Exam 2: CKD And Nephrotic Syndrome Flashcards

1
Q

What defines CKD?

A

Decreased kidney function or kidney damage for 3 months or more

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2
Q

What is the hallmark of progressive kidney disease?

A

Declining GFR

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3
Q

What are the leading causes of kidney failure?

A

DM and HTN

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4
Q

What is uremic syndrome?

A

Accumulation of metabolic waste products or uremic toxins

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5
Q

What is uremic syndrome often seen with?

A

A profound decrease in GFR (10-15)

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6
Q

Patient presents with fatigue, malaise, pericarditis, encephalitis, and a GFR of 15. What are you converted about?

A

Uremic syndrome

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7
Q

What finding on renal US supports diagnoses of CKD?

A

Small kidneys bilaterally (<9-10cm)

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8
Q

What defines the kidney function/damage seen with CKD?

A

Kidney function: GFR <60

Kidney damage: Albuminuria (urine albumin to creatinine ratio >30), abnormal imaging, abnormal urinary sediment, and hx of kidney transplant

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9
Q

What is CKD stage 1?

A

GFR >90, kidney damage with normal or increased GFR

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9
Q

What is CKD stage 2?

A

GFR 60-89, kidney damage with mildly decreased GFR

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10
Q

What is CKD stage 3a?

A

GFR 45-59, mildly-moderately decreased GFR

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11
Q

What is CKD stage 3b?

A

GFR 30-44, moderately-severely decreased GFR

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12
Q

What is CKD stage 4?

A

GFR 15-29, severely decreased GFR

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13
Q

What is CKD stage 5?

A

GFR <15, kidney failure

** add D if treated with Dialysis

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14
Q

What is albuminuria stage 1?

A

ACR (albumin to creatinine ratio) < 30, normal to mildly increased

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15
Q

What is albuminuria stage 2?

A

ACR 30-300, moderately increased

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16
Q

What is albuminuria stage 3?

A

ACR >300, severely increased

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17
Q

What is the pathogenesis of CKD?

A

Progressive decline of GFR, typically over months to years, due to the irreversible destruction of nephrons independent of the cause

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18
Q

What does destruction of nephrons often lead to?

A

Compensatory hypertrophy and supranormal GFR of the remaining nephrons.
-This leads to overwork injury and progressive glomerular sclerosis and interstitial fibrosis

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19
Q

What labs should you order for patients who are at high risk of developing CKD?

A
  • ACR

- Serum creatinine to estimate GFR

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20
Q

What are some of the complications that may arise from CKD?

A
  • CVD
  • HTN
  • Dyslipidemia
  • anemia
  • Mineral and bone disorders
  • fluid and electrolyte abnormalities
  • uremia
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21
Q

What are the bone disorders that can occur as a complication from CKD?

A

Osteitis fibrosa cystica, adynamic bone disease, and osteomalacia

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22
Q

What is the typical pattern seen on labs in patients who are developing bone disorders secondary to CKD?

A

-Hyperphosphatemia, hypocalcemia, decreased vitamin D. This is called secondary hyperparathyroidism!!

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23
Q

What are the reversible factors that cause CKD?

A
  • Infection
  • UTI
  • Decreased renal perfusion
  • nephrotoxic agents
  • HF
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24
Q

What is the vital treatment measure in regards to CKD?

A

Treatment of underlying disease

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25
Q

Why are ACE inhibitors and ARBs used for CKD?

A
  • renal protective

- helpful in slowing the progression of proteinuric CKD (decreases albumin)

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26
Q

What is the target BP in CKD patients without proteinuria?

A

< 140/90

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27
Q

What is the target BP in CKD patients with Proteinuric CKD?

A

< 130/80

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28
Q

What it is the one indication that is common to most guidelines about when to refer to patient for CKD?

A

GFR < 30

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29
Q

Who is dialysis reserved for?

A

Patients with kidney failure/ESRD.

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30
Q

What are the acute complications of hemodialysis?

A

-Hypotension, cramps, nausea/vomiting, HA, CP, back pain, itching, fever, and chills

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31
Q

How does hemodialysis work?

A
  • Requires a constant flow of blood along one side of a semipermeable membrane with a cleaning solution (or a dialysate) along the other.
  • Diffusion and convection allow the dialysate to remove unwanted substances from the blood while adding back needed components
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32
Q

What are the complications of peritoneal dialysis?

A
  • Peritonitis
  • exit site infection
  • Poor dialysate drainage
33
Q

What is the treatment of choice for ESRD?

A

Kidney transplant

34
Q

What are the 3 chronic tubulointerstitial diseases of the kidney?

A

Obstructive uropathy, reflex nephropathy, and analgesic nephropathy

35
Q

When can ACE inhibitors and ARBs be harmful in CKD?

A
  • Caution in acute kidney injury, may see acute reduction in GFR and hyperkalemia
  • Contraindicated in bilateral renal artery stenosis
36
Q

What are the indications for dialysis?

A
  • uremic symptoms
  • fluid overload unresponsive to diuresis
  • Refractory hyperkalemia, acidosis, and hyperphosphatemia
37
Q

You should prepare to initiate dialysis if the GFR is ***.

A

<30

38
Q

What is the “dialyzer” in peritoneal dialysis?

A

The peritoneal membrane

39
Q

What is tubulointerstitial disease?

A

Broadly refers to kidney disease that involve tubules and/or interstitium of the kidney and spares the glomeruli

40
Q

What is tubulointerstitial disease characterized by?

A

Interstitial scarring, fibrosis, and tubular atrophy leading to chronic renal insufficiency

41
Q

What are the underlying etiologies of chronic tubulointerstitial disease?

A

Obstructive uropathy, reflux neuropathy, medications (analgesics), and heavy metals

42
Q

What are the clinical findings with chronic tubulointerstitial disease?

A

-polyuria, hyperkalemia (decreased GFR and distal tubules are aldosterone resistant), and urinalysis is nonspecific (proteinuria <2 and broad waxy casts)

43
Q

What is obstructive uropathy?

A

Prolonged (or recurrent) obstruction of the urinary tract

-chronic reduction in GFR and impaired tubular function

44
Q

What is the clinical presentation of obstructive uropathy?

A

Pain, change in urine output, HTN, hematuria, increased serum creatinine

45
Q

What is seen on UA in a patient with obstructive uropathy?

A

Hematuria, pyuria, and bacteriuria is often bland

46
Q

What is seen on US of obstructive uropathy?

A

Used to detect masses, hydroureter, and hydronephrosis

47
Q

What is reflux nephropathy?

A

The consequence of VUR or other urologic anomalies in childhood

48
Q

What is the sequence of events in reflux nephropathy?

A

1) retrograde passage of urine from the bladder to the upper urinary tract
2) urine can extravasate into the interstitium
3) Inflammatory response develops
4) Fibrosis occurs

49
Q

Who is reflux nephropathy typically diagnosed in?

A

Young children with a history of recurrent UTIs

50
Q

What two tests are helpful in diagnosing reflux nephropathy?

A

renal US (evaluate for scarring and hydronephrosis) and Voiding Cystourethrogram (VCUG, helpful for evaluating VUR and the anatomy of the lower urinary tract)

51
Q

What is the pathogenesis in obstructive uropathy?

A

Tubular atrophy, interstitial fibrosis, and eventually irreversible renal injury

52
Q

What can cause obstruction and lead to obstructive uropathy?

A

Prostatic disease, ureteral calculus in a single functioning kidney, bilateral urethral calculus, carcinoma of the cervix colon or bladder, and retroperitoneal tumors or fibrosis

53
Q

What are the abnormal labs you will see with analgesic nephropathy?

A

-Elevated serum creatinine, UA showing hematuria or sterile pyuria, mild proteinuria, and anemia

54
Q

What can be seen in CT scan in a patient with Analgesic nephropathy?

A

Renal papillary necrosis and calcification

55
Q

What is analgesic nephropathy?

A

CKD caused by long term consumption of analgesic, often when taken in combination with other medications (Tylenol and NSAIDs)

56
Q

What is the treatment for chronic tubulointerstitial disorders?

A
  • ID underlying disorder
  • Medical management
  • Relief of obstruction
  • Withdrawal of all analgesics
  • Referral to nephrology
57
Q

What is nephrotic syndrome?

A

Non inflammatory damage to the glomerular capillary wall (podocyte or GBM).

Can be primary or in association with systemic disease

Distinct constellation of clinical and lab features of renal disease

58
Q

What is the nephrotic spectrum?

A

Diseases that present primarily with proteinuria and bland urine sediment

59
Q

What are the abnormal labs that are seen with nephrotic syndrome?

A

Nephrotic range proteinuria (<3.5), hypoalbuminemia, edema, and hyperlipidemia

60
Q

What are the signs of nephrotic syndrome?

A
  • Edema
  • Ascites
  • foamy urine
61
Q

What are the symptoms of nephrotic syndrome?

A
  • Malaise
  • Anorexia
  • Dyspnea
  • Abdominal distention
  • Weight gain
  • Orthostatic hypotension
62
Q

What are some of the complications seen with nephrotic syndrome?

A
  • Protein malnutrition
  • hypercoagulability
  • Vitamin D deficiency and hypocalcemia
  • infection
  • anemia
63
Q

What will be seen on urine microscopy in a patient that with nephrotic syndrome?

A

Oval fat body

64
Q

What is the management of nephrotic syndrome?

A
  • ACE and ARB
  • Statin therapy
  • Loop diuretics
  • sodium and fluid restriction
  • Anticoagulants
  • Immunosuppresive therapy
  • Nephrology referral
65
Q

What is the most common cause of nephrotic syndrome in children?

A

MInimal change disease (MCD)

66
Q

What is MCD often associated with?

A

Following a URI, hypersensitivity reactions, medications (lithium) and malignancies

67
Q

What is the first line treatment for MCD?

A

Prednisone

68
Q

What is the etiology of primary Membranous nephropathy (MN)?

A

Thought to be immune mediated, autoantibodies directed against antigen found on podocytes

69
Q

What is the etiology of secondary MN?

A

Hep B, autoimmune disease, thyroid is its, malignancy, drugs, etc

70
Q

Patients with MN are at high risk for ***.

A

Hypercoagulable state

71
Q

What is the treatment for MN?

A

Supportive, immunosuppresive agents, transplant

72
Q

What is pathogenesis of MCD?

A

Primarily affects podocytes, diffuse podocyte foot process fusion

73
Q

Focal segmental glomerulosclerosis (FSGS) has a *** pattern of kidney injury.

A

Histological

74
Q

What is the clinical presentation of FSGS?

A

> 70% present with nephrotic syndrome

75
Q

Patients with MN are at higher risk for *** vein thrombosis.

A

Renal

76
Q

What is the pathogenesis of FSGS?

A

Glomerular injury resulting from damage to podocytes.

Sclerosis in parts of at least on glomerular

77
Q

What is the etiology of primary and secondary FSGS?

A

Primary- idiopathic

Secondary- obesity, infections, inflammation, toxins, healed previous glomerular injury, reflex nephropathy, HTN, etc

78
Q

What is the treatment for FSGS?

A
  • supportive
  • immunosuppresive antes (primary)
  • Disease specific treatment (secondary )
79
Q

What patients have poor outcomes with FSGS?

A

Patients with nephrotic range proteinuria, African American Race, and renal insufficiency

80
Q

What is the most common cause fo ESRD in the US?

A

Diabetic nephropathy