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X Clin Med II Exam 3 > CKD and Nephrotic syndrome > Flashcards

CKD and Nephrotic syndrome Flashcards

1
Q

What is the most common comorbid condition of CKD?

A

Diabetes

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2
Q

What is the link b/w CKD, CVD and diabetes?

A

They increase the risk for all-cause mortality, CV mortality and ESRD

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3
Q

What is the definition of CKD?

A

Decreased kidney function of kidney damage for 3+ months

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4
Q

What lab values classify CKD?

A

GFR<60 ml/min/1.73m2
Evidence of kidney damage (albumineria-albumin creatinine ratio>30, abnormal imaging/urinary sediment, hx of kidney transplant)

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5
Q

What is the best marker of kidney function?

A

GFR (serum creatinine is poor)

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6
Q

Hallmark of progressive kidney disease

A

Declining GFR

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7
Q

Stage 1 of CKD

A

Kidney damage with normal or increased GFR

>90

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8
Q

Stage 2 of CKD

A

Kidney damage with mildly decreased GFR

60-89

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9
Q

Stage 3a of CKD

A

Mildly-moderately decreased GFR

45-59

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10
Q

Stage 3b of CKD

A

Moderately-severely decreased GFR

30-44

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11
Q

Stage 4 of CKD

A

Severely decreased GFR

15-29

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12
Q

Stage 5 of CKD

A 
Kidney failure (add D if dialysis also)
<15
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13
Q

Albumineria categories of CKD

A 
Stage 1A (normal to mildly increased, ACR<30, negative to trace on protein dipstick)
Stage A2 (moderately increased, ACR 30-300, trace to 1+ protein dipstick)
Stage A3 (severely increased, ACR>300, greater than 1+ on protein dipstick)
*must see persistent albumineria over 6 mo period
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14
Q

What causes a progressive decline in GFR in CKD?

A

Irreversible destruction of nephrons independent of cause

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15
Q

What happens when some nephrons get destroyed?

A

Compensatory hypertrophy and supranormal GFR of remaining nephrons (leads to an overwork injury)–progressive glomerular sclerosis and interstitial fibrosis

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16
Q

In general what does GFR loss lead to?

A

Abnormalities in water, electrolyte and pH balance (metabolic acidosis)
Accumulation of waste products normally excreted
Abnormalities in production and metabolism of some hormones (erythropoietin and calcitrol)

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17
Q

Causes of CKD

A 
Diabetes
HTN
Glomerular disease
Polycystic kidney disease
Chronic tubulointerstitial disorders
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18
Q

Who might be at risk for CKD?

A 
60+
Diabetes, HTN, CVD, cancer, recurrent UTIs, nephrolithiasis, autoimmune
History of AKI
Nephrotoxic drugs
FHx
Ethnic minority
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19
Q

What should you worry about with nonspecific sxs of CKD like fatigue?

A

Uremic syndrome

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20
Q

What causes uremic syndrome?

A

Accumulation of metabolic waste products or uremic toxins (profound decrease in GFR)

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21
Q

Sxs of uremic syndrome

A 
Fatigue, malaise, anorexia, n/v
Pruritus, bruising
Metallic taste
SOB
DOE, pericarditis
Restless legs, seizures, encephalopathy
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22
Q

What supports diagnosis of CKD on renal U/S?

A

Small kidneys bilaterally (<9-10cm) due to decline of renal mass/atrophy (may see normal or enlarged too)

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23
Q

When are complications of CKD more likely to occur?

A

In later stages (may lead to death before the progression to ESRD)

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24
Q

Leading cause of death in pts with CKD

A

CVD

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25
Q

Other common complications of CKD

A

HTN, dyslipidemia, anemia, mineral/bone disorders, fluid and electrolyte abnormalities, uremia, malnutrition

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26
Q

Typical pattern of mineral and bone disorders associated with CKD (CKD-MBD)

A 
Hyperphoshatemia
Hypocalcemia
Decreased vitamin D
Secondary hyperparathyroidism
Usually detectable by Stage 3!!
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27
Q

First step in the management of CKD

A

ID the cause

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28
Q

What are some reversible factors of kidney injury?

A

Infection (urine C&S)
Obstruction (bladder cath, renal US)
Volume depletion (BP, pulse, orthostatic measurements)
Nephrotoxic agents (drug history, recent imaging)
HF (physical exam, CXR)
*will see acute increase in serum creatinine

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29
Q

Ways to slow the disease progression of CKD

A

Glycemic control
BP control (ACEs and ARBS to reduce proteinuria)
Low sodium diet
Weight management
CV risk factor management (statin therapy and smoking cessation)

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30
Q

Use of Ace-I or ARBs in CKD

A

Renoprotective! By slowing progression of preoteinuric CKD and decrease albumineria
Dilate the efferent arteriole to decrease glom pressure

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31
Q

When might Ace-Is or ARBs be harmful in CKD

A

May see an acute reduction in GFR and hyperkalemia so caution in AKI (b/c goal is to increase filtration here)

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32
Q

Contraindication of Ace-Is and ARBS

A

Bilateral renal artery stenosis (will see huge jump in serum creatinine)

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33
Q

Target BP in CKD pts without proteinuria

A

<140/90

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34
Q

Target BP in CKD pts with proteinuric CKD

A

<130/80

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35
Q

Most common guideline for referral in CKD

A

GFR<30

36
Q

Why should you refer with CKD?

A

Determine cause
Manage complications (EPO therapy, phosphate binders in CKD-MBD, resistant HTN)
Prepare for dialysis
Transplant eval

37
Q

When is renal replacement therapy needed?

A

For pts with kidney failure/ESRD

Hemodialysis, peritoneal dialysis, kidney transplant

38
Q

Indications for dialysis with CKD

A

GFR<30

Uremic sxs, fluid overload unresponsive to diuresis, refractory hyperkalemia, acidosis and hyperphosphatemia

39
Q

What is hemodialysis?

A

Constant BF along one side of semipermeable membrane with cleansing solution or a dialysate along the other
Remove unwanted substances

40
Q

Acute complications of hemodialysis

A 
Hypotension (most common)
Cramps
N/v
HA
Chest pain
Back pain
Itching
Fever and chills
41
Q

Peritoneal dialysis

A

Peritoneal membrane is dialyzer b/c semipermeable
Dialysate instilled into peritoneal cavity with cath
Diffusion and osmosis drive waste products and excess fluid through peritoneum into dialysate
Then it is drained and replaced with fresh dialysate (exchange)

42
Q

Complications of peritoneal dialysis

A

Peritonitis (mostly)
Exit site infection
Poor dialysate exchange

43
Q

Treatment of choice for ESRD

A

Kidney transplant (improves quality of life)

44
Q

Does dialysis or kidney transplant reduce mortality risk more?

A

Kidney transplant

45
Q

What characterizes chronic tubulointerstitial disease?

A

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

46
Q

Causes of chronic tubulointerstitial disease

A

Obstructive uropathy
Reflux nephropathy
Analgesic nephropathy, heavy metals, lithium

47
Q

General findings of chronic tubulointerstitial disease

A 
Polyuria (can't concentrate urine)
Hyperkalemia (b/c decreased GFR and DT aldosterone resistant)
Nonspecific UA (proteinuria, broad waxy casts)
48
Q

What is obstructive uropathy?

A

Prolonged obstruction of urinary tract leading to decreased GFR, renal BF and impaired tubular function
Tubular atrophy, intersitial fibrosis and irreversible renal injury over time

49
Q

Obstructions that can lead to obstructive uropathy

A 
Prostatic disease
Ureteral calculus in single functioning kidney
Bilateral ureteral calculi
Carcinoma of cervix, colon, bladder
Retroperitoneal tumors or fibrosis
50
Q

Diagnostics in obstructive uropathy

A

UA might have hematuria, pyuria and bacteriuria (benign)

US might show pass, hydroureter or hydronephrosis

51
Q

What is reflux nephropathy?

A

Consequence of vesicoureteral reflux other another anomalies in childhood
Incompetent vesicoureteral sphincter–urine extravasates into interstitium–inflammatory response–fibrosis

52
Q

When do you diagnose reflux nephropathy?

A

In young kids with recurrent UTIs (but maybe not til adulthood and just see HTN)

53
Q

What is seen on renal US in reflux nephropathy?

A

Renal scarring and hydronephrosis

54
Q

Analgesic nephropathy

A

CKD caused by long term consumption of analgesics, often when taken in combo meds (acetaminophen, NSAIDs)
*when have chronic HA, muscular pains, arthritis

55
Q

UA and CT scan in analgesic nephropathy

A

UA- hematuria, mild proteinuria, steril pyuria

Ct- papillary microcalcifications/necrosis

56
Q

Tx of chronic tubulointerstitial disorders

A 
ID underlying disorder
Med management
Relieve obstruction
Withdraw analgesics
Refer
57
Q

Definition of nephrotic syndrome

A

Noninflammatory damage to glomerular capillary wall (podocyte and GBM)

58
Q

What is on the nephrotic spectrum>

A

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

59
Q

What is nephrotic syndrome?

A 
Nephrotic range proteinuria (>3.5 g/d)
Hypoalbuminemia
Edema (O face)
Hyperlipidemia (donut)
*foamy/oval fat bodies in urine
60
Q

Primary vs secondary disease of nephrotic syndrome

A

Primary causes are minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis
Secondary causes are diabetic nephropathy or amyloidosis

61
Q

Signs and sxs of nephrotic syndrome

A

Edema (periorbital, pedal, anasarca)
Ascites
Foamy urine
Malaise, anorexia, dyspnea, abd distention, weight gain, hypovolemia

62
Q

Complications of nephrotic syndrome

A 
Protein malnutrition
Hypercoagulability (loss antithrombin, protein C/S, increased platelet activation)
Vit D deficiency and hypocalcemia
Infection (loss Igs in urine)
Anemia (loss EPO and transferrin)
63
Q

What are oval fat bodies?

A

Grape like clusters of fatty casts in urine

64
Q

Management of nephrotic syndrome

A 
ACE-Is and ARBS
Statins, loop diuretics
Sodium and fluid restriction
Anticoagulants when indicated
Immunosuppression
Refer
65
Q

Most common cause of nephrotic syndrome in kids

A

Minimal change disease (peaks at age 2)

66
Q

Most common cause of minimal change disease

A

Idiopathic (primary)

67
Q

Secondary associations with minimal change disease

A

Following URI
Hypersensitivity
Meds
Malignancies

68
Q

Most common presentation of minimal change disease

A

Edema (puffy) with sudden onset over days to a week or 2

69
Q

Histopathology of minimal change disease

A

No changes on light microscope

Mostly affect podocyte (diffuse podocyte foot process fusion on electron microscopy)

70
Q

1st line tx of minimal change disease

A

Prednisone (up to 6 mos)

71
Q

When does membranous nephropathy usually peak?

A

fourth and fifth decades (mostly male)

72
Q

Primary vs secondary membranous nephropathy

A

Primary: usually idiopathic immune mediated destruction due to antigen on podocytes
Secondary (hep b, autoimmune, thyroiditis, malignancy, drugs)

73
Q

How does membranous nephropathy present?

A

Features of nephrotic syndrome (gradual onset)

Higher risk of hypercoagulability

74
Q

Tx of membranous nephropathy

A

Support
Maybe immunosuppression
Transplant (but can see reoccurrence)

75
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Cause of primary glomerular disease in adults
Histologic lesion not just disease entity
Present on nephrotic syndrome usually

76
Q

Who is at greater risk of FSGS?

A

African Americans (men)

77
Q

Why does FSGS occur?

A

Glomerular injury from damage to podocytes (sclerosis in parts of at least one glomerulus so focal)

78
Q

Tx for FSGS

A

Support
Immunosuppression (primary)
Disease specific (secondary)

79
Q

Who will have a poor outcome with FSGS?

A

Nephrotic range proteinuria
African American
Renal insufficiency

80
Q

Most common cause of ESRD in US

A

Diabetic nephropathy

81
Q

What is nearly universal in type 1 DM with nephropathy?

A

Retinopathy (peak when have had DM for 10-20 yrs)

82
Q

What causes diabetic nephropathy?

A

The effect of HTN and metabolic abnormalities (hyperglycemia and dyslipidemia)
Morphologic changes in kidney leading to increased filtration of serum proteins in urine
Albumineria >300

83
Q

Tx for diabetic nephropathy

A

Glycemic and BP control
ACEis and ARBs
Statin therapy
Dialysis and transplant when indicated

84
Q

What cause renal amyloidosis?

A

Deposition of amyloid in the glomerulus (abnormally folded proteins)

85
Q

2 etiologies of renal amyloidosis

A

Primary/AL: monoclonal light chain

Secondary/AA: chronic inflammatory disease or infection

86
Q

What is the renal involvement in amyloidosis?

A

Proteinuria, decreased GFR and nephrotic syndrome

87
Q

What is a good screening test for amyloidosis?

A

Serum and urine protein electrophoresis (SPEP or UPEP) to see spikes due to light chains

X Clin Med II Exam 3 (6 decks)

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