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Step 1 (Steffanie) > Renal > Flashcards

Renal Flashcards

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1
Q

In metabolic acidosis there is increased urinary excretion of which substances?

A

H+, NH4+, and H2PO4-

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2
Q

What happens to the concentrations of PAH, creatinine, inulin, and urea as fluid runs along the proximal tubule?

A

They increase

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3
Q

What happens to the concentrations of bicarb, glucose, and amino acids as fluid runs along the proximal tubule?

A

They decrease

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4
Q

How does CKD with mineral bone disease present?

A

Hyperphosphatemia, secondary hyperparathyroidism, and decreased calcitriol levels. Pts can be asymptomatic or develop weakness, bone pain, and fractures

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5
Q

Vasopressin and Desmopressin cause increased permeability of which substances?

A

Increase in water and urea permeability at the inner medullary collecting duct

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6
Q

Filtration fraction equation

A

FF=GFR/RPF

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7
Q

What is responsible for the thrombotic and thromboembolic complications of nephrotic syndrome?

A

Loss of anticoagulant factors, especially antithrombin III

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8
Q

Linear deposits of immunoglobulin along the glomerular basement membrane

A

anti-glomerular basement membrane disease

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9
Q

What are the immunoglobulin deposits composed of in anti-glomerular membrane disease

A

IgG and C3

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10
Q

What is seen on light microscopy in anti-GBM disease?

A

Glomerular crescents composed of proliferating parietal cells with an infiltration of monocytes and macrophages

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11
Q

Renal failure and pulmonary hemorrhage in patients with anti-GBM antibodies

A

Goodpasture syndrome

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12
Q

Immunofluorescence microscopy in poststreptococcal glomerulonephritis

A

Granular deposits of IgG, IgM and C3 in the mesangium and basement membranes

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13
Q

Membranous glomerulonephropathy

A

A cause of nephrotic syndrome. Can occur secondary to underlying malignant tumors, infections, and certain meds.

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14
Q

Findings on imaging with membranous glomerulopathy

A

Diffuse increased thickness of the glomerular basement membrane on light microscopy, spike and dome appearance on methenamine silver stain, and granular deposits on immunofluorescence

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15
Q

Presentation of minimal change disease

A

Weight gain, pitting edema, significant proteinuria, hypoalbuminemia, hyperlipidemia

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16
Q

Findings in minimal change disease

A

Biopsy specimen will show no obvious glomerular lesions on light microscopy and will be negative for immune deposits on immunofluorescence. Electron microscopy shows effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes

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17
Q

What other conditions are associated with ADPKD?

A

Berry aneurysms, hepatic cysts, mitral valve prolapse

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18
Q

Urine findings in acute tubular necrosis

A

Brown, granular casts

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19
Q

Which parts of the kidney are particularly susceptible to ischemia?

A

Proximal tubule and medullary segment of thick ascending limb

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20
Q

Which part of the kidney is susceptible to nephrotoxic ATN?

A

Proximal tubule

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21
Q

What are key causes of acute interstitial nephritis?

A

NSAIDs, PCN, diuretics

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22
Q

Oliguria, fever, and rash days to weeks after starting a new drug. Eosinophils found in the urine

A

Acute interstitial nephritis

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23
Q

Presentation of renal papillary necrosis

A

Gross hematuria, flank pain

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24
Q

Causes of renal papillary necrosis

A

Chronic analgesic abuse, diabetes mellitus, sickle cell disease, severe acute pyelonephritis

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25
What cancer is minimal change disease associated with?
Hodgkin lymphoma
26
Normal glomeruli on H&E stain, effacement of foot processes on EM, negative IF
Minimal change disease
27
How is minimal change disease treated?
Corticosteroids
28
What mediates the damage in minimal change disease
Cytokines
29
What is the most common cause of nephrotic syndrome in Hispanics and African Americans?
Focal segmental glomerulosclerosis
30
segmental sclerosis and hyalinosis on H&E, effacements of foot processes on EM, negative IF
Focal segmental glomerulosclerosis
31
Most common cause of nephrotic syndrome in Caucasian adults
Membranous nephropathy
32
Diffuse capillary and GBM thickening on H&E, granular IF due to immune complex deposition, "spike and dome" appearance on EM
Membranous nephropathy
33
Thick capillary membranes with "tram track appearance" on H&E, granular IF
Membranoproliferative glomerulonephritis
34
Type I MPGN
Associated with hepatitis B or C. Subendothelial IC deposits
35
Type II MPGN
Associated with C3 nephritic factor IgG antibody that stabilizes C3 convertase leading to persistent compliment activation and decreased C3 levels. Intramembranous deposits
36
Hematuria and RBC casts
Nephritic syndrome
37
~2-4 weeks after group A strep infection. Peripheral and periorbital edema, cola-colored urine, HTN.
Acute poststreptococcal glomerulonephritis
38
Nephritogenic strains of group A strep
Carry M protein virulence factor
39
"Starry sky" granular appearance on IF due to IgM, IgG, and C3 deposition along GMB and mesangium. Subepithelial IC humps on EM
Acute poststreptococcal glomerulonephritis
40
What makes up the crescents in rapidly progressive glomerulonephritis?
Fibrin and plasma proteins with glomerular parietal cells, monocytes, macrophages
41
Linear IF in RPGN
Antibodies against collagen in GBM and alveolar basement membrane. Seen in Goodpasture syndrome - hematuria/hemoptysis.
42
Treatment for Goodpasture syndrome?
Plasmapheresis
43
Granular IF in RPGN
PSGN or DPGN
44
Negative IF (pauci-immune) in RPGN
Wegener granulomatosis - also nasal/sinus symptoms (PR3-ANCA/c-ANCA), microscopic polyangiitis (MPO-ANCA/p-ANCA), Churg-Strauss syndrome - asthma, eosinophilia, granulomas (MPO-ANCA/p-ANCA)
45
Episodic hematuria that occurs concurrently with respiratory or GI infections
IgA nephropathy (Berger Disease)
46
IgA immune complex deposition in mesangium on IF
IgA nephropathy (Berger Disease)
47
Isolated hematuria, sensorineural deafness, ocular disturbances
Alport Syndrome
48
Inheritance pattern of Alport Syndrome
X-linked dominant mutation in type IV collagen
49
"wire looping" of capillaries on H&E, granular IF, subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
Diffuse proliferative glomerulonephritis
50
What is a common cause of diffuse proliferative glomerulonephritis?
SLE
51
WBC casts
Pyelonephritis
52
Most common type of kidney stone in adults?
Calcium oxalate or calcium phosphate, oxalate more common
53
What kind of kidney stones are seen with Crohn disease?
Calcium oxalate
54
Treatment for calcium stones
Thiazides - calcium sparing diuretic, decrease calcium in urine
55
Kidney stone associated with infection with urease + bugs (Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella)
Struvite/Ammonium magnesium phosphate
56
Staghorn calculi
Adult - struvite/ammonium magnesium phosphate stone | Child - Cysteine stone
57
Clinical features of uremia
Nausea and anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction
58
Consequences of renal failure
Metabolic acidosis, dyslipidemia, hyperkalemia, uremia, sodium and water retention, growth retardation and developmental delay, erythropoietin failure (anemia), and renal osteodystrophy
59
Angiomyolipoma
Hamartoma comprised of blood vessels, smooth muscle, and adipose tissue. Increased frequency in tuberous sclerosis
60
Hematuria, palpable mass, flank pain = classic triad. May also present with fever, weight loss, paraneoplastic syndrome (EPO, renin, PTHrP, ACTH)
Renal cell carcinoma
61
May present with left sided vericocele
Renal cell carcinoma
62
Pathogenesis of renal cell carcinoma
Loss of VHL tumor suppressor gene - increased IGF-1 (promotes growth) and HIF transcription factor (increases VEGF and PDGF)
63
Von Hippel-Lindau Disease
Aut. dominant disorder associated with inactivation of VHL gene. Increased risk for hemangioblastoma of the cerebellum and renal cell carcinoma
64
Which lymph nodes does renal cell carcinoma classically go to?
Retroperitoneal lymph nodes
65
Malignant kidney tumor comprised of blastema, primitive glomeruli and tubules, and stromal cells. Average age 3 years.
Wilms tumor
66
Large unilateral flank mass with hematuria and HTN
Wilms tumor presentation
67
WT1 mutation
Wilms tumor - especially syndromic cases such as WAGR syndrome or Beckwith-Wiedemann syndrome
68
Most common type of lower urinary tract cancer
Urothelial carcinoma - malignant tumor arising from uroethelial lining of renal pelvis, ureter, bladder, or urethra. Usually from bladder
69
Risk factor for urothelial carcinoma
Cigarette smoke, naphthylamine, azo dyes, long term cyclophaospahmide or phenacetin
70
Squamous cell carcinoma of the urinary tract usually involves?
The bladder
71
Risk factors for squamous cell carcinoma of the bladder?
Chronic cystitis, schistosoma hematobium, long standing nephrolithiasis
72
Adenocarcinoma of the bladder arises from?
Urachal remnant (at dome of bladder), cystitis glandularis, exstrophy
73
Waxy casts
End stage renal disease/chronic renal failure
74
Urgency incontinence
Overactive bladder (detrusor instability) - leak with urge to void immediately.
75
Treatment for urgency incontinence
Kegel exercises, bladder training, antimuscarinics (oxybutinin)
76
Overflow incontinence
Incomplete emptying (detrusor underactivity or outlet obstruction) - leak with overfilling
77
Treatment of overflow incontinence
Catheterization, relieve obstruction (alpha blockers for BPH)
78
Mannitol
Acts on proximal convoluted tubule and descending limb. Osmotic diuretic. Use - drug overdose, elevated intracranial/intraocular pressure
79
Acetazolamide
Acts on proximal convoluted tubule.Carbonic anhydrase inhibitor. Causes self limited NaHCO3 diuresis and decreased total body HCO3- stores. Use - glaucoma, metabolic alkalosis, altitude sickness, pseudotumor cerebri
80
Adverse effects of acetazolamide
Proximal renal tubular acidosis, parasthesias, promotes calcium phosphate stone formation
81
Name the loop diuretics
Furosemide, bumetanide, torsemide
82
Mechanism of loop diuretics
Act on thick ascending limb of the loop of Henle. Inhibit cotransport system (Na+/K+/2Cl-).
83
Adverse effects of loop diuretics
Ototoxicity, hypokalemia, hypomagnesemia, dehydration, sulfa allergy, metabolic alkalosis, interstitial nephritis, gout
84
Name the thiazide diuretics
Hydrochlorothiazide, chlorthalidone, metolazone
85
Mechanism of thiazide diuretics
Inhibit NaCl reabsorption in early DCT - causes decreased diluting capacity of nephron. Decrease calcium excretion.
86
Adverse effects of thiazide diuretics
Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy
87
Name the potassium sparing diuretics
Spironolactone, eplerenone, amiloride, triamterene
88
Mechanism of spironolactone and eplerenone
Competitive aldosterone receptor agonists in cortical collecting tubule
89
Mechanism of triamterene and amiloride
Act on cortical collecting tubule by blocking Na+ channels
90
Adverse effects of potassium sparing diuretics
Hyperkalemia
91
Aliskiren
Direct renin inhibitor. Used for HTN. Contraindicated in pts already taking ACE inhibitor or ARB. Contraindicated in pregnancy

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