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Unit 3 Clin Med II > L19: CKD + Nephrotic syndrome > Flashcards

L19: CKD + Nephrotic syndrome Flashcards

1
Q

What’s the most common comorbid condition with CKD and the most common cause of ESRD?

A

CKD: diabetes
ESRD: diabetic nephropathy

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2
Q

“The link” 3 things that increase risk for all-cause mortality, CVD mortality, and ESRD

A 
***
CKD
CVD
DM
***
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3
Q

Who’s most likely to get CKD

A

Non-hispanic blacks

gender don’t matter

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4
Q

Serology for CKD should include

A

lipid profile
Phosphate, Alk phosphatase
intact PTH
25-hydroxyvitamin D

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5
Q

Definition of CKD

A

Decreased kidney function OR kidney damage

>3 months

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6
Q

GFR that defines CKD

A

GFR <60

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7
Q

Kidney damage is defined by

A

albuminuria: ACR: >30 mg/g
Abnormal imaging, urinary sediment
Hx of kidney transplant

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8
Q

An ultrasound of CKD is ~most likely~ to show

A

Small kidneys bilaterally <9-10 cm

however, normal/enlarged can also be seen

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9
Q

CKD pathogenesis

A

Progressive decline in GFR over months/years:
Irreversible destruction of nephrons→ compensatory hypertrophy, supranormal GFR of remain nephrons → overwork injury → progressive glomerular sclerosis and interstitial fibrosis

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10
Q

CKD is caused by:

A

Diabetes
HTN
Glomerular disease
Polycystic kidney disease
Chronic tubulointerstitial disorders

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11
Q

Eventually, kidney dysfuntion in CDK will cause

A

→ abnormalities in water, electrolyte, pH balance
→ accumulation of waste products
→ decreased EPO→ anemia
→ calcitriol (vit D) abnormalities

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12
Q

Calcitriol aka

A

Vitamin D

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13
Q

Nephron loss leads to increased

A

ATII → Increased pressure glomerular capillary→ injury and proteinuria

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14
Q

Kidney damage due to increased Angiotensin II can be treated by

A

ACE-I or ARB

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15
Q

Early CKD presentation

A

Asymptomatic

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16
Q

Advanced CKD presentation

A

this may be the first manifestation of symptoms

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17
Q

How to screen for CKD

A

Urine Albumine to creatinine ratio (ACR)

Serum creatinine to estimate GFR (eGFR)

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18
Q

Nephrotoxic drugs

A

NSAIDS

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19
Q

Nephrotoxic drugs

A

NSAIDS

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20
Q

Nonspecific symptoms that should make you worry about UREMIC SYNDROME

A 
**fatigue**
malaise
N/V/A
pruritus
easy bruisability
metallic taste
SOB
dyspnea on exertion
resltess legs
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21
Q

Uremic syndrome is

A

Profound decrease in GFR (10-15) → Accumulation of metabolic waste products: uremic toxins

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22
Q

Uremic syndrome can eventually cause

A

seizures
Pericarditis
encephalopathy

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23
Q

Leading cause of death in CKD

A

Cardiovascular disease
***

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24
Q

Complications of CKD in general

A

More likely at later stages
May lead to death before the progression to end-stage kidney disease
May arise from adverse effects of interventions

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25
Q

Specific complications of CKD

A 
*CVD*
HTN, dyslipidemia
Anemia
Hyperkalemia, hyperphosphatemia, hypocalcemia
Metabolic acidosis
Malnutrition (Low serum albumin)
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26
Q

Mineral and bone disorders are clinically detectable ____

A

starting at stage 3 CKD

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27
Q

Mineral and bone disorders (CKD-MBD) are characterized by

A

Spectrum of bone disorders

Pattern: Hyperphosphatemia, hypocalcemia, decreased vitamin D, secondary hyperparathyroidism

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28
Q

How is hyperparathyroidism secondary in CKD-MBD?

A

Decreased GFR causes decrease 1,25 Vit D

Decreased 1,25 vit D causes increased PTH

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29
Q

Albuminuria

A

urine albumin urine creatinine ration (ACR) > 30 mg/g

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30
Q

The best marker of kidney function

A

GFR

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31
Q

Is serum creatinine a good marker of kidney function?

A

NO

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32
Q

Obstruction labs

A

Rise in creatinine and difficulty urinating

seen on renal US

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33
Q

Volume depletion signs/symptoms

A

Decreased BP and pulse

orthostatic hypotension

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34
Q

The goal of ACE-I or ARBs it to

A

slow progression of proteinuria

renoprotective

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35
Q

Angiotensin II vasoconstricts

A

the efferent arteriole

inhibiting it dilates the efferent arteriole and decreases glomerular pressure

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36
Q

ACE-I/ARBs are contraindicated

A

Acute kidney injury: can cause acute reduction in GFR and hyperkalemia

Bilateral renal artery stenosis

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37
Q

Target BP in patients with CKD+proteinuria

A

130/80

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38
Q

Target BP in patients with CKD and NO proteinuria

A

140/90

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39
Q

BP control in the elderly

A

should be tailored

they may get dizzy or lightheaded

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40
Q

If your patient has a GFR<30

A

REFER

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41
Q

Other reasons to refer a patient with CKD

A 
Determine cause of CKD
Manage complications: 
→ EPO therapy (Hgb <10) 
→ CKD-MBD: phosphate binders
→ resistant HTN
Dialysis or transplant
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42
Q

CKD-MBD treatment

A

phosphate binders

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43
Q

Anemia treatment

A

when Hgb <10

Erythropoitin therapy

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44
Q

Indications for dialysis

A

GFR<30
Uremic syndrome
Refractory fluid overload
Refractory hyperkalemia, acidosis, hyperphosphatemia

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45
Q

Fluid overload 1st line

A

Diuresis

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46
Q

What’re the benefits of Kidney transplant for end-stage renal disease?

A

Improved quality of life

Reduces mortality risk compared to dialysis

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47
Q

Complications of hemodialysis

A 
cramps
N/V
HA
chest pain
back pain
itching
fever
chills
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48
Q

Complications of peritoneal dialysis

A

peritonitis
exit site infection
poor dialysate drainage

49
Q

Hemodialysis vs peritoneal dialysis: dialyzer

A

Hemodialysis: a machine with a semipermeable membrane

Peritoneal dialysis: Peritoneal membrane (partially permeable)

50
Q

Hemodialysis vs peritoneal dialysis: dialysate

A

Hemodialysis: in the machine on the other side of the semi-permeable membrane flowing in the opposite direction
Peritoneal dialysis: instilled into peritoneal cavity via indwelling catheter, “dwells” as waste products diffuse in, drained and replaced

51
Q

Chronic Tubulointerstitial Disease is caused by

A

Insults from an acute factor OR progressive insults without any obvious acute cause

52
Q

Chronic Tubulointerstitial Disease is characterized by

A

Interstitial scarring, fibrosis, and tubular atrophy → progressive decrease in eGFR (CDK)

53
Q

5 main etiologies of Chronic Tubulointerstitial Disease

A 
Obstructive uropathy
Reflux nephropathy
Analgesic nephropathy
Heavy metals (lead)
Lithium
54
Q

General findings in Chronic Tubulointerstitial Disease

A

Tubular damage→ inability to concentrate urine → polyuria

Decreased GFR→ hyperkalemia

Distal tubules become aldosterone resistant→ hyperkalemia

Urinalysis: proteinuria (<2g/d), broad waxy casts
→ nonspecific

55
Q

If you see a nonspecific urinalysis with dilute urine and waxy casts and serum hyperkalemia, think

A

Chronic Tubulointerstitial Disease

56
Q

Causes of obstructive uropathy

A 
Prostatic disease
Ureteral calculus in single functioning kidney
Bilateral ureteral calculi
Carcinoma: cervix, colon, bladder
Retroperitoneal tumors or fibrosis
57
Q

Obstructive uropathy pathophysiology

A

Prolonged obstruction of urinary tract
→ decreased GFR
→ decreased renal blood flow
→ impaired tubular function

→ tubular atrophy and interstitial fibrosis→ irreversible kidney injury (eventually)

58
Q

Urinalysis of obstructive uropathy

A

often benign +/- hematuria, pyuria, bacteriuria

59
Q

Ultrasound of obstructive uropathy

A

mass
Hydroureter*
Hydronephrosis

60
Q

Reflux nephropathy pathophysiology

A

Incompetent vesicoureteral sphincter→ urine an extravasate into interstitium → inflammatory response to bacteria or urine → fibrosis

61
Q

Reflux nephropathy is caused by

A

Vesicoureteral reflux
OR
Other urologic anomalies

In early childhood

62
Q

Seen on RUS of reflux nephropathy

A

scarring

hydronephrosis

63
Q

Reflux nephropathy may be undetected until early adulthood and presents with

A

HTN

64
Q

Reflux nephropathy is usually diagnosed in young children due to

A

recurrent UTIs

65
Q

Long term use of analgesics such as ______ can cause analgesic nephropathy

A

NSAIDS
Acetaminophen
Aspirin

66
Q

Urinalysis of analgesic nephropathy shows

A

hematuria
mild proteinuria
sterile pyuria (WBC present without bacteria)

67
Q

CT scan of analgesic nephropathy

A

Papillary micro-calcifications/necrosis

68
Q

Sterile pyuria

A

analgesic nephropathy

69
Q

Papillary micro-calcifications/necrosis on CT

A

Analgesic nephropathy

70
Q

Nephritic vs nephrotic: pathogenesis

A

Nephritic: inflammatory
NephrOtic: non-inflammatory

71
Q

Nephritic vs nephrotic: hematuria

A

Nephritic: ++
NephrOtic: +/-

72
Q

Nephritic vs nephrotic: proteinuria

A

Nephritic: <3.0 g/day
NephrOtic: >3.5 g/day

73
Q

Nephritic vs nephrotic: urine

A

Nephritic: cola-colored, RBC casts
NephrOtic: foamy (protein) + Oval fat bodies

74
Q

Classic tetrad for nephrotic syndrome

A

Nephrotic range proteinuria >3.5g/d
Hypoalbuminemia
Edema
Hyperlipidemia

75
Q

Nephrotic ~spectrum~ diseases are defined as

A

diseases that present with proteinuria and bland urine sediment (no cells or cellular casts)

76
Q

Nephrotic syndrome is defined as

A

Noninflammatory damage to the glomerular capillary wall (podocyte and basement membrane)

may be primary or second

77
Q

Primary nephrotic syndromes

A

Minimal change disease
Membranous nephropathy
Focal Segmental glomerulosclerosis

78
Q

Nephrotic syndrome can be secondary to

A

DM

Amyloidosis

79
Q

Signs of nephrotic syndrome

A

Edema: periorbital, pedal, anasarca (extreme)
Ascites
Foamy urine

80
Q

Symptoms of nephrotic syndrome

A 
Malaise
Anorexia
Dyspnea
Abdominal distention
Weight gain
Hypovolemia → orthostatic hypotension
81
Q

Complications of nephrotic syndrome

A

Protein malnutrition (proteinuria)
Hypocalcemia
Infection
Anemia

82
Q

Why does hypocalcemia occur in nephrotic syndrome?

A

Urinary loss of vitamin D binding protein, 25-hydroxyvitamin D→ vitamin D deficiency, hypocalcemia

83
Q

Why does infection occur in nephrotic syndrome?

A

Urinary loss of immunoglobulins, defects in complement cascade

84
Q

Why does anemia occur in nephrotic syndrome?

A

Urinary loss of UPO and transferrin

85
Q

Management of nephrotic syndrome

A 
ACE-I/ARBS
Statins
Loop diuretics
\+/- anticoagulants
Corticosteroids (immunosuppressants) 
Cytotoxic agents (immunosuppressants) 
Nephrology referral
Sodium + fluid restriction
86
Q

Minimal change disease is caused by

A

we don’t know

87
Q

Minimal change disease as seen on microscopy

A

Light microscopy: no changes (hence the name)

Electron microscopy: diffuse podocyte foot process fusion

88
Q

Most common nephrotic syndrome in children

A

Minimal change disease

Males, ~2 years old

89
Q

Minimal change disease in adults

A

Rare

40 years, M=F

90
Q

Treatment of minimal change disease

A

prednisone

91
Q

Sudden onset edema in a kiddo following a URI

A

minimal change disease

92
Q

Minimal change disease prognsosi

A

very few progress to ESRD

93
Q

Membranous nephropathy affects

A

Adults, males, 4th and 5th decades

94
Q

Primary membranous nephropathy

A

immune-mediated autoantibodies against podocyte antigen

95
Q

Secondary membranous nephropathy

A 
Hep B
autoimmune
thyroiditis
malignancy
drugs
96
Q

Presentation of membranous nephropathy

A

Gradual development of nephrotic syndrome

Higher risk of hypercoagulable state→ renal vein thrombosis

97
Q

Slow onset edema

A

membraneous nephropathy

“Gradual development of nephrotic syndrome

98
Q

Renal vein thrombosis

A

membranous nephropathy

99
Q

Diagnosis of membranous nephropathy

A

serology

biopsy

100
Q

Treatment of membranous nephropathy

A

Supportive
+/- immunosuppressive agents
Transplant, but risk of recurrence

101
Q

Prognosis of membranous nephropathy

A

Prognosis depends on renal function and amount of proteinuria

Adverse risk: Male, >50 years

102
Q

Who gets focal Segmental glomerulosclerosis?

A

Adults
African Americans
M>F
18-45 years (usually)

Accounts for 35% of all cases of idiopathic nephrotic syndromes

103
Q

Focal Segmental glomerulosclerosis pathophysiology

A

Histologic lesion
Glomerular injury from damage to podocytes
→ sclerosis in parts (segmental)
→ at least one glomerulus (focal)

104
Q

Most Minimal change disease is

A

Idiopathic/primary (most)

105
Q

Secondary minimal change disease

A

URI esp peds
hypersensitivity: bee stings, NSAIDs
lithium
Hodgkin disease

106
Q

Types of Focal Segmental glomerulosclerosis

A

Primary (idiopathic)

Secondary: obesity, infection, inflammation, toxins, healed previous glomerular injury, reflex nephropathy

107
Q

Presentation of Focal Segmental glomerulosclerosis

A

VARIES GREATLY

But most present with nephrotic syndrome (primary disease)

108
Q

Treatment of primary Focal Segmental glomerulosclerosis

A

immunosuppressants

109
Q

Poor outcomes in Focal Segmental glomerulosclerosis

A

Nephrotic-range proteinuria (>3.5)
African American
renal insufficiency

110
Q

Peak incidence of diabetic nephropathy

A

10-20 years after having diabetes

in T2DM, nephropathy may be present at time of diagnosis

111
Q

Nearly universal in T1DM with nephropathy

A

retinopathy

112
Q

Diabetic nephropathy occurs due to

A

HTN
Hyperglycemia
Hyperlipidemia

113
Q

Progression of diabetic nephropathy

A
  1. Early disease: hyperfiltration
  2. Albuminuria
    30-300mg/g → >300mg/g
  3. Slow progressive decline in GFR
114
Q

Diabetic nephropathy treatment

A

Strict BP and Glycemic control
ACE-I/ARBS
Statin or Statin+Ezetimibe
+/- dialysis, transplant

115
Q

AL amyloidosis

A

monoclonal light chain

116
Q

AA amyloidosis

A

chronic inflammatory disease or infection

117
Q

Renal amyloidosis causes

A

proteinuria
decreased GFR
nephrotic syndrome

118
Q

Screening for renal amyloidosis

A

Serum and Urine protein electrophoresis (SPEP/UPEP)

119
Q

Treatment of renal amyloidosis

A

Refer to nephrology+treat underlying cause

Prognosis varies depending on nature, number, and extent of organ involvement

Unit 3 Clin Med II (8 decks)

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