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
When do you order a renal biopsy for nephrotic syndrome?
If there is new-onset idiopathic nephrotic syndrome Not ordered in people with long standing DM, because we know what it is coming from
26
How do you manage nephrotic syndrome?
Eat more protein Restrict salt
27
What doses do you need for thiazide/loop diuretics?
MORE because they are protein-bound and more likely to get peed out
28
How do you manage hypercoagulabitilty?
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
29
What is the MCC of nephrotic syndrome in kids and how does it present?
Minimal Change Disease often full-blown nephrotic syndrome Thromboembolic events, hyperlipidemia, protein malnutrition
30
What is the treatment of nephrotic syndrome?
Prednisone Rarely progresses to ESRD
31
What is the MCC of primary nephrotic syndrome in adults?
Membranous Nephropathy Often frothy urine (like a protein shake) and edema
32
How do you treat Membranous Nephropathy?
ACE/ARBs, immunosuppression, transplant varying results
33
What is a secondary nephrotic syndrome and how does it present?
Amyloidosis, d/t EC deposition of amyloid Large kidneys d/t holding too much amyloid
34
What is the MC of ESRD?
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
What is chronic tubulointerstitial disease?
Like AIN Present with tubular dysfunction
36
What is the MCC of Chronic Tubulointerstitial Disease
obstructive uropathy Vesicoureteral Reflux - mainly in childhood -Analgesic Nephropathy
37
What is the pathophys of obstructive uropathy?
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
What are the s/s of obstructive uropathy?
Hydronephrosis that is asymptomatic, somtimes have symptoms
39
What are the labs of obstructive uropathy?
Vary like crazy, so use imaging instead
40
What imaging do you use 1st line for obstructive uropathy?
US non-contrast CT if non-diagnostic or suspected stone
41
How do you treat obstructive uropathy?
Get rid of obstruction RIGHT AWAY (once nephrons are gone, they are gone) wanna protect the nephrons that we already have
42
What is vesicoureteral reflux?
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
What does vesicoureteral reflex typically seen in?
Frequent UTIs (kids and men) Urine: mild-moderate proteinuria
44
How do you diagnose Vesicoureteral Reflux?
put in radiopaque dye instilled in bladder; pt then voids while x-ray is taken (should not back up, but should void)
45
What do you see in US of Vesicoureteral Reflux?
Hydronephrosis (often times) and renal scarring see dilated urters
46
How do you treat Vesicoureteral Reflux?
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
What is analgesic nephropathy caused by?
Normally caused by phenacetin Chronic use of aspirin, NSAIDs, acetaminophen at least 1 g/d for 3+ years
48
Where do we see the worst effects of Analgesic Nephropathy?
10x higher in renal papillae (concentrates here) than in renal cortex
49
What findings do you see in Analgesic Nephropathy?
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
How do you treat Analgesic Nephropathy?
Stop Analgesics if possible renal function may stabilize
51
What is chronic AIN typically caused by?
multiple autoimmune disorders often see small scarred kidneys d/t long-term damage
52
What is nephrocalcinosis?
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
What typically causes nephrocalcinosis?
Increased calcium excretion hypercalcemia, hyperphosphatemia, or increased excretion of calcium, phosphate or oxalate in urine Hyperparathyroidism
54
s/s of nephrocalcinosis
asymptomatic in most cases (incidental finding) May see s/s of underlying cause
55
What is the MCC renal masses?
Solitary renal cysts 65-70% high Bosniak score = fine normally benign
56
What are the two different types of medullary cystic kidney diseases (MCKD)?
When dx in childhood - Juvenile Nephronophthisis Childhood (Juvenile NPH) - autosomal recessive Adult (MCKD) - autosomal dominant
57
What does MCKD cause
multiple small renal cysts at corticomedullary junction and in medulla Cortex becomes fibrotic → interstitial inflammation, glomerular sclerosis only cysts in the inner portion
58
What kidney disease typically cause flank pain?
Autosomal dominant PKD hx of UTI and nephrolithiasis common + hx of HTN in >50 % + family hx of PKD in 75%
59
What happens to the size of kidneys in AD PKD?
Large, palpable kidney - leading to flake pain
60
Where are cysts also seen a lot of times in AD PKD?
In spleen and liver d/t higher predisposition of cysts
61
How do you treat AD PKD?
Pain management If hematuria, hydration HTN with ACE/ARBs Cerebral aneurysm
62
If there is recurrent hematuria in ADPKD, what should you be sus of?
Cell carcinoma
63
What does an infected cyst in ADPKD present?
flank pain, fever, +WBC
64
How do you treat ADPKD with fever and inc WBCs?
Bactrim, quinolones pentrate into cysts
65
How do you stop progression of ADPKD?
Tolvaptan (vasopressin V2 receptor antagonist) slows renal decline use if GFR at least 25 possibly avoid caffeine
66
What does tolvaptan do?
Reduce urine osmality, leading to less cyst formation SE: hypernatremia CI: liver disease
67
What is the presentation of autosomal recessive (AR) PKD?
Enlarged kidneys w/ small cysts on COLLECTING TUBULES only Impaired urine concentration Metabolic acidosis HTN common
68
How to differentiate ARPKD from early-onset ADPKD
both parents will not have cysts
69
Renal artery stenosis MC
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
What is the common cause of renal artery stenosis (RAS)?
HTN, may have audible abdominal bruit (because of back-up of blood flow)
71
What is imaging of RAS look like?
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
How do you treat RAS?
often angioplasty to reduce meds (stenting) can do surgical bypass
73
What leads to nephrosclerosis?
poorly controlled HTN for years aka Hypertensive nephropathy
74
What do you see in Nephrosclerosis
Sclerosis of arteries and arterioles Interstitial fibrosis and decreased glomerular tuft Up to 27% of ESRD pts have HTN as cause of CKD
75
What patients are most likely to have Nephrosclerosis?
5x more common in AA don't know why, likely genetic predisposition
76
How do you treat Nephrosclerosis?
Manage HTN Typically need multiple anti-HTN drugs
77
Cholesterol Atheroembolic Disease pathophys + seen in
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
How do you treat Cholesterol Atheroembolic Disease
statins sometimes biopsy
79