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Clin Med II Exam 3 > CKD and Nephrotic Syndrome > Flashcards

CKD and Nephrotic Syndrome Flashcards

1
Q

Leading cause of ESRD

A

Diabetes

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2
Q

Components that increase risk of mortality with CKD

A

DM, CVD, & CKD

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3
Q

Most likely to get CKD

A

Black females

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4
Q

CKD Definition

A

Decreased kidney function OR kidney damage for 3 or more months

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5
Q

Clinical evidence CKD

A
  1. GFR <60

2. Evidence of kidney damage

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6
Q

Evidence of kidney damage

A
  1. Albuminuria - Urine albumin-to-Cr ratio >30*
  2. Abnormal imaging test
  3. Abnormal urinary sediment
  4. History of kidney transplant
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7
Q

Best marker for kidney function

A

GFR

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8
Q

Poor measure of kidney function

A

Serum creatinine

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9
Q

Hallmark of progressive kidney disease

A

Declining GFR

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10
Q

Staging CKD

A 
Based on GFR:
G1. >90
G2. 60-89
G3a. 45-59
G3b. 30-44
G4. 15-29
G5. <15 (Kidney failure - Add "D" if treated by dialysis)
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11
Q

What is classification of CKD based on?

A

Cause, GFR, and albuminuria

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12
Q

Classifying CKD

A

Stage A1) ACR<30; neg to trace protein dipstick
Stage A2) ACR 30-300; trace to 1+ protein dipstick
Stage A3) ACR>300; >1+ protein dipstick

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13
Q

Low risk of CKD progression

A

A1 with G1 or G2

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14
Q

Mod risk of CKD progression

A

1) A1 with G3a

2) A2 with G1 or G2

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15
Q

High risk of CKD progression

A

1) A1 with G3b
2) A2 with G3a
3) A3 with G1 or G2

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16
Q

Very high risk of CKD progression

A

1) A2 with G3b
2) A3 with G3a and G3b
3) ALL G4 and G5 (no matter the albumin)

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17
Q

Progression of CKD

A

Destruction of nephrons&raquo_space;
Compensatory hypertrophy of working nephrons&raquo_space; Overwork of remaining nephrons&raquo_space;
Progressive glomerular sclerosis and fibrosis

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18
Q

Causes of CKD

A 
DM*
HTN*
Glomerular disease
Polycystic kidney disease
Chronic tubulointerstitial disorders
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19
Q

Screening for CKD

A
  1. First determine risk for ALL patients
  2. At risk patients should be screened by checking: Urine albumin-to-creatinine ratio and serum creatinine to estimate GFR
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20
Q

Patients “at risk” for CKD

A 
>60 YO
DM
HTN
CVD
FHx of kidney disease
Ethnic minority
Cancer
Systemic infection (HIV or Hep C)
Recurrent UTIs
Nephrolithiasis
Nephrotoxic drug exposure
Autoimmune disorders
History of AKI
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21
Q

Clinical Presentation of CKD

A

Depends on underlying cause and stage. Asymptomatic early and may not have symptoms until kidney failure is advanced!

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22
Q

Uremic syndrome

A

Accumulation of metabolic waste products typically seen with GFR <15

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23
Q

S/Sx of uremic syndrome

A

Fatigue, malaise, pericarditis, encephalopathy

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24
Q

Renal U/S findings for CKD

A

Small kidneys, bilaterally (<9-10cm)

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25
Q

Leading cause of death in CKD patients

A

Cardiovascular disease

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26
Q

Complications of CKD

A 
CVD*
HTN
Dyslipidemia
Anemia
Mineral/Bone disorders
Fluid and electrolyte abnormalities
Uremia
Malnutrition
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27
Q

CKD-MBD labs

A

Hyperphosphatemia, hypocalcemia, decreased Vitamin D - Secondary hyperparathyroidism*

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28
Q

When is CKD-MBD clinically detectable

A

Stage 3 CKD

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29
Q

Important to managing CKD

A

Treat the underlying cause!

  • Glycemic control (if DM)
  • BP control (ACE or ARBs)
  • Weight management
  • Control CV factors (ie. lipids, smoking cessation)
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30
Q

Slowing progression of proteinuric CKD

A

ACE or ARB

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31
Q

Caution of ACE and ARB

A

Acute reduction in GFR - Caution in AKI

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32
Q

Contraindication for ACE and ARB in CKD

A

Bilateral renal artery stenosis

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33
Q

Target BP in CKD patients

A

W/out proteinuria - <140/90

W/ proteinuria - <130/80

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34
Q

When to refer CKD

A 
GFR <30
Determine cause of CKD
Mange complications
Preparation/initiation of dialysis
Transplant eval
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35
Q

When to refer based on GFR and albumin classifications

A
  1. Always if ACR >300 (A3)
  2. Always if GFR <30 (G4 and G5)
  3. For all other patients, MONITOR (unless in low risk of progression - ACR <30 and GFR >60 (A1 with G1 or G2))
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36
Q

What is renal replacement therapy (RRT)

A

Dialysis (hemo or peritoneal) or Kidney transplant

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37
Q

RRT is used for

A

Patients with kidney failure/ESRD

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38
Q

Indications for dialysis

A

Uremic symptoms
Fluid overload refractory to diuresis
Refractory hyperkalemia, acidosis, hyperphosphatemia

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39
Q

When to start preparing for dialysis

A

GFR <30

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40
Q

Acute complications of hemodialysis

A 
HYPOTENSION (25-55% of treatments)
Cramps
N/V
HA
CP
Back pain
Pruritus
Fever/chills
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41
Q

Fluid used to “clean” the blood in dialysis

A

Dialysate

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42
Q

Complications of peritoneal dialysis

A

PERITONITIS
Exit site infection
Poor dialysate drainage

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43
Q

Treatment of choice for ESRD

A

Kidney transplant

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44
Q

Chronic Tubulointerstitial Disease

A

Interstitial scarring, fibrosis, and tubular atrophy –> progressive decrease in GFR (CKD)

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45
Q

Underlying etiologies of chronic tubulointerstitial disease

A 
Obstructive neuropathy
Reflux nephropathy
Analgesic nephropathy
Heavy metals (lead)
Lithium
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46
Q

General findings of chronic tubulointerstitial disease

A

Polyuria (can’t concentrate urine secondary to damage)
Hyperkalemia (tubules become aldosterone resistant)
Urinalysis is nonspecific (proteinuria <2g/d, broad waxy casts)

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47
Q

Obstructive uropathy definition

A

Prolonged obstruction of the urinary tract leads to:
1. Decreased GFR
2. Decreased renal blood flow
3. Impaired tubular function
Eventually leads to irreversible renal injury

48
Q

Causes of obstruction

A 
Prostatic disease
Ureteral calculus in a single kidney
Bilateral ureteral calculi
Carcinoma of cervix, colon, or bladder
Retroperitoneal tumors or fibrosis
49
Q

Labs/Diagnostics for obstruction

A

UA, U/S

50
Q

UA findings with obstruction

A

Often BENIGN - may show hematuria, pyuria, or bacteriuria

51
Q

U/S findings with obstruction

A

Possible mass, hydroureter, hydronephrosis

52
Q

Cause of reflux nephropathy

A

Vesicoureteral reflux (VUR) or other urologic anomalies in early childhood. Leads to inflammation and fibrosis of kidney.

53
Q

Reflux nephropathy in kids

A

History of recurrent UTIs

54
Q

Reflux nephropathy in adults

A

Present with HTN

55
Q

Imaging for reflux nephropathy

A

U/S, VCUG

56
Q

U/S findings in reflux nephropathy

A

Renal scarring and hydronephrosis

57
Q

VCUG findings in reflux nephropathy

A

Often have VUR

58
Q

What is analgesic nephropathy

A

CKD caused by LONG-TERM consumption of analgesics (ie. acetaminophen, NSAIDS)

59
Q

Labs/diagnostics for analgesic nephropathy

A

UA, CT scan

60
Q

UA findings for analgesic nephropathy

A

Hematuria, mild proteinuria, sterile pyuria (WBC w/out bacteria)

61
Q

CT findings for analgesic nephropathy

A

Papillary microcalcifications/necrosis

62
Q

Treating chronic tubulointerstitial disease

A

Treat underlying cause and refer to nephrology or urology

63
Q

What is nephrotic syndrome

A

Noninflammatory damage to the glomerular capillary wall

64
Q

Nephrotic spectrum vs syndrome

A

Spectrum - Diseases that present primarily with proteinuria and a bland urine sediment (no cells or casts)
Syndrome - Distinct clinical and laboratory features of renal disease

65
Q

Clinical and lab features of nephrotic syndrome

A

Proteinuria (>3.5 g/d)
Hypoalbuminemia
Edema
Hyperlipidemia

66
Q

Nephrotic vs Nephritic (pathogenesis)

A

Nephrotic: Non-inflammatory
Nephritic: Inflammatory

67
Q

Nephrotic vs Nephritic (hematuria)

A

Nephrotic: +/-
Nephritic: ++

68
Q

Nephrotic vs Nephritic (proteinuria)

A

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

69
Q

Nephrotic vs Nephritic (urine)

A

Nephrotic: “Foamy”/oval fat bodies*
Nephritic: Colar-colored urine; RBC casts

70
Q

Nephrotic vs Nephritic (edema)

A

Nephrotic: ++++
Nephritic: ++

71
Q

Cola-colored urine

A

Nephritic

72
Q

Foamy urine

A

Nephrotic

73
Q

Oval fat bodies

A

Nephrotic

74
Q

RBC casts

A

Nephritic

75
Q

Nephrotic syndrome primary etiologies

A 
Minimal change disease (MCD)
Membranous nephropathy (MN)
Focal Segmental Glomerulosclerosis (FSGS)
76
Q

Nephrotic syndrome secondary etiologies

A

Diabetic nephropathy

Amyloidosis

77
Q

S/Sx of nephrotic syndrome

A 
Edema
Ascites
"Foamy urine"
Malaise
Anorexia
Dyspnea
Weight gain
Orthostatic hypotension (hypovolemia)
78
Q

Anasarca

A

Massive, generalized edema

79
Q

Complications of nephrotic syndrome

A 
HYPERCOAGULABILITY*
INFECTION*
Protein malnutrition
Vitamin D deficiency and hypocalcemia
Anemia
80
Q

Work-up for nephrotic syndrome

A 
UA (ACR, proteinuria, lipiduria)
Urine microscopy (few cells/casts, OVAL FAT BODIES)
Serology
U/S
Biopsy if indicated
81
Q

Management of nephrotic syndrome

A 
ACE/ARBs
Statins
Loops
Sodium/fluid restriction
Anticoagulants (when indicated)
Immunosuppressants (corticosteroids, cytotoxic agents)
Nephrology referral
82
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease (MCD)

83
Q

Causes of MCD

A 
Most are IDIOPATHIC
Secondary MCD following: 
-URI* (esp in children)
-Hypersensitivity reactions (NSAIDs &amp; bee stings)
-Medications (lithium)
-Malignancies (hodgkins)
84
Q

MCD presentation

A

Sudden onset (days to week or two) of EDEMA

85
Q

MCD histopathology

A

No changes on light microscopy

Primarily effects the PODOCYTE

86
Q

MCD 1st line treatment

A

Prednisone

87
Q

MCD prognosis

A

Good (w/ treatment) - Very few progress to ESRD

88
Q

MN epidemiology

A

M>F; Adults - peak around 4th and 5th decades

89
Q

Primary MN causes

A

Most are IDIOPATHIC

Thought to be immune-mediated against podocytes

90
Q

Secondary MN causes

A 
Hep B
Autoimmune diseases
Thyroiditis
Malignancy
Drugs
91
Q

Nephrotic syndrome with higher risk for hypercoagulable state

A

MN

92
Q

MN Presentation

A

Presents with features of nephrotic syndrome (80%):

  • GRADUAL development
  • Higher risk for hypercoagulable state
93
Q

Diagnosing MN

A

Serology, biopsy

94
Q

Treating MN

A

Supportive
+/- immunosuppressive agents
Transplant

95
Q

MN prognosis

A

Depends on renal function and amount of proteinuria

96
Q

Adverse risk factors for MN prognosis

A

Male, >50 YO

97
Q

Most common cause of PRIMARY glomerular diseases in adults

A

Focal Segmental Glomerulosclerosis (FSGS)

98
Q

Presentation of FSGS

A 
VARIES a great deal
Nephrotic syndrome (>70%)
99
Q

FSGS Epidemiology

A

Black
Male
18-45 YO (no age group exempt)

100
Q

FSGS pathogenesis

A

Glomerular injury resulting from damage to PODOCYTES

101
Q

Cause of primary FSGS

A

Idiopathic

102
Q

Cause of secondary FSGS

A 
Obesity
Infection
Inflammation
Toxins
Healed previous glomerular injury
Reflex nephropathy
103
Q

FSGS treatment

A

Supportive
Immunosuppressive agents (primary)
Disease-specific treatment (secondary)

104
Q

Adverse risk factors for FSGS prognosis

A

Nephrotic-range proteinuria (>3.5 g/day)
African-American
Renal insufficiency

105
Q

Most common cause of ESRD in the US

A

Diabetic Nephropathy

106
Q

Common comorbidity in Type I DM with nephropathy

A

Retinopathy

107
Q

Peak incidence diabetic nephropathy

A

DM for 10-20 years (esp if uncontrolled)

108
Q

Progression of diabetic nephropathy

A

Hyperfiltration»Albuminuria»Declined GFR

109
Q

Diabetic nephropathy treatment

A

Glycemic and BP control
ACE/ARBs
Statins (may add ezetimibe)
Dialysis and transplant (when indicated)

110
Q

Abnormally folded/shaped proteins

A

Amyloid

111
Q

Pathophysiology of Renal Amyloidosis

A

Deposition of amyloid in the GLOMERULUS

112
Q

AL Amyloidosis

A

Monoclonal light chain

113
Q

AA Amyloidosis

A

Chronic inflammatory disease (RA) or infection

114
Q

Presentation of renal amyloidosis

A

Proteinuria
Decreased GFR
Nephrotic syndrome

115
Q

Screening test for renal amyloidosis

A

Serum/urine protein electrophoresis (SPEP & UPEP)

116
Q

Renal amyloidosis prognosis

A

VARIES depending on the nature, number, and extent of other organ involvement

117
Q

Treatment for renal amyloidosis

A

Treat underlying cause

Refer to nephrology

Clin Med II Exam 3 (2 decks)

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