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USMLE HY notes > Nephrology + Acid Base > Flashcards

Nephrology + Acid Base Flashcards

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USMLE® Step 1 flashcards
1
Q

Hyponathremia + plasms OSm normal

A

think about lipids / proteins

hyperlipidemia or MM

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2
Q

Hyponathremia + plasms OSm high

A

Glucose
mannitol

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3
Q

What is the only reason for Hyponathremia hypervolemic + Urine Na > 20

A

Acute or chronic kidney disease

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4
Q

What are could be the reasons for high ADH in the present of hypovulemia?

A
  1. CHF
  2. Chirrosis
  3. Volume loss
  4. Disease in thyroid / adrenal
  5. SIADH

SIADH is true only when the rest are not

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5
Q

SIADH
volume status?
kidney function?
Urine OSm?

A

Volume- euovolumic
Kidney function- normal
Urine Osm > 100

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6
Q

what are the 3 main reasons for Hyponathremia with normal / low ADH

A
  1. Renal failure- cannot dilute urine proparly. Urine OSm ~250
  2. Pshycogenic polydypsia- drink lots of water
  3. Special diet- Beer potomania / Tea & toasts

for PSychogenic + diet- UOsm is normal which means&raquo_space; less Osmoles or lots of water eauvolemic

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7
Q

Which causes for Hyponathremia hypervoluemic + low Na in urine?

A

CHF
Chirrosis
Nephrotic syndrome

Renal failure- Hyponathremia Hypervolemic + high Na in Urine

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8
Q

What is the Defintion of Psuedo-hyponathremia?

A

low Na in blood when serum osmolality is normal ( > 275)

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9
Q

What is the correction of Na with Glucose

A

Add 1.6 for every 100 glucose above 100

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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

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11
Q

What is the rate of correction of hyponathremia

A

8-10 in 24 hours.

no more then 18 in 48 hours

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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

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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!

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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

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15
Q

Tx for Hyponathremia hypervoulemic?

A

Water restriction + fusid

Chirrosis, Renal failure, CHF

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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&raquo_space; Quadraplagia and loss of face muscles.
lock in syndrome

Give desmopressin or free water (D5W)

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17
Q

Which electrolyte disbalance cause the highest mortality rate?

A

Hypernathremia (40-60%)

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18
Q

What are the 2 things present in hypernathremia?

in the pt

A
  1. inability acess to water freely
  2. loss of water- diarrhea, fabrile ilness, burning, diuretics, DKA (osmotic )

figure out why the pt is not drinking and why he is loosing water

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19
Q

what are the main reasons for kidney water loss in hypernathremia

A

> 3 liter a day

  1. Osmotic diuresis- Hyperglycemia, mannitol, urea. **UOsm > 750 **
  2. Water diuresis DI - Uosm ~50-200
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20
Q

Nephrogenic DI causes

A
  1. Lithum / Amp B
  2. Hypercacemia
  3. Severe hyponathremia
  4. Fusid- rare, only when theres 0 acess to water

same for chronic interstitial nephritis and CKD

Central- problem in secrete ADH

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21
Q

First line tx in hypernathremia

A

Free water (PO or Zonda)
* if signs of hypovulemia&raquo_space; IV isotonic seline

Not exceed 12mEq per day- cerebral edema

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22
Q

Tx for nephrogenic DI

A
  1. Thiazides
  2. correct electrolyte disbalance- hypercalcemia / hypokalemia
  3. NSAIDS
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23
Q

Tx for Central DI

A

Desmopressin - ADH analog w/o the vasoconstriction affect

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24
Q

How to calculate Total body water

A

TBW= weight X 0.5women
or
0.6man

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25
Q

Drugs that cause Hypokalemia

A
  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

Vomiting - Hypokalmia hypochloremic alkelosis
Diarrhea- Hypokalemia hyperchrolermic acidosis

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26
Q

What are the causes of psuedohyperaldo?

A
  1. peochromocytome
  2. Cushing - mmic MRC activity
  3. Liqrich consumption
  4. Liddle synd- GOF in ENaC
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27
Q

Barter and Gitelman are presented like which type of diuretics?

A

Barter- Fusid
Gitelman- Thiazide

Hypokalemia. Hypomagnesmia, Alkelosis

Barter- Hypocalcemia
Gitelman- Hypcercalcemia

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28
Q

Which typr of RTA cause hypokalemia wnad which hyperkalemia

A

Hypokalemia- type RTA I/ II
Hyperkalemia- Type IV

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29
Q

Thyrotoxicosis can cause Hyperkalemia/ hypo?

A

Hypokalemia- cell shift

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30
Q

What can cause Hypokalemia resist to Tx?

A

Hypomagnesemia

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31
Q

Acid base abnormalitiy in diarrhea

A

Metabolic acidosis hyperchloremic + low Na and K in urine

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32
Q

הסנפת דבק מגע
תיאזידים
פניצילן
הקאות / ניקוז קיבה

באיזה הפרעה אלקטרוליטרית יתבטאו ובאיזה מנגנון, מה יהיה כמות האלקטרוליט בשתן

A

Hypokalemia due to loss by the kidney

in urine- high K

contrast to Diarrhea - low K in urine

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33
Q

how can we figure out if hypokalemia is due to intra-kidney or extra-kidney mechanism?

A

Urine k/U cratinine < 15
lead as to think of Extrea renal reasons

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34
Q

a loss of 400-800 mmol in body will be reasult in decrease of ————— mmil/dL in Serum

A

around 2 mmol/dL

soo by that if we see for exmaple a decrease of 1600 ~ around 4 mmol difference

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35
Q

How to correct hypokalemia?

adjust the concentration in central and periphral line

A

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

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36
Q

Which electrolyte disbalace can cause digosxin toxicity?

A

Hypokalemia
Hypomagnesemia
Hypercalcemia

prolongation of QT, U wave.

like Thiazid doing

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37
Q

Drugs that cause hyperkalemia

A

NSAIDS
Cyclosporins
ACEi/ARBS
Spironolactone
Amiloride
SMP-TMX
Heparin
Ketoconazole

also- substance with high osmolality
contrast substance
mannitol

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38
Q

Which type of RTA will cause Hyperkalemia

A

Type VI
(resistance to aldo)

Hyperkalemia + acidos + low BP

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39
Q

Tx for Hyperkalemia

A

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

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40
Q

What are the main causes for high AG metanolic acidosis

A

MUD-PILES

methanol
Uremia
DKA or Alceholic ketoacidosis
Prophylene
Iron / Isoniazide
Lactic acidosis
Ethyele glycol
Siaclytic acid - aspirin

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41
Q

2 Causes of low AG

A

Hypoalbumenia
MM

increase cations- Lithum

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42
Q

Which type of acid-base disbalance can cause malaria and cholera

A

Lactic acidosis (high Ag)

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43
Q

Tx for Aspirin toxicity?

A

mixed disorder- high AG metabolic acidosis + respiratoy alkelosis

Tx
HCO3.
if alkelosis- add acetozolamide (Carbonic anhydrase inhibitor = secrete HCO3)

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44
Q

Methanol toxicity will cause which clinical presentation

A

Vision damage &raquo_space; coma

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45
Q

Tx for Ethylene glycol

A

IV Fomepizole
or
Ethanol IV

for happy be-zol

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46
Q

Indication for Dialysis in Ethylene glycol toxicity

A
  1. PH < 7.3
  2. Osmolar Gap >20
  3. Evidanve of organ demege
  4. Acidosis with high AG
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47
Q

in Adv. chronic kidney disease what will be the acid-base disbalance?

and what is the tx

A

Metabolic acidosis with high AG

usually PH > 7.32

Tx- PO HCO3 . remain levels > 22

due to increase uremia = low excretion of organic acids in urine

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48
Q

When we will give HCO3-

A
  • 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
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49
Q

What is define RTA type II

A

loss of HCO3- in urine

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50
Q

Side effect of Tx ewith HCO3

A
  • Hypokalemia
  • AKI
  • tissue ischemia
  • Cerebral edema
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51
Q

DDx for Metabolic acidosis with normal AG?

A
  • Diarrhea
  • RTA I/II
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52
Q

Which electrolyte will always be high in Normal AG metabolic acidosis

A

Clhoride

hyperchloremic metabolic acidosis

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53
Q

How to differiant between normal AG metabolic acidosis from GI or kidney?

A

2 options

1. Calculate Urine AG
if negetive &raquo_space; GI source
שלילי = שלשול
If positive&raquo_space; kidney

2. Urine K/Ucreatinine-
if high > 13 = kidney
if low < 13 = GI
kidney is higer then the ass

Diarrhea / RTA I / II

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54
Q

what is the mechanism of type 1 RTA

Which 2 medicaion can cause it

A

Distal RTA= no H excrete in DCT&raquo_space; more K + Ca will secrete = hypokalemia, hypercalciurea

Amp B / Iposophomide

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55
Q

what is the mechanism of type 2 RTA

A

Proximal RTA = no HCO- reabsorb in PCT&raquo_space; Hypokalemia

56
Q

Which type of RTA can present as part of fanconi syndrome?

and main cause of Fanconi in adults

A

RTa II

Fanconi- no reabsorbtion in PCT = secrete glucose, amino acids, phosphate. acid urine.

main cause in adults- MM

hypokalemia + hypophosphatemia

57
Q

Which acid base disbalance is seen in Vomiting / Zonda

And what we will see in the urine in the vomiting phase and the hypovulemic phase?

regarding to Cl , NA, K in urine

A

Hypochloremic hypokalemic metabolic alkelosis

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
Q

What is contraction alkelosis

and when we will see it?

A

.loss of volume + Na Cl&raquo_space; RAAS + Symp.&raquo_space;
* HCO3- reabsoprb
* K + H excrete (aldosterone)

Chirrosis, CHF, diuretics (loop, thiazide)

59
Q

What is the Tx for Metabolic alkelosisin the presance of hypervoulemia

A

Acetazolamide = CAi = loss of HCO3 in urine

60
Q

Definition of AKI

A
  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

in AKI we base Cr calculation on Urine output and no GFR
anuric pt < 100 ml/day = GFR almost 0

61
Q

What will see in TINU syndrome
what is the Tx?

A

Ant. uvieteis + tubuloiterstitial nephritis- WBC in urine

Steroids

62
Q

AKI

When we will see RBC casts / dysmorphic RBC?

A

Glomerulonephritis- all things related to the glomeruli

alsosmall vessel vasculitis, Thrombotic microangiopathy, malignant HTN

63
Q

AKI

When we will see White casts / WBC

A

Interstitial nhpritis

64
Q

When we will see AKI with normal urine output

A
  1. Nephrogenic DI
  2. Cisplatin
  3. Aminoglycosides
  4. Amp B

In Aminoglycosides + Amp B- both present with hypomagnesemia

Amp B- Hypocalcemia
AG- Hypokalemia

both cause ATN Fena > 1%

65
Q

Pre- Renal AKI

BUN/Cr ratio
FeNa%
UOsm
Casts

A
  • BUN/Cr ratio > 20
  • FeNa% < 1%
  • Urine Na < 20
  • UOsm > 500
  • Casts- normal /hyaline
66
Q

When we will see low FeNa?

A
  • Pre-renal
  • Rhabdomyolysis
  • Hemolysis
  • Contrast nephropathy

if FeNa > 2% -ATN

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
Q

Cr level during a week after Contrast induce nephropathy

A

Cr level will rse after 1-2 days&raquo_space; peak in 3-5 days&raquo_space; decrease within a week

Pre-renal

68
Q

What are the indications for urgent dialysis?

A
  • Hypervulemic, hyperkalemic, acidosis- refactory to treatment
  • curtain toxicity
  • severe complication of uremia- astrerxis, encephalopaty, paericardial effusion, uremic bleeding
69
Q

Which type of crystals we see after TLS

A

oxalate

also in Ethylene glycol- high AG + high osmolar gap

70
Q

Drugs Etiologies for AIN?

A

most common- drug reaction (ellergic)
* PPI
* Penecillin
* Cheplocporin
* refampin
* resprim- TMP-SMX
* cyprofluxacin -fleuroquinolone

הכל עם פיפי&raquo_space; יוצא בפיפי תאי דם לבנים
ppI, פניצלין, צפלוספורונים, ריפמפין, ריספפרים , ציפרופלוקסצין

71
Q

which type of kidney damge lithum cause

A

Chronic Interstitial nephritis

72
Q

Which type of medication we will always give in AIN

A

Steroids

after Tb ruled out

73
Q

Extra menefistation of PCKD?

A
  • SAH (anurysms in circle of willis)
  • MVP
  • Divertoculosis
  • hernia of abdominal wall
  • liver cyts- most common presentation
74
Q

Dgx of PCKD
Tx for PCKD

A

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
Q

Which type of kidney disorder is correlate with lithum?

A

Naphrogenic DI

Tx- Amiloride

76
Q

How does hypercalcemia affect Nephrogenic DI?

A

Worsen it

77
Q

What is a major risk factor for developing Chronic TIN for lithum

A

Reccurent episodes of high levels of lithum.

mainly in prolong use (10-20 years)

78
Q

Tx for Chrnic Nephrogenic DI secondary to lithum

A
  • **Amiloride
  • Drinking water
  • Thiazides**

DI will cause hypernathremia

79
Q

מתי נצטרך להתאים מינון לכליות (בתרופות)

A

כל מה שמתפנה בכליה ב-30% ומעלה

80
Q

מהי אחת מהאנדיקציות הבודדות להגבלת מים בחולים עם
CKD

A

היפונתרמיה

81
Q

What is the Tx for Acidosis in CKD?

A

Sodium- biarbonate PO- when HCO3 < 23-20

82
Q

Which type of medication can be given in CKD when theres indication for RAS inhibitors in the presance of hyperkalemia

A

use lowring K medications:
Patiromer with the RAS inhibitors

83
Q

Which type of complication in the preseance of hyperparathyrodisim can be seen in CKD?

and which hormone will become in resistant

A

ostitis fibrosa cystica
» can lead to EPO resistance

84
Q

inc CKD pt who is taking to much Vitamin D and Ca supplaments, what can we see?

A

A-dynamic bone disease

could lead to ca deposition in other tissues&raquo_space; tumoral calcinosis

persistant inhibiton of PTH

more in DM pt

85
Q

What are severe adverse effectof A-dynami bine diesease

due to prolong inhibiton of PTH

A
  1. Tumoral calcinosis
  2. acclerate calcinosis of CV system
86
Q

What severe adverse effect is unique to CKD and a/w stoping to take warfarin?

A

Calciphylaxis

painful libido-reticularis (marvke skin)&raquo_space; necrotic ischemic of the skin (legs, abdomen , breasts)

indication for stop tx of comadin

87
Q

Target levels of PTH in CKD

A

levels 150-300

which are pi 2-9 from upper limit of normal

prevent advenace inhibition&raquo_space; A-dynamic bone disease

88
Q

Tx for bone mineral disorder in ckd , what are the 4 groups of drugs

A
  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
Q

Treatment for decrease production of EPO

and what is the HB target

A

ESA - EPO analogs

Iron supplements
B12 and folate supplements.

HB target- 11-10.5

the body could develop resistance to ESA

90
Q

Which type of periacrditis is a/w CKD?

Tx?

A

Uremic pericarditis

Dialysis w/o heparin

91
Q

What is the mediation to treat CKD with protinurea (high glomerular pressure)

A

ACEi / ARBs
if not stand it- CCB (non- dhydro= Verpamil/ dilitazem)

92
Q

What are the criteria for starting dialysis in CKD

A

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

Toxic Lithum, metformin, Aspirin

93
Q

Major risk factor in
* Hemodyalysis
* Peritoneal dialysis

A

Hemo-Hypotension
Peritoneal- peritonitis

94
Q

Dgx of peritonitis in pt with peritonaldylysis

A

WBC >100, at least 50% PMN

Intra-peritoneal Abx

95
Q

Which type of thrombosis is highly a/w Nephrotic syndrome

A

Renal vein thrombosis

96
Q

Nephroetic syndrome

True or False?

theres a connection between the level of hypoalbuminemia to the complication of the diease

A

true

97
Q

What we will see in histology of minimal change?

and what is the Tx

Which type of disease is a/w in adults?

A

light microscopy- flatting of the podocytes legs

Tx- Steroids

could see in types for lymphoma

98
Q

What is the most common cause of nephrotic syndrome in adults?

A

Focal segmented GN
1/3 of nephrotic syndromes

99
Q

Etilogies for FSGN

A
  1. HIV
  2. HBV
  3. HTN
  4. Cholesterol emboli
  5. Sickle cells
  6. Heroin
  7. Bi-phosphonate
  8. Fabry’s
100
Q

Tx for FSGN

A
  • RAS inhibitors- ARBS/ ACEi
  • Steroids- in primary FSGN
  • treat the underline cause
101
Q

What is the Tx for recurance of FSGN in kidney transplant?

A

plasmaphersis

30% of pt

102
Q

nephrotic syndrome

Most common cause of Membranous GN?

A

idiopathy 0 70-80%

103
Q

What are etiologies for
Most common cause of Membranous GN?

A

solid malignancy
infections- HBV, HCV, shypilis
Sys.disease- IgG4, sarcoidosis, chron, DM
Drugs- anti-TNF, NSAIDS, Lithum, biphosphanate

104
Q

Which type of test every pt with Membranous GN must check

A

level of Ab for PLA2R

directed against podocytes&raquo_space; primary MGN

105
Q

Histology in Membranous GN

A

עיבוי אחיד של ממברנת הבסיס
אימיונופלורנציה- IgG + C3 deposition = Granular iamge

106
Q

how many pt with Membranous GN will present with nephrotic syndrome

A

80% + non-selective protinurea

107
Q

Which type subtype of nephrotic syndrome is the highly a/w thrombotic complications?

A

Membranous GN

108
Q

What is the expected prognosis of pt with Membranous GN

A

1/3 spontanous remission
1/3 w/o worsening of kidney function
1/3 ESRD

109
Q

What is a patognemonic sign of diabetic nephropathy on biopsy

A

Kimmelstein wilson
nodular glumerolosclerosis

110
Q

What is the most common cause of CKD worlwide?

A

DM

40% of pt will develop diabetic nephropathy

111
Q

How many pt with retinopathy will also present with nephropathy

in
DM I
DM II

A

DM I- 90%
DM II- 60%

112
Q

Tx for Diabetic nephroapthy?

A

SGLTi + ACEi / ARBs

מאטים את ההתקדמות של אי ספיקת כליות

113
Q

Fabry’s disease

Heritance
Dgx
Tx

A

X-linked
def. in alpha-galactosidase &raquo_space; buildup of globotrioaosylceramide in endothelium

**Dgx- **Zebra bodies (vacoules in epithelium )&raquo_space; FSGN
Genetic testing + levels of alpha-galactosidase

Tx
ACEi/ARBs
enzyme replacement/ migalastat

male, around his 30’s with peripahral nephropathy , cataract in the past, CV problems and nephrotic syndrome

114
Q

Alport Syndrome

organ that effected
Heritance

A

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
Q

A pt after PCI / aortic surgey / under the use of anti-coagulants present with acute AKI

what can be the most common cause?

A

Cholesterol emboli

116
Q

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?

A

Cholesterol emboli

Kidney bopsy- mononuclear infiltrate around blood vessels

117
Q

What we will see in Cholesterol emboli regards:
Complement levels
WBC?

A

Eosinophilia + eosinophylurea
+
low complement

118
Q

Which medication must be stop if Cholestrol emboli is present?

A

Anti-coagulation therapy.

no defentive tx for Cholestrol emboli

119
Q

Which SLE Ab has good correlation to the probability of a pt to develop Lupus nephritis

A

Ds-DNA ab

120
Q

what are the 6 classes of lupus nephritis?

A

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

low complement in 70-90% of cases

121
Q

Tx for Calss I +II of lupus nephritis

A

no tretment

Minimal chnges +masengial proliferation

122
Q

Tx for class III + IV lupus nephritis

A

focal + diffuse

Induction : steroids high dose + MMF/ cyclophospamide 2-6 months&raquo_space; maintenace with low sterods + MMF/ AZA

123
Q

How man ypt with lupus nephritis will ends up with ESRD

A

20%

124
Q

which GN disease is presented with anti-GBM + hemoptysis?

A

Goodpasture syndrome

alpha3-NC1 collagen Ab on basal membrane

125
Q

Anti-GBM

which are the 2 peaks of the disease?
prevelance ages

A

young males - on their 20’s. mainly goodpasture
females/males- 60-70. just kidney involves.

126
Q

Dgx of Anti-GBM disease

A
  1. Kidney biopsy
    Immunofluresence- שקיעה לינארית של הנוגדנים מסוג IgG
  2. Serum Ab against Anti-GBM- alpha3-NCI1
127
Q

What are the good prognostic factors and the bad ones in anti-GBM disease

A
  • good- ANCA ab, Goodpasutre
  • Bad- > 50% creasent and fibrosis on biopsy, Cr 5-6, oliguria, need for acute dialysis
128
Q

Tx for Anti-GBM disease

A

Plasmaphersis + prednisone + cyclophospamide

wait with tranplant at least 6 month- until Ab can’t be measurable in serum

129
Q

episodic Hematuria right after or at URTI
can raise suspucion to which type of disease?

A

IgA nephropathy

episodic hematuria with sedemantion of IgA in masenguim is seen in

130
Q

How to Dgx IgA nephropathy

A

Kidney biopsy - immune complex with IgA

131
Q

IgA nephropathy

Waht are the risk factors for damge the kidney?

A
  1. Protinurea- most predictable
  2. HTN
  3. no reccurent episodes of macrohematuria
  4. male
  5. old age at presentation
132
Q

Tx for RPGN?

A

Steroids + plasmaphersis + cytotoxic medications

133
Q

MPGN

nephrotic or nephritic?
complement levels
what are the 3 types

A

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
Q

How many pt with MPGN will present with RPGN?

A

25%

135
Q

What is the tX for all kideny disease with protinurea?

A

ACEi / ARBs

136
Q

Which medication can be given if theres a problem in complement system

A

**Eculizumab **- Ab against activated C5 (by C3)

C3 GN

137
Q

What is the Tx for primary MPGN

A

Steroids

USMLE HY notes (34 decks)

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