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GU > CKD - Part 2 - Exam 1 > Flashcards

CKD - Part 2 - Exam 1 Flashcards

1
Q

What is the difference between nephritic and nephrotic? What is the proteinuria cut off?

A

nephritIc is for INFLAMMATION/IMMUNE and the urine sediment tends to be heavier on the bleeding (hematuria) +/- RBC casts

LESS than 3 grams is nephritic and MORE than 3 grams is nephrotic

Nephrotic: think PROTEIN in the urine, more than 3 grams with “bland” urine sediment

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2
Q

“bland” urine sediment is associated with _______. What does it mean? May see ______ in the urine

A

nephrotic spectrum of CKD

Bland= no cells or casts

may see oval fat bodies

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3
Q

HTN
oliguria
cola-colored urine

What am I?

A

nephritic syndrome

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4
Q

hypoalbuminemia
hyperlipidemia
peripheral edema
massive proteinuria

What am I?

A

nephrotic syndrome

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5
Q

What is the MC cause of primary glomerulonephritis?

A

berger’s dz ( IgA nephropathy)

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6
Q

What are the 5 causes of glomerulonephritis?

A

C3 glomerulopathy
Anti-glomerular basement membrane
Monoclonal Ig
Pauci-immune
Immune complex deposition

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7
Q

What is happening in Immune complex deposition GN? What is the MC cause?

A

Antigen-antibody complexes lodge in glomerular basement membrane (GBM)
Complement activation to resolve complexes → GBM destruction

**IgA nephropathy (Berger disease)- MC
Infections
endocarditis
LUPUS
Strep!

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8
Q

What is happening in Anti-GBM-associated glomerulonephritis? _______ is a type of anti-GM. What systems does it involve?

A

Autoantibodies against GBM

Goodpasture’s Syndrome

kidneys and lungs

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9
Q

What is happening in C3 Glomerulopathy ? What is it caused by?

A

C3 complement proteins lodge in the glomerular basement
membrane (GBM) → GBM destruction
aka C3 gets stuck and activate and destroys GBM

Causes - abnormal alternative complement pathway

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10
Q

What is happening in Monoclonal Ig-mediated glomerulonephritis? What is it caused by?

A

Excessive antibodies lodge in GBM and/or tubular basement membrane

causes monoclonal gammopathies (multiple myeloma, MGUS)

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11
Q

What is MGUS? What type of GN is it associated with?

A

monoclonal gammopathy of unknown significance, B cells that make antibody

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12
Q

What is happening in Pauci-Immune Glomerulonephritis? What is it caused by? What is important to note?

A

small-vessel vasculitis associated with ANCAs

cell-mediated autoimmune processes

CELL MEDIATED!!

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13
Q

What are some common PE findings in GN?

A

GFR decreases
edema in scrotal and periorbital regions
cola-colored urine

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14
Q

If a pt has GN, what will their BUN:Cr ratio be? What will their urinalysis look like? Urine sediment?

A

BUN:Cr ratio will be higher than 20

hematuria, moderate proteinuria (usually LESS 3 g/d)

RBC (often dysmorphic), RBC casts

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15
Q

What are RBC casts a sign of? What type of kidney injury are they associated with?

A

sign of heavy glomerular bleeding, tubular stasis

GN

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16
Q

When would it be common to see low complement levels in what types of GN? What is the exception?

A

complement levels are low in C3 complex and Immune complex GN (except Berger’s dz)

Immune complex GN (except Berger’s dz)

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17
Q

When would you order an renal biopsy in GN? What are the CI?

A

to find the underlying cause by revealing the patten of inflammation related to the cause if it is not CI

CI: bleeding disorder and uncontrolled HTN

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18
Q

What is the tx for GN?

A

Management of HTN
Management of volume overload - if present
Antiproteinuric therapy (ACE/ARB) - NOT IN AKI GN
steroids
cytotoxic agent
plasma exchange for Goodpasture dz and P Pauci-immune glomerulonephritis

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19
Q

What 2 types of GN do you treat with plasma exchange?

A

Pauci-immune glomerulonephritis

Goodpastures dz (Anti-GBM)

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20
Q

Postinfectious Glomerulonephritis is usually due to ______. What will the serum blood test reveal? What will the urine show?

A

GABHS

Low complement; high ASO titer (unless previous abx)

hematuria, subnephrotic proteinuria (<3 g/d), RBC casts

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21
Q

_____ helps definitive dx of Postinfectious Glomerulonephritis. What will it reveal? What is the tx?

A

Biopsy

“humps” of immune complex deposits

PCN, antihypertensives, salt restriction, diuretics

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22
Q

What should you NOT give in Postinfectious Glomerulonephritis? Why?

A

steroids

do NOT improve outcomes

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23
Q

_______ is the MC PRIMARY glomerular dz worldwide. What is the common pt population?

A

IgA Nephritis (Berger’s Disease)

2-3x more common in males; MC in children and young adults

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24
Q

How does Berger’s dz commonly present?

A

episode of gross hematuria often with an viral URI

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25
Q

What is the serum test you would want to order to confirm berger’s dz? What will the urinalysis look like?

A

there is NO confirming test

hematuria (micro or gross), proteinuria (varies)

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26
Q

What is the tx for berger’s dz? low risk and high risk

A

Low risk - no HTN, normal GFR, minimal proteinuria - monitor yearly

High risk - proteinuria >1.0 g/d, decreased GFR, HTN - ACE or ARB

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27
Q

What is Henoch-Schönlein Purpura? What is the MC pt population?

A

Systemic small-vessel vasculitis, with IgA deposition in vessel walls

MC in males and children

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28
Q

_______ is the MC systemic vasculitis of childhood.

A

Henoch-Schönlein Purpura

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29
Q

What is the serum test you would want to order to confirm Henoch-Schönlein Purpura? What is the normal presenation?

A

No confirming serum test!

Palpable purpura in lower extremities and butocks; arthralgias, abdominal symptoms (nausea, colic, melena)

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30
Q

What is the tx for Henoch-Schönlein Purpura?

A

no specific tx, supportive care

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31
Q

In US _____ is MCC of nephrotic glomerular disease. What is the proteinuria range? ______ is a very common PE finding

A

DM

GREATER than 3 grams/day

peripheral edema!!, dyspnea, pleural effusions, ascities

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32
Q

______ test only detects albumin so need to order ______ and/or _______ in nephrotic syndrome. Which one is the most accurate?

A

urine dipstick

Spot urine protein:urine Cr ratio

24-hr urine for protein- more accurate

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33
Q

What will the urine sediment show in nephrotic syndrome? If marked HLD will show ________

A

few cells/casts
“Grape clusters” (light microscopy)
“Maltese crosses” (polarized light)

oval fat bodies

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34
Q

What will serum labs show for a pt who has nephrotic syndrome?

A

hypoalbuminemia
hypoproteinemia
hyperlipidemia
elevated ESR
decreased levels of Vit D, zinc and copper

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35
Q

Why is hyperlipidemia seen in greater than 50% of nephrotic syndrome pts?

A

low protein due to peeing it all out decreases oncotic pressure which increased hepatic lipid production

and lower clearance rate of VLDL leads to hypertriglyceridemia

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36
Q

______ is done in adults with new-onset idiopathic nephrotic syndrome but NOT done if DM or another obvious cause is present

A

renal biopsy

NOT done in real life

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37
Q

if nephrotic syndrome is mild ______ dietary protein. If greater than 10mg protein lost per day need to _______ dietary protein

A

mild restrict protein intake

greater than 10mg protein lost per day need to increased protein consumption

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38
Q

What are the medication tx options for nephrotic syndrome?

A

1st- ACE/ARB

2nd- SGLT2 inhibitors (-flozin)

3rd- Nonsteroidal mineralocorticoid receptor antagonists (nsMRAs) (finerenone)
- MRAs: eplerenone, spironolactone would be next best option if finerenone is not covered

thiazide and loops in large doses

statins to reduce hyperlipidemia

anticoags

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39
Q

Why do you give an ACE/ARB in nephrotic syndrome?

A

lower urine protein excretion by reducing glomerular capillary pressure; antifibrotic effects

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40
Q

Why would you give a SGLT2 inhibitor in nephrotic syndrome?

A

lower urine protein excretion by lowering intraglomerular pressure (tubuloglomerular feedback), reducing renal oxidative stress and improving oxygenation of cortex

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41
Q

Why would you give a Nonsteroidal mineralocorticoid receptor antagonists (nsMRAs) in nephrotic syndrome? What is the drug name specifically? What are the alternatives?

A

reduce effects of aldosterone, lowering intraglomerular pressure and therefore proteinuria

finerenone (Kerendia)

eplerenone, spironolactone just normal mineralocorticoid receptor antagonists (MRAs)

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42
Q

_____ is a common PE finding in nephrotic syndrome. How do you tx it?

A

edema

dietary salt restriction and thiazide and loop diuretics at high doses

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43
Q

What is the tx for hyperlipidemia in nephrotic syndrome?

A

diet and exercise with lipid-lowering drugs

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44
Q

When is hypercoagulability seen in nephrotic syndrome? Why? What does it lead to? What is the tx?

A

Usually seen if serum albumin <2 g/dL

because increased urinary loss of antithrombin, protein C, protein S

leads to increased platelet activation

tx: anticoag for 3-6 months if evidence of thrombosis and need to be for life if multiple clots are present

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45
Q

**_______ is the MC cause of proteinuric renal dz in children. What are the s/s?

A

Minimal Change Disease

often full-blown nephrotic syndrome
Thromboembolic events, hyperlipidemia, protein malnutrition

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46
Q

What is the tx for minimal change dz? How long do you continue tx in children and adults?

A

high dose Prednisone, 60 mg/m2/d

8 weeks in kids and 16 weeks in adults

need to taper dose after course is complete

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47
Q

**_______ is the MC cause of PRIMARY nephrotic syndrome in adults. What is the caused by?

A

Membranous Nephropathy

immune complex deposition

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48
Q

_______ may be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril

A

membranous nephropathy

49
Q

membranous nephropathy PE findings may be ______, ______ and _____. What are they at an increased risk for?

A

asymptomatic; may see edema, frothy urine

Higher risk of hypercoagulable state, esp. renal vein thrombosis

50
Q

What is the tx for membraneous nephropathy?

A

ACE/ARB
immunosuppressive agents
kidney transplant

51
Q

______ is a type of secondary nephrotic syndrome that occurs as a result of extracellular deposits of ______ protein. When visualizing the kidneys that are often ______. Why?

A

Amyloidosis

amyloid protein

large kidneys due to protein deposits that are very big

52
Q

What is the tx for amyloidosis? What is the prognosis?

A

very limited options, manage underlying dz

Overall 5-year survival - <20% soooo NOT GREAT

53
Q

______ is the MC cause of ESRD in the US. Is it primary or secondary?

A

diabetic nephropathy

secondary nephrotic syndrome

54
Q

When does Diabetic Nephropathy usually develop after the dx of DM? What does early and later diabetic nephropathy look like lab wise? When do you need to tx it? What is the tx?

A

usually develops about 10 years after DM onset

Early - hyperfiltration with increased GFR
Later - microalbuminuria (30-300 mg/d)
Progression - albuminuria 300+ mg/d

Treatment - as soon as microalbuminuria is found!!!

tx: strict gylcemic control
ACE/ARB
SGLT2

55
Q

_____ changes happen before _____ changes

A

urine changes happen before blood changes

when thinking about changes in lab values

56
Q

Define Focal Segmental Glomerular Sclerosis (FSGS)? Is it a common cause of _______

A

some, but not all (focal) glomeruli are scarred, and each involved glomerulus is only partially scarred (segmental)

nephrotic syndrome

57
Q

What are some primary causes of Focal Segmental Glomerular Sclerosis (FSGS)?

A

Idiopathic; associated with cytokines, other glomerular conditions (IgA nephropathy, minimal change disease)

58
Q

Give the genetic reasoning behind Focal Segmental Glomerular Sclerosis (FSGS)?

A

associated with specific mutated genes resulting in malformed proteins that reduce the integrity of the glomerular filtration barrier

59
Q

What are some secondary causes of Focal Segmental Glomerular Sclerosis (FSGS)? What are the 2 highlighted ones from lecture?

A

analgesics, heroin, lithium, steroids, chemo
HBV, HCV, HIV, Parvovirus B19, CMV, SARS-CoV-2, solitary kidney, vesicoureteral reflux, obesity, sickle cell, HTN, Alport syndrome, Sarcoidosis

heroin and obesity

60
Q

How do you definitively dx FSGS? Can suspect FSGS with _____ and _______

A

renal bx!!

proteinuria and probable cause

61
Q

What is Tubulointerstitial Disease? What is NOT involved?

A

Disorders mainly affecting renal tubules and interstitium

Glomeruli and renal vessels are relatively spared

62
Q

70% of acute interstitial nephritis is due to ______. How does it present?

A

medications!!

acute renal failure: reduced urine output, SOB, swelling, fatigue, confusion, HTN, arrthymias etc etc

63
Q

What are the two main pathologies of chronic Tubulointerstitial Disease?

A

interstitial fibrosis and tubular atrophy

64
Q

What is the MC cause of chronic tubulointerstitial dz?

A

obstructive uropathy due to kidney stones, prostate dz, cancer of cervix, colon or bladder, retroperitoneal tumors/fibrosis

65
Q

What is the 2nd MC cause of chronic tubulointerstitial disease? What is it?

A

Vesicoureteral Reflux

urine flow back up the tubule when voiding

66
Q

Analgesic Nephropathy is what type of kidney disease? What is the about you need to consume a day to put yourself at risk?

A

Chronic Tubulointerstitial Disease

ingest min 1 g/d for 3+ yrs

67
Q

What are the 5 categories of Chronic Tubulointerstitial Disease?

A

Obstructive Uropathy
Vesicoureteral Reflux
Analgesic Nephropathy
Autoimmune Interstitial
Nephritis
Nephrocalcinosis

68
Q

What are some potential causes of obstructive uropathy?

A

enlarged prostate, renal calculi, cancer, retroperitoneal fibrosis or mass

69
Q

in obstructive uropathy ______ are almost always asymptomatic. How do you dx?

A

hydronephrosis

imaging!!! US is preferred then CT for more detailed info. CT is NOT first line

70
Q

How will an obstructive uropathy present?

A

oliguria, anuria or polyuria if urine is unconcentrated due to damage caused by the tubules

UA: benign, may see hematura and pyuria

serum creatinine may be elevated

71
Q

If you suspect a nephrocalcinosis: what is the imaging of choice?

A

US

Can also be visualized with CT

72
Q

What is the tx for an obstructive uropathy? Will the pt regain normal function?

A

find and remove obstruction ASAP!!!

will NOT restore renal function or stop progression to ESRD because the damage has already occured!

73
Q

Vesicoureteral Reflux primarily occurs during ______. ______ sphincter is damaged. What is the common presentation?

A

childhood

vesicoureteral sphincter

frequent UTIs especially in young children!! HTN and proteinuria in adults

74
Q

________ are very helpful in dx Vesicoureteral Reflux because xrays are taken while the pt is urinating. ______ will show hydronephrosis and renal scarring. Will the kidneys be larger or smaller?

A

Voiding cystourethrogram

US

asymmetric small kidneys due to scarring and atrophy

75
Q

What is the tx for Vesicoureteral Reflux?

A

maintain sterile urine -> low dose abx

surgical reimplantation of ureters in kids

control of HTN- ACE/ARB

76
Q

Analgesic Nephropathy was especially associated with ______. Name 3 additional meds that can cause this. What dose?

A

phenacetin

ASA, NSAIDs, acetaminophen

Ingestion of at least 1 g/d for 3+ years

77
Q

Why is taking too much analegesics bad for your kidneys?

A

Tubulointerstitial inflammation and papillary necrosis. Analgesics can be concentrated up to 10x higher in renal papillae than in renal cortex

78
Q

_____ may be found in the urine of a pt with Analgesic Nephropathy. What are common CT findings?

A

Sloughed papillae

small, scarred kidney with papillary calcifications

79
Q

What is IVP? Why is it not used more? What will you find on a pt with Analgesic Nephropathy?

A

Intravenous Pyelogram: imaging test that uses contrast dye used to look at the kidneys and ureters.

because the contrast is VERY bad for the kidneys

“ring shadow” or “golfball on a tee” sign

80
Q

What is the tx for analgesic nephropathy?

A

stop taking analgesic

Renal function may stabilize or mildly improve if analgesic stopped in a timely manner

81
Q

What is Autoimmune Interstitial Nephritis
due to?

A

multiple AI disorders!

Amyloidosis
Cryoglobulinemia
IgA nephropathy
Renal transplant rejection
Anti-GBM-Antibody syndrome (Goodpasture syndrome)
Sarcoidosis
Sjogren Syndrome
SLE

82
Q

Polyuria, decreased urinary concentrating ability
Volume depletion due to salt-wasting
Hyperkalemia
Hyperchloremic metabolic acidosis

What am I?
What will imaging look like?
What is the tx?

A

Autoimmune Interstitial Nephritis

small, scarred kidneys

control the underlying AI cause

83
Q

What is nephrocalcinosis? What does it cause?

A

Deposition of calcium in renal parenchyma and tubules

can cause AKI, CKD or do not cause any harm at all!

most do NOT progress to ESRD

84
Q

What is nephrocalcinosis caused by? What is the MC cause?

A

Caused by increase in urinary excretion of calcium, phosphate, and/or oxalate

MCC - increased urinary calcium excretion

85
Q

having _____, ______ and ______ increases your risk of nephrocalcinosis

A

hyperparathyroid

vit D therapy

high dose loop diuretics for a long time

86
Q

What is the imaging of choice for Nephrocalcinosis? What is the tx?

A

US

correct underlying metabolic disorder

87
Q

______ is 65-70% of all renal masses. Where are they usually found?

A

single renal cyst

Generally in outer cortex, may be in medulla

renal size will be normal and usually asympotmatic

88
Q

If you do find a renal cyst, need to reference the _____ score. When would finding one be a problem?

A

Bosniak score

If develop after onset of dialysis → potential for adenocarcinoma

89
Q

when Medullary Cystic Kidney Disease
is dx in childhood, what is it called? How is it inherited?

A

Juvenile Nephronophthisis

autosomal recessive

90
Q

How is adult Medullary Cystic Kidney Disease inherited? Where are the cysts located?

A

autosomal dominant

multiple small renal cysts at corticomedullary junction and in medulla

91
Q

Polyuria
pallor
lethargy
renal salt wasting
HTN in later dz
hyperuricemia

What am I?
What is the tx?

A

Medullary Cystic Kidney Disease

adequate salt and water intake
no meds to STOP progression
can give allopurinol if pt is hyperuricemic
RENAL TRANSPLANT

92
Q

How common is Autosomal Dominant Polycystic Kidney Disease (ADPKD)? 90% are from _______ inheritance. 10% from ______

A

affects 1 in 400 to 1 in 1000 pts

90% from autosomal dominant inheritance

10% from spontaneous mutations

93
Q

What 2 genes are associated with Autosomal Dominant Polycystic Kidney Disease (ADPKD)? Which one is worse?

A

ADPKD-1 - 85% of pts - more severe course

ADPKD-2 - 15% of pts - slower progression, later onset in life

94
Q

abdominal or flank pain
hx of UTI and nephrolithiasis
hx of HTN in >50%
large kidneys

What am I?
What is the imaging of choice?

A

Autosomal Dominant PKD

US confirms dx; can use CT if unclear

95
Q

In Autosomal Dominant PKD, where are two additional places that is common to see cysts?

A

liver and spleen

96
Q

What is the tx for ADPKD?

A

Tolvaptan (Jynarque, Samsca)- to slow renal decline

ocreotide: decreased cyst growth; no improvement of kidney function

avoid caffeine

2L/water a day

HTN tx and protein RESTRICT

97
Q

In ADPKD may see hematuria due to ______. These pts are at a higher chance of ______. They also have ____ and ____ complications

A

rupture of cyst

Cerebral aneurysms in the circle of willis

heart: mitral valve prolapse, aortic aneurysms, aortic valve disease

GI: colonic diverticula

98
Q

What should you do if ADPKD pt has an infected cyst? What will it present like?

A

Blood/urine culture and maybe CT to help dx:

tx with abx: bactrim or fluoroquinolones

flank pain, fever, ↑ WBC

99
Q

______ tx for ADPKD slows rate of change in kidney volume, lower rate of renal decline. What is the drug class? What effect does it have on urine osmo?

A

Tolvaptan (Jynarque, Samsca)

Vasopressin receptor antagonists

Greater reduction in urinary osmolality = greater impairment of cyst growth

100
Q

______ tx for ADPKD decreased cyst growth; no improvement of kidney function

A

Ocreotide

101
Q

thirst/polydipsia, polyuria/nocturia, hypernatremia, increased liver enzymes are the SE of ______. What is the BBW? What do you need to monitor?

A

tolvaptan

should be initiated and reinitiated in patients only in a hospital where serum sodium can be closely monitored

monitor LFTs and electrolytes

102
Q

What part of the kidney does Autosomal Recessive PKD effect? What is the common pt population?

A

Enlarged kidneys with small cysts on collecting tubules only

commonly first found in neonates

103
Q

Enlarged kidneys (bilateral abdominal masses)
Impaired urine concentration
Metabolic acidosis
HTN common

What am I?

A

Autosomal Recessive PKD

104
Q

Autosomal Recessive PKD up to 50% of neonates die from ______. ____ of surviving neonates live to ____ or longer but 1/3 will develop ____ by age 10. And may develop ______

A

pulmonary hypoplasia

80%

age 10

ESRD

portal hypertension from periportal fibrosis

105
Q

How do you dx Autosomal Recessive PKD?

A

large, echogenic kidneys (kidney that appears bright on an US)

cysts are only visible after birth

106
Q

How do you distinguish ARPKD from ADPKD? What is the tx for ARPKD?

A

absence of renal cysts in either parents = autosomal recessive

manage HTN, dialysis and kidney transplant

107
Q

80-90% of renal artery stenosis is due to ______. 10-15% is due to _______

A

atherosclerotic occlusive disease

fibromuscular dysplasia

108
Q

What is fibromuscular dysplasia? What is the classic pt?

A

Fibromuscular dysplasia (FMD) affects the artery walls, making them either too weak or too stiff making them narrow or bulge

HTN in females who are less than 40

109
Q

_____ of all pts with HTN have RAS. Who are the MC pts?

A

5%

MC - >45 yrs with atherosclerotic disease hx

110
Q

What is the MC PE finding for a pt with renal artery stenosis? What is the gold standard imaging of choice? What is the real world answer?

A

HTN!! may have audible abdominal bruit

Renal angiography

Doppler US

111
Q

If a pt gets an AKI after starting an ACE inhibitor, what are you thinking?

A

renal artery stenosis

112
Q

What is the tx for renal artery stenosis?

A

meds for HTN and surgery (but NOT proven better than medical management)

angioplasty or stenting

113
Q

What is nephrosclerosis?

A

Hypertensive nephropathy Sclerosis of arteries and arterioles

Interstitial fibrosis and decreased glomerular tuft

114
Q

What are risk factors for nephrosclerosis? What is the major one? What is the tx?

A

African American race - 5x more common
Increased age, smoking, hypercholesterolemia
Longstanding uncontrolled HTN

tx the HTN!!! thiazides and ACE/ARB

115
Q

What is Cholesterol Atheroembolic Disease? When does it usually occur?

A

Emboli to kidneys → usually due to cholesterol
crystals breaking free of vascular plaque and lodging in downstream microvessels

following some sort of event: vascular surgery, trauma, heparin, thrombolytics

116
Q

What are the risk factors for Cholesterol Atheroembolic Disease?

A

male, DM, HTN, ischemic cardiac disease

117
Q

May see livedo reticularis and localized gangrene. What kidney disease are these associated with?

A

Cholesterol Atheroembolic Disease

118
Q

How do you definitively dx Cholesterol Atheroembolic Disease? What is the tx? What will the labs look like?

A

kidney biopsy

statins to stabilize the plaque and supportive care

increased Cr, eosinophilia (60-80%), elevated ESR, low complement

119
Q
A

GU (13 decks)

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