Nephrology + Acid Base Flashcards
(137 cards)
1
Q
Hyponathremia + plasms OSm normal
A
think about lipids / proteins
hyperlipidemia or MM
2
Q
Hyponathremia + plasms OSm high
A
Glucose
mannitol
3
Q
What is the only reason for Hyponathremia hypervolemic + Urine Na > 20
A
Acute or chronic kidney disease
4
Q
What are could be the reasons for high ADH in the present of hypovulemia?
A
- CHF
- Chirrosis
- Volume loss
- Disease in thyroid / adrenal
- SIADH
SIADH is true only when the rest are not
5
Q
SIADH
volume status?
kidney function?
Urine OSm?
A
Volume- euovolumic
Kidney function- normal
Urine Osm > 100
6
Q
what are the 3 main reasons for Hyponathremia with normal / low ADH
A
- Renal failure- cannot dilute urine proparly. Urine OSm ~250
- Pshycogenic polydypsia- drink lots of water
- Special diet- Beer potomania / Tea & toasts
for PSychogenic + diet- UOsm is normal which means»_space; less Osmoles or lots of water eauvolemic
7
Q
Which causes for Hyponathremia hypervoluemic + low Na in urine?
A
CHF
Chirrosis
Nephrotic syndrome
Renal failure- Hyponathremia Hypervolemic + high Na in Urine
8
Q
What is the Defintion of Psuedo-hyponathremia?
A
low Na in blood when serum osmolality is normal ( > 275)
9
Q
What is the correction of Na with Glucose
A
Add 1.6 for every 100 glucose above 100
10
Q
What is the relations between ADH and urine Osmolarity?
A
UOsm > 100
testimony of ADH in the system
the main causes of hyponathemia with UOsm < 100:
1. Renal failure
2. Psycogenic polydipsia
3. Spaciel diet
11
Q
What is the rate of correction of hyponathremia
A
8-10 in 24 hours.
no more then 18 in 48 hours
12
Q
What is the rate of correction in severe symptomatic hyponathremia? and which type of fluid will we use?
A
fluid- Hypertonic seline 3%
rate- 1-2 an hour and up to 4-6 in the first hours.
do not correct over 8-10 in 24h
must check Na levels evey 2-4 hrs
13
Q
Why we do not give normal Seline for SIADH
and what is the Tx for SIADH
A
Normal seline- can worse the hyponathremia
Tx SIADH
* Treat underline cause
* restrict water intake
* Na tablets
* Correct hypokalemia
if not worked:
Fusid
* Demecyclocycline- mainly for chronic
* ADH antagonists- VAPTAN suffix in hospitelized pt with CHF and hyponathremia only!
14
Q
How we asses the efficacy excpected from water restriction?
A
ratio of electrolyte in urine vs Bloos
Urine Na + Urine K / Na in blood
when high ratio > 1 = more aggresive restriction
> 1 = up to 500 ml / day. less ~ 1 liter a day
15
Q
Tx for Hyponathremia hypervoulemic?
A
Water restriction + fusid
Chirrosis, Renal failure, CHF
16
Q
Etiology for Osmotic demyelination syndrome and presentation
option of tx?
A
From low to high your pons will die
when correction is above 8-10 in 24h or 18 in 48h.
de-meylinaiton of the pontine»_space; Quadraplagia and loss of face muscles.
lock in syndrome
Give desmopressin or free water (D5W)
17
Q
Which electrolyte disbalance cause the highest mortality rate?
A
Hypernathremia (40-60%)
18
Q
What are the 2 things present in hypernathremia?
in the pt
A
- inability acess to water freely
- loss of water- diarrhea, fabrile ilness, burning, diuretics, DKA (osmotic )
figure out why the pt is not drinking and why he is loosing water
19
Q
what are the main reasons for kidney water loss in hypernathremia
A
> 3 liter a day
- Osmotic diuresis- Hyperglycemia, mannitol, urea. **UOsm > 750 **
- Water diuresis DI - Uosm ~50-200
20
Q
Nephrogenic DI causes
A
- Lithum / Amp B
- Hypercacemia
- Severe hyponathremia
- Fusid- rare, only when theres 0 acess to water
same for chronic interstitial nephritis and CKD
Central- problem in secrete ADH
21
Q
First line tx in hypernathremia
A
Free water (PO or Zonda)
* if signs of hypovulemia»_space; IV isotonic seline
Not exceed 12mEq per day- cerebral edema
22
Q
Tx for nephrogenic DI
A
- Thiazides
- correct electrolyte disbalance- hypercalcemia / hypokalemia
- NSAIDS
23
Q
Tx for Central DI
A
Desmopressin - ADH analog w/o the vasoconstriction affect
24
Q
How to calculate Total body water
A
TBW= weight X 0.5women
or
0.6man
25
Drugs that cause Hypokalemia
1. **Renal-** **Diuretics** =Fusid / Thiazide - Hypokalemia, hypomagnesemia, metabolic alkelosis
fusid- Hypocaclemia
Thiazide- Hypercalcemia
**RTA type IV- aldo resistance**
2. **Re-distbution-** high insulin (re-feeding), Beta agonists (albuterol, dubetumine, terbatuline), psuedo-ephedrin,
3. **Consumption-** B12 + GCSF
4. **Penecillin**
5. **Alkelosis**
6. **Hyperaldo**- alkelosis, HTN, hypokalemia
## Footnote
Vomiting - Hypokalmia hypochloremic alkelosis
Diarrhea- Hypokalemia hyperchrolermic acidosis
26
What are the causes of psuedohyperaldo?
1. peochromocytome
2. Cushing - mmic MRC activity
3. Liqrich consumption
4. Liddle synd- GOF in ENaC
27
Barter and Gitelman are presented like which type of diuretics?
Barter- Fusid
Gitelman- Thiazide
## Footnote
Hypokalemia. Hypomagnesmia, Alkelosis
Barter- Hypocalcemia
Gitelman- Hypcercalcemia
28
Which typr of RTA cause hypokalemia wnad which hyperkalemia
Hypokalemia- type RTA I/ II
Hyperkalemia- Type IV
29
Thyrotoxicosis can cause Hyperkalemia/ hypo?
**Hypokalemia- cell shift**
30
What can cause Hypokalemia resist to Tx?
**Hypomagnesemia**
31
Acid base abnormalitiy in diarrhea
Metabolic acidosis hyperchloremic + low Na and K in urine
32
הסנפת דבק מגע
תיאזידים
פניצילן
הקאות / ניקוז קיבה
באיזה הפרעה אלקטרוליטרית יתבטאו ובאיזה מנגנון, מה יהיה כמות האלקטרוליט בשתן
**Hypokalemia due to loss by the kidney**
in urine- **high K**
## Footnote
contrast to Diarrhea - low K in urine
33
how can we figure out if hypokalemia is due to intra-kidney or extra-kidney mechanism?
Urine k/U cratinine < 15
**lead as to think of Extrea renal reasons**
34
a loss of 400-800 mmol in body will be reasult in decrease of --------------- mmil/dL in Serum
around 2 mmol/dL
## Footnote
soo by that if we see for exmaple a decrease of 1600 ~ around 4 mmol difference
35
How to correct hypokalemia?
| adjust the concentration in central and periphral line
**K in normoseline**
Central line- 20-100 in 100 ml (up to 20 in 1 hr)
Peripheral line- 40 for liter (up to 10 in 1 hr)
| prefer femoral line for central
36
Which electrolyte disbalace can cause digosxin toxicity?
Hypokalemia
Hypomagnesemia
Hypercalcemia
| prolongation of QT, U wave.
## Footnote
like Thiazid doing
37
Drugs that cause hyperkalemia
NSAIDS
Cyclosporins
ACEi/ARBS
Spironolactone
Amiloride
SMP-TMX
Heparin
Ketoconazole
also- substance with high osmolality
contrast substance
mannitol
38
Which type of RTA will cause Hyperkalemia
Type VI
(resistance to aldo)
| Hyperkalemia + acidos + low BP
39
Tx for Hyperkalemia
K > 6.5 or ECG changes = **Calcium gluconate**
1. Insulin + dextrose
2. Ventolin i inhaleation
3. K-exlate PO / PR- few hrs till effect
4. Fusid / Thizide
5. **Dialysis**
40
What are the main causes for high AG metanolic acidosis
**MUD-PILES**
methanol
Uremia
DKA or Alceholic ketoacidosis
Prophylene
Iron / Isoniazide
Lactic acidosis
Ethyele glycol
Siaclytic acid - aspirin
41
2 Causes of low AG
Hypoalbumenia
MM
| increase cations- Lithum
42
Which type of acid-base disbalance can cause malaria and cholera
Lactic acidosis (high Ag)
43
Tx for Aspirin toxicity?
mixed disorder- high AG metabolic acidosis + respiratoy alkelosis
**Tx**
HCO3.
if alkelosis- add acetozolamide (Carbonic anhydrase inhibitor = secrete HCO3)
44
Methanol toxicity will cause which clinical presentation
Vision damage >> coma
45
Tx for Ethylene glycol
IV Fomepizole
or
Ethanol IV
| for happy be-zol
46
Indication for Dialysis in Ethylene glycol toxicity
1. PH < 7.3
2. Osmolar Gap >20
3. Evidanve of organ demege
4. Acidosis with high AG
47
in Adv. chronic kidney disease what will be the acid-base disbalance?
| and what is the tx
Metabolic acidosis with high AG
usually PH > 7.32
| **Tx**- PO HCO3 . remain levels > 22
## Footnote
due to increase uremia = low excretion of organic acids in urine
48
When we will give HCO3-
* PH < 7 - ketoacidosis
* when pt does not have functional HCO3 in plasma like- toxicity/ CKD
* RTA type II or Diarrhea- loss of HCO3 in urine /stool
* Aspirin toxicity- help eliminate medication trough the urine
49
What is define RTA type II
loss of HCO3- in urine
50
Side effect of Tx ewith HCO3
* Hypokalemia
* AKI
* tissue ischemia
* Cerebral edema
51
DDx for Metabolic acidosis with normal AG?
* Diarrhea
* RTA I/II
52
Which electrolyte will **always** be high in Normal AG metabolic acidosis
**Clhoride**
| hyperchloremic metabolic acidosis
53
How to differiant between normal AG metabolic acidosis from GI or kidney?
**2 options**
**1. Calculate Urine AG**
if negetive >> GI source
**שלילי = שלשול**
If positive >> kidney
**2. Urine K/Ucreatinine-**
if high > 13 = kidney
if low < 13 = GI
**kidney is higer then the ass**
## Footnote
Diarrhea / RTA I / II
54
what is the mechanism of type 1 RTA
| Which 2 medicaion can cause it
Distal RTA= no H excrete in DCT >> more K + Ca will secrete = **hypokalemia, hypercalciurea**
| Amp B / Iposophomide
55
what is the mechanism of type 2 RTA
Proximal RTA = no HCO- reabsorb in PCT >> Hypokalemia
56
Which type of RTA can present as part of fanconi syndrome?
| and main cause of Fanconi in adults
**RTa II**
Fanconi- no reabsorbtion in PCT = secrete glucose, amino acids, phosphate. acid urine.
| main cause in adults- MM
## Footnote
hypokalemia + hypophosphatemia
57
Which acid base disbalance is seen in Vomiting / Zonda
## Footnote
And what we will see in the urine in the vomiting phase and the hypovulemic phase?
regarding to Cl , NA, K in urine
Hypochloremic hypokalemic metabolic alkelosis
## Footnote
In the vomiting phase- both k, NA high
in the hypovulemic stage- both low
in both low Cl in urine - we lost it in the GI
58
What is contraction alkelosis
| and when we will see it?
.loss of volume + Na Cl >> RAAS + Symp. >>
* HCO3- reabsoprb
* K + H excrete (aldosterone)
| Chirrosis, CHF, diuretics (loop, thiazide)
59
What is the Tx for Metabolic alkelosisin the presance of hypervoulemia
**Acetazolamide = CAi = loss of HCO3 in urine**
60
Definition of AKI
1. increase of Cr > 0.3 from baseline in 48 hrs
2. increase of Cr > 50% from baseline in a week
3. urine output < 0.5 ml/kg/hr for at least 6 hours
## Footnote
in AKI we base Cr calculation on Urine output and no GFR
**anuric pt < 100 ml/day = GFR almost 0**
61
What will see in TINU syndrome
what is the Tx?
Ant. uvieteis + tubuloiterstitial nephritis- WBC in urine
Steroids
62
# AKI
When we will see RBC casts / dysmorphic RBC?
Glomerulonephritis- all things related to the glomeruli
| alsosmall vessel vasculitis, Thrombotic microangiopathy, malignant HTN
63
# AKI
When we will see White casts / WBC
Interstitial nhpritis
64
When we will see AKI with normal urine output
1. Nephrogenic DI
2. Cisplatin
3. Aminoglycosides
4. Amp B
## Footnote
In Aminoglycosides + Amp B- both present with hypomagnesemia
Amp B- Hypocalcemia
AG- Hypokalemia
**both cause ATN Fena > 1%**
65
# Pre- Renal AKI
BUN/Cr ratio
FeNa%
UOsm
Casts
* **BUN/Cr ratio** > 20
* **FeNa%** < 1%
* **Urine Na** < 20
* **UOsm** > 500
* **Casts**- normal /hyaline
66
When we will see low FeNa?
* Pre-renal
* Rhabdomyolysis
* Hemolysis
* Contrast nephropathy
| if FeNa > 2% -ATN
## Footnote
Fractional excretion of sodium is the amount of salt (sodium) that leaves the body through urine compared to the amount filtered and reabsorbed by the kidney
67
Cr level during a week after Contrast induce nephropathy
Cr level will rse after 1-2 days >> peak in 3-5 days >> decrease within a week
| Pre-renal
68
What are the indications for urgent dialysis?
* Hypervulemic, hyperkalemic, acidosis- refactory to treatment
* curtain toxicity
* severe complication of uremia- astrerxis, encephalopaty, paericardial effusion, uremic bleeding
69
Which type of crystals we see after TLS
oxalate
| also in Ethylene glycol- high AG + high osmolar gap
70
Drugs Etiologies for AIN?
most common- drug reaction (ellergic)
* PPI
* Penecillin
* Cheplocporin
* refampin
* resprim- TMP-SMX
* cyprofluxacin -fleuroquinolone
## Footnote
הכל עם פיפי >> יוצא בפיפי תאי דם לבנים
ppI, פניצלין, צפלוספורונים, ריפמפין, ריספפרים , ציפרופלוקסצין
71
which type of kidney damge lithum cause
**Chronic** Interstitial nephritis
72
Which type of medication we will always give in AIN
Steroids
| after Tb ruled out
73
Extra menefistation of PCKD?
* SAH (anurysms in circle of willis)
* MVP
* Divertoculosis
* hernia of abdominal wall
* **liver cyts- most common presentation**
74
Dgx of PCKD
Tx for PCKD
Dgx- imaging and clinical Hx
Tx:
BP < 140/90- RAS inhibitors
Tolvapatin
cysts infections- Abx like Resprim / quinolones, sinto (4-6weeks)
| same abx as pyelonephritis
75
Which type of kidney disorder is correlate with lithum?
**Naphrogenic DI**
Tx- Amiloride
76
How does hypercalcemia affect Nephrogenic DI?
**Worsen it**
77
What is a major risk factor for developing Chronic TIN for lithum
Reccurent episodes of high levels of lithum.
mainly in prolong use (10-20 years)
78
Tx for Chrnic Nephrogenic DI secondary to lithum
* **Amiloride
* Drinking water
* Thiazides**
## Footnote
DI will cause hypernathremia
79
מתי נצטרך להתאים מינון לכליות (בתרופות)
כל מה שמתפנה בכליה ב-30% ומעלה
80
מהי אחת מהאנדיקציות הבודדות להגבלת מים בחולים עם
CKD
היפונתרמיה
81
What is the Tx for Acidosis in CKD?
Sodium- biarbonate PO- when HCO3 < 23-20
82
Which type of medication can be given in CKD when theres indication for RAS inhibitors in the presance of hyperkalemia
use lowring K medications:
**Patiromer** with the RAS inhibitors
83
Which type of complication in the preseance of hyperparathyrodisim can be seen in CKD?
| and which hormone will become in resistant
ostitis fibrosa cystica
>> **can lead to EPO resistance**
84
inc CKD pt who is taking to much Vitamin D and Ca supplaments, what can we see?
**A-dynamic bone disease**
could lead to ca deposition in other tissues >> **tumoral calcinosis**
| persistant inhibiton of PTH
## Footnote
more in DM pt
85
What are severe adverse effectof A-dynami bine diesease
| due to prolong inhibiton of PTH
1. Tumoral calcinosis
2. acclerate calcinosis of CV system
86
What severe adverse effect is unique to CKD and a/w stoping to take warfarin?
**Calciphylaxis**
painful libido-reticularis (marvke skin) >> necrotic ischemic of the skin (legs, abdomen , breasts)
**indication for stop tx of comadin**
87
Target levels of PTH in CKD
levels 150-300
which are pi 2-9 from upper limit of normal
## Footnote
prevent advenace inhibition >> A-dynamic bone disease
88
Tx for bone mineral disorder in ckd , what are the 4 groups of drugs
1. **סופחי סידן- **prefer those without Ca, Sevelamer or Lanthanum
2. **Active vitamin D**- Calcitriol , could cause hypercalcemia and hyperphospatemia
3. **Calcimimetic -** decrease PTH and Ca in blood. (for secondary hyper-para PTH(
89
Treatment for decrease production of EPO
| and what is the HB target
ESA - EPO analogs
Iron supplements
B12 and folate supplements.
| **HB target- 11-10.5**
## Footnote
the body could develop resistance to ESA
90
Which type of periacrditis is a/w CKD?
Tx?
Uremic pericarditis
Dialysis w/o heparin
91
What is the mediation to treat CKD with protinurea (high glomerular pressure)
**ACEi / ARBs**
if not stand it- **CCB (non- dhydro= Verpamil/ dilitazem)**
92
What are the criteria for starting dialysis in CKD
**AEIOU**
A-acidosis- uncontrolled
O- volume overload
E- hyperkalemia
I- itoxicity
U-uremia with pericarditis / Enephalopathy/ bleeding
GFR < 10
| GFR 5-15 with AOEIU or GFR < 10
## Footnote
Toxic Lithum, metformin, Aspirin
93
Major risk factor in
* Hemodyalysis
* Peritoneal dialysis
Hemo-Hypotension
Peritoneal- peritonitis
94
Dgx of peritonitis in pt with peritonaldylysis
WBC >100, at least 50% PMN
| Intra-peritoneal Abx
95
Which type of thrombosis is highly a/w Nephrotic syndrome
Renal vein thrombosis
96
# Nephroetic syndrome
True or False?
theres a connection between the level of hypoalbuminemia to the complication of the diease
**true**
97
What we will see in histology of minimal change?
| and what is the Tx
## Footnote
Which type of disease is a/w in adults?
**light microscopy-** flatting of the podocytes legs
| **Tx- Steroids**
## Footnote
could see in types for lymphoma
98
What is the most common cause of nephrotic syndrome in adults?
**Focal segmented GN**
1/3 of nephrotic syndromes
99
Etilogies for FSGN
1. HIV
2. HBV
3. HTN
4. Cholesterol emboli
5. Sickle cells
6. Heroin
7. Bi-phosphonate
8. Fabry's
100
Tx for FSGN
* RAS inhibitors- ARBS/ ACEi
* Steroids- in primary FSGN
* treat the underline cause
101
What is the Tx for recurance of FSGN in kidney transplant?
plasmaphersis
| 30% of pt
102
# nephrotic syndrome
Most common cause of Membranous GN?
idiopathy 0 70-80%
103
What are etiologies for
Most common cause of Membranous GN?
solid malignancy
infections- HBV, HCV, shypilis
Sys.disease- IgG4, sarcoidosis, chron, DM
Drugs- anti-TNF, NSAIDS, Lithum, biphosphanate
104
Which type of test every pt with Membranous GN must check
**level of Ab for PLA2R**
## Footnote
directed against podocytes >> primary MGN
105
Histology in Membranous GN
עיבוי אחיד של ממברנת הבסיס
אימיונופלורנציה- IgG + C3 deposition = Granular iamge
106
how many pt with Membranous GN will present with nephrotic syndrome
80% + non-selective protinurea
107
Which type subtype of nephrotic syndrome is the highly a/w thrombotic complications?
**Membranous GN**
108
What is the expected prognosis of pt with Membranous GN
1/3 spontanous remission
1/3 w/o worsening of kidney function
1/3 ESRD
109
What is a patognemonic sign of diabetic nephropathy on biopsy
**Kimmelstein wilson**
nodular glumerolosclerosis
110
What is the most common cause of CKD worlwide?
DM
| 40% of pt will develop diabetic nephropathy
111
How many pt with retinopathy will also present with nephropathy
in
DM I
DM II
DM I- 90%
DM II- 60%
112
Tx for Diabetic nephroapthy?
SGLTi + ACEi / ARBs
| מאטים את ההתקדמות של אי ספיקת כליות
113
Fabry's disease
Heritance
Dgx
Tx
**X-linked**
def. in **alpha-galactosidase** >> buildup of **globotrioaosylceramide** in endothelium
**Dgx- **Zebra bodies (vacoules in epithelium ) >> **FSGN**
Genetic testing + levels of alpha-galactosidase
**Tx**
ACEi/ARBs
**enzyme replacement/ migalastat**
## Footnote
male, around his 30's with peripahral nephropathy , cataract in the past, CV problems and nephrotic syndrome
114
Alport Syndrome
organ that effected
Heritance
Triad of:
* Eyes- lenticonus / retinpoathy
* Kidneys- hematuria + chronic glomerolusclerosis
* hearing loss (senso-nuerologic)
85% X linked- alpha5
15% AR - alpha3/alpha 4
of collagen IV
Tx:
ACEi
Kidney transplent
115
A pt after PCI / aortic surgey / under the use of anti-coagulants present with acute AKI
what can be the most common cause?
Cholesterol emboli
116
a pt present with
FSGS with hematuria and light protenuria with AKI. also presented with TIA, blue toes and libido retiularis (marble rash)
he is taking AG therapy.
what could be the reason?
| and how can we dgx in definite?
Cholesterol emboli
| **Kidney bopsy-** mononuclear infiltrate around blood vessels
117
What we will see in Cholesterol emboli regards:
Complement levels
WBC?
Eosinophilia + eosinophylurea
+
low complement
118
Which medication must be stop if Cholestrol emboli is present?
Anti-coagulation therapy.
| no defentive tx for Cholestrol emboli
119
Which SLE Ab has good correlation to the probability of a pt to develop Lupus nephritis
Ds-DNA ab
120
what are the 6 classes of lupus nephritis?
Class I- minimal change
Class II- Mesengial proliferation
Class III- Focal nephritis
Class IV- Diffuse nephritis
Class V- membranous nephritis
Class VI- sclerotic nephritis
| Mini messi focus on defintliy productive member of soccer
## Footnote
low complement in 70-90% of cases
121
Tx for Calss I +II of lupus nephritis
no tretment
Minimal chnges +masengial proliferation
122
Tx for class III + IV lupus nephritis
focal + diffuse
Induction : steroids high dose + MMF/ cyclophospamide 2-6 months >> maintenace with low sterods + MMF/ AZA
123
How man ypt with lupus nephritis will ends up with ESRD
20%
124
which GN disease is presented with anti-GBM + hemoptysis?
**Goodpasture syndrome**
| alpha3-NC1 collagen Ab on basal membrane
125
Anti-GBM
which are the 2 peaks of the disease?
prevelance ages
young males - on their 20's. mainly goodpasture
females/males- 60-70. just kidney involves.
126
Dgx of Anti-GBM disease
1. **Kidney biopsy**
Immunofluresence- שקיעה לינארית של הנוגדנים מסוג IgG
2. Serum Ab against Anti-GBM- **alpha3-NCI1**
127
What are the good prognostic factors and the bad ones in anti-GBM disease
* good- ANCA ab, Goodpasutre
* Bad- > 50% creasent and fibrosis on biopsy, Cr 5-6, oliguria, need for acute dialysis
128
Tx for Anti-GBM disease
Plasmaphersis + prednisone + cyclophospamide
**wait with tranplant at least 6 month- until Ab can't be measurable in serum**
129
episodic Hematuria right after or at URTI
can raise suspucion to which type of disease?
IgA nephropathy
## Footnote
episodic hematuria with sedemantion of IgA in masenguim is seen in
130
How to Dgx IgA nephropathy
Kidney biopsy - immune complex with IgA
131
# IgA nephropathy
Waht are the risk factors for damge the kidney?
1. Protinurea- most predictable
2. HTN
3. no reccurent episodes of macrohematuria
4. male
5. old age at presentation
132
Tx for RPGN?
Steroids + plasmaphersis + cytotoxic medications
133
MPGN
nephrotic or nephritic?
complement levels
what are the 3 types
Nephritic
low complement levels
type 1- most common, immune complex apperance of **Tram Tracks**. chronic inf.HBV/ HCV, SLE, Cryoglobulinemia, MM.
Type 2+ 3- mainly idioathic. a/w complement
134
How many pt with MPGN will present with RPGN?
25%
135
What is the tX for all kideny disease with protinurea?
ACEi / ARBs
136
Which medication can be given if theres a problem in complement system
**Eculizumab **- Ab against activated C5 (by C3)
| **C3 GN**
137
What is the Tx for primary MPGN
Steroids
