Chronic Kidney Disease. Large Group 5. -Barnes Flashcards

1
Q

What is the number one cause of ESRD?

A

Diabetes (43%)

HTN (26%)

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2
Q

What are the stages of CKD?

A

I=GFR >90 (w/evidence of kidney damage)

II=GFR 60-90

III=GFR 30-60 (moderate)

IV=GFR 15-29 (severe)

V=<15 =ESRD

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3
Q

What are the stages of Diabetic Nephropathy?

A

1=hyperfunction and hypertrophy (increase in GFR)

2=silent (thickened BM and normal GFR)

3=incipient—> microalbuminuria (slight decrease in GFR)

4=overt Diabetic Nephropathy–> macroalbuminuria (>300) (large decrease in GFR)

5=uremia

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4
Q

Will microalbuminuria be seen on a urine dipstick?

A

NO!

Only measures >300 (macroalbuminuria)

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5
Q

What is UACR? What is it used to determine? Why?

A

Urine albumin: urine creatinine ratio

Microalbuminuria–> ratio >30=CKD

urine dipsticks will not detect it and 24 hour urine samples are often not accurate

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6
Q

What is microalbuminuria a risk marker for? Why?

A

other small vasculature problems because the kidney small vessels are affected

HTN progression, CV disease, CKD

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7
Q

What histological changes can be seen before the onset of microalbuminuria in diabetic nephropathy?

A

GBM thickening

mesangial expansion

Kimmelstiel-wilson lesion

glomerular sclerosis

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8
Q

When do we want to catch Diabetic Nephropathy?

A

before the albuminuria is >300

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9
Q

What are the PE findings in Diabetic Retinopathy?

A

micro aneurysms and cotton wool spots on fundoscopic exam

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10
Q

What is the treatment of Diabetic Nephropathy?

A
  • slow progression of CKD
  • RAAS suppression/Albuminuria therapy (ACE Is and ARBS) (proteinuria <100)
  • Discontinue smoking, Na+ restriction, weight loss
  • protein restriction (.8g/kg/day)
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11
Q

What physiological changes take place in the nephron of a Diabetic Nephropathy patient? What medication can help with this?

A

AGE damage the afferent arteriole –> decrease perfusion of the glomerulus–> macula densa senses less Na+ flow and more renin is secreted –> AgII increases–>
constricted efferent arteriole–> increased pressure –> dilated afferent arteriole –> glomerular loss of proteins

kidneys can become very large

ACE inhibitors and ARBs decrease efferent pressure to minimize this but can also decrease GFR

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12
Q

What will present with a waxy cast?

A

CKD

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13
Q

Why can anemia (normochromic and normocytic) develop due to CKD?

A

decreased erythropoietin released from the kidney due to decreased renal mass

inflammation can lead to decrease iron release from the liver –> iron deficiency

hyperparathyroidism

hemoglobinopathies

inadequate dialysis

can also get platelet dysfunction

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14
Q

What is the treatment goal for CKD (hemodynamics)?

A

hemoglobin 10-12

TSAT >20%

ferritin >100

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15
Q

What mineral bone disorders can result from CKD? Why?

A

Vitamin D deficiency (kidneys have 1 alpha hydroxyls that converts vitamin D to the active form normally)

Hypocalcemia

Hyperphosphatemia (inc retention from the kidneys and bones inc)

Hyperparathyrodism (from low active vitamin D)

increase in FGF-23 –> causes changes in phosphorous and vitamin D–> allow phosphorous to appear normal

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16
Q

What are the clinical features of bone mineral disorders in CKD pts?

A
Asymptomatic 
Bone pain 
Proximal myopathy
Fractures
Vascular medial wall calcification
Soft tissue calcification
Calciphylaxis
17
Q

What is uremic fetor? When can this be seen?

A

stale urine smell coming from mouth

can be seen in uremia

18
Q

What neurologic symptoms can be seen in uremia/CKD?

A

Tremors
Encephalopathy
Seizures
Peripheral and autonomic neuropathy

19
Q

What is calciphylaxis? What causes it?

A

caused by chronic hyperphosphatemia in CKD pts

get Ca2+ in the small vessels that feed the skin–> necrosis

20
Q

What lab changes could be found in CKD?

A
Hyperkalemia 
Hypocalcemia 
Hyperphosphatemia
Metabolic acidosis
AGMA (from uremia) +NAGMA (from decreased distal perfusion)
21
Q

What will the US of a CKD kidney show?

A

long shrunken kidney

loss of cortex

22
Q

At what GFR should dialysis be initiated?

A

non-DM: <15

23
Q

What are the indications of dialysis?

A

AEIOU

 Acidosis
 Electrolyte (highK+ mostly)
 Intoxication 
 Overload (volume)
 Uremia

refractory to medical treatment

24
Q

What type of medication do renal transplant pts have to be on forever?

A

immunosuppressants

25
Q

What is the diagnostic criteria for autosomal dominant polycystic kidney disease?

A

Two renal cysts unilaterally or bilaterally before age 30 years by renal ultrasound.

Two cysts in each kidney between the ages of 30 and 59 years by renal ultrasound.

Four or more cysts in each kidney after age 60 years by renal ultrasound.

26
Q

What is the most common genetic disruption in ADPKD?

A

PKD1

it also progresses more rapidly

27
Q

What are the extra renal associations with ADPKD?

A

cysts in liver

heart valve abnormalities (mitral valve prolapse)

aneurysms

28
Q

How is the progression of ADPKD monitored?

A

kidney and cyst volume are monitored by MRI

get a decrease in GFR once the kidneys become significantly enlarged

29
Q

What is the treatment of ADPKD?

A

V2 receptor antagonists prevent ADH from binding and promoting fluid secretion –> decrease cyst size

30
Q

Which ADPKD pt should be screened for intracranial aneurysm?

A

Patients with a family history of SAH

High risk occupation such as pilots

Prior to major elective surgeries with anticipated hemodynamic instability.

31
Q

What is the treatment of asymptomatic aneurysms?

A

Under 10 mm in diameter - Observation and follow-up (at 6 months initially and then yearly)

For >10 mm - surgical clipping is indicated.