some degree of renal failure will almost always present with enlarged kidneys

A

Polycystic kidney disease

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57
Q

In the patient with bilaterally small kidneys, renal biopsy is not advised because (3)

A

(1) it is technically difficult and has a greater likelihood of causing bleeding and other adverse consequences
(2) there is usually so much scarring that the underlying disease may not be apparent
(3) the window of opportunity to render disease-specific therapy has passed

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58
Q

Contraindications to kidney biopsy (4)

A
bilaterally small kidneys
uncontrolled hypertension
active urinary tract infection
bleeding diathesis (including ongoing anticoagulation)
severe obesity
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59
Q

favored approach for kidney biosy

A

Ultrasound-guided percutaneous biopsy

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60
Q

In the CKD patient in whom a kidney biopsy is indicated (e.g., suspicion of a concomitant or super-imposed active process such as interstitial nephritis or in the face of accelerated loss of GFR), the bleeding time should be measured, and if increased,_________ should be administered immediately prior to the procedure

A

desmopressin

or brief run of HD without heparin

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61
Q

The most important initial diagnostic step in approach to kidney disease management

A

to distinguish newly diagnosed CKD from acute or subacute renal failure

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62
Q

Among the calcium channel blockers, ______ and_______ may exhibit superior antiproteinuric and renoprotective effects

A

diltiazem and verapamil

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63
Q

Two human kidneys harbor nearly how many glomerular capillary tufts

A

1.8 million

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64
Q

The glomerular capillaries filter how many liters of plasma water

A

120–180 L/d

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65
Q

Humans with normal nephrons excrete on average how many mg of albumin in daily voided urine

A

8–10 mg

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66
Q

Persistent glomerulonephritis that worsens renal function is always accompanied by (3)

A

interstitial nephritis
renal fibrosis
tubular atrophy

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67
Q

T or F: Renal failure in glomerulonephritis best correlates histologically with the type of inciting glomerular injury

A

False. It best correlates histologically with the appearance of tubulointerstitial nephritis rather than with the type of inciting glomerular injury

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68
Q

Glomerular diseases often present as microscopic hematuria except for these 2 conditions wherein gross hematuria is common.

A

IgA nephropathy

sickle cell disease

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69
Q

Microalbuminuria is how much albumin in the urine?

A

30–300 mg/24 h

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70
Q

Frank proteinuria is how much albumin in the urine?

A

> 300 mg/24 h

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71
Q

Sustained proteinuria value

A

> 1–2 g/24 h

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72
Q

Foaming urine on voiding is indicative of

A

proteinuria

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73
Q

Class of proteinuria that is nonsustained, generally <1 g/24 h

A

benign proteinuria
sometimes called functional or transient proteinuria

caused by fever, exercise, obesity, sleep apnea, emotional stress, and congestive heart failure

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74
Q

Proteinuria only seen with upright posture

A

orthostatic proteinuria

benign prognosis

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75
Q

T or F: In children with minimal change disease (MCD), the proteinuria is non-selective and composed of albumin and a mixture of other serum proteins

A

False. selective, composed largely of albumin

Proteinuria in most adults with glomerular disease is nonselective, containing albumin and a mixture of other serum proteins

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76
Q

Glomerular syndrome producing 1–2 g/24 h of proteinuria, hematuria with red blood cell casts, pyuria, hypertension, fluid retention, and a rise in serum creatinine associated with a reduction in glomerular filtration

A

acute nephritic syndrome

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77
Q

If glomerular inflammation causes the serum creatinine rises quickly, particularly over a few days, this acute nephritis is called

A

rapidly progressive glomerulonephritis (RPGN)

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78
Q

Pathologic equivalent of the clinical presentation of RPGN

A

crescentic glomerulonephritis

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79
Q

When patients with RPGN present with lung hemorrhage from Goodpasture’s syndrome, antineutrophil cytoplasmic antibodies (ANCA)-associated small-vessel vasculitis, lupus erythematosus, or cryoglobulinemia, they are often diagnosed as

A

pulmonary-renal syndrome

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80
Q

Describes the onset of heavy proteinuria (>3.0 g/24 h), hypertension, hypercholesterolemia, hypoalbuminemia, edema/anasarca, and microscopic hematuria

A

Nephrotic syndrome

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81
Q

Only large amounts of proteinuria (>3.0 g/24 h) are present without clinical manifestations

A

nephrotic-range proteinuria

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82
Q

Describes patients with vascular injury producing hematuria and moderate proteinuria

A

Glomerular–vascular syndrome

Affected individuals can have vasculitis, thrombotic microangiopathy, antiphospholipid syndrome, or, more commonly, a systemic disease such as atherosclerosis, cholesterol emboli, hypertension, sickle cell anemia, and autoimmunity

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83
Q

The most common infectious causes of glomerulonephritis throughout the world (2)

A

subacute bacterial endocarditis
malaria and schistosomiasis

closely followed by HIV and chronic hepatitis B and C

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84
Q

The kidney biopsy uses this stain to assess cellularity and architecture

A

hematoxylin and eosin (H&E)

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85
Q

The kidney biopsy uses this stain to stain carbohydrate moieties in the membranes of the glomerular tuft and tubules

A

periodic acid–Schiff (PAS)

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86
Q

The kidney biopsy uses this stain to enhance basement mem- brane structure

A

Jones-methenamine silver

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87
Q

The kidney biopsy uses this stain for amyloid deposits

A

Congo red

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88
Q

The kidney biopsy uses this stain to identify collagen deposition and assess the degree of glomerulo- sclerosis and interstitial fibrosis

A

Masson’s trichrome

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89
Q

Ideal number of glomeruli that are reviewed individually for discrete lesions in kidney biopsy

A

20

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90
Q

How many percent of glomeruli is involved in focal lesion? diffuse lesion?

A

<50%

>50%

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91
Q

When cells in the capillary tuft proliferate, it is called

A

endocapillary

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92
Q

when cellular proliferation extends into Bowman’s space

A

extracapillary

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93
Q

formed when epithelial podocytes attach to Bowman’s capsule in the setting of glomerular injury

A

Synechiae

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94
Q

develop when fibrocellular/ fibrin collections fill all or part of Bowman’s space

A

crescents

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95
Q

acellular, amorphous accumulations of proteinaceous material throughout the tuft with loss of functional capillaries and normal mesangium in the glomerulus

A

sclerotic glomer- uli

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96
Q

Histopathologic finding that is an ominous sign of irreversibility and progression to renal failure

A

Interstitial fibrosis

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97
Q

prototypical for acute endocapillary proliferative glomerulonephritis

A

Poststreptococcal glomerulonephritis

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98
Q

PSGN is common in what ages

A

2-14 years old

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99
Q

Infection prior to development of PSGN and the cause

A

Skin and throat infections with particular M types of streptococci (nephritogenic strains) antedate glomerular disease

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100
Q

Post- streptococcal glomerulonephritis due to impetigo develops ______ after skin infection and ________ after streptococcal pharyngitis

A

2–6 weeks

1–3 weeks

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101
Q

On renal biopsy, this condition demonstrates hypercellularity of mesangial and endothelial cells, glomerular infiltrates of polymorphonuclear leukocytes, granular subendothelial immune deposits of IgG, IgM, C3, C4, and C5–9, and subepithelial deposits (which appear as “humps”)

A

poststreptococcal glomerulonephritis

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102
Q

Acute nephritic syndrome with hematuria, pyuria, red blood cell casts, edema, hypertension, and oliguric renal failure, and manifests as headache, malaise, anorexia, and flank pain

A

PSGN

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103
Q

Increased titers of these antibodies can help confirm the diagnosis of PSGN (3)

A

ASO (30%)
anti-DNAse (70%)
antihyaluronidase antibodies (40%)

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104
Q

Kidneys have subcapsular hemorrhages with a “flea-bitten” appearance, and microscopy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial immune deposits of IgG, IgM, and C3

A

Subacute bacterial endocarditis

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105
Q

Predominant organism causing glomerulonephritis in subacute bacterial endocarditis

A

Staphylococcus

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106
Q

The most common clinical sign of renal disease in lupus nephritis

A

proteinuria

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107
Q

Antibodies that correlate best with the presence of renal disease in lupus

A

Anti-dsDNA

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108
Q

the only reliable method of identifying the morphologic variants of lupus nephritis

A

renal biopsy

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109
Q

Class of lupus nephritis with minimal mesangial

A

Class I

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110
Q

Class of lupus nephritis with normal histology with mesangial deposits

A

Class I

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111
Q

Class of lupus nephritis with mesangial proliferation

A

Class II

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112
Q

Class of lupus nephritis with mesangial hypercellularity with expansion of the mesangial matrix

A

Class II

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113
Q

Class of lupus nephritis with focal nephritis

A

Class III

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114
Q

Class of lupus nephritis with focal endocapillary ± extracapillary proliferation with focal subendothelial immune deposits and mild mesangial expansion

A

Class III

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115
Q

Class of lupus nephritis with diffuse nephritis

A

Class IV

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116
Q

Class of lupus nephritis with diffuse endocapillary ± extracapillary proliferation with diffuse subendothelial immune deposits and mesangial alterations

A

Class IV

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117
Q

Class of lupus nephritis with membranous nephritis

A

Class V

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118
Q

Class of lupus nephritis with thickened basement membranes with diffuse subepithelial immune deposits; may occur with class III or IV lesions and is sometimes called mixed membranous and proliferative nephritis

A

Class V

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119
Q

Class of lupus nephritis with sclerotic nephritis

A

Class VI

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120
Q

Class of lupus nephritis with global sclerosis of nearly all glomerular capillaries

A

Class VI

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121
Q

Class of lupus nephritis that describes focal lesions with proliferation or scarring, often involving only a segment of the glomerulus

A

Class III

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122
Q

Class of lupus nephritis that have the most varied course

A

Class III

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123
Q

Class of lupus nephritis that describes global, diffuse proliferative lesions involving the vast majority of glomeruli

A

Class IV

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124
Q

Without treatment, this aggressive lesion has the worst renal prognosis among the classes of lupus nephritis

A

Class IV

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125
Q

Class of lupus nephritis that describes subepithelial immune deposits producing a membranous pattern

A

Class V

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126
Q

Patients with this class of lupus nephritis are predisposed to renal-vein thrombosis and other thrombotic complications

A

Class V

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127
Q

Lupus patients with this class of lupus nephritis have >90% sclerotic glomeruli and ESRD with interstitial fibrosis

A

Class VI

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128
Q

When do you do renal transplantation in renal failure from lupus?

A

Usually performed after ~6 months of inactive disease

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129
Q

When anti-GBM disease present with lung hemorrhage and glomerulonephritis, they have a pulmonary-renal syndrome called

A

Goodpasture’s syndrome

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130
Q

The target epitopes for the anti-GBM disease lie in the quaternary structure of

A

α3 NC1 domain of collagen IV

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131
Q

T or F: In Goodpasture’s syndrome, hemoptysis is largely confined to smokers

A

True

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132
Q

T or F: In Goodpasture’s sydrome, those who present with lung hemorrhage as a group do better than older populations who have prolonged, asymptomatic renal injury

A

True

presentation with oliguria is often associated with a particularly bad outcome

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133
Q

Renal biopsies typically show focal or segmental necrosis that later, with aggressive destruction of the capillaries by cellular proliferation, leads to crescent formation in Bowman’s space

A

Goodpasture’s syndrome / anti-GBM disease

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134
Q

Prognosis at presentation of anti-GBM disease is worse if (4)

A
  • > 50% crescents on renal biopsy with advanced fibrosis
  • serum creatinine is >5–6 mg/dL
  • oliguria is present
  • need for acute dialysis
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135
Q

In the management of Goodpasture’s syndrome, aside from dialysis, patients with advanced renal failure who present with hemoptysis should still be treated for their lung hemorrhage with

A

Plasmapheresis

can be life-saving
8-10 treatments
accompanied by oral prednisone and cyclophosphamide in the first 2 weeks

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136
Q

It is classically characterized by episodic hematuria associated with the deposition of IgA in the mesangium

A

IgA nephropathy

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137
Q

Henoch-Schönlein purpura is distinguished clinically from IgA nephropathy by (4)

A
  • prominent systemic symptoms
  • a younger age (<20 years old)
  • preceding infection
  • abdominal complaints.
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138
Q

An immune complex–mediated glomerulonephritis defined by the presence of diffuse mesangial Ig deposits often associated with mesangial hypercellularity

A

IgA nephropathy

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139
Q

In IgA nephropathy, IgA deposited in the mesangium is typically polymeric and of what subclass

A

IgA1

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140
Q

Recurrent episodes of macroscopic hematuria during or immediately follow- ing an upper respiratory infection often accompanied by proteinuria or persistent asymptomatic microscopic hematuria

A

IgA nephropathy

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141
Q

T or F: IgA nephropathy is a benign disease for the majority of patients

A

True

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142
Q

Renal failure seen in how many percent of patients with IgA nephropathy over 20–25 years

A

25–30%

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143
Q

Treatment of IgA nephropathy

A

ACE inhibitors

steroid and immunosuppressive therapy have conflicting results in the studies
Tonsillectomy and fish oil have also been suggested in small studies to benefit select patients

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144
Q

The 2 types of antibodies in ANCA small-vessel vasculitis

A

anti-proteinase 3 (PR3)

anti-myeloperoxidase (MPO)

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145
Q

Vasculitis syndromes that are ANCA-positive and have a pauci-immune glomerulonephritis with few immune complexes in small vessels and glomerular capillaries (4)

A

Granulomatosis with polyangiitis
Microscopic polyangiitis
Churg-Strauss syndrome
Renal-limited vasculitis

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146
Q

Induction therapy of ANCA small-vessel vasculitis (3)

A

Glucocorticoids

Rituximab or cyclophosphamide

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147
Q

Recommended treatment in rapidly progressive renal failure or pulmonary hemorrhage in ANCA small-vessel vasculitis

A

Plasmapheresis

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148
Q

Patients with this disease classically present with fever, purulent rhinorrhea, nasal ulcers, sinus pain, polyarthralgias/arthritis, cough, hemoptysis, shortness of breath, microscopic hematuria, and 0.5–1 g/24 h of proteinuria; occasionally there may be cutaneous purpura and mononeuritis multiplex

A

Granulomatosis with Polyangiitis

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149
Q

Biopsy of involved tissue will show a small-vessel vasculitis and adjacent noncaseating granulomas.

A

Granulomatosis with Polyangiitis

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150
Q

Renal biopsies during active disease demonstrate segmental necrotizing glomerulonephritis without immune deposits and have been classified as focal, mixed, crescentic or sclerotic

A

Granulomatosis with Polyangiitis

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151
Q

Small-vessel vasculitis that is more common in patients exposed to silica dust and those with α1-antitrypsin deficiency, which is an inhibitor of PR3

A

Granulomatosis with Polyangiitis

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152
Q

Αmong the ANCA small-vessel vasculitis, relapse is most common in

A

Granulomatosis with Polyangiitis

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153
Q

Clinically, these patients look somewhat similar to those with granulomatosis with polyangiitis, except they rarely have significant lung disease or destructive sinusitis

A

Microscopic Polyangiitis

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154
Q

Small-vessel vasculitis is associated with peripheral eosinophilia, cutaneous purpura, mononeuritis, asthma, and allergic rhinitis, often accompanied by hypergammaglobulinemia, elevated levels of serum IgE, or the presence of rheumatoid factor

A

Churg-Strauss Syndrome

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155
Q

Lung inflammation, including fleeting cough and pulmonary infiltrates, often precedes the systemic manifestations of this small-vessel vasculitis by years; lung manifestations are rarely absent

A

Churg-Strauss Syndrome

156
Q

Small-vessel vasculitis and focal segmental necrotizing glomerulonephritis can be seen on renal biopsy, usually absent eosinophils or granulomas

A

Churg-Strauss Syndrome

157
Q

defined morphologically with dense deposits forming ribbons in the GBM

A

dense deposit disease

158
Q

sometimes called mesangiocapillary glomerulonephritis or lobar glomerulonephritis

A

membranoproliferative glomerulonephritis

159
Q

It is an immune-mediated glomerulonephritis characterized by thickening of the GBM with mesangioproliferative changes; 70% of patients have hypocomplementemia

A

membranoproliferative glomerulonephritis

160
Q

MPGN that is commonly associated with persistent hepatitis C infections, autoimmune diseases like lupus or cryoglobulinemia, or neoplastic diseases

A

Type I

161
Q

The most proliferative of the three types of MPGN

A

Type I

162
Q

Shows mesangial proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane and endothelial cells, producing a double contour sometimes called tram-tracking

A

Type I MPGN

163
Q

Low serum C3 and a dense thickening of the GBM containing ribbons of dense deposits and C3

A

type II MPGN, dense deposit disease

164
Q

Classically, the glomerular tuft has a lobular appearance; intramesangial deposits are rarely present and subendothelial deposits are generally absent. What type of MPGN?

A

Type II

165
Q

MPGN that has the least proliferation and is often focal; mesangial interposition is rare, and subepithelial deposits can occur along widened segments of the GBM that appear laminated and disrupted.

A

Type III

166
Q

MPGN that is secondary to glomerular deposition of circulating immune complexes or their in situ formation

A

Type I

167
Q

____ percent of patients with MPGN develop ESRD 10 years after diagnosis, and ____ percent have renal insufficiency after 20 years

A

50%

90%

168
Q

Characterized by expansion of the mesangium, sometimes associated with mesangial hypercellularity; thin, single contoured capillary walls; and mesangial immune deposits.

A

Mesangioproliferative glomerulonephritis

169
Q

Mesangioproliferative disease may be seen in what conditions (4)

A

IgA nephropathy
Plasmodium falciparum malaria
Resolving postinfectious glomerulonephritis
Class II nephritis from lupus

170
Q

Nephrotic syndrome classically presents with (6)

A
Heavy proteinuria
Minimal hematuria
Hypoalbuminemia
Hypercholesterolemia
Edema
Hypertension
171
Q

Minimal change disease is sometimes known as

A

nil lesion

172
Q

Renal biopsy shows no obvious glomerular lesion by light microscopy and is negative for deposits by immunofluorescent microscopy, or occasionally shows small amounts of IgM in the mesangium

A

Minimal change disease

173
Q

Electron microscopy demonstrates an effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes.

A

Minimal change disease

174
Q

Presents clinically with the abrupt onset of edema and nephrotic syndrome accompanied by acellular urinary sediment. Average urine protein excretion reported in 24 h is 10 g with severe hypoalbuminemia.

A

Minimal change disease

175
Q

In minimal change disease, adults are not considered steroid-resistant until after ______ of therapy

A

4 months

176
Q

First-line therapy for minimal change disease

A

Prednisone

177
Q

Refers to a pattern of renal injury characterized by segmental glomerular scars that involve some but not all glomeruli

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

178
Q

the clinical findings of FSGS largely manifest as

A

proteinuria

179
Q

The pathologic changes of FSGS are most prominent in glomeruli located at the

A

corticomedullary junction

so if the renal biopsy specimen is from superficial tissue, the lesions can be missed, which sometimes leads to a misdiagnosis of MCD

180
Q

T or F: Steroids and other immunosuppressive agents may be used in the treatment of both primary and secondary FSGS

A

False. There is no role for steroids or other immunosuppressive agents in secondary FSGS

181
Q

Accounts for ~20% of cases of nephrotic syndrome in adults, with a peak incidence between the ages of 30 and 50 years and a male to female ratio of 2:1

A

Membranous glomerulonephritis

182
Q

Most common cause of nephrotic syndrome in the elderly

A

Membranous glomerulonephritis

rare in children

183
Q

Uniform thickening of the basement membrane along the peripheral capillary loops is seen by light microscopy on renal biopsy

A

Membranous glomerulonephritis

184
Q

Immunofluorescence demonstrates diffuse granular deposits of IgG and C3, and electron microscopy typically reveals electron-dense subepithelial deposits

A

Membranous glomerulonephritis

185
Q

T or F: The stage of glomerular disease in membranous glomerulonephritis is predictive of its progression

A

False. degree of tubular atrophy or interstitial fibrosis is more predictive of progression than is the stage of glomerular disease

186
Q

Factors that are associated with worse prognosis in membranous glomerulonephritis (4)

A

Male gender
older age
hypertension
persistence of proteinuria

187
Q

Nephrotic syndrome that has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep-vein thrombosis

A

Membranous glomerulonephritis

188
Q

The single most common cause of chronic renal failure

A

Diabetic nephropathy

189
Q

A sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy

A

Thickening of the GBM

190
Q

Some DM nephropathy patients develop eosinophilic, PAS+ nodules called

A

nodular glomerulosclerosis or Kimmelstiel-Wilson nodules

191
Q

Microalbuminuria appears ____ years after the onset of diabetes

A

5–10

192
Q

Feature of DM nephropathy that is a potent risk factor for cardiovascular events and death in patients with type 2 diabetes

A

Microalbuminuria

193
Q

The absence of this condition in type 1 patients with proteinuria should prompt consideration of a diagnosis other than diabetic nephropathy

A

retinopathy

90% of patients with type 1 diabetes and nephropathy have diabetic retinopathy

194
Q

It usually takes ____ years for DM nephropathy to reach ESRD

A

10–20

195
Q

Specific pattern of renal injury caused by nephrotoxic light chain that causes renal failure but not heavy proteinuria or amyloidosis

A

cast nephropathy

196
Q

Specific pattern of renal injury caused by nephrotoxic light chain that produces nephrotic syndrome with renal failure

A

light chain deposition disease

197
Q

Result of primary fibrillar deposits of immunoglobulin light chains known as amyloid L (AL), or secondary to fibrillar deposits of serum amyloid A (AA) protein fragments

A

renal amyloidosis

198
Q

T or F. Primary and secondary amyloidosis may both present as nephrotic syndrom

A

True

199
Q

The treatment for primary amyloidosis that can delay the course of renal amyloidosis in about 30% of patients

A

melphalan

also autologous hematopoietic stem cell transplantation

200
Q

Characterized by glomerular accumulation of nonbranching randomly arranged fibrils.

A

Fibrillary-Immunotactoid Glomerulopathy

201
Q

Fibrillar/microtubular deposits of oligoclonal or oligotypic immunoglobulins and complement appear in the mesangium and along the glomerular capillary wall, and stain negative to Congo red

A

Fibrillary-Immunotactoid Glomerulopathy

202
Q

An X-linked inborn error of globotriaosylceramide metabolism secondary to deficient lysosomal a-galactosidase A activity, resulting in excessive intracellular storage of globotriaosylceramide

A

Fabry’s disease

203
Q

Presents in childhood in males with acroparesthesias, angiokeratoma, and hypohidrosis

A

Fabry’s disease

204
Q

Renal biopsy reveals enlarged glomerular visceral epithelial cells packed with small clear vacuoles containing globotriaosylceramide; vacuoles may also be found in parietal and tubular epithelia

A

Fabry’s disease

205
Q

Vacuoles of electron-dense materials in parallel arrays (zebra bodies) are seen on electron microscopy

A

Fabry’s disease

206
Q

Fabry’s disease renal biopsy reveal features of

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

207
Q

Urinalysis may reveal oval fat bodies and birefringent glycolipid globules under polarized light (Maltese cross)

A

Fabry’s disease

208
Q

Empiric and temporizing treatment for pulmonary-renal syndrome until results of testing are available (2)

A

plasmapheresis and methylprednisolone

209
Q

Classically, patients with this condition develop hematuria, thinning and splitting of the GBMs, mild proteinuria (<1–2 g/24 h), which appears late in the course, followed by chronic glomerulosclerosis leading to renal failure in association with sensorineural deafness.

A

Alport’s syndrome

210
Q

Approximately 85% of patients with Alport’s syndrome have an X-linked inheritance of mutations in the

A

α5 (IV) collagen chain on chromosome Xq22–24

15% of patients have autosomal recessive disease of the α3(IV) or α4(IV) chains on chromosome 2q35–37

211
Q

Τypically have thin basement membranes on renal biopsy, which thicken over time into multilamellations surrounding lucent areas that often contain granules of varying density—the so-called split basement membrane

A

Alport’s syndrome

212
Q

Characterized by persistent or recurrent hematuria and is not typically associated with proteinuria, hypertension, or loss of renal function or extrarenal disease

A

Thin basement membrane disease (TBMD)

213
Q

Thin basement membrane disease (TBMD) is also known as

A

benign familial hematuria

it usually presents in childhood in multiple family members

214
Q

Thin basement membrane disease (TBMD) is caused by a defect in what collagen

A

Collagen type IV

215
Q

Develop iliac horns on the pelvis and dysplasia of the dorsal limbs involving the patella, elbows, and nails, variably associated with neural-sensory hearing impairment, glaucoma, and abnormalities of the GBM and podocytes, leading to hematuria, proteinuria, and FSGS

A

nail-patella syndrome

216
Q

The syndrome is autosomal dominant, with haploinsufficiency for the LIM homeodomain transcription factor LMX1B

A

nail-patella syndrome

217
Q

On renal biopsy there is focal sclerosing glomerulonephritis with specific lucent damage to the lamina densa of the GBM, an increase in collagen III fibrils along glomerular capillaries and in the mesangium, and damage to the slit-pore membrane, producing heavy proteinuria not unlike that seen in congenital nephrotic syndrome

A

nail-patella syndrome

218
Q

Approximately ___ of glomeruli are normally sclerotic by age 40, rising to ___ by age 60 and ___ by age 80

A

10%
20%
30%

219
Q

The lesion associated with HIV-associated nephropathy is

A

FSGS

220
Q

HIV patients with FSGS typically present with nephrotic-range proteinuria and hypoalbuminemia, but unlike patients with other etiologies for nephrotic syndrome, they do not commonly have (3)

A

hypertension
edema
hyperlipidemia.

221
Q

The lesion associated with syphilis-associated nephropathy is

A

membranous glomerulonephritis

222
Q

Schistosoma that is most commonly associated with clinical renal disease

A

Schistosoma mansoni

223
Q

Most common kidney stone

A

Calcium oxalate

224
Q

2nd most common kidney stone

A

Calcium phosphate

225
Q

T or F. A UTI in the setting of an obstructing stone requires urgent intervention to reestablish drainage

A

True. A UTI in the setting of an obstructing stone is a urologic emergency

226
Q

The point at which the concentration product exceeds the solubility product

A

Supersaturation

227
Q

The most clinically important inhibitor of calcium-containing stones

A

Urine citrate

228
Q

The majority of calcium oxalate stones grow on calcium phosphate at the tip of the renal papilla forming

A

Randall’s plaque

229
Q

Dietary factors that are associated with an increased risk of nephrolithiasis (6)

A
  • Animal protein
  • Oxalate
  • Sodium
  • Sucrose
  • Fructose
230
Q

Dietary factors associated with a lower risk of nephrolithiasis (4)

A
  • Calcium
  • Potassium
  • Magnesium
  • Phytate
231
Q

T or F. Higher dietary calcium intake is related to a higher risk of stone formation

A

False. Lower risk. May be due to a reduction in intestinal absorption of dietary oxalate that results in lower urine oxalate

232
Q

T or F. Supplemental calcium may increase the risk of kidney stone formation

A

True. May be due to the timing of supplemental calcium intake or to higher total calcium consumption leading to higher urinary calcium excretion

233
Q

T or F. Dietary oxalate is a strong risk factor for kidney stone formation.

A

False Dietary oxalate is a weak risk factor for stone formation, BUT urinary oxalate is a strong risk factor

234
Q

Vitamin C supplements will increase risk of what type of kidney stone?

A

Calcium oxalate

235
Q

Urine output which doubly increase the risk of stone formation

A

<1L/day

236
Q

T or F. Higher urine citrate excretion increases the risk of stone formation

A

False. Lower urine citrate

237
Q

Urine pH that promotes uric acid stones formation

A

≤ 5.5

238
Q

Urine pH that promotes calcium phosphate stone formation

A

≥6.5

239
Q

Formation of this stone is not influenced by urine pH

A

Calcium oxalate stones

240
Q

2 most common monogenic disorders that lead to stone formation

A

Primary hyperoxaluria

Cystinuria

241
Q

Sudden onset of unilateral flank pain then intensity of pain increase rapidly often accompanied by nausea and vomiting that radiate to ipsilateral testicle in men or ipsilateral labium in women

A

Renal colic

242
Q

2 most common presentation of acute stone event

A
  • Renal colic

* Painless gross hematuria

243
Q

Nephrolithiasis mimic acute cholecystitis if stone is at the

A

right ureteral pelvic junction

244
Q

Nephrolithiasis mimic acute appendicitis if stone is at the

A

blocks the ureter as it crosses over the right pelvic brim

245
Q

Nephrolithiasis mimic acute diverticulitis if stone is at the

A

left pelvic brim

246
Q

T or F: Absence of hematuria exclude the diagnosis of stone

A

False

247
Q

Preferred imaging and highly sensitive for nephrolitiasis

A

Helical computed tomography

248
Q

Drugs that may increase the rate of spontaneous kidney stone passage

A

Alpha blocker

249
Q

Indications for urologic intervention (3)

A
•	Evidence of UTI
•	Low probability of spontaneous stone passage
o	Stone measuring ≥6 mm 
o	Anatomic abnormality
•	Intractable pain
250
Q

The least invasive option for nephrolithiasis

A

Extracorporeal shockwave lithotripsy (ESWL)

251
Q

Uses shock waves generated outside the kidney body to fragment the stone

A

Extracorporeal shockwave lithotripsy (ESWL)

252
Q

Serve as the cornerstone on which therapeutic recommendations for nephrolithisis are based

A

24-h urine collection

253
Q

The “gold standard” diagnostic test for nephrolithiasis

A

Helical CT without contrast

254
Q

For all kidney stone types, consistently _____ reduces the likelihood of crystal formation

A

diluted urine

Urine volume should be at least 2 L/d

255
Q

Antihypertensive drugs that can lower urine Ca in doses higher than those used to treat HPN

A

Thiazide diuretic (Most commonly chlorthalidone)

256
Q

The only strategy that reduces endogenous oxalate production

A

Avoiding high-dose Vit C supplements

257
Q

Supplemental alkali that may be given to kidney stone patients (2)

A

potassium citrate or bicarbonate

258
Q

2 main risk factors for uric acid stone formation

A
  • Persistently low urine pH

* Higher uric acid excretion

259
Q

The focus for cystine kidney stone prevention

A

Increasing cystine solubility

260
Q

Medication that covalently binds to cystine (2)

A

Tiopronin

Penicillamine

261
Q

Preferred medication that covalently binds to cystine

A

Tiopronin

262
Q

AKA infection stones

A

Struvite

263
Q

AKA triple-phosphate stones

A

Struvite

264
Q

Struvite forms only when the upper urinary tract is infected with

A

urease-producing bacteria

265
Q

3 bacteria that most commonly cause struvite

A
  • Proteus mirabilis
  • Klebsiella pneumoniae
  • Providencia species
266
Q

Urease produced by urease-producing bacteria hydrolyzes urea and may elevate the urine pH to

A

> 8.0

267
Q

Struvite stones may grow quickly and fill the renal pelvis causing

A

staghorn calculi

268
Q

2 management for staghorn calculi

A

Complete removal

Acetohydroxamic acid

269
Q

Imaging that is often used for long-term follow-up of nephrolithiasis

A

Plain abdominal radiography (KUB)

270
Q

The first tolerable and effective agent for the treatment of UTI

A

Nitrofurantoin

271
Q

The most common manifestation of UTI

A

Acute cystitis

272
Q

Refers to acute cystitis or pyelonephritis in nonpregnant outpatient women without anatomic abnormalities or instrumentation of the urinary tract

A

Uncomplicated UTI

273
Q

Prevalence of UTI during the neonatal period according to sex

A

male>female

274
Q

Prevalence of UTI after 50 years of age according to sex

A

male=female

275
Q

Prevalence of UTI between 1-50 years of age

A

female > male

276
Q

How many percent of women in the general population acquire at least one UTI during their lifetime

A

50–80%

277
Q

Independent risk factors for acute cystitis (3):

A
  • Recent use of a diaphragm with spermicide
  • Frequent sexual intercourse
  • History of UTI
278
Q

Risk factors of UTI in healthy postmenopausal women (3):

A
  • Sexual activity
  • Diabetes mellitus
  • Incontinence
279
Q

Factors independently associated with pyelonephritis in young healthy women (6)

A
  • Frequent sexual intercourse
  • New sexual partner
  • A UTI in the previous 12 months
  • Maternal history of UTI
  • Diabetes
  • Incontinence
280
Q

Independent risk factors of UTI recurrence in premenopausal women (5)

A
  • Frequent sexual intercourse
  • Use of spermicide
  • New sexual partner
  • First UTI before 15 years of age
  • Maternal history of UTI
281
Q

Major risk factors of recurrent UTI in postmenopausal women (2)

A
  • History of premenopausal UTI

* Anatomic factors affecting bladder emptying

282
Q

Most common cause of UTI in men

A

urinary obstruction secondary to prostatic hypertrophy

283
Q

UTI due to lack of circumcision is due to what organism

A

Escherichia coli

284
Q

Most common organisms causing UTI

A

enteric gram-negative rods (most common: E. coli)

285
Q

Most common route of infection in UTI

A

Ascending from the urethra to the bladder

286
Q

Hematogenous route is present in how many % of documented UTIs

A

<2%

287
Q

Hematogenous route of UTI is most commonly seen in these 3 organisms

A
  • Salmonella
  • S. aureus
  • Candida
288
Q

The critical initial step in the pathogenesis of UTI among women

A

Colonization of the vaginal introitus and periurethral area with organisms from the intestinal flora

289
Q

Inhibition of ureteral peristalsis and decreased ureteral tone leads to this condition which is important in the pathogenesis of pyelonephritis in pregnant women

A

Vesicoureteral reflux

290
Q

The primary reason why UTI is predominantly an illness of young women rather than of young men

A

Distance of the urethra from the anus

291
Q

Virulence factor of E. coli that mediate binding to specific receptors on the surface of uroepithelial cells

A

Surface adhesins

292
Q

Virulence factor of E. coli described as hair-like protein structures that interact with a specific receptor on renal epithelial cells

A

P fimbriae

293
Q

Virulence factor of E. coli that is important in the pathogenesis of pyelonephritis and subsequent bloodstream invasion from the kidney

A

P fimbriae

294
Q

Play a key role in initiating E. coli bladder infection that mediate binding to mannose on the luminal surface of bladder uroepithelial cells

A

Type 1 pilus

295
Q

The most important issue to be addressed when a UTI is suspected is the

A

characterization of the clinical syndrome

296
Q

An indication that the upper urinary tract is involved in UTI

A

Unilateral back or flank pain

297
Q

An indication of invasive infection of either the kidney or the prostate

A

Fever

298
Q

Severe pyelonephritis is characterized by these clinical manifestations (5)

A
  • High fever
  • Rigors
  • Nausea
  • Vomiting
  • Flank and/or loin pain
299
Q

the main feature distinguishing cystitis from pyelonephritis

A

Fever

300
Q

Fever in pyelonephritis typically exhibits this pattern

A

high spiking “picket-fence” pattern

301
Q

Complication of pyelonephritis seen in patients with diabetes that present as obstructive uropathy when sloughed papillae obstruct the ureter

A

Acute papillary necrosis

302
Q

A particularly severe form of the pyelonephritis that is associated with the production of gas in renal and perinephric tissues

A

Emphysematous pyelonephritis

303
Q

Emphysematous pyelonephritis occurs almost exclusively in what group of patients

A

Diabetic patients

304
Q

Occurs when chronic urinary obstruction (often by staghorn calculi) together with chronic infection causes this suppurative destruction of renal tissue

A

Xanthogranulomatous pyelonephritis

305
Q

Causes yellow coloration of kidney with infiltration by lipid-laden macrophages

A

Xanthogranulomatous pyelonephritis

306
Q

When to you suspect the abscess as complication of pyelonephritis?

A

when a patient has continued fever and/or bacteremia despite antibacterial therapy

307
Q

Presents as fever, chills, dysuria, frequency, and pain in the pelvic or perineal area in men

A

Acute bacterial prostatitis

308
Q

In women presenting with at least one symptom of UTI (dysuria, frequency, hematuria, or back pain) and without complicating factors, the probability of acute cystitis or pyelonephritis is

A

50%

309
Q

If vaginal discharge and complicating factors are absent and risk factors for UTI are present, then the probability of UTI is close to___, and no laboratory evaluation is needed

A

90%

310
Q

Combination of dysuria and urinary frequency (in the absence of vaginal discharge) increases the probability of UTI to

A

96%

311
Q

Laboratory tests that provide point-of-care information for UTI

A

Urine dipstick test

Urinalysis

312
Q

Only members of the family ______ convert nitrate to nitrite that can be detected in urine dipstick test

A

Enterobacteriaceae

313
Q

Enough ______ must accumulate in the urine to reach the threshold of detection

A

Nitrite

314
Q

Diagnostic gold standard for UTI

A

Urine culture

315
Q

In symptomatic women, colony count threshold of ______ can be diagnostic of UTI

A

≥10^2 bacteria/mL

316
Q

T or F. Men with febrile UTI for the first time should have imaging performed

A

True

CT or ultrasound

317
Q

Microbiologic criterion for asymptomatic bacteriuria

A

≥10^5 bacterial CFU/mL of urine

318
Q

The predominant multilocus sequence type found worldwide as the cause of multidrug-resistant UTI

A

E. coli ST131

319
Q

previously recommended as first-line treatment for acute cystitis

A

TMP-SMX

320
Q

Organisms that are intrinsically resistant to this nitrofurantoin (5)

A
  • Proteus
  • Pseudomonas
  • Serratia
  • Enterobacter
  • Yeasts
321
Q

T or F. Nitrofurantoin may be used in the treatment of pyelonephritis

A

False

322
Q

Most fluoroquinolones are highly effective as short-course therapy for cystitis, except

A

moxifloxacin – may not reach adequate urinary levels

323
Q

Rare but potentially serious adverse effects of fluoroquinolones in >60 years of age

A

Increased risk of Achilles tendon rupture

324
Q

Widely used urinary analgesics but can cause significant nausea

A

Phenazopyridine

325
Q

First-line therapy for acute uncomplicated pyelonephritis

A

Fluoroquinolones

Oral ciprofloxacin (500 mg twice daily, with or without an initial IV 400-mg dose)

326
Q

UTI medications that are relatively safe in early pregnancy (3)

A
  • Nitrofurantoin
  • Ampicillin
  • Cephalosporins
327
Q

2 drugs of choice for UTI in pregnancy

A

Ampicillin

Cephalosporins

328
Q

Standard of care for overt pyelonephritis in pregnancy

A

parenteral β-lactam therapy with or without aminoglycosides

329
Q

For acute bacterial prostatitis, what is the recommended treatment and duration?

A

fluoroquinolone or TMP-SMX

2-4 weeks

330
Q

For chronic bacterial prostatitis, what is the recommended treatment and duration?

A

fluoroquinolone or TMP-SMX

4-6 weeks

331
Q

For recurrent bacterial prostatitis, what is the recommended treatment and duration?

A

fluoroquinolone or TMP-SMX

12 weeks

332
Q

Treatment for xanthogranulomatous pyelonephritis

A

nephrectomy

333
Q

Initial treatment for emphysematous pyelonephritis

A

Percutaneous drainage

Elective nephrectomy on follow-up

334
Q

Treatment of asymptomatic bacteriuria is given only in (4)

A
  • Pregnant women
  • Persons undergoing urologic surgery
  • Neutropenic patients
  • Renal transplant recipients
335
Q

Accepted threshold for bacteriuria to meet the definition of CAUTI

A

≥10^3 CFU/mL of urine

336
Q

Risk factors for candiduria (3)

A
  • ICU patients
  • Those taking broad-spectrum antimicrobial drugs
  • Those with underlying diabetes mellitus
337
Q

Therapy for candiduria is recommended for patients who (5)

A
  • Have symptomatic cystitis or pyelonephritis
  • Neutropenia
  • Undergoing urologic manipulation
  • Clinically unstable
  • Low-birth-weight infants

(At high risk for disseminated disease)

338
Q

First-line regimen for Candida infections of the urinary tract

A

Fluconazole – (200–400 mg/d for 7–14 days)

339
Q

Three prophylactic strategies for recurrent UTI in women

A

Continuous therapy (6 months)
Postcoital therapy
Patient-initiated therapy

340
Q

Most common cause of bacterial cystitis

A

Escherichia coli

341
Q

An unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with lower urinary tract symptoms of more than 6 weeks’ duration, in the absence of infection or other identifiable causes

A

INTERSTITIAL CYSTITIS/BLADDER PAIN SYNDROME

342
Q

Ulcer in the bladder

A

Hunner lesion

343
Q

How many % of interstitial cystitis/bladder pain syndrome has Hunner lesion?

A

≤10%

344
Q

Most common site of interstitial cystitis/bladder pain syndrome

A

Suprapubic (80% of women) – most severe pain

345
Q

In 95% of patients, bladder filling exacerbates the pain and/or bladder emptying relieves it

A

interstitial cystitis/bladder pain syndrome

346
Q

Functional somatic syndromes that can accompany IC/BPS (3):

A

a. Gynecologic chronic pelvic pain
b. Irritable bowel syndrome
c. Fibromyalgia

347
Q

Oral medications for interstitial cystitis/bladder pain syndrome:

A

a. NSAIDs
b. Amitriptyline
c. Pentosan polysulfate

348
Q

Treatment of hunner lesion in interstitial cystitis/bladder pain syndrome:

A

Fulguration (solutions containing lidocaine, hyaluronic acid, or dimethyl sulfoxide can be instilled into the bladder)

349
Q

Normal points of narrowing are common sites of urinary tract obstruction (4)

A
  • Ureteropelvic junction
  • Ureterovesical junction
  • Bladder neck
  • Urethral meatus
350
Q

Most common cause of utinary tract obstruction in childhood

A

Congenital malformations

  • Narrowing of the ureteropelvic junction
  • Abnormal insertion of the ureter into the bladder
351
Q

Most common cause of bilateral hydronephrosis in boys

A

Posterior urethral valves

352
Q

Most common causes of urinary tract obstruction in adults (3)

A
  • Pelvic tumors
  • Calculi
  • Urethral stricture
353
Q

Symptom that most commonly leads to medical attention in urinary tract obstruction

A

Flank pain

354
Q

Flank pain that occurs only with micturition is pathognomonic of

A

vesicoureteral reflux

355
Q

Partial bilateral UTO often results in (3)

A
  1. Acquired distal renal tubular acidosis
  2. Hyperkalemia
  3. Renal salt wasting
356
Q

Struvite is made of what mineral/compound?

A

Magnesium ammonium phosphate

357
Q

Used for the diagnosis of vesicoureteral reflux and bladder neck and urethral obstructions

A

Voiding cystourethrography

358
Q

T or F. Even in obstruction without infection, immediate surgical intervention must be done to avoid complications

A

False. When infection is not present, surgery is often delayed until acid-base, fluid, and electrolyte status is restored

359
Q

Functional obstruction secondary to neurogenic bladder may be decreased with the combination of (2)

A

frequent voiding and cholinergic drugs

360
Q

Duration of obstruction wherein kidney function recovery is unlikely

A

After 8 weeks of obstruction

361
Q

Imaging performed after a prolonged period of decompression and to predict the reversibility of renal dysfunction

A

Renal radionuclide scan

362
Q

Total body water is composed of ____ intracellular, and ____ extracellular

A

2/3

1/3

363
Q

Extracellular fluid is composed of ___ plasma, and ___ interstitial edema

A

¼

3/4

364
Q

Fluid is returned from the interstitial space into the vascular system through the

A

Lymphatic system

365
Q

A parameter that represents the filling of the arterial tree and that effectively perfuses the tissues

A

Effective arterial blood volume

366
Q

Decrease effective arterial blood volume will _____ renin release

A

Increase

Decreased effective arterial blood volume -> diminished renal blood flow -> translated by the renal juxtaglomerular cells (specialized myoepithelial cells surrounding the afferent arteriole) into a signal -> increased renin release

367
Q

Specialized myoepithelial cells surrounding the afferent arteriole that detects diminished renal blood flow

A

juxtaglomerular cells

368
Q

Angiotensinogen is synthesized in the

A

Liver

369
Q

Angiotensin II has generalized vasoconstrictor properties, particularly on the

A

renal efferent arterioles

370
Q

Aldosterone acts on the _____ by _____

A

Collecting tubule

Enhances sodium reabsorption and potassium excretion

371
Q

RAAS effect on Na and water

A

Retention

372
Q

Arginine vasopressin is secreted by

A

posterior pituitary gland

373
Q

Arginine vasopressin secretion occurs in response to

A

increased intracellular osmolar concentration

374
Q

AVP stimulates what receptors

A

V2 receptors

375
Q

Site of action of AVP in the kidney

A

distal tubules and collecting ducts

376
Q

Action of AVP on the kidney

A

increases the reabsorption of free water

377
Q

Potent peptide vasoconstrictor released by endothelial cells

A

Endothelin-1

Elevated in patients with severe heart failure

378
Q

Stimulates release of ANP

A

Atrial distention

379
Q

ANP and BNP are stored in these sites respectively

A

Atrial myocytes

Ventricular myocytes

380
Q

Stimulates release of BNP

A

When ventricular diastolic pressure rises

381
Q

Effects of ANP and BNP on Na and water

A

Excretion of sodium and water

Augmenting glomerular filtration rate
Inhibiting sodium reabsorption in the proximal tubule
Inhibiting release of renin and aldosterone

382
Q

Primary alteration in the nephrotic syndrome causing edema

A

diminished colloid oncotic pressure

383
Q

Causes of edema in hepatic cirrhosis (4)

A
  1. Hepatic venous outflow obstruction leading to increase splanchnic blood volume
  2. Hepatic lymph formation
  3. Hypoalbuminemia
  4. Peripheral artery vasodilation
384
Q

Multiple peripheral arteriovenous fistulae result in reduced effective systemic perfusion and effective arterial blood volume and leading enhancing edema formation in this condition

A

Beriberi heart disease

385
Q

Edema develops or becomes intensified when famished subjects are first provided with an adequate die

A

Refeeding edema