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Clin Med > Renal: Glomerular diseases > Flashcards

Renal: Glomerular diseases Flashcards

1
Q

what proteins are lost in PU

whats not lost

A
  • MAINLY albumin (LMW protein)
  • clotting factors
  • immunoglobulins

NOT LOST=lipoproteins

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2
Q

Orthostatic Proteinuria

-PU findings

A

PU= 1-2gm/day

  • 2-5% of adults
  • more common in adolescents and uncommong after 30YO
  • etiology= hemodynamic, subtle glomerular change, entrapment of renal vein on left side by aorta and superior mesenteric artery
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3
Q

Glomerulonephritis

-list the causes that have low complement

A

SLE
MPGN
post infectious GN
endocarditis

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4
Q

list the overall types of glomerulonephritis

A

post infecitous gn
IGA nephritis
MPGN–membranoprolifertive GN
PRGN–rapidly proliferative GN–>goodpasture’s dz, HUS, Vasuclitis

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5
Q

Acute Glomerulonephritis

  • causes
  • CM
A

post infectious
vasculitis–>Lupus, Wegners granulomatosis, HUS, goodpastures, IGA

CM

  • HTN
  • edema
  • proteinuria at non-nephrotic levels <3,000
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6
Q

post-infectious GN latent period

A

GN occurs after strep of URT or skin infection

8-14 days latent period***

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7
Q

Post-infectious GM

  • etiologies
  • CM
  • Labs
  • urine sedement
  • tx
A

ETIOLOGIES:

  • MCC= beta-hemolytic GAS skin or respiratory source
  • others=hep b, hep c, HIV, malaria, syphilis

CM–>asympto post infection to full blown nephritis

  • Hematuria (microscopic to gross) 10-14 days after infection–>TEA COLOR or COCOLA URINE
  • facial puffiness, edema (peripheral)
  • fever
  • oliguria —- <400
  • HTN
  • abd pain

LABS

  • (+) ASO titers if hx of URI–> 50% in skin and 90% in strep URI
  • LOW C3 C4 complements

URINE
+RBCs
+RBC casts
+PU non-nephrotic

TX

  • manage the renal effects—renal insuff, HTN (Nifedipine)
  • ABX –>PCN for strep
  • NO STEROIDS
  • referral to nephrology might need HD
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8
Q

how many days psot infectious would a PT see s/s of GN
in general
-for strep
-for skin infection

A

8-14 days

STREP URI: 1-3 weeks
SKIN (ex impetigo): 3-6 weeks

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9
Q

what drugs are reno-protecrtive and good to give for PT with HTN in nephritic syndrome

A

ACEI/ARBs

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10
Q

what anti-hypertensive drug is used speficailly in poststreptococcal GN

A

Nifedipine–instead of ACEI —– bc the ACEI can cause hyperK

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11
Q

IgA Nephropathy

  • etiology
  • timing of dz
  • MC affects what popuation and gender
  • CM
  • how do we diagnose
  • prognosis
  • tx
  • RF for poorer prognosis
A

24-48 HRS (1-3days) after URI or GI infection
**young males ** 2nd-3rd decade

CM

  • asympto
  • 1/2 cases present with gross hematuria 1-5 days post URI/GI infection
  • HTN and peripheral edema RARE
  • +/- flank pain, fever,

URINE

  • RBCs
  • proteinuria <3grams
  • Hematuria 1-3 days after URI or GI infection

DX=biopsy of skin or kidney— will see IGA deposits
*inds for biopsy–>p.u >1 gram, HTN, edema, decr renal function

Prognosis
30%=benign
40-60% progressive renal dz over the nxt 20 yrs

TX

  • ACEI, ARGS
  • lipid lowering therapy
  • corticosteroids 6 MO

RF for bad prognosis

  • microscopic hemturia*******
  • older age at onset
  • renal dysunfction at presentation
  • PU > 1 gm/day
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12
Q

Membranoproliferative GN

  • types and what they are assoc wth
  • urine sed findings
A

TYPE 1

  • secondary to ag-ab exposure–> HEP C, endocarditis, SLE
  • monoclonal gammopathies—myelomas

type 2
*complement activation

URINE

  • Hematuria
  • dysmorphic RBCs
  • red cell casts
  • variable proteinuria
  • serum creatiine normal-elevated
TX
*underlying cause--- HEP C etc 
-monoclonal gammopathy 
-ACEI 
-
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13
Q

HUS

  • cm
  • dx
  • blood smear
  • MCC
  • tx
A

CM

  • abd pain
  • bloody diarrhea
  • fever
  • seixures

DX
-Ecoli H7:0157–>shiga like toxin—verotoxin
BLOOD SMER=shcistocytes, thrombocytopenia,

MCC=e coli shia prod toxin

TX=supportive, HD, plasma infusion and exchange
DO NOT NOT NOT NOT NOT NOT NOT GIBE ABX****

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14
Q

Rapidly progressive GN (RPGN)

  • types
  • clinical pres
  • UA
A

TYPES
*Anti-GBM aka Goodpasture’s syndrome

*Pauci-immune: ANCA assoc. vasculitis–> Wegners aka Granulomatosis Polyangiitis, and Microscopic Polyangiitis

CM

  • rapidly progressive decline in renal function
  • most insidious—fatigue and edema

UA
*active sedements—RBCs, RBC casts, PU variable

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15
Q

Wegners aka Granulomatosis Polyangiitis

  • invovles wht parts of body
  • labs
  • CM
  • tx
A
  • necrotizing vasculitis of small and medium vessels
  • UPPER»»» lower resp tract + kidneys mainly involved
  • LABS= (+) ANCA-C
CM 
***persistent rhinorrhea, purulent nasal disx, sinus pain 
**nasal and oral ulcers************* 
Hoarseness, stridor, earache, conductive & sensorineural hearing loss or otorrhea
Eyes: conjunctivitis, corneal ulcers
Skin: palpable purpura
Nervous System: mononeuritis multiplex
Less commonly: GI, heart, GU, thyroid

TX

  • steroids alone–mild
  • moderate-severe: steroids + immune modulators
  • severe pulmonary hemorrahge/renal dz or not respoidng to above tx–> Plasma exchange
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16
Q

Microscopic polyangiitis

A

P-ANCA +

NO granulomatosis on biopsy

and no ulcers

17
Q

Goodpastures

  • population
  • CM
  • urine
  • tx
A

-antigens to typeiv collagne on GBM and alveolar BM in lungs

MC M>F
MALES= both lung and kidney issues
FEMALES=renal only

*3rd — 6th deade of life—bimodal

CM

  • pulm HTN in 2/3rds of PTs» more in men——- pulm hemorrahge— they basically exsanguinate
  • renal dz: acute renal failure with RPGN
  • LATE CM: HTN, oliguria
  • later age mc renal s/s only
  • malaise
  • wt loss

*URINE: RBCs, RBC casts, mild-mod PU

TX

  • plasmaphoresis + prednisone
  • anti-GBM abs
18
Q

Nephrotic syndrome overview:

  • features
  • urine
  • CM
  • tx
  • prone to?
A
  • **excretion of 3.0 g or more PU in 24 hours due to glomerular injury
  • urine= BLAND—>no significant active sedement
  • renal dysfunction can be insidious

CM

  • hypoalbuminemia in serumm from very high PU
  • peripheral edema
  • prone to infections
  • Lipiduria and hyperlipidemia

TX

  • normal-protei and low fat diet
  • salt restriction
  • diuretics
  • immunosuppression and potential thrombosis prophylaxis
  • ACEI

PRONE TO:

  • infections
  • clots
19
Q

list systemic dz assoc with nephrotic syndrome

A 
DM 
SLE 
Amyloidosis 
CA 
HBV 
HIV

MPGN is commonly seen with nephrotic syndrome

20
Q

two main etiologies for nephrotic syndrome

A

RENAL ISSUE—PRIMARY CAUSE

  1. minimal change dz
  2. focal segmental glonerulogsclerosis
  3. idiopathic membranous nephropathy

SYSTEMIC EXTRA RENAL CAUSE—SECONDARY

  • DM
  • SLE
  • HBV
  • HIV
  • amyloidosis
21
Q

nephrotic syndrome complications

A
  • PU
  • edema from incr NA/H20 retention and decr oncotic pressure
  • interstitial fluid
  • malnutrition
  • loss of clotting factors
  • hyperlipidemia
  • athlersclerosis
  • thrombosis—decr anti-thrombin III levels
  • diminished immunity
  • homrone loss—thyroid, vit d
  • decr vit C
22
Q

where is the edema typically in nephrotic syndome:

-kids vs adults

A

KIDS=facial
ADULTS=peripheral dependent
***BUT BOTH CAN LEAD TO ANASARCA

23
Q

urine sed findings in nephrotic

A

MIGHT have hematuria but usually NO RBC CASTS—— but can see a few RBCs +/-

***FATTY CASTS–> (+) Lipiduria—->OVAL FAT BODIES —>maltese cross under polorized light
urine=bland

“frothy” urine

24
Q

general tx for nephrotic syndrome

-1st line tx for minimal change dz

A
  1. immunosupresive therapy
    * steroids
    * immunomodulators
  2. PU
    * goal=lower intra glomerular pressure–>reduction in protein excretion
    * ACEI* or ARBS
    * want efferent arteriolar diltion–>reduces renal blood flow, GFR and protein loss
  3. Hyperlipidemia
    * diet mod
    * statins
  4. Edema
    * thiazides or loops
    * 1 liter fluid and NA restriction

MINIMAL CHANGE
1st line=glucocorticoids

25
Q

Minimal Change Dz

  • mc in who
  • assoc with
  • prognosis
  • CM
  • pathology results
  • labs
  • tx
A

MCC in kids
M>F
*assoc with: viral infections, allergies, Hodgkin, NSAIDS, Lithium
*

if it occurs in adults– we are highly suspicious of lymphoma

prognosis=long term very good

CM

  • abrupt onset of Nephrotic syndrome
  • HTN uncommon
  • Hematuria uncommon
  • renal failure uncommon
  • HTN IS CMMON in eldelry + NSAID use

PATHOLOGY
*fusion of visceral epithelial cell foot processes

LABS

  • severe PU
  • sed rate increased
  • low albumin
  • incr cholesterol and trigs
  • normal RF

tx
VERY responsive to corticos–>prednisone

26
Q 
Membranous Nephropathy 
-mc in who 
-urine findings 
-CM 
-can be assoc with > 
-complications 
-what are the prognostic factors 
-
A

most common cause of nephrotic syndrome in adults—esp WHITE MALES >40 YO
**20-30 g PU PER DAY!!!!!

**HTN in 13-55%

complication=pe, dvt, thrombosis in renal vein

assoc with:

  • SLE
  • viral hep
  • malaria
  • meds like PCN
  • hypocomplementemia
  • *BAD PROGNOSTIC INDICATORS=
    1. persistant PU
    2. renal insuff
    3. male
    4. older age
    5. uncontrolled HTN
27
Q

Focal Segmental Glomerulosclerosis (FSGS)

  • common in who
  • etioloies
  • assoc with
  • cm
  • types—worst? best?
A

*commin in pt with ESRD
*MC GN leading to ESRD
M>F
AA 4x lileky to develop ESRD vserus white or asian

ETIOLOGIES

  • idiopathic
  • secondary–>due to another glomerular dz–>nephron loss, hyperfiltration, chronic pyelonephritis, reflux, DM, SLE**

Assoc with:

  • heroin abuse
  • hiv
  • obesity

CM

  • acute or subacute nephrotic syndrome with PU >3.5 g/day
  • secondary presents isidiously with increasing non-nephorotic PU with renal insuff——normal albumin levels– and wihtout edema

TYPES

  • collapsing worst
  • tip lesion best

DX

  • biopsy
  • circulating factor

TX
-steroids—prenisone 1st line
ACEI to reduce PU

Clin Med (52 decks)

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