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Clin med A 2 > CKD part 2 > Flashcards

CKD part 2 Flashcards

1
Q

what is included in the nephritic spectrum

A
  • urine sediment with hematuria, +/- RBC casts
  • Proteinuria (< 3 g/d)
  • Nephritic - i for inflammation/immune, which is often involved
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2
Q

what is included in the nephrotic syndrome

A
  • “Bland” urine sediment - no cells or casts (May see oval fat bodies)
  • Proteinuria (at least 300 mg/d, often > 3 g/d)
  • Nephrotic - o for protein
  • hypertriglyceridemia/hyperlipidemia
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3
Q

what are general findings of glomerulonephritis

A
  • decreased GFR
  • edema and HTN
  • smoky/coca cola colored urine (hematuria)
  • uremic s/s
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4
Q

lab findings in glomerulonephritis

A
  • high serum Cr
  • hematuria and protein in urinalysis
  • RBC, WBC, RBC casts on urine sediment
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5
Q

I skipped all of the causes because we learned these in AKI

A

sorry:(

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6
Q

what is treatment for glomerulonephritis

A
  • management of HTN and volume overload
  • ACE/ARB for proteinuria
  • immunosuppressive agents (high dose corticosteroids or cytotoxic agents)
  • plasma exchange for goodpasture or pauci-immune glomerulonephritis.
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7
Q

what is postinfectious glomerulonephritis

A

glomerulonephritis due to bacteria or pathogens. usually GABHS

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8
Q

what test helps make the definitive diagnosis for postinfectious glomerulonephritis

A

biopsy showing “humps” of immune complex deposits.

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9
Q

what is the treatment for postinfectious glomerulonephritis

A
  • treat infection
  • supportive (antiHTN, diuretics, salt restriction)
  • NO steroids (doesnt show improvement)
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10
Q

what is the MC primary glomerular disease worldwide

A

IgA nephritis (Berger’s Disease)

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11
Q

what is the demographics MC in Berger’s disease

A

2-3x more common in males; MC in children and young adults

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12
Q

what is the MC symptom in berger’s disease

A

Episode of gross hematuria.
(often in onjunction with URI)

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13
Q

what is considered low risk bergers disease and how would you treat it?

A

no HTN, normal GFR, minimal proteinuria

tx: monitor yearly

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14
Q

what is considered high risk bergers disease and how would you treat it?

A

proteinuria>1.0, decreased GFR, HTN

tx: ACE/ARB

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15
Q

what is the prognosis for bergers disease

A

33% spontaneous remission

20-40% progress to ESRD (especially if > 1 g/d proteinuria)

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16
Q

what is Henoch-Schonlein purpura

A

systemic small-vessel vasculitis assicaited with IgA deposition in vessel walls

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17
Q

what is the S/S of henoch schonlein purpura

A
  • palpable purpura in LE and buttocks
  • arthralgias
  • abdominal symptoms (nausea, colic, melena)
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18
Q

what is the treatment for henoch schonlein purpura

A

no tx only supportive care (hydration, rest, sleep)

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19
Q

what is prognosis for henoch scholein purpura

A

make full recovery over several weeks. may progress to CKD

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20
Q

what is pictured

A

henoch scholein purpura

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21
Q

what is the MCC of nephrotic glomerular disease in US

A

DM

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22
Q

what are the general S/S of nephrotic syndrome

A

subnephrotic proteinuria - little to no s/s
nephrotic syndrome (peripheral edema, dyspnea, pleural effusions, ascites)

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23
Q

what does urinalysis show in nephrotic syndrom

A

proteinuria 300mg/d or more

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24
Q

what is the urine sediment showing in nephrotic syndrome

A
  • If marked HLD - oval fat bodies
    “Grape clusters” (light microscopy) or “Maltese crosses” (polarized light)
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25
Q

what do serum labs show for nephrotic sydrome

A

hypoalbuminemia (<3)
hypoproteinemia (<6)
hyperlipidemia
elevated ESR
possible Vit D, zinc and copper deficiency

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26
Q

what is the pathophysiology of hyperlipidemia in nephrotic syndrome

A
  • Low protein → Low oncotic pressure → increased hepatic lipid production
  • Lower clearance of VLDL → hypertriglyceridemia
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27
Q

What is the treatment for protein loss in nephrotic syndrome

A
  • if mild decrease intake
  • if severe (>10g/day) increase protein
  • ACE/ARB to lower urine protein excretion
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28
Q

what is the treatment for edema in nephrotic syndrome

A
  • dietary salt restriction
  • thiazides and loops are protein bound so larger doses would be needed
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29
Q

what is the treatment for hyperlipidemia in nephrotic syndrome

A

diet and exercise, lipid lowering drugs

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30
Q

what is the treatment for hypercoagulability in nephrotic syndrome

A

anticoagulation for 3-6 months minimum if evidence of thrombosis.

Continue if renal vein thrombosis, PE, or recurrent thromboemboli

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31
Q

at what protein level is hypercoagulability usually seen in nephrotic syndrome

A

serum albumin <2g/dL

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32
Q

what is the MCC of proteinuric renal disease in children

A

minimal change disease in children (80%)

(this makes up 20-25% of proteinuric renal disease in adults)

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33
Q

what are s/s of minimal change disease

A

full blown nephrotic syndrome:
- thromboembolic events
- hyperlipidemia
- protein malnutrition

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34
Q

what is treatment for minimal change disease?

A

corticosteroids - specifically prednisone

for up to 8 weeks in children and 16 weeks in adults. taper off when done.

RARELY progresses to ESRD

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35
Q

what is the MCC of primary nephrotic syndrom ein adults

A

membranous nephropathy due to immune complex deposition

nephrotic syndrome could also be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril

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36
Q

what are the s/s of membranous nephropathy

A

may be asymptomatic or may see edema and frothy urine.

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37
Q

what is treatment for membranous nephropathy

A

ACE/ARB, immunosuppression, transplant.

50% progress to ESRD
30% spontaneous remission

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38
Q

what is amyloidosis

A

extracellular deposition of amyloid protein

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39
Q

what are s/s of amyloidosis

A
  • proteinuria, decreased GFR, nephrotic syndrome
  • enlarged kidneys
  • s/s of other chronic inflammatory disease
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40
Q

what is the treatment for amyloidosis

A
  • manage underlying disease

treatment options are limited and 5 year survival rate is <20% :( sad day

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41
Q

what is the MCC of ESRD in the US

A

diabetic nephropathy!

20 year risk - 40% (higher risk in T2DM)

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42
Q

how does diabetic nephropathy present

A

developes about 10 years after DM onset
- early - hyperfiltration with increased GFR
- Later - microalbuminuria (30-300 mg/d)
- Progression - albuminuria 300+ mg/d

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43
Q

what is the treatment for diabetic nephropathy

A
  • strict glycemic control
  • treat HTN to goal - ACE/ARB can be used
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44
Q

What is tubulointerstitial disease?

A

disorder affecting renal tubules and interstitium (glomeruli and renal vessels not generally affected)

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45
Q

what is the main pathology of acute tubulointerstitial disease

A

acute interstitial nephritis

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46
Q

what are the main pathologies of chronic tubulointerstitial disease

A

interstitial fibrosis
tubular atrophy

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47
Q

what is the main cause of acute interstitial nephritis

A

70% due to medication

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48
Q

What are the causes of chronic tubulointerstitial disease

A

Obstructive uropathy (1st MCC)
vesicouretal reflux (2nd MCC)
analgesic nephropathy (1g/day 3+ yrs)
Autoimmune interstitial nephritis
nephrocalcinosis

can also be:
renal ischemia
glomerular disease
but we dont really go into these i dont think

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49
Q

what is obstructive uropathy

A

prolonged obstruction of the urinary tract leading to backflow of urine, movement of fluid into interstitium and then inflammation and fibrosis

this leads to damage and scarring

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50
Q

what are causes of obstructive uropathy

A

enlarged prostate
renal calculi
cancer
retroperitoneal fibrosis or mass

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51
Q

what are the s/s of obstructive uropathy

A

hydronephrosis
pain
bladder distension
HTN
Urine - oliguria, anuria or polyuria :/

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52
Q

what is hydronephrosis

A

this picture was just good for my brain to make sense of it.

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53
Q

what do UA and serum creatinine show in obstructive uropathy

A

UA - benign, may see hematuria or pyuria
serum Cr - elevated

54
Q

what is the preferred imaging of study for obstructive uropathy and what does it show

A

US - may show dilation of collecting system.

only use CT if suspected stone!

55
Q

how do you treat obstructive uropathy

A

relieve obstruction ASAP

if not removed quickly could lead to tubular damage and renal scarring

56
Q

what is vesicouretal reflux disease and who is it MC in

A

primarily occurs in children

incompetent or misplaced vesicouretal sphincter leads to retrograde flow of urine while voiding.

this causes inflammatory responses and scarring

57
Q

what is the presentation of vesicouretal reflux disease

A
  • frequent UTIs (esp in children)
  • may not be dx until later in life when HTN and proteinuria develope:(
58
Q

what do labs show in vesicouretal reflux disease

A
  • varying elevations in BUN/Cr
  • mild-mod proteinuria
59
Q

what imaging modalities can be used to assess vesicouretal reflux disesae

A
  • voiding cystourethrogram (dye instilled in bladder, pt pees while xray is taken)
  • US to assess for hydronephrosis and renal scarring
60
Q

what would a US show in vesicouretal reflux disease

A
  • hydronephrosis and renal scarring

Adults -
- asymmetric small kidneys
- irregular outlines
- thin cortices
- areas of compensatory hypertrophy

61
Q

how do you describe dilation of the kidneys

A

idk if we need to know this tbh

62
Q

how do you treat vesicouretal reflux disease

A
  • maintain sterile urine in children
  • surgical implantation of ureters (for children with persisten high grade reflux, NOT for adolescents or adults)
  • control of HTN with ACE/ARB
63
Q

what is analgesic nephropathy

A

tubulointerstitial inflammation and papillary necrosis in patients who ingest at least 1g/day of analgeics for 3+ years

64
Q

what is the highest associated analgesic with analgesic nephropathy? what are some other common analgesics?

A

phenacetin!

may also be caused by:
NSAIDS, aspirin, tylenol!

65
Q

why do analgesics cause papillary necrosis.

A

Analgesics can be concentrated up to 10x higher in renal papillae than in renal cortex

66
Q

what is seen in urine of analgesic nephropathy

A

hematuria
proteinuria
polyuria
pyuria
sloughed papillae!!

67
Q

what are image findings in analgesic nephropathy?

A

CT - small, scarred kidney with papillary calcifications
IVP - contrast will fill area of sloughed papillae, causing a “ring shadow” or “golfball on a tee” sign

NOTE: IVP rarely used d/t risk of constrast nephropathy

68
Q

how do you treat analgesic nephropathy

A

discontinue analgesics

69
Q

what is the cause of autoimmune interstitial nephritis

A

a combination of multiple autoimmune disorders as seen below!

70
Q

what are clinical findings of autoimmune interstitial nephritis

A
  • could be asymptomatic ¯_(ツ)_/¯
  • polyuria
  • volume depletion d/t salt wasting
  • hyperkalemia
  • hyperchloremic metabolic acidosis
71
Q

what does immaging show in autoimmune interstitial nephritis.

A

small, scarred kidneys

72
Q

what is the treatment for autoimmune interstitial nephritis

A

control underlying cause

73
Q

what is nephrocalcinosis

A

deposition of calcium in renal parenchyma and tubules

74
Q

what isthe prognosis of neophrocalcinosis

A
  • Can cause AKI, CKD
  • May also have normal renal function
  • Most pts do not progress to ESRD
75
Q

what is the cause of nephrocalcinosis

A

increased in urinary excretion of calcium (MCC), phosphate and/or oxalate

76
Q

what is a risk factor for nephrocalcinosis

A

conditions that cause hypercalcemia, hyperphosphatemia or increased excretion of Ca, PO, or oxalate in urine
such as:
- hyperparathyroidism
- vit D therapy
- loops

77
Q

what are lab findings in nephrocalcinosis

A
  • hypercalcemia and hyperphosphatemia
  • urine with sterile pyuria or hematuria
  • proteinuria
  • 24 hour urine may show increase Ca, PO or oxalate
78
Q

what are s/s of nephrocalcinosis

A

usually asymptomatic, often found incidentally

79
Q

what is the treatment for nephrocalcinosis

A

correct underlying metabolic disorder

80
Q

what makes up 65-70% of all renal masses

A

single or solitary renal cysts, generally found in the outer cortex or medulla.

81
Q

what is the management of a single or solitary renal cyst

A

if benign then routine follow up is acceptable.

refer to bosiak score for whether or not a cyst is benign!:)

82
Q

what could a cyst developing after onset of dialysis suggest

A

potential for adenocarcinoma

83
Q

what are the two types of cystic kidney disease and what causes them?

A
  • juvenile nephronophthisis (in children) - autosomal recessive gene
  • Adult medullary cystic kidney disease - autosomal dominant gene
84
Q

what is the result of jevenile NPH and adult MCKD

A

multiple small renal cysts at corticomedullary junction and in medulla.

85
Q

what are the s/s of medullary cystic kidney disease

A

polyuria, pallor, lethargy, renal salt wasting

later in disease:
HTN, hyperuricemia, growth restriction in juvenile NPH

86
Q

what ages does ESRD occur in juvenile NPH and in MCKD

A

Juvenile NPH - <20 years
MCKD - ages 20-70

87
Q

what is the treatment for medullary cystic kidney diseases

A
  • adequate salt and water intake
  • no therapy known to stop progression
  • allopurinol if hyperuricemic
  • does not recur in renal transplants.
88
Q

what is the cause of Autosomal Dominant polycystic kidney disease

A

mutation of genes ADPKD-1 or ADPKD-2 via autosomal dominant inheritance (90%) or spontaneous mutation (10%)

89
Q

what gene is more severe and more common in ADPKD

A

ADPKD-1 - 85% of patients.

ADPDK-2 15% of patients with slower progression and later onset in life.

90
Q

what are s/s of ADPKD

A
  • abdominal pain
  • flank pain
  • hx of UTI
  • hx of HTN in >50% of patients
  • family hx of PKD in 75%
  • enlarged palpable kidneys!
91
Q

what will labs show in ADPKD

A

hematuria and proteinuria

H&H is normal

92
Q

what confirms the diagnosis of ADPKD

A

US showing:
- Age < 30 - 2+ renal cysts
- Age 30-59 - 2+ cysts in each kidney
- Age 60 + - 4+ cysts in each kidney

93
Q

where else might cysts be seen in ADPKD

A
  • liver
  • spleen
94
Q

what is the cause of pain in ADPDK? how do you treat it

A

cause - infection, bleeeding, nephrolithiasis

tx - bed rest, analgesics, cyst decompression

95
Q

what is the cause of hematuria in ADPKD? How do you treat it?

A

Cause - MC due to rupture of cyst but could be Kidney stone, UTI

tx - bed rest, hydration, resolves in 1 week.

96
Q

what could recurrent hematuria in ADPKD mean

A

possible renal cell carcinoma

97
Q

How do you treat nephrolithiasis in ADPKD

A

pain control
hydration of 2-3L/day

98
Q

how do you treat HTN in ADPKD

A
  • ACE/ARB preferred
  • cyst decompression
99
Q

how does an infected cyst present in ADPKD and how do you treat it

A

presents with flank pain, fever and increased WBC
- cultures (blood and urine)
- TX with cystic penetration ABX
and continue with 2 weeks of IV ABX and long term oral ABX

100
Q

what are other complications that can occur with ADPKD

A
  • Cerebral aneurysms on circle of willis
  • mitral valve prolapse
  • aortic aneurysms
  • aortic valve disease
  • colonic diverticula
101
Q

How do you treat ADPKD Cyst growth

A
  • vasopressin receptor antagonists (slow progression)
  • ocreotide ( decreased cyst growth)
  • tolvaptan (slows renal decline)
102
Q

what drug class is tolvaptan

A

vasopressin V2 receptor antagonist

103
Q

when is tolvaptan recommended in ADPKD

A

in all patients 18+ with GFR of 25+ and 1+ risk marker which includes:
1. mayo class 1C, 1D, 1E
2. age <55 and eGFR <65
3. kidney length >16.5 cm in patient <50 y/o
4. PROPKD score of >6

104
Q

what may help and/or slow progression of ADPKD

A

avoidance of caffeine
tx of HTN and proteinuria

105
Q

How does tolvaptan aid in treatment of ADPKD

A

reduces urinary osmolality which impairs cyst growth

106
Q

what are SE of tolvaptan

A

thirst
polydipsia
polyuria
nocturia
hypernatremia!!
increased liver enzymes
BBW!!! - should be initiated and reinitiated only in a hospital where serum sodium can be CLOSELY monitored!

107
Q

what are CI for tolvaptan

A

liver disease
pts on strong CYP3A4 inhibitors
allergy

108
Q

How does Autosomal recessive PDK present

A
  • enlarged tubules with small cysts on collecting tubules only
  • impaired urine concentration
  • metabolic acidosis
  • HTN common
109
Q

what is the MCC of death in autosomal recessive PKD

A

pulmonary hypoplasia due to oligohydramnios (amniotic fluid abnormality)

110
Q

what age do people with autosomal recessive PKD tend to live until? what complications will they have?

A
  • 80% of surviving neonates live to 10 or longer

they will have complications such as:
- 1/3 with ESRD by 10
- portal HTN
- periportal fibrosis

111
Q

what is the diagnosis for autosomal recessive PKD

A

large echogenic kidneys with cysts visible after birth.

absence of renal cysts in either parent confirms or denies ARPKD

112
Q

what is treatment for ARPKD

A

manage HTN
dialysis
kidney transplant

113
Q

what is the MCC of renal artery stenosis? what is the only other cause we learned?

A

80-90% d/t atherosclerotic occlusive disease

10-15% - fibromuscular dysplasia

114
Q

when would you suspect fibromuscular dysplasia

A

unexplained HTN in woman <40

115
Q

what are risk factors for RAS

A

HTN
atherosclerosis
CKD
DM
Tobacco use

116
Q

what are the s/s of RAS

A

HTN
pulmonary edema
AKI after starting ACEI

may present with abdominal bruits!

117
Q

what labs are seen in RAS

A

elevated BUN/Cr if significant ischemia

118
Q

what does US reveal in RAS

A

asymmetric kidneys if unilateral or small hyperechoic kidneys if bilateral

119
Q

what would an MRA reveal in RAS

A

turbulent blood flow with false positive results

120
Q

what is the gold standard for RAS diagnosis

A

renal angiography

121
Q

How do you treat RAS

A
  • manage HTN
  • angioplasty (reduces HTN meds needed but doesnt slow disease)
  • surgical bypass (risky and not better than angioplasty)
122
Q

what is nephrosclerosis

A

hypertensive nephropathy leading to sclerosis of arteries and arterioles. also causes interstitial fibrosis and decreased glomerular tuft!

123
Q

what are risk factors for nephrosclerosis

A

African American race - 5x more common
Increased age, smoking, hypercholesterolemia
Longstanding uncontrolled HTN

124
Q

what is treatment for nephrosclerosis

A

management of HTN with mulitple anti-HTN

thiazides and ACE/ARB are MC

125
Q

what is cholesterol atheroembolic disease

A

emboli to kidneys usually d/t cholesterol crystals breaking free of vascular plaque and lodging in downstream microvessels

126
Q

when might you see cholesterol atheroembolic disease

A

vascular surgery
trauma
heparin use
thromoblytic use

127
Q

what are risk factors for cholesterol atheroembolic disease

A

male
DM
HTN
ischemic cardiac disease

128
Q

what are the s/s of cholesterol atherembolic disease

A

onset 1-14 days after inciting event
- worsening HTN and renal function with fever, abdominal pain and wt loss.

may also see livedo reticularis and localized gangrene!

129
Q

what labs are seen in cholesterol atheroembolic disease

A

increased Cr
eosinophilia
elevated ESR
low complement

130
Q

what is definitive diagnosis for cholesterol atheroembolic disease

A

kidney biopsy

131
Q

what is treatment for cholesterol atheroembolic disease

A

no specific effective therapy but can use:
- statins
- steroids (contraversial)
- supportive

132
Q

oh ma lort that was a lot good luck yall

A

byeeeeeeee

Clin med A 2 (30 decks)

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