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FA17 Nephrology > GN 2 > Flashcards

GN 2 Flashcards

1
Q

nephrotic syndrome hallmark clinical findings

A

proteinuria >3g/day

peripheral edema

hypoalbuminuria

(may have just the proteinuria)

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2
Q

etiologies of nephrotic syndrome

A

1/3 = systemic disease with renal manifestations

2/3 = idiopathic

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3
Q

systemic diseases causing nephrotic syndrome

A

amyloidosis

diabetic nephropathy

HIV nephropathy

SLE

hep C

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4
Q

types of idiopathic nephrotic syndrome

A

minimal change dz
membranous nephropathy
focal segmental glomerulosclerosis

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5
Q

amyloidosis nephrotic syndrome

A

associated with multiple myeloma (AL) or RA, IBD, and chronic infection (AA)

misfolded non-fxnl proteins

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6
Q

diabetic nephropathy

A

MC in type I

DM pts are prone to other renal dz (papillary necrosis and nephritis)

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7
Q

nephrotic syndrome s/s (6)

A

peripheral edema

abdominal fullness

dyspnea

increased infection

hypercoagulability

protein calorie malnutrition

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8
Q

peripheral edema nephrotic syndrome

A

LOW serum albumin causes drop in oncotic pressure shift to 3rd space

this also causes abdominal fullness (ascites) and dyspnea

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9
Q

dyspnea nephrotic syndrome

A

due to pulmonary edema, pleural effusion, ascites on diaphragm

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10
Q

infection nephrotic syndrome

A

due to urinary loss of Ig and complement

also have increased susceptibility to pneumococcus

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11
Q

hypercoagulability

A

increased likelihood of arterial and venous thromboemoboli

particular FVT and renal vein thrombosis

renal vein thrombosis - be sure to distinguish from stone

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12
Q

protein calorie malnutrition

A

negative protein balance

more is being excreted than is being taken in

catabolic state may be masked by weight gain from edema

causes vitamin deficiencies (loss of binding proteins)

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13
Q

lab derangements off nephrotic syndrome

A

decreased serum albumin

hyperlipidemia

vitamin deficiencies

elevated ESR (increased fibrinogen)

hypocalcemia

U/A - proteinuria and oval fat bodies

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14
Q

hyperlipidemia nephrotic syndrome

A

hepatic production of lipids increases to maintain oncotic pressure despite losing so much protein in urine

decreased VLDL clearance

inflammation also exists - accelerated CAD

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15
Q

hypocalcemia why in nephrotic syndrome

A

vitamin D deficiency

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16
Q

tests used to elucidate etiology of nephrotic syndrome

A

ANA

C3/C4/complement

SPEP/UPEP

infectious dz work up

renal biopsy

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17
Q

general management of nephrotic syndrome

A

Diet and Edema control

hyperlipidemia management

anticoagulation

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18
Q

diet and edema nephrotic syndrome

A

SALT restriction

diuretics (loop and TZD will be higher doses)

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19
Q

hyperlipidemia management nephrotic syndrome

A

diet and exercise don’t help

aggressive pharmacotherapy

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20
Q

hypercoaguable state nephrotic syndrome

A

prone to membranous glomerulopathy and Afib

anticoagulant 3-6 months for thrombosis or until dz is controlled

consider prophylactic anticoagulation

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21
Q

minimal change dz (Nil Dz)

A

mc in children, can affect adults

adults: M=F, children: M>F

may be idiopathic, follow URI, or paraneoplastic syndrome (Hodgkin), associated with drugs (NSAID)

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22
Q

manifestations of Nil Dz

A

susceptible to infection

tendency to thromboembolic events

CAN cause acute renal failure

severe hyperlipidemia, protein malnutrition

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23
Q

Nil Dz renal biopsy

A

tissue looks almost completely normal

little disposition of immune complexes

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24
Q

minimal change disease tx

A

prednisone 1mg/kg/day
adults longer

some patients become resistant to corticosteroid

majority of patients will relapse and req steroid again - ESRD progression rare

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25
membranous nephropathy etiology
common cause of nephrotic syndrome in adults (idiopathic) in children usually secondary disorder
26
membranous nephropathy disease
AutoAb against phospholipid receptor (PLA2-R) on podocyte of glomerulus immune complex deposition in glomerular capillary walls and thickening of GBM no hypercellularity on biopsy
27
membranous nephropathy medication induced
medications for another disease cause issue malignancies: Lung and GI infections: HBV, endocarditis, syphilis autoimmune dz: SLE, thyroiditis, mixed connective tissue drug exposure: NSAID
28
membranous nephropathy
typical symptoms and signs of nephrotic syndrome AKI is rare normal BP and normal GFR
29
membranous nephropathy diagnosis
serologic assays for PLA2R Abs does not req. renal biopsy
30
disease conditions in membranous nephropathy
higher incidence of neoplasm - usual age appropriate screenings (Chest CT, colonoscopy, PSA, mammogram, pap/pelvic) high risk of thromboembolic event high risk of renal vein thrombosis
31
treatment of membranous nephropathy
risk stratification based on 24 hr urine protein level and Cr clearance Low: ACE/ARB, BP/hyperlipidemia to goal Moderate/HR: same +immunosuppression excellent for renal transplant
32
treatment membranous nephropathy low risk
proteinuria <3.5 g/day low salt diet, strict BP control, ACE inhibitor
33
treatment membranous nephropathy moderate risk
3.5-8 g/day normal renal fxn low salt diet, strict BP control, ACE inhibitor +/- immunosuppression
34
treatment membranous nephropathy high risk
8 g/day normal renal fxn low salt diet, strict BP control, ACE inhibitor +immunosuppression
35
Focal Segmental Glomeurlosclerosis (FSGS)
primary idiopathic/ secondary to DM, GIV, vesicurethral reflux nephrotic syndrome + evidence nephritic symptoms (microscopic hematuria at diagnosis, HTN)
36
FSGS renal biopsy
segmental areas of mesangial sclerosis | cloppase in some of glomeruli
37
primary FSGS presents + Tx
rapid decline of renal function more likely to have nephrotic syndrome Tx: high dose steroids for 2-3 months, taper
38
secondary FSGS presents + Tx
gradual decline in renal function over years proteinuria may reach nephrotic levels, rarely develop nephrotic syndrome supportive care + ACE inhibitors
39
tubulointerstitial disease
disease of kidney outside glomerulus acute or chronic
40
acute tubulointerstitial disease (AIN)
hypersensitivity to medications toxins/ischemia interstitial edema, PMN infiltration, tubular cell necrosis
41
drugs that often cause AIN
ABX (PCN, Cephalosporins, sulfa) NSAIDs Rifampin PPI
42
AIN patho
begins abruptly, AKI within days of exposure subset of DRESS (drug rash with eosinophilia and systemic syndromes)
43
NSAID AIN
BEGINS WEEK TO MONTHS AFTER USE mc in elderly nephrotic syndrome
44
AIN presentation
``` rash fever eosinophilia eosinophiluria elevated IgE (allergic) ```
45
rifampin AIN
DOESN'T cause EOSINOPHILIA usually occurs following reintroduction DRSS
46
other causes of AIN besides drugs
immunologic disease acute renal transplant rejection infections (any type of infection will cause)
47
AIN treatment
promptly DC offending drug or treat underlying disease document allergy can hive high dose of steroid over 4-6 weeks excellent supportive care
48
chronic tubulointerstitial disease
acute insult or progressive insult without acute cause interstitial fibrosis and atrophy are often seen
49
main causes of chronic tubulointerstitial disease
obstructive uropathy vesicoureteral reflux analgesics heavy metals
50
obstructive uropathy
prolonged obstruction of urinary tract (BPH, stone, carcinoma, retroperitoneal tumor/fibrosis) UO alternates bt polyuria and oliguria HTN + azotemia back flow of uric into kidney
51
obstructive uropathy treatment
BPH and stones - usual tx pelvic tumor: stent, tx underlying cause
52
retroperitoneal fibrosis
rare, encases ureters and abdominal organs in fibrotic tissue can be caused by meds, biologic agents, cancers diagnose by CT + contrast, CT biopsy secondary = tx underlying dz + steroid primary = steroid, tamoxifen, immunosuppressive
53
vesicoureteral reflux
urine passes retrograde during voiding due to incompetent vesicoureteral sphincter disorder of child hood (typically renal damage before 5 y/o) inflammatory response + fibrosis progressing to ESRD
54
VUR epidemiology
caucasian, red head, male neonates, female mc children
55
diagnosis of vesicoureteral reflux
voiding cystourethrogtaphy (VCUG) recommended in children with UTI and siblings of persons with VUR
56
VUR treatment
keeping patient infection free significantly decrease risk of renal damage (prophylactic ABX and monitored) young patents - conservative tx,
57
analgesics chronic tubulointerstitial disease
ingestion of large quantities of analgesics for chronic pain (esp. combo pills) MC in women hematuria, mild proteinuria, polyuria, anemia, sterile pyuria
58
analgesics chronic tubulointerstitial disease patho
kidney tries to excrete large quantities become concentrated at papillary tip (10x that of serum) cause inflammation and papillary tip necrosis - sloughing
59
heavy metals that cause analgesics chronic tubulointerstitial disease
lead cadmium mercury bismuth accumulate and cause cell scaring, fibrosis
60
other causes of chronic tubulointerstitial disease
Lithium imunologic dz neoplasia atherosclerotic kidney dz genetics metabolic d
61
general manifestations of chronic tubulointerstitial disease
polyuria due to inability to concentrate urine may also have dehydration and salt wasting hyperkalemia due to aldosterone restance hyperCl due to renal tubular acidosis (decreased ammonia, inability to acidly, bicarb wasting)
62
diagnosis of chronic tubulointerstitial disease
UA non specific - brand waxy casts + proteinuria ID underlying disorder quantify degree of fibrosis on biopsy

FA17 Nephrology (13 decks)

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