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Clin Med GI > CKD Lecture 2 > Flashcards

CKD Lecture 2 Flashcards

1
Q

What makes up the glomerulus and what can cause damage to this?

A

Epithelium, podocytes, basement membrane, endothelium

Many different ways to damage - overworking, inflammation, deposition

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2
Q

What typically is acute kidney disease (nephritic or nephrotic)

A

Nephritic (I = inflammation, immune system)

Urine sediment with hematuria, +/- RBC casts
Proteinuria (< 3 g/d)

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3
Q

What is nephrotic kidney disease?

A

Typically no urine sediment

PrOteinuria = nephrOtic

> 3 g of protein peed our per day

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4
Q

What blood abnormality is common in nephrotic kidney disease?

A

Hypoalbumunia (because you pee out albumin)

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5
Q

What causes chronic glomerulonephritis?

A

Same causes as acute, but it just progresses to scarring

  1. Immune complex deposition
  2. Pauci-immune (vasculitis)
  3. Anti-glomerular basement membrane
  4. C3 glomerulopathy
  5. Monoclonal Ig (too much IgG)
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6
Q

What is the MC chronic glomerulonephritis?

A

Immune complex deposition, with Berger disease often

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7
Q

What are the general findings of glomerulonephritis?

A

Fall in GFR (fast if acute, slower if chronic)

Edema and HTN

Smoky, cola-colored urine d/t heavy glomerular bleeding

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8
Q

What is BUN:Cr mainly used for chronic GN?

A

mainly hydration status

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9
Q

What urine sediment is typically seen in GN?

A

RBCs and RBC casts

RBCs often dysmorphic from crossing damaged glomerulus (squeezed through)

RBC casts - sign of heavy glomerular bleeding, tubular stasis (they clump together)

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10
Q

What is a CI to renal biopsy for GN?

A

Bleeding disorder
Uncontrolled HTN (damaging kidneys makes them increase RAAS system)

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11
Q

How do you manage chronic HTN for GN?

A

ACE/ARB in order to reduce proteinuria

Also corticosteroids, cytotoxic agent

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12
Q

Do you use ACE/ARB in AKI?

A

NO

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13
Q

What often causes post-infectious GN

A

GABHS
typically history of pharyngitis and impetigo

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14
Q

What is the treatment of post-infectious GN?

A

treatment of infection
Supportive - antihypertensives, salt restriction, diuretics
Steroids do not generally improve outcome

children recover, adults maybe progress to CKD

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15
Q

Who are the MC with IgA nephritis (berger’s disease)?

A

Males, children/young adults

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16
Q

What are the MC presenting symptom of Berger’s disease?

A

episode of gross hematuria

normal serum
33% spontaneous remission

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17
Q

How do you treat Berger’s disease?

A

Low risk - no HTN, normal GFR, minimal proteinuria - monitor yearly
High risk - proteinuria >1.0 g/d, decreased GFR, HTN - ACE or ARB

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18
Q

What is Henoch-Schönlein Purpura?

A

Systemic small-vessel vasculitis - MC systemic vasculitis of childhood

s/s Palpable purpura in lower extremities and butocks; arthralgias, abdominal symptoms

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19
Q

What is the treatment of Henoch-Schönlein Purpura?

A

no direct treatment proven successful
Supportive care - hydration, rest, pain relief

may make full recovery over several weeks; may progress to CKD

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20
Q

What is the MCC of nephrotic syndrome and what is it?

A

DM
“Nephrotic range” proteinuria - >3 g/day

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21
Q

What are the s/s of nephrotic syndrome?

A

Subnephrotic proteinuria - little to no s/s
Nephrotic Syndrome - peripheral edema (MC), can also have edema in other areas as well

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22
Q

What is the Urinalysis of nephrotic syndrome?

A

Proteinuria - 300 mg/d or more

must order specifically for protein

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23
Q

What is the urinary sediment of nephrotic syndrome?

A

few cells/casts
If marked HLD - oval fat bodies
“Grape clusters” (light microscopy) or “Maltese crosses” (polarized light)

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24
Q

What are the serum labs of nephrotic syndrome?

A

hypoalbuminemia
hypoproteinemia
hyperlipidemia (in order to try to increase osmotic pressure lost from peeing out protein)
Possible deficiencies d/t not having protein carriers

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25
Q

When do you order a renal biopsy for nephrotic syndrome?

A

If there is new-onset idiopathic nephrotic syndrome

Not ordered in people with long standing DM, because we know what it is coming from

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26
Q

How do you manage nephrotic syndrome?

A

Eat more protein
Restrict salt

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27
Q

What doses do you need for thiazide/loop diuretics?

A

MORE because they are protein-bound and more likely to get peed out

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28
Q

How do you manage hypercoagulabitilty?

A

Usually seen if serum albumin <2 g/dL
Urinary loss of antithrombin, protein C, protein S
Increased platelet activation
Anticoagulation x 3-6 months min. if evidence of thrombosis
Ongoing - if renal vein thrombosis, PE, recurrent thromboemboli

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29
Q

What is the MCC of nephrotic syndrome in kids and how does it present?

A

Minimal Change Disease

often full-blown nephrotic syndrome
Thromboembolic events, hyperlipidemia, protein malnutrition

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30
Q

What is the treatment of nephrotic syndrome?

A

Prednisone
Rarely progresses to ESRD

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31
Q

What is the MCC of primary nephrotic syndrome in adults?

A

Membranous Nephropathy

Often frothy urine (like a protein shake) and edema

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32
Q

How do you treat Membranous Nephropathy?

A

ACE/ARBs, immunosuppression, transplant

varying results

33
Q

What is a secondary nephrotic syndrome and how does it present?

A

Amyloidosis, d/t EC deposition of amyloid

Large kidneys d/t holding too much amyloid

34
Q

What is the MC of ESRD?

A

DM neuropathy

Early - hyperfiltration with increased GFR
Later - microalbuminuria (30-300 mg/d)
Progression - albuminuria 300+ mg/d
Treatment - as soon as microalbuminuria is found
Strict glycemic control

35
Q

What is chronic tubulointerstitial disease?

A

Like AIN
Present with tubular dysfunction

36
Q

What is the MCC of Chronic Tubulointerstitial Disease

A

obstructive uropathy

Vesicoureteral Reflux - mainly in childhood

-Analgesic Nephropathy

37
Q

What is the pathophys of obstructive uropathy?

A

Prolonged obstruction of urinary tract
Backflow of urine → extravasation into interstitium → inflammation, fibrosis
Prolonged reflux of urine causes damage, scarring
Causes - enlarged prostate, renal calculi, cancer, retroperitoneal fibrosis or mass

38
Q

What are the s/s of obstructive uropathy?

A

Hydronephrosis that is asymptomatic, somtimes have symptoms

39
Q

What are the labs of obstructive uropathy?

A

Vary like crazy, so use imaging instead

40
Q

What imaging do you use 1st line for obstructive uropathy?

A

US
non-contrast CT if non-diagnostic or suspected stone

41
Q

How do you treat obstructive uropathy?

A

Get rid of obstruction RIGHT AWAY (once nephrons are gone, they are gone)

wanna protect the nephrons that we already have

42
Q

What is vesicoureteral reflux?

A

Urine flows back up into kidney because one side of the ureter sphincter is not able to contract.

Leads to inflammatory response and scarring

43
Q

What does vesicoureteral reflex typically seen in?

A

Frequent UTIs (kids and men)
Urine: mild-moderate proteinuria

44
Q

How do you diagnose Vesicoureteral Reflux?

A

put in radiopaque dye instilled in bladder; pt then voids while x-ray is taken (should not back up, but should void)

45
Q

What do you see in US of Vesicoureteral Reflux?

A

Hydronephrosis (often times) and renal scarring

see dilated urters

46
Q

How do you treat Vesicoureteral Reflux?

A

Maintaining sterile urine with prophylactic AB to reduce scarring

surgical reimplantation or urters (ineffective in adolescence/adults, because there is already too much scar tissue, need a transplant)

Control HTN w/ ACE/ARBs

47
Q

What is analgesic nephropathy caused by?

A

Normally caused by phenacetin

Chronic use of aspirin, NSAIDs, acetaminophen

at least 1 g/d for 3+ years

48
Q

Where do we see the worst effects of Analgesic Nephropathy?

A

10x higher in renal papillae (concentrates here) than in renal cortex

49
Q

What findings do you see in Analgesic Nephropathy?

A

Sloughed papillae in urine

CT - small, scarred kidney with papillary calcifications (seen w/out contrast as well)
IVP - contrast will fill area of sloughed papillae, causing a “ring shadow” or “golfball on a tee” sign
IVP rarely used due to risk of contrast nephropathy

50
Q

How do you treat Analgesic Nephropathy?

A

Stop Analgesics if possible

renal function may stabilize

51
Q

What is chronic AIN typically caused by?

A

multiple autoimmune disorders

often see small scarred kidneys d/t long-term damage

52
Q

What is nephrocalcinosis?

A

Deposition of calcium in renal parenchyma and tubules
Can cause AKI, CKD
May also have normal renal function
Most pts do not progress to ESRD

53
Q

What typically causes nephrocalcinosis?

A

Increased calcium excretion

hypercalcemia, hyperphosphatemia, or increased excretion of calcium, phosphate or oxalate in urine
Hyperparathyroidism

54
Q

s/s of nephrocalcinosis

A

asymptomatic in most cases (incidental finding)
May see s/s of underlying cause

55
Q

What is the MCC renal masses?

A

Solitary renal cysts 65-70%

high Bosniak score = fine

normally benign

56
Q

What are the two different types of medullary cystic kidney diseases (MCKD)?

A

When dx in childhood - Juvenile Nephronophthisis
Childhood (Juvenile NPH) - autosomal recessive
Adult (MCKD) - autosomal dominant

57
Q

What does MCKD cause

A

multiple small renal cysts at corticomedullary junction and in medulla
Cortex becomes fibrotic → interstitial inflammation, glomerular sclerosis

only cysts in the inner portion

58
Q

What kidney disease typically cause flank pain?

A

Autosomal dominant PKD

hx of UTI and nephrolithiasis common
+ hx of HTN in >50 %
+ family hx of PKD in 75%

59
Q

What happens to the size of kidneys in AD PKD?

A

Large, palpable kidney - leading to flake pain

60
Q

Where are cysts also seen a lot of times in AD PKD?

A

In spleen and liver d/t higher predisposition of cysts

61
Q

How do you treat AD PKD?

A

Pain management
If hematuria, hydration
HTN with ACE/ARBs
Cerebral aneurysm

62
Q

If there is recurrent hematuria in ADPKD, what should you be sus of?

A

Cell carcinoma

63
Q

What does an infected cyst in ADPKD present?

A

flank pain, fever, +WBC

64
Q

How do you treat ADPKD with fever and inc WBCs?

A

Bactrim, quinolones

pentrate into cysts

65
Q

How do you stop progression of ADPKD?

A

Tolvaptan (vasopressin V2 receptor antagonist)

slows renal decline
use if GFR at least 25

possibly avoid caffeine

66
Q

What does tolvaptan do?

A

Reduce urine osmality, leading to less cyst formation

SE: hypernatremia
CI: liver disease

67
Q

What is the presentation of autosomal recessive (AR) PKD?

A

Enlarged kidneys w/ small cysts on COLLECTING TUBULES only

Impaired urine concentration
Metabolic acidosis
HTN common

68
Q

How to differentiate ARPKD from early-onset ADPKD

A

both parents will not have cysts

69
Q

Renal artery stenosis MC

A

80-90% due to atherosclerotic occlusive disease
10-15% - fibromuscular dysplasia
Suspect if unexplained HTN in woman < 40
5% of all pts with HTN have RAS
MC - >45 yrs with atherosclerotic disease hx
Other risks - CKD, DM, tobacco use, HTN

70
Q

What is the common cause of renal artery stenosis (RAS)?

A

HTN, may have audible abdominal bruit (because of back-up of blood flow)

71
Q

What is imaging of RAS look like?

A

US can reveal asymmetric kidneys (if unilateral RAS) or small hyperechoic kidneys (if bilateral RAS)

Doppler US - >90% sensitive and specific with good sonographer
Very operator and pt dependent
Poor choice - obese pt, interfering bowel gas, or if pt cannot lie supine

Imaging - US can reveal asymmetric kidneys (if unilateral RAS) or small hyperechoic kidneys (if bilateral RAS)
MRA - excellent but expensive
Turbulent blood flow = false + results
Contrast can cause problems in pts with low GFR
Renal angiography - gold standard

72
Q

How do you treat RAS?

A

often angioplasty to reduce meds (stenting)

can do surgical bypass

73
Q

What leads to nephrosclerosis?

A

poorly controlled HTN for years

aka Hypertensive nephropathy

74
Q

What do you see in Nephrosclerosis

A

Sclerosis of arteries and arterioles
Interstitial fibrosis and decreased glomerular tuft
Up to 27% of ESRD pts have HTN as cause of CKD

75
Q

What patients are most likely to have Nephrosclerosis?

A

5x more common in AA

don’t know why, likely genetic predisposition

76
Q

How do you treat Nephrosclerosis?

A

Manage HTN

Typically need multiple anti-HTN drugs

77
Q

Cholesterol Atheroembolic Disease pathophys + seen in

A

Emboli to kidneys → usually due to cholesterol crystals breaking free of vascular plaque and lodging in downstream microvessels

Often follow angiographic procedures
May see with vascular surgery, trauma, heparin, thrombolytics

78
Q

How do you treat Cholesterol Atheroembolic Disease

A

statins

sometimes biopsy

79
Q
A

Clin Med GI (10 decks)

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