Renal: Glomerular diseases Flashcards
what proteins are lost in PU
whats not lost
- MAINLY albumin (LMW protein)
- clotting factors
- immunoglobulins
NOT LOST=lipoproteins
Orthostatic Proteinuria
-PU findings
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
Glomerulonephritis
-list the causes that have low complement
SLE
MPGN
post infectious GN
endocarditis
list the overall types of glomerulonephritis
post infecitous gn
IGA nephritis
MPGN–membranoprolifertive GN
PRGN–rapidly proliferative GN–>goodpasture’s dz, HUS, Vasuclitis
Acute Glomerulonephritis
- causes
- CM
post infectious
vasculitis–>Lupus, Wegners granulomatosis, HUS, goodpastures, IGA
CM
- HTN
- edema
- proteinuria at non-nephrotic levels <3,000
post-infectious GN latent period
GN occurs after strep of URT or skin infection
8-14 days latent period***
Post-infectious GM
- etiologies
- CM
- Labs
- urine sedement
- tx
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
how many days psot infectious would a PT see s/s of GN
in general
-for strep
-for skin infection
8-14 days
STREP URI: 1-3 weeks
SKIN (ex impetigo): 3-6 weeks
what drugs are reno-protecrtive and good to give for PT with HTN in nephritic syndrome
ACEI/ARBs
what anti-hypertensive drug is used speficailly in poststreptococcal GN
Nifedipine–instead of ACEI —– bc the ACEI can cause hyperK
IgA Nephropathy
- etiology
- timing of dz
- MC affects what popuation and gender
- CM
- how do we diagnose
- prognosis
- tx
- RF for poorer prognosis
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
Membranoproliferative GN
- types and what they are assoc wth
- urine sed findings
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 -
HUS
- cm
- dx
- blood smear
- MCC
- tx
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****
Rapidly progressive GN (RPGN)
- types
- clinical pres
- UA
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
Wegners aka Granulomatosis Polyangiitis
- invovles wht parts of body
- labs
- CM
- tx
- 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
Microscopic polyangiitis
P-ANCA +
NO granulomatosis on biopsy
and no ulcers
Goodpastures
- population
- CM
- urine
- tx
-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
Nephrotic syndrome overview:
- features
- urine
- CM
- tx
- prone to?
- **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
list systemic dz assoc with nephrotic syndrome
DM SLE Amyloidosis CA HBV HIV
MPGN is commonly seen with nephrotic syndrome
two main etiologies for nephrotic syndrome
RENAL ISSUE—PRIMARY CAUSE
- minimal change dz
- focal segmental glonerulogsclerosis
- idiopathic membranous nephropathy
SYSTEMIC EXTRA RENAL CAUSE—SECONDARY
- DM
- SLE
- HBV
- HIV
- amyloidosis
nephrotic syndrome complications
- 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
where is the edema typically in nephrotic syndome:
-kids vs adults
KIDS=facial
ADULTS=peripheral dependent
***BUT BOTH CAN LEAD TO ANASARCA
urine sed findings in nephrotic
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
general tx for nephrotic syndrome
-1st line tx for minimal change dz
- immunosupresive therapy
* steroids
* immunomodulators - 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 - Hyperlipidemia
* diet mod
* statins - Edema
* thiazides or loops
* 1 liter fluid and NA restriction
MINIMAL CHANGE
1st line=glucocorticoids
