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

L19: CKD + Nephrotic syndrome Flashcards

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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
Specific complications of CKD
``` *CVD* HTN, dyslipidemia Anemia Hyperkalemia, hyperphosphatemia, hypocalcemia Metabolic acidosis Malnutrition (Low serum albumin) ```
26
Mineral and bone disorders are clinically detectable ____
starting at stage 3 CKD
27
Mineral and bone disorders (CKD-MBD) are characterized by
Spectrum of bone disorders | Pattern: Hyperphosphatemia, hypocalcemia, decreased vitamin D, *secondary hyperparathyroidism*
28
How is hyperparathyroidism secondary in CKD-MBD?
Decreased GFR causes decrease 1,25 Vit D | Decreased 1,25 vit D causes increased PTH
29
Albuminuria
urine albumin urine creatinine ration (ACR) > 30 mg/g
30
The best marker of kidney function
GFR
31
Is serum creatinine a good marker of kidney function?
NO
32
Obstruction labs
Rise in creatinine and difficulty urinating | seen on renal US
33
Volume depletion signs/symptoms
Decreased BP and pulse | orthostatic hypotension
34
The goal of ACE-I or ARBs it to
slow progression of proteinuria | renoprotective
35
Angiotensin II vasoconstricts
the efferent arteriole | inhibiting it dilates the efferent arteriole and decreases glomerular pressure
36
ACE-I/ARBs are contraindicated
Acute kidney injury: can cause acute reduction in GFR and hyperkalemia Bilateral renal artery stenosis
37
Target BP in patients with CKD+proteinuria
130/80
38
Target BP in patients with CKD and NO proteinuria
140/90
39
BP control in the elderly
should be tailored | they may get dizzy or lightheaded
40
If your patient has a GFR<30
REFER
41
Other reasons to refer a patient with CKD
``` Determine cause of CKD Manage complications: → EPO therapy (Hgb <10) → CKD-MBD: phosphate binders → resistant HTN Dialysis or transplant ```
42
CKD-MBD treatment
phosphate binders
43
Anemia treatment
when Hgb <10 | Erythropoitin therapy
44
Indications for dialysis
GFR<30 Uremic syndrome Refractory fluid overload Refractory hyperkalemia, acidosis, hyperphosphatemia
45
Fluid overload 1st line
Diuresis
46
What're the benefits of Kidney transplant for end-stage renal disease?
Improved quality of life | Reduces mortality risk compared to dialysis
47
Complications of hemodialysis
``` cramps N/V HA chest pain back pain itching fever chills ```
48
Complications of peritoneal dialysis
**peritonitis** exit site infection poor dialysate drainage
49
Hemodialysis vs peritoneal dialysis: dialyzer
Hemodialysis: a machine with a semipermeable membrane | Peritoneal dialysis: Peritoneal membrane (partially permeable)
50
Hemodialysis vs peritoneal dialysis: dialysate
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
Chronic Tubulointerstitial Disease is caused by
Insults from an acute factor OR progressive insults without any obvious acute cause
52
Chronic Tubulointerstitial Disease is characterized by
Interstitial scarring, fibrosis, and tubular atrophy → progressive decrease in eGFR (CDK)
53
5 main etiologies of Chronic Tubulointerstitial Disease
``` Obstructive uropathy Reflux nephropathy Analgesic nephropathy Heavy metals (lead) Lithium ```
54
General findings in Chronic Tubulointerstitial Disease
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
If you see a nonspecific urinalysis with dilute urine and waxy casts and serum hyperkalemia, think
Chronic Tubulointerstitial Disease
56
Causes of obstructive uropathy
``` Prostatic disease Ureteral calculus in single functioning kidney Bilateral ureteral calculi Carcinoma: cervix, colon, bladder Retroperitoneal tumors or fibrosis ```
57
Obstructive uropathy pathophysiology
Prolonged obstruction of urinary tract → decreased GFR → decreased renal blood flow → impaired tubular function → tubular atrophy and interstitial fibrosis→ irreversible kidney injury (eventually)
58
Urinalysis of obstructive uropathy
often benign +/- hematuria, pyuria, bacteriuria
59
Ultrasound of obstructive uropathy
mass Hydroureter* Hydronephrosis
60
Reflux nephropathy pathophysiology
Incompetent vesicoureteral sphincter→ urine an extravasate into interstitium → inflammatory response to bacteria or urine → fibrosis
61
Reflux nephropathy is caused by
Vesicoureteral reflux OR Other urologic anomalies In early childhood
62
Seen on RUS of reflux nephropathy
scarring | hydronephrosis
63
Reflux nephropathy may be undetected until early adulthood and presents with
HTN
64
Reflux nephropathy is usually diagnosed in young children due to
recurrent UTIs
65
Long term use of analgesics such as ______ can cause analgesic nephropathy
NSAIDS Acetaminophen Aspirin
66
Urinalysis of analgesic nephropathy shows
hematuria mild proteinuria sterile pyuria (WBC present without bacteria)
67
CT scan of analgesic nephropathy
Papillary micro-calcifications/necrosis
68
Sterile pyuria
analgesic nephropathy
69
Papillary micro-calcifications/necrosis on CT
Analgesic nephropathy
70
Nephritic vs nephrotic: pathogenesis
Nephritic: inflammatory NephrOtic: non-inflammatory
71
Nephritic vs nephrotic: hematuria
Nephritic: ++ NephrOtic: +/-
72
Nephritic vs nephrotic: proteinuria
Nephritic: <3.0 g/day NephrOtic: >3.5 g/day
73
Nephritic vs nephrotic: urine
Nephritic: cola-colored, RBC casts NephrOtic: foamy (protein) + Oval fat bodies
74
Classic tetrad for nephrotic syndrome
Nephrotic range proteinuria >3.5g/d Hypoalbuminemia Edema Hyperlipidemia
75
Nephrotic ~spectrum~ diseases are defined as
diseases that present with proteinuria and bland urine sediment (no cells or cellular casts)
76
Nephrotic syndrome is defined as
Noninflammatory damage to the glomerular capillary wall (podocyte and basement membrane) may be primary or second
77
Primary nephrotic syndromes
Minimal change disease Membranous nephropathy Focal Segmental glomerulosclerosis
78
Nephrotic syndrome can be secondary to
DM | Amyloidosis
79
Signs of nephrotic syndrome
Edema: periorbital, pedal, anasarca (extreme) Ascites Foamy urine
80
Symptoms of nephrotic syndrome
``` Malaise Anorexia Dyspnea Abdominal distention Weight gain Hypovolemia → orthostatic hypotension ```
81
Complications of nephrotic syndrome
Protein malnutrition (proteinuria) Hypocalcemia Infection Anemia
82
Why does hypocalcemia occur in nephrotic syndrome?
Urinary loss of vitamin D binding protein, 25-hydroxyvitamin D→ vitamin D deficiency, hypocalcemia
83
Why does infection occur in nephrotic syndrome?
Urinary loss of immunoglobulins, defects in complement cascade
84
Why does anemia occur in nephrotic syndrome?
Urinary loss of UPO and transferrin
85
Management of nephrotic syndrome
``` ACE-I/ARBS Statins Loop diuretics +/- anticoagulants Corticosteroids (immunosuppressants) Cytotoxic agents (immunosuppressants) Nephrology referral Sodium + fluid restriction ```
86
Minimal change disease is caused by
we don't know
87
Minimal change disease as seen on microscopy
Light microscopy: no changes (hence the name) Electron microscopy: diffuse podocyte foot process fusion
88
Most common nephrotic syndrome in children
Minimal change disease | Males, ~2 years old
89
Minimal change disease in adults
Rare | 40 years, M=F
90
Treatment of minimal change disease
prednisone
91
Sudden onset edema in a kiddo following a URI
minimal change disease
92
Minimal change disease prognsosi
very few progress to ESRD
93
Membranous nephropathy affects
Adults, males, 4th and 5th decades
94
Primary membranous nephropathy
immune-mediated autoantibodies against podocyte antigen
95
Secondary membranous nephropathy
``` Hep B autoimmune thyroiditis malignancy drugs ```
96
Presentation of membranous nephropathy
Gradual development of nephrotic syndrome | Higher risk of hypercoagulable state→ renal vein thrombosis
97
Slow onset edema
membraneous nephropathy | "Gradual development of nephrotic syndrome
98
Renal vein thrombosis
membranous nephropathy
99
Diagnosis of membranous nephropathy
serology | biopsy
100
Treatment of membranous nephropathy
Supportive +/- immunosuppressive agents Transplant, but risk of recurrence
101
Prognosis of membranous nephropathy
Prognosis depends on renal function and amount of proteinuria Adverse risk: Male, >50 years
102
Who gets focal Segmental glomerulosclerosis?
Adults African Americans M>F 18-45 years (usually) Accounts for 35% of all cases of idiopathic nephrotic syndromes
103
Focal Segmental glomerulosclerosis pathophysiology
Histologic lesion Glomerular injury from damage to podocytes → sclerosis in parts (segmental) → at least one glomerulus (focal)
104
Most Minimal change disease is
Idiopathic/primary (most)
105
Secondary minimal change disease
URI ***esp peds*** hypersensitivity: bee stings, NSAIDs lithium Hodgkin disease
106
Types of Focal Segmental glomerulosclerosis
Primary (idiopathic) Secondary: obesity, infection, inflammation, toxins, healed previous glomerular injury, reflex nephropathy
107
Presentation of Focal Segmental glomerulosclerosis
VARIES GREATLY | But most present with nephrotic syndrome (primary disease)
108
Treatment of primary Focal Segmental glomerulosclerosis
immunosuppressants
109
Poor outcomes in Focal Segmental glomerulosclerosis
Nephrotic-range proteinuria (>3.5) African American renal insufficiency
110
Peak incidence of diabetic nephropathy
10-20 years after having diabetes | *in T2DM, nephropathy may be present at time of diagnosis*
111
Nearly universal in T1DM with nephropathy
retinopathy
112
Diabetic nephropathy occurs due to
HTN Hyperglycemia Hyperlipidemia
113
Progression of diabetic nephropathy
1. Early disease: hyperfiltration 2. Albuminuria 30-300mg/g → >300mg/g 3. Slow progressive decline in GFR
114
Diabetic nephropathy treatment
Strict BP and Glycemic control ACE-I/ARBS Statin or Statin+Ezetimibe +/- dialysis, transplant
115
AL amyloidosis
monoclonal light chain
116
AA amyloidosis
chronic inflammatory disease or infection
117
Renal amyloidosis causes
proteinuria decreased GFR nephrotic syndrome
118
Screening for renal amyloidosis
Serum and Urine protein electrophoresis (SPEP/UPEP)
119
Treatment of renal amyloidosis
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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