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Clincial Medicine > Nephrology/Urology > Flashcards

Nephrology/Urology Flashcards

1
Q

Which glomerular disease is represented by this clinical presentation:

Proteinuria 150mg - 3 g/day
Hematuria > 2 RBCs/high power field in spun urine

A

Asymptomatic glomerular disease

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2
Q

Which glomerular disease is represented by this clinical presentation:

Brown/red painless hematuria (no clots); typically coincides with intercurrent infection

A

Macroscopic hematuria

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3
Q

Which glomerular disease is represented by this clinical presentation:

Proteinuria: adult > 3.5 g/day; child > 40mg/hr/m^2
Hypoalbuminemia (

A

Nephrotic syndrome

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4
Q

Which glomerular disease is represented by this clinical presentation:

Oliguria
Hematuria: may see casts
Proteinuria (usually

A

Nephritic syndrome

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5
Q

Which glomerular disease is represented by this clinical presentation:

Renal failure over days/weeks
Proteinuria (usually

A

Rapidly progressive glomerulonephritis

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6
Q

Which glomerular disease is represented by this clinical presentation:

Hypertension
Renal insufficiency
Proteinuria (> 3g/day)
Shrunken, smooth kidneys

A

Chronic glomerulonephritis

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7
Q

What urine protein measurement could be indicative of glomerular disease?

A

Spot urine protein:creatinine >200mg

Spot urine albumin:creatinine >30mg

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8
Q

What are some clinical features seen with heavy proteinuria and nephrotic syndrome?

A

Most cases are primary renal disease
Leg and facial edema
Xanthelasma

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9
Q

Five Primary renal diseases discussed:

A

1) Minimal change disease
2) Focal segmental glomerular sclerosis
3) Membranous nephropathy
4) Membranoproliferative GN
5) Mesangial GN

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10
Q

What is the standard for diagnosing primary renal diseases?

A

Renal biopsy

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11
Q

Which primary renal disease involves diffuse fusion of foot processes of podocytes, doesn’t normally progress to renal failure, and usually responds to steroids (prednisone)?

A

Minimal change disease

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12
Q

What is the ddx for MCD?

A

NSAIDs, Hodgkin’s lymphoma

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13
Q

What are the most common causes of nephrotic syndrome in adults?

A

Focal Segmental Glomerular Sclerosis
and
Membranous Nephropathy

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14
Q

Secondary causes of FSGS?

A

HIV, IVDA, ureteral reflux, morbid obesity, unilateral agenesis of kidney

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15
Q

How is FSGS treated? How is that different than MCD?

A

FSGS is treated with Prednisone for longer than MCD and is more resistant to steroid tx.

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16
Q

If FSGS patient exhibits minimal to no response to steroids, what comes next?

A

Cyclosporine or cytoxan

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17
Q

Which antibodies are seen in 80% of cases of membranous nephropathy?

A

Phospholipase A2 receptor antibodies

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18
Q

What is seen histologically with membranous nephropathy?

A

Thickened basement membranes with subepithelial immune deposits

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19
Q

What is the typical natural history of membranous nephropathy? (3)

A

1/3 remission
1/3 same
1/3 worse

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20
Q

How is membranous nephropathy treated?

A

Steroids with either cytoxan or cyclosproine

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21
Q

What medications may act as secondary causes of membranous GN?

A

Gold, D-penicillaminne, NSAIDs, captopril

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22
Q

What infections commonly act as secondary causes of membranous GN?

A

Hep B, syphilis, schistosomiasis, malaria, Hep C

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23
Q

What consistency of malignancy is commonly associated as a secondary cause of membranous GN?

A

Solid tumors

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24
Q

Which autoimmune diseases can be secondary causes of membranous GN?

A

SLE, RA, thyroiditis

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25
Q

Which is the least common primary glomerular disease?

A

Membranoproliferative GN

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26
Q

Histologically, MPGN presents with:

A

Thick glomerular BM due to immune complex deposition and mesangial cell interposition

Increased mesangial and endocapillary cellularity

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27
Q

MPGN can be mediated two different ways:

A

Immune complexes or complement

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28
Q

MPGN is less commonly caused by the alternative complement pathway, but if glomerulus only stains for complement, one should consider

A

congenital or acquired defects in complement cascade.

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29
Q

Examples of chronic immune complex diseases associated with MPGN in the following categories:

Autoimmune, infections, thrombotic microangiopathy, other

A

Autimmune: SLE, sjogren’s, RA, compelement deficiency

Infection: Hep C, SBE, chronic visceral abscess, Hep B

Thrombotic microangiopathy: renal transplant glomerulopathy, antiphospholipid antibody syndrome, TTP/HUS, scleroderma

Other: CLL, melanoma, non-Hodgkins lymphoma, renal cell Ca, a-1-antitrypsin deficiency, partiel lipodystrophy

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30
Q

Which serologies are tested during work up for glomerular disease?

A 
ANA
ASO
C3, C4
Hep B and C
SPEP or UPEP
Cryglobulin, HIV, rheumatoid factor, ANCA, anti-GBM
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31
Q

Which glomerular disease presents with:

Preceded by a latent period of 1 - 2 weeks with pharyngitis or 3 - 6 weeks with skin infection.

Then: Edema, hematuria, back pain, oliguria, HTN, may progress to RPGN.

A

Post streptococcal GN

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32
Q

What are the 4 S’s of GN associated with low complement?

The other two?

A 
SLE
SBE
(Post) Strep
Shunt nephritis
\+MPGN and cryoglobulinemia
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33
Q

Which GN presents with:

Hematuria, proteinuria, ARF, nephrotic syndrome, RPGN, diffuse mesangial deposits of IgA and may progress to ESRD in 20 - 30% of patients over years?

A

IgA nephropathy/Berger’s disease

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34
Q

For IgA nephropathy, what is the interval between the synpharyngitic flare and the gross hematuria? How is this different from Post strep GN?

A

24 - 48 hours. In post strep, latent period is 1 - 2 weeks. Also, C3 and C4 are normal in IgA GN.

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35
Q

How is IgA GN treated?

A

Prednisone (with fish oil if proteinuria >1g)

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36
Q

Three types of kidney disease associated with SLE:

A
  1. Lupus GN/Lupus nephritis
  2. Tubulointerstitial nephritis
  3. Antiphospholipid antibody syndrome
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37
Q

Lupus nephritis classes with good prognosis include:

A

Class I (normal) and class II (mesangial GN)

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38
Q

Lupus nephritis classes with poor prognosis in any form:

A

Class IV (Diffuse and membrano- proliferative GN, >50% glomerular involvement with capillary hypercellularity)

Class VI (sclerosis, >90%, progresses to ESRD)

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39
Q

Lupus nephritis classes with poor prognosis if severe form:

A

Class III (focal,

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40
Q

Three classes of lupus nephritis require aggressive treatment

A

Severe Class III (focal proliferation)
All Class IV (diffuse prolif)
Some Class V (membranous)

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41
Q

What treatment options are available for cases of lupus nephritis that require aggressive therapy?

A

Steroids (prednisone) plus cytoxan in monthly pulses for 3 - 6 mos

Cellcept! and low dose steroids

Rituximab

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42
Q

Systemic vasculitis involving granulomatous inflammation of the respiratory tract and necrotizing vasculitis of small and medium vessels

A

Wegener’s/granulomatosis with polyangiitis (GPA)

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43
Q

Systemic vasculitis involving eosinophil rich and granulomatous inflammation of respiratory tract with necrotizing vasculitis of small and medium vessels, associated with asthma and blood eosinophilia.

A

Churg-Strauss/Eosinophilic granulomatosis with polyangiitis (EGPA)

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44
Q

Systemic vasculitis involving necrotizing vasculitis with few or no immune deposits affecting small vessels. Necrotizing arteritis may also be present.

A

Microscopic polyangiitis (MPA)

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45
Q

Systemic vasculitis involving IgA dominant immune deposits in small blood vessels

A

Henoch-Schonlein Purpura

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46
Q

Systemic vasculitis involving proteins that precipitate in the cold

A

Cryoglobulinemia

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47
Q

Organ system manifestations consistent with which vasculitis?

Cutaneous, Renal, Musculoskeleta, GI

A

HSP

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48
Q

Organ system manifestations consistent with which vasculitis?

Cutaneous, Renal, Musculoskeletal

A

Cryoglobulinemia

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49
Q

Organ system manifestations consistent with which vasculitis?

Renal, pulmonary, ENT, musculoskeletal, neurologic/GI, least often cutaneous

A

Wegener granulomatosis (GPA)

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50
Q

Organ system manifestations consistent with which vasculitis?

Renal, musculoskeletal, pulmonary/GI, least often cutaneous

A

Microscopia polyangiitis

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51
Q

Organ system manifestations consistent with which vasculitis?

Pulmonary, neurologic, cutaneous, ENT/MS/GI

A

Churg-Strauss syndrome

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52
Q

What complication can develop within 5 years of the onset of Scleroderma?

A

Scleroderma renal crisis

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53
Q

What is the DOC for treating scleroderma renal crisis?

A

ACE inhibitors, though a significant number of pts require dialysis

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54
Q

What disorders result in deposits of abnormal proteins?

A

Amyloid, myeloma, light chain nephropathy, fibrillary GN, immunotactoid glomerulopathy

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55
Q

What pathological pattern is seen with amyloid deposition in the kidney?

A

Fibrils of beta pleated sheets

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56
Q

What symptoms are specific to amyloid disease? What’s seen on U/A? Renal ultrasound?

A

Anorexia, orthostasis, edema, purpura…

U/A: benign

Ultrasound: large kidneys

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57
Q

How is amyloid visualized upon biopsy?

A

Congo red stain: apple-green birefringence with polarized light

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58
Q

How is amyloid disease of the kidney treated?

A

Prednisone, melfalan.

Colchicine may be used for 2ndary amyloid.

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59
Q

What is the distribution of TBW between ICF, ECF and intravascular space?

A 
ICF = 2/3
ECF = 1/3
intravascular = 1/4 ECF
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60
Q

Addition of a normal saline solution will add to which portion of TBW?

A

ECF

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61
Q

What is the normal range of serum sodium?

A

135 mEq/L - 145 mEq/L

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62
Q

Equation for plasma osmolality:

Posm = 2[Na+] +

A

Posm = 2[Na+] + (BUN/2.8) + (Glucose/18)

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63
Q

What types of hyponatremia result from drawing water out of cells into the blood and what substances may cause this? Is the osmolality considered normal?

A

Translocational hyponatremia; caused by addition of glucose, mannitol, glycine, or maltose

Pseudohyponatremia; caused by elevated proteins or lipids

Plasma osmolality may be normal or elevated

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64
Q

What states may cause a hyponatremia with a low plasma osmolality and normally dilute urine? What is the osmolarity of normally dilute urine?

A

Psychogenic polydipsia
Infants fed dilute formula
Low solute intake

Normal:

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65
Q

What state may result in a hyponatremic patient with low plasma osmolality and a concentrated urine?

A

Elevated vasopressin (results in hypovolemia with decreased TBW and severely decreased TB Na+)

Uosm: >100 mOsm/kg

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66
Q

What disorders should one consider with a hypovolemia patient that has a decreased TBW, an even more decreased TB sodium, and urine sodium >20mEq/L?

A

Renal losses:

diuretic excess
mineralcorticoid deficiency
salt-losing deficiency
bicarbonaturia
ketonuria
osmotic diuresis
cerebral salt wasting
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67
Q

What disorders should one consider with a hypovolemia patient that has a decreased TBW, an even more decreased TB sodium, and urine sodium

A

Extra renal losses:

vomiting or diarrhea
third spacing of fluids
burns
pancreatitis
trauma
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68
Q

What might cause a patient with euvolemia to have hyponatremia with a urine sodium >20 mEq/L?

A 
Glucocorticoid deficiency
Hypothyroidism
Stress
Drugs
SIADH
Aging
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69
Q

What classes of drugs may cause hyponatremia?

A

Vasopressin analogs (DDAVP, oxytocin, chlorpropamide, carbamazepine, nicotine, narcotics, antidepressants)

Renal vasopressin potentiators (chlorpropamide, cyclophosphamide, NSAIDs, acetaminophen)

Unknown mechanisms (haloperidol, fluphenazine, amitriptyline, thioradazine, fluoxetine, MDMA, sertraline)

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70
Q

What are the clinical features of SIADH?

A

Euvolemic, Uosm > 100 mOsm/kg, urine sodium = intake, low BUN and low uric acid

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71
Q

What is the time frame for acute hyponatremia? What is a possible immediate result? Symptoms?

A
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72
Q

What are risk factors for neurologic complications from acute hyponatremia?

A

Post-op menstruant females, psychiatric polydipsic patients, marathon runners, elderly women on thiazides, children, hypoxemic pts

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73
Q

Which are more sensitive to correction rate: chronic or acute hyponatremic patients?

A

Chronic patients are more sensitive to correction rate. Acute hyponatremia can be rapidly corrected.

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74
Q

What are symptoms of chronic hyponatremia?

A

Nausea, vomiting, cramps and weakness, ataxia, confusion and mental status change, seizures

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75
Q

How should acute symptomatic hyponatremia be treated?

A

Intubate if O2 desaturating
Hypertonic saline (3%) or mannitol
Furosemide

Goal: 2 mEq/L/hr

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76
Q

What patients are at risk for ODS?

A 
Chronic hyponatremia
alcoholism
malnutrition
liver disease
burns
hypokalemia
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77
Q

How should chronic symptomatic hyponatremia be treated?

A

Furosemide
Replace Na and K
No more than 1.5/mM/L/hr or 12mM in 24 hours

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78
Q

What might be some reasons for impaired thirst or osmoreceptor lesions?

A 
Tumor
Granulomatous diseases
Ischemia
Primary hyperaldosteronism
Age
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79
Q

Three types of renal water losing disorders:

A 
Neurogenic DI (decreased vasopressin secretion)
Gestational DI (increased degradation)
Nephrogenic DI (renal resistance to vasopressin)
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80
Q

Autosomal recessive DI normally involves mutations in the region coding for what protein? What syndrome is this most commonly a part of?

A

Mutation in region coding for neurophysin II.

Part of Wolfram syndrome (DIDMOAD)

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81
Q

How does one treat neurogenic DI?

A

DDAVP nasal or oral

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82
Q

How does one treat partial neurogenic DI?

A

Chlorpropamide or carbamezapine

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83
Q

How does one treat gestational DI?

A

DDAVP nasal

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84
Q

How does one treat nephrogenic DI?

A

HCTZ and low Na diet to reduce GFR and lower ECFV

or

NSAID to decrease GFR

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85
Q

Water deficit =

A

Water deficit = 0.6 x body weight x [(SNa/140)-1]

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86
Q

What is a normal range of TBK?

A

50(m) - 40(f) mEq/kg

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87
Q

What factors increase K+ uptake in cells?

A

Insulin
B-catecholamines
Alkalosis

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88
Q

What factors decrease uptake or increase efflux of K+ in cells?

A

a-catecholamines
acidosis
Hyperosmolarity (efflux)

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89
Q

What are common etiologies for renal K+ loss?

A

Diuretics
Magnesium deficiency
ATN

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90
Q

What might be some consequences of hypokalemia?

A 
HTN
Arrhythmias
Muscle weakness
Metabolic alkalosis
Insulin resistance
AKI, ESRD
Polydipsia, polyuria
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91
Q

What are the clinical manifestations of hypokalemia?

A 
Muscle weakness
Arrhythmias
Resp failure
Ileus
Hypokalemic nephropathy
Increased ammonia formation
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92
Q

In treating hypokalemia, what is the first step?

A

Replete magnesium

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93
Q

What conditions make patients high risk with hypokalemia (at

A

Severe hepatic disease
HF
Ischemic HD or MI
On digoxin or antiarrhythmics

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94
Q

What might cause pseudohyperkalemia?

A

Leukocytosis > 50k wbc
Thrombocytosis >1m plts
Hemolysis
Prolonged tourniquet

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95
Q

What are four causes of true hyperkalemia?

A

Impaired renal excretion
Excessive intake
Cellular shift
tissue destruction

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96
Q

What can be given to move K+ into cells with hyperkalemic patients?

A

Glucose & insulin
NaHCO3 for acidemic pts
Beta agonists

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97
Q

What can be given to oppose the electrical abnormalities in a hyperkalemic patient?

A

Ca2+ gluconate

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98
Q

What can be given to remove excess K+ from a hyperkalemic patient?

A

Kayexalate
Diuretics
Florinef
Dialysis

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5
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99
Q

What are some clues with hematuria that it might be a UTI?

A

Dysuria and/or pyuria

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100
Q

What clue with hematuria suggests that it might be glomerulonephritis?

A

A recent URI

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101
Q

What might lead one to think that hematuria is a result of hereditary nephritis or PKD?

A

Positive family hx of renal disease

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102
Q

What might lead to the diagnosis of a kidney stone (calculus) with hematuria?

A

Unilateral flank pain with radiation

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103
Q

What symptoms accompanying hematuria might suggest BPH?

A

Hesitancy and dribbling

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104
Q

What are some other possible causes of hematuria?

A

Malignancy, recent vigorous exercise or trauma, endometriosis, medications, sickle cell, TB

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105
Q

What is a normal excretion of albumin?

A

Up to 30mg/day

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106
Q

What are ways to measure protein excretion?

A

24 hour urine collection

Random urine protein:creatinine
normal: 0.1 - 0.15

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107
Q

What are possible etiologies of transient proteinuria?

A 
Fever
Exercise
UTI
Malignant HTN
CHF
108
Q

Acute kidney injury is defined as a reduction in kidney function that occurs in a period less than ___ hours, consists of:
Absolute increase in serum creatinine of >/= ___mg/dl
Percentage increase in serum creatinine >/= ____ %
Reduction in urine output of __ hours.

A

> 48 hours

Serum creatinine increase >/= 0.3 mg/dl
Percentage serum creatinine increase >/= 50%
Reduction in urine output 6 hours

109
Q

The RIFLE criteria defines degree of kidney disease based on GFR and urine output. RIFLE:

A 
Risk
Injury
Failure
Loss
ESKD
110
Q

According to the RIFLE criteria, Injury is defined as:
SCreat =
GFR =

A 
SCreat = x2
GFR = decrease > 50%
111
Q

According to the RIFLE criteria, Risk is defined as:
SCreat =
GFR =

A 
SCreat = x1.5
GFR = decrease > 25%
112
Q

According to the RIFLE criteria, Failure is defined as:
SCreat =
GFR =

A 
SCreat = x3 or >/= 4mg/dl
GFR = decrease > 75%
113
Q

According to the RIFLE criteria, Loss is defined as:

A

Persistent ARF with complete loss of kidney function >4 weeks

114
Q

According to the RIFLE criteria, ESKD is diagnosed after __ months

A

> 3 months

115
Q

Anuria is UO of

A
116
Q

Oliguria is UO of

A

100 - 400cc/24 hrs

117
Q

Polyuria is UO of >

A

> 3000cc/24 hrs

118
Q

How much of ARF is iatrogenic?

A

50%

119
Q

Symptoms common with uremic milieu of AKI:

General, fluid, CV, pulm, abd, neuro, heme

A
  • Nausea, vomiting, malaise, altered taste and sensorium
  • Fluid imbalance (hypo or hypervolemia)
  • Pericardial effusion, tamponade
  • Rales with hypervolemia
  • Diffuse abd pain and ileus
  • Encephalopathic changes (asterixis), confusion, seizures, hiccups
  • Platelet dysfx
120
Q

A sudden and severe drop in BP or interruption of blood flow to kidneys from severe injury or illness is which type of etiology for ARF?

A

Pre-renal

121
Q

Direct damage to the kidneys by inflammation, toxins, drugs, infection or reduced blood supply is which type of etiology for ARF?

A

Intrarenal

122
Q

Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury represents which type of etiology for ARF?

A

Post-renal

123
Q

Prerenal ARF resulting from intravascular volume depletion can be associated with:

A

Dehydration, hemorrhage, renal fluid loss (diuresis), skin loss, third space loss (cirrhosis, CHF, nephrotic syndrome)

124
Q

Prerenal ARF resulting from inadequate cardiac output can be associated with:

A

Cardiogenic shock, CHF, pericardial effusion with tamponade, massive PE

125
Q

Prerenal ARF resulting from systemic vasodilation can be associated with:

A

Sepsis syndrome

126
Q

Prerenal ARF resulting from renal vasoconstriction can be associated with:

A

PG inhibitors, aspirin, NSAIDs, cyclosporine, tacrolimus, radiocontrast

127
Q

Intrarenal causes for ARF can be divided into (4) causes

A

Vascular, glomerular, interstitial, and tubular causes

128
Q

Intrarenal ARF resulting from vascular disease can be associated with:

A

Bilateral renal artery stenosis/thrombosis/embolism

Bilateral renal vein thrombosis

Small vessel disease: thrombotic microangiopathy (HUS/TTP, scleroderma, malignant HTN, HELLP syndrome), atheroembolic disease

129
Q

Atheroembolism may cause ARF by:

A

cholesterol emboli following a procedure or anticoagulation that presents as pt with blue toes and levido reticularis, eosinophilia/eosinophiluria, low C3 and C4

130
Q

Rapidly Progressive glomerulonephritis histologically looks like:

A

Crescentic GN

131
Q

RPGN is classified with ________ on biopsy

A

Immunofluorescence

132
Q

RPGN can be attributed to:

A

Immune complex deposition (linear or granular), Pauci-immune diseases

133
Q

RPGN associated with Linear immune complex deposition includes two diseases:

A

Good pasture’s

Anti-GBM renal limited disease

134
Q

RPGN associated with granular immune complex deposition includes 6 diseases:

A 
Post-infectious GN
Infective endocarditis
Lupus nephritis
IgA nephropathy
Henoch-Schonlein purpura
Membranoproliferative GN
135
Q

RPGN associated with no immune deposits (Pauci-immune) includes two diseases:

A

C-ANCA disease (Wegener’s granulomatosis)

P-ANCA diseases (Churgg-Strauss, polyarteritis nodosa)

136
Q

RPGN immune complex GN with Low C3/C4

A

SLE, SBE, MPGN, PIGN, cryo, shunt nephritis, heavy chain dz, HBV

137
Q

RPGN immune complex GN with normal C3/C4

A

IgA nephropathy

138
Q

Intrarenal ARF resulting from interstitial diseases such as:

A

Bacterial pyelonephritis

Drug induced acute allergic

139
Q

What is the classic triad of drug-induced acute allergic interstitial nephritis?

A

Fever, rash, urine eosinophilia

140
Q

What drugs are common etiologies of drug induced AIN?

A

Abx, anti-TB meds, diuretics, NSAIDs, anticonvulsants, allopurinol, many more

141
Q

Intrarenal ARF resulting from tubular diseases such as:

A

Renal ischemia, exogenous toxins and drugs, endogenous toxins

142
Q

Common exogenous agents that can cause ATN:

A
  • Amphotericin B (direct nephrotoxic fx)
  • Aminoglycosides (proximal tubule damage, hypomagnesemia)
  • Cisplatin (magnesuria and hypomagnesemia)
  • Radiocontrast
  • Ethylene glycol
143
Q

How does one prevent ATN associated with contrast dye?

A

Volume loading with NSS before and after study, oral acetylcystine before and after, stop diuretics/ACEI/ARB/NSAIDs 24 - 28 hrs before, iso-osmolar contrast agents

144
Q

How quickly does ATN associated with contrast dye occur?

A

Within 12 hours of study

145
Q

Post-renal etiologies for ARF are divided into three locations:

A

Intraureteral
Extraureteral
Urether and bladder outlet

146
Q

Intraureteral causes of ARF include:

A

Stones, blood clots, papillary necrosis, vesicoureteral reflux, stricture

147
Q

Extraureteral causes of ARF include:

A

Cancer, retroperitoneal fibrosis, pregnant uterus

148
Q

Urethral and bladder outlet causes of ARF include:

A

Phimosis, stricture, BPH, neurogenic bladder, calculi, trauma, blood clot, spasm, malignancy of prostate/bladder/cervix/colon

149
Q

Post-renal etiologies of ARF present with symptoms such as:

A

Suprapubic or flank pain, decreased UO, oliguria and polyuria, hesitancy, intermittency, dribbling, nocturia, frequency

150
Q

Post-renal etiologies of ARF may be associated wiith:

A

Hx of UTI
Indwelling catheter
Anticholinergics or alpha antagonists
Autonomic dysfx

151
Q

Findings upon physical exam with post-renal causes of ARF may include:

A 
Enlarged kidneys
Palpable bladder
Abd mass, distension
Pelvic mass
BPH, prostatic induration
Aortic dilitation
Edema
152
Q

Post-renal ARF should be expected if

A

bladder or prostate are enlarged or there is evidence of tumor or UA is non-diagnostic

153
Q

What is the first step if ARF is suspected to be obstruction-related?

A

Bladder scan for post-void residual (normal

154
Q

Urine eosinophilia is associated with which two nephritic conditions?

A

Allergic interstitial nephritis

Atheroembolism

155
Q

What is the FeNa?

A

Fractionoal Excretion of Sodium

FeNa = [(U/P Na)/(U/P Cr)] x 100

Measures resorption activity of tubules

156
Q

Chronic kidney disease is defined as presence of damage or decreased function for:

A

three months or more, regardless of cause

157
Q

CKD staging based on GFR stages ranges from G1, corresponding to a GFR of ___ and G5, corresponding to a GFR of ___.

A

G1; GFR = > 90 mL/min/1.73m^2 (normal)

G5; GFR =

158
Q

CKD staging based on albuminuria stages ranges from A1, corresponding to AER of ___, to A3, corresponding to ___.

A

A1; AER = 300 mg/day (severely increased)

159
Q

CKD staging w/r/t comorbidities: Stage I:

A

Treat comorbidities. Goal is to slow progression of disease. Reduce CV risk.

160
Q

CKD staging wrt comorbidities: Stage II:

A

Determining prognosis. Keep an eye on PTH.

161
Q

CKD staging wrt comorbidities: Stage III:

A

Focus is treating complications like hypocalcemia and anemia and malnutrition.

162
Q

CKD staging wrt comorbidities: Stage IV:

A

Preparing pt for transplant. Monitoring phosphate in blood. Managing metabolic acidosis. Managing hyperkalemia.

163
Q

CKD staging wrt comorbidities: Stage V:

A

Transplant is goal. Managing uremia.

164
Q

The normal GFR for women and men is ___ and ___ respectively.

A

Women: 120 mL/min/1.73m^2
Men: 130 mL/min/1.73m^2

165
Q

Problem with using serum creatinine to estimate GFR?

A

Can only rely upon in in individuals with stable kidney function.

166
Q

Creatinine is ____ filtered and not metabolized, but it is ____ in the proximal tubule.

A

Freely filtered, secreted in proximal tubule.

167
Q

The Cockcroft-Gault equation results in how much of an overestimate of creatinine clearance?

A

10 - 40 percent.

168
Q

The equation used to estimate kidney function in patients with CKD

A

MDRD equation

169
Q

The equation used to estimate GFR that is best used with normal or mildly reduced GFR (>60mL/etc)

A

CKD-EPI

170
Q

Other conditions commonly associated with CKD (5):

A 
Anemia
HTN
CVD
Mineral bone disease
Hyperkalemia
171
Q

Uremic cardiomyopathy in patients with advanced CKD is characterized by:

A

diastolic dysfunction, heart failure, and LVH

172
Q 
Dipstick values for albuminuria corresponding to:
\+1
\+2
\+3
\+4
A 
\+1 = 30 mg/dl
\+2 = 100 mg/dl
\+3 = 300 mg/dl
\+4 = >1000 mg/dl
173
Q

Two erythropoiesis-stimulating agents that can be given to predialysis patients with anemia:

A

Procrit

Arenesp

174
Q

Target Hg levels for patients with CRF:

A

10 - 11 g/dL

175
Q

Metabolic acidosis resulting from CKD becomes overt when GFR reaches:

A
176
Q

Metabolic acidosis with CKD results in what response on the PTH-calcium axis? Muscle?

A

Bone buffering and skeletal muscle break down

177
Q

Patients who are oliguric with CKD will develop problems with elevated _____ in the blood.

A

Potassium

178
Q

Sodium and intravascular volume balance is maintained in patients with CKD until GFR reaches

A
179
Q

The target serum PTH in patients with CKD ranges from ___ in stage II to ____ in stage V

A

Stage II: 35 - 70 pg/ml

Stage V: 150 - 300 pg/ml

180
Q

Four things to manage in slowing the progression of CKD:

A

Blood pressure
Protein restriction
Glycemic control in DM
Dyslipidemia

181
Q

The AEIOU of indications for dialysis:

A 
Acidosis
Electrolytes
Ingestions/Intoxications
Overload of volume
Uremia
182
Q

Uremia signs and symptoms

A

Fatigue, weakness, decreased appetite, weight gain, nausea, vomiting, bizarre dreams, altered mental status, seizures

Hiccups, diffuse pruritis, twitching

183
Q

Complications of uremia:

A

Pericarditis, pleuritis, encephalopathy, bleeding diathesis, nausea, vomiting, malnutrition, hiccups, pruritis

184
Q

Anion gap equation

A

Anion gap = Na - (HCO3 + Cl)

[Normal = 10 - 12]

185
Q

In respiratory compensation for metabolic acidosis, for every Mmole of bicarb BELOW normal ,the PCO2 falls ___ and H+ increases about ___

A

PCO2 falls 1.2

H+ increases 1

186
Q

In respiratory compensation for metabolic alkalosis, for every bicarb ABOVE normal, PCO2 increases ____ and H+ decreases ____

A

PCO2 inc 0.7 Mmole

H+ dec 0.5 Mmole

187
Q

In renal compensation for acute respiratory _______, H+ increaeses by 0.8 nmole for each mmHg pCO2

A

Acidosis

188
Q

In renal compensation for chronic respiratory ______, HCO3 decreases by 5 for a pCO2 decrease of 10 and H+ decreases by 0.25 nMole for each mmHg pCO2

A

Alkalosis

189
Q

Winter’s formula

A

Evaluates respiratory compensation

pCO2 = 1.5 x HCO3 + 8 +/- 2

190
Q

Distal RTA Type 1 is a dysfunction of ______ cells

A

Intercalated

191
Q

In Distal RTA type 1, urine pH is _____, blood potassium is _____ and urine calcium is _____

A

Alkaline
Low
High

192
Q

Distal RTA type 1 is diagnosed with:

A

Tests of H+ excretion (NH4):
Urinary AG
Urinary OG
Blood pCO2

193
Q 
Proximal RTA type 2 is characterized by: 
HCO3 wasting for TCO2 \_\_\_\_\_
HCO3 in urine that \_\_\_\_ with TCO2
K+ is \_\_\_\_
Urine pH is \_\_\_\_
Other things in urine (3):
A

> 17mEq/L
inc/dec
K+ = Low
Urine pH = low

Phosphaturia, glycosuria, proteinuria?

194
Q

RTA type IV involves low levels of

A

Renin and aldosterone

195
Q

Four principal cell disorders:

A

Liddle’s
Pseudohypoaldo I
Pseudohypoaldo II
Hyporenin/hypoaldo

196
Q

Liddle’s syndrome mimics primary hypoaldosteronism but with increased volume and is caused by:

A

Open Na+ channel in principal cells and low renin

197
Q

Pseudohypoaldosteronism I presents with increased K+, Na+ wasting, RTA and is caused by

A

closed Na+ channels in principal cells

198
Q

Pseudohypoaldosteronism II (Gordon’s syndrome) presents with increased K+, increased Na+ reabsorption, RTA, and is caused by

A

Increased Chloride shunt

199
Q

Hyporenin/hypoaldo presents with

A

Hyperkalemia, Na+ wasting, RTA

200
Q

Bartter’s acid base disorder has a _____ effect

A

Loop-diuretic-like effect

NaCl wasting, K+ wasting, hypercalciuria, hypomangesuria

201
Q

Gitelman’s acid base disorder has a _______ defect

A

Thiazide-like defect

NaCl wasting, K+ wasting, hypocalciuria, hypermagnesuria

202
Q

UTI is defined by the presence of a pure growth of more than _____ colony forming units of bacteria per ml

A

10^5 CFUs

203
Q

MC UTI:

A

e. coli

204
Q

Recurrent UTI tests get a urologic work up that consists of:

A 
Unspun urine
Urinalysis
Culture
KUB
U/S
205
Q

Bacteriuria CFU/mL for acute cystitis

A

> 10^3

206
Q

Bacteriuria CFU/mL for acute pyelonephritis

A

> 10^4

207
Q

Bacteriuria CFU/mL for UTI in men

A

> 10^4

208
Q

Bacteriuria CFU/mL asymptomatic

A

> 10^5 x 2

209
Q

Microalbuminuria is defined as ____mg / day albumin

A

30 - 300 mg / day

210
Q

Macroalbuminuria is defined as ____mg / day albumin

A

> 300 mg / day albumin

211
Q

Of the 10% of T1DM patients that develop diabetic nephropathy, __% of them develop ESRD within 30 years if untreated

A

75%

212
Q

Stage 1 of diabetic nephropathy

A

Rernal hypertrophy and hyperfunction: GFR increases, risk stratification difficult

213
Q

Stage 2 of diabetic nephropathy

A

Latency: detectable glomerular lesions but urinary albumin and bp are normal

214
Q

Stage 3 of diabetic nephropathy

A

Microalbuminuria: usually 5+ years after disease onset, declining GFR, HTN mor prevalent, vascular complications (retinopathy, neuropathy, PVD, CAD, CVA)

215
Q

Stage 4 of diabetic nephropathy

A

Macroalbuminuria: GFR declines monthly (1.2mL/min), ESRD in 5 - 15 years, 3/4 with HTN

216
Q

Stage 5 of diabetic nephropathy

A

Progression to ESRD

217
Q

In type 1 diabetics, _______ universally precedes nephropathy

A

Retinopathy

218
Q

Why might one with stage 1 diabetic nephropathy have increased GFR?

A

Increased activation of renin-angiotensin-aldosterone system, resulting in elevated pressure that eventually damages glomerulus

219
Q

_____ bind cell surfaces and induce cytokine release, oxidative stress, and free radical formation in diabetic nephropathy

A

Advanced Glycation End products

220
Q

In diabetic nephropathy, increased activity of ________ results in increased sorbitol which induces free radicals and ECM synthesis

A

Aldose reductase

221
Q

In diabetic nephropathy, ______ is increased, resulting in free radicals and hydrogen peroxide

A

Nitric oxide synthase

222
Q

In diabetic nephropathy, mesangial cell nuclei form palisades around masses of mesangial matrix and glomerular capillaries form microaneurysms in a presentation known as _____

A

Kimmelstein-Wilson nodules (Nodular Glomerulosclerosis)

223
Q

Immunofluorescence staining for diabetic nephropathy has a _____ pattern for the GBM, TBM, and Bowman’s capsule for Ig_

A

Linear, IgG

224
Q

_____ is the earliest clinical finding of diabetic nephropathy

A

Increased urinary protein excretion

225
Q

In patients with the microalbuminuria stage of diabetic nephropathy, __% will remain microalbuminuric and ______% will progress to frank proteinuria after ten years

A

40% remain, 20 - 45% progress

226
Q

What is the gold standard test for proteinuria?

A

24 hour collection of urine for albumin

227
Q

How often should a diabetic patient have a urinalysis?

A

Yearly starting 5 years after diagnosis/onset

228
Q

The most important points of control in preventing diabetic nephropathy are:

A

Glycemic and blood pressure, especially blood pressure!

229
Q

The drug class(es) used to treat diabetic nephropathy:

A

ACEIs and ARBs, low does aspirin

230
Q

ACEIs and ARBs promote dilation of ____ arterioles more than ____ arterioles.

A

Efferent > afferent

231
Q

Treatment options for a patient with diabetic nephropathy that develops ESRD:

A

Hemodialysis
Peritoneal dialysis
Transplant

232
Q

Examples of endogenous antigens involved in AIN

A

TBM glycoproteins (3M-1, TIN1)
Tamm-Horsfall tubular protein
Immune complexes

233
Q

Before antibiotics, AIN was mainly induced by:

A

scarlet fever, diphtheria

234
Q

Medications commonly implicated in AIN

A

Methicillin, Rifampin, Allopurinol, NSAIDs, COX2I, PPI, HAART

235
Q

AIN manifests clinically after a few days to weeks and presents with:

A

ARF, mild proteinuria, hematuria, pyuria, leukocyte casts, possible flank pain, fever, maculopapular rash, and arthralgia

236
Q

For best prognosis with drug-induced AIN, treatment should start with:

A

Removing aggravating agent

237
Q

Poor prognostic findings for drug-induced AIN are associated with:

A 
Delayed improvement (1 week)
Prolonged exposure (>2 - 3 weeks)
Pre-existing CKD
Biopsy findings of diffuse interstitial infiltrates, granulomas, fibrosis, or tubular atrophy
238
Q

Systemic diseases associated with AIN:

A

Sarcoidosis
SLE
Sjogren’s

239
Q

Malignancies associated with AIN:

A

Lymphoma, leukemia

240
Q

Possible general causes of chronic interstitial nephritis:

A

Toxins, drugs, crystals, infections, obstructions, immunologic mechanisms, ischemia

241
Q

Histology findings for CIN:

A

Tubular dilation, hypercellularity, noncaseating granulomas, crystals

242
Q

CIN clinical manifestation:

A

Loss of GFR over time, mild proteinuria, proximal and distal tubular dysfx, concentrating defect, salt wasting

243
Q

Mechanism for Lithium-induced diabetes insipidus:

A

Inhibits ADH signaling and decreases expression of AQP2 in collecting ducts

244
Q

Treatment for Lithium renal toxicity:

A

Discontinue cautiously, K-sparing diuretics (amilioride, triamterene), possibly hemodialysis

245
Q

Analgesic nephropathy may be caused by prolonged use of ______ and ______ and is a result of:

A

Aspirin and acetaminophen, result of decreased BF to renal medulla

246
Q

MC complications of analgesic nephropathy:

A

Renal papillary necrosis

247
Q

Papillary necrosis is associated with (6) conditions and will present on CT with ______ or _____

A

Analgesic nephropathy, diabetic nephropathy, APN, sickle cell, UT obstruction, renal TB

Bumpy contours or papillary calcifications

248
Q

In rhabdomyolytic nephrotoxic injury, muscle destruction releases ______ and ______ which cause injury via:

A

Myoglobin: vasoconstriction, NO scavenging, oxidative injury
Hemoprotein: direct tubular cytotoxicity

249
Q

With rhabdomyolysis and ATN will see upon UA:

A

Muddy brown casts, granular casts but no RBCs

250
Q

Renal perfusion autoregulation mechanisms impaired when .. BP? drops below

A

80?

251
Q

ATN phases involve:
Ischemic injury, disruption of polarity and sloughing of cells causing _______ ____________ , then maintenance of injury followed by recovery which often presents with initial post-ATN _______

A

tubular obstruction, diuresis

252
Q

By definition, a complicated UTI involves:

A

a structural or functional impairment that reduces efficacy of antimicrobial therapy

253
Q

Most common urinary pathogen in community UTI:

A

E. coli

254
Q

Nosocomial UTI often caused by:

A

Proteus
Klebsiella
Enterococcus
S. saprophyticus

255
Q

Hematogenous spread of infection to UT usually associated with

A

s. aureus or candidal fungemia

256
Q

What bacterial virulence factor seems to be instrumental in pathogenesis of bacterial cystitis by attaching to vaginal and bladder mucosae?

A

Type 1 pili

257
Q

Risk factors for UTI in young women include

A 
Frequency of sexual intercourse
Previous UTI
Condom
Diaphragm
Abx 2 - 4 weeks earlier
258
Q

A UTI may be complicated by pre-existing conditions such as:

A

DM
Transplant
Granulocytopenia
HIV/AIDS

259
Q

Treating a mild infectious pyelonephritis with a compliant patient:

A

7 - 14 days
12 - 24 hr observation
Quinolone, TMP/SMZ
Gram positive cocci: amox or amox/clav

260
Q

Treating moderate to severe infectious pyelonephritis or non-compliant pt:

A

Parenteral:
Quinolone
Aminoglycoside +/- ampicillin
Extended spectrum cephalosporin +/- aminoglycoside

261
Q

MC instrumental complication for UTI in men:

A

Foley catheter

262
Q

Treatment duration for uncomplicated UTI in women

A

Cystitis: 3 days
APN: 7 days

263
Q

Treatment duration for complicated UTI in women

A

Cystitis: 7 - 10 days
APN: >2 weeks

264
Q

Post-menopausal women have a decrease in _____ and an increase in ______ in their vaginal flora, associate with:

A

Lactobacilli, e.coli

Decreased estrogen

265
Q

Mechanism of cranberry juice in managing a UTI

A

Proanthocyandins inhibit bacterial adherence to epithelial cells

266
Q

What antibiotic is preferred DOC for treating gram negative infections with ESBL?

A

Carbapenem

Clincial Medicine (10 decks)

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