Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GU: Clin Med IIA > CKD pt 2 > Flashcards

CKD pt 2 Flashcards

1
Q

2 categories of processes that lead to abnormal glomerular function

A
  1. nephritic spectrum
  2. nephrotic spectrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Urine sediment with hematuria, +/- RBC casts
Proteinuria (< 3 g/d)
inflammation/immune is often involved
what type of glomerular disease?

A

nephritic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

“Bland” urine sediment - no cells or casts
May see oval fat bodies
Proteinuria (at least 300 mg/d, often > 3 g/d)
what type of glomerular disease

A

nephrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Broad term for glomerular diseases in the nephritic spectrum
Generally - inflammatory process affecting glomeruli, causing renal dysfunction

A

Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

causes of glomerulonephritis

A
  • Immune complex deposition
  • Pauci-immune
  • Anti-glomerular basement membrane
  • C3 glomerulopathy
  • Monoclonal Ig
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

causes of immune complex deposition in CKD

A

IgA nephropathy (Berger disease), infections, endocarditis, lupus nephritis, membranoproliferative (MPGN), cryoglobulinemic (seen with HCV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what specific pathogen is associated particularly in immune complex deposition glomerulonephritis

A

strep infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pt comes in with edema, HTN and smoky colored urine
what could they possibly have?

A

glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

labs seen in glomerulonephritis

CKD

A
  • sCr rises over days - months - BUN:Cr ratio primary helpful to assess volume
  • Urinalysis - hematuria, moderate proteinuria (usually < 3 g/d)
  • Urine sediment - RBCs, WBCs, RBC casts
  • RBCs dysmorphic from crossing damaged glomerulus
  • RBC casts - sign of heavy glomerular bleeding, tubular stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

additional lab findings for glomerulonpehritis

CKD

A
  • Complement levels - may be low in C3 complex and immune complex glomerulonephritis (except Berger’s disease)
  • ASO titers - help evaluate for recent streptococcal infection
  • anti-GBM antibodies
  • P-ANCA and C-ANCA levels - pauci-immune glomerulonephritis
  • SPEP - monoclonal gammopathies
  • Inflammatory markers - ESR, CRP, ANA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what could reveal patterns of inflammation related to cause of glomerulonephritis
not commonly done

A

Renal biopsy - consider if no CI (bleeding disorder, uncontrolled HTN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tx for glomerulonephritis

CKD

A
  • Management of HTN
  • Management of volume overload - if present
  • Antiproteinuric therapy (ACE/ARB) - if no AKI
  • Immunosuppressive agents - High-dose corticosteroids, Cytotoxic agents may be used
  • Plasma exchange - Goodpasture disease, Pauci-immune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Postinfectious Glomerulonephritis is usually due to ?

A

GABHS - Often after pharyngitis or impetigo
May occur with other bacteria, viral (Hep B/C, CMV, EBV), syphilis, malaria, fungal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

s/s of Postinfectious Glomerulonephritis

A

1-3 wks after infection, avg. 7-10 d
S/S - vary from asx hematuria to nephritic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pt with recent GABHS infection presents with
Serum - Low complement; high ASO titer (unless previous abx)
Urine - hematuria, subnephrotic proteinuria (< 3 g/d), RBC casts
what could this patient might have?

A

Postinfectious Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

a renal biopsy comes back with “humps” of immune complex deposits. what is the dx?

A

Postinfectious Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tx for Postinfectious Glomerulonephritis? What medication is NOT recommended due to not improving outcome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Most common primary glomerular disease worldwide

A

IgA Nephritis (Berger’s Disease)
Can be primary (renal-limited) or secondary to cirrhosis, celiac disease, HIV, CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

IgA Nephritis (Berger’s Disease)
is MC in who?

A

males
children and young adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

10 yr old male pt comes in with an episode of gross hematuria and URI, what is their probable dx?

A

IgA Nephritis (Berger’s Disease)

Often in conjunction with mucosal viral infection (i.e., URI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

lab findings of IgA Nephritis (Berger’s Disease)

A

Serum - Normal complement; no confirming serum test
Urine - hematuria (micro or gross), proteinuria (varies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

tx for IgA Nephritis (Berger’s Disease)

A
  • varies depending on risk for progression
  • Low risk - no HTN, normal GFR, minimal proteinuria - monitor yearly
  • High risk - proteinuria >1.0 g/d, decreased GFR, HTN - ACE or ARB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Systemic small-vessel vasculitis - MC systemic vasculitis of childhood

A

Henoch-Schönlein Purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Associated with IgA deposition in vessel walls
Often associated with inciting infection (such as GABHS)
More common in males; more common in children

A

Henoch-Schönlein Purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Palpable purpura in lower extremities and butocks; arthralgias, abdominal symptoms (nausea, colic, melena)
what is this dx

A

Henoch-Schönlein Purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what lab findings would you find with Henoch-Schönlein Purpura

A

Serum - Normal complement; no confirming serum test
Urine - hematuria , proteinuria (varies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

tx for Henoch-Schönlein Purpura

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MCC of nephrotic glomerular disease

A

DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the “Nephrotic range” proteinuria?

value

A

> 3 g/d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

s/s of Subnephrotic proteinuria

A

asx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

s/s of Nephrotic Syndrome

A

peripheral edema
* May be in dependent regions
* May be generalized (including periorbital edema)
* Dyspnea, pleural effusions, ascites can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

oval fat bodies
grape clusters (light microscopy)
maltese crosses (polarized light)
are seen in what glomerular disease

A

nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what urinalysis could you do for nephrotic syndrome

A

dipstick - only detects albumin
spot urine protein:urine Cr ratio
24-hr urine for protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

serum labs of nephrotic syndrome

A
  • depends on amount of protein lost
  • Hypoalbuminemia - < 3 g/dL
  • Hypoproteinemia - < 6 g/dL
  • Hyperlipidemia - >50% of early nephrotic pts (hypertriglyceridemia)
  • Elevated ESR - due to altered plasma components
  • Possible deficiencies - Vitamin D, zinc, copper deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

an adult pt has a new onset idiopathic nephrotic syndrome, what could you do?

A

renal bx
Rarely done if long-standing DM or other obvious cause is present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

tx for nephrotic syndrome

A
  1. Protein restriction - if subnephrotic/mild
    - If > 10 g/d lost - INCREASE protein instead
    - ACE/ARB - lower urine protein excretion by reducing glomerular capillary pressure; antifibrotic effects
  2. Edema - dietary salt restriction; diuretics
    - Thiazide, loops - larger doses needed
  3. Hyperlipidemia - diet and exercise; lipid-lowering rx
  4. Hypercoagulability - anticoagulation
    - seen if serum albumin < 2 g/dL
    - Anticoag x 3-6 months min. if evidence of thrombosis
    - Ongoing - if renal vein thrombosis, PE, recurrent thromboemboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

why do we see hypercoagulability in nephrotic syndrome

A

Urinary loss of antithrombin, protein C, protein S
increased platelet activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

MCC proteinuric renal disease in children

A

Minimal Change Disease

20-25% of primary nephrotic disease in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

s/s of minimal change disease

A
  • often full-blown nephrotic syndrome
  • Thromboembolic events, hyperlipidemia, protein malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

tx for minimal change disease

A

Corticosteroids - Prednisone, 60 mg/m2/d
* < 8 wks for children, < 16 wks for adults
* Continue for several wks after proteinuria remission
* Taper dose after course is complete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MCC primary nephrotic syndrome in adults

A

Membranous Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

causes of Membranous Nephropathy

A

Due to immune complex deposition
May be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

pt comes in with edema and frothy urine. other than those he is asx, what could be their condition?

A

Membranous Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

membranous nephropathy have a Higher risk of hypercoagulable state, esp. where?

A

renal vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

tx for Membranous Nephropathy

A

ACE/ARB, immunosuppressive agents, transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Extracellular deposition of amyloid protein
Proteinuria, decreased GFR, nephrotic syndrome
what is this dx

A

Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

pt comes in with some inflammation and palpable kidneys
no abd or flank pain
what could be thier dx

A

Amyloidosis

Kidneys are often enlarged
May see other chronic
inflammatory dz
Treatment - limited options

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MC cause of ESRD in the US

A

Diabetic Nephropathy
20 year risk: About 40% (higher risk in T2DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Diabetic Nephropathy usually develop when after DM onset?

A

10 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

presentation of diabetic nephropathy

A
  • Early - hyperfiltration with increased GFR
  • Later - microalbuminuria (30-300 mg/d)
  • Progression - albuminuria 300+ mg/d
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

when to tx diabetic nephropathy

A

as soon as microalbuminuria is found

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Disorders mainly affecting renal tubules and interstitium

A

Tubulointerstitial Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

difference between acute vs chronic Tubulointerstitial Disease

A
  1. Acute - Acute Interstitial Nephritis
    * Presents with acute renal failure
    * 70% - due to meds
  2. Chronic - more indolent onset
    * May manifest with tubular dysfunction
    * Predominant pathology - interstitial fibrosis, tubular atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

causes of chronic tubulointerstitial disease

A
  • Obstructive Uropathy - MCC
  • Vesicoureteral Reflux - 2nd MCC
  • Analgesic Nephropathy - ingest min 1 g/d for 3+ yrs
  • May also be due to renal ischemia, glomerular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

causes of obstructive uropathy

A

Prolonged obstruction of urinary tract
* Prostatic disease
* Ureteral calculi
* Cancer of cervix, colon, or bladder
* Retroperitoneal tumors or fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how does obstructive uropathy cause damage?

A

Backflow of urine → extravasation into interstitium → inflammation, fibrosis
Prolonged reflux of urine causes damage, scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

obstructive uropathy s/s

A

vary with underlying cause, location/degree of obstruction

  • Hydronephrosis - asx
  • Pain - if acute complete obstruction (e.g., stone)
  • Bladder distension - +/-
  • HTN - +/-
  • Urine output - +/-
  • May present with oliguria or anuria
  • May present with polyuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

UA and serums of obstructive uropathy

A

often benign; may see hematuria, pyuria
Serum creatinine - typically elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Imaging shows dilation of collecting system
what is the dx

A

Obstructive Uropathy

60
Q

when should imaging be done with kidney disease? (Acute and chronic)

A

all pts with AKI of unknown cause
all CKD pts to r/o obstruction

61
Q

preferred imaging study for obstructive uropathy? what other imagings can be done

A

US - preferred imaging study
CT - more detailed information, not first-line
If suspected stone, PCKD - noncontrast CT

62
Q

tx for Obstructive Uropathy

A

relief of obstruction ASAP
Prolonged obstruction → further tubular damage, especially in distal nephron
Longstanding obstruction → renal scarring

63
Q

Vesicoureteral Reflux is MC in who?

A

children

Primarily occurs during childhood

64
Q

cause of Vesicoureteral Reflux

A

Incompetent, misplaced vesicoureteral sphincter → retrograde flow of urine while voiding
Inflammatory response and scarring

65
Q

child with hx of UTIs comes in with complaint of a UTI. what could be their dx?

A

Vesicoureteral Reflux
Especially young children with history of recurrent UTIs
Adults may give hx of frequent UTIs

66
Q

Vesicoureteral Reflux may not be dx until later in life until when?

A

HTN and proteinuria develop

67
Q

presentation of vescoureteral reflux (s/s, labs, urine)

A
  • S/S - HTN, hx of frequent UTIs
  • Labs - varying elevations in BUN/Cr
  • Urine - mild-moderate proteinuria, no sediment unless current infection
68
Q

imaging of choice for vesicoureteral reflux

A

Voiding cystourethrogram - radiopaque dye instilled in bladder; pt then voids while x-ray is taken

69
Q

upon US what would be seen with vesicoureteral reflux? what 3 things could be found in an adult?

A

hydronephrosis, renal scarring

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

70
Q

tx for Vesicoureteral Reflux

A
  • Maintaining sterile urine in childhood - Reduces severity of scarring
  • Surgical reimplantation of ureters - for children with persistent high-grade reflux - Ineffective in adolescents/adults
  • Control of HTN - ACE/ARB
71
Q

Usually seen in pts who ingest large amounts of analgesics
what type of chronic Tubulointerstitial Disease

A

Analgesic Nephropathy

72
Q

what meds MC cause Analgesic Nephropathy

A
  • phenacetin (banned in 1983)
  • ASA, NSAIDs, acetaminophen
73
Q

how much analgesics must be consumed to cause analgesic nephropathy?

A

at least 1 g/d for 3+ years

74
Q

Analgesic Nephropathy
causes damage how?

A
  • Tubulointerstitial inflammation and papillary necrosis
  • Analgesics can be concentrated up to 10x higher in renal papillae > renal cortex
75
Q

Urine presents hematuria, proteinuria, polyuria, pyuria
Sloughed papillae found
what is this dx

A

Analgesic Nephropathy

76
Q

small, scarred kidney with papillary calcifications
seen on CT, what is the dx?

A

Analgesic Nephropathy

77
Q

IVP shows contrast will fill area of sloughed papillae, causing a “ring shadow” or “golfball on a tee” sign
what is this dx

A

Analgesic Nephropathy
IVP rarely used due to risk of contrast nephropathy

78
Q

tx for Analgesic Nephropathy

A

DC of offending agent
* Renal decline expected to progress if analgesics continued
* Renal function may stabilize or mildly improve if analgesic stopped in a timely manner

79
Q

Autoimmune Interstitial Nephritis can be a complication of multiple autoimmune disorders:

A
  • Amyloidosis
  • Cryoglobulinemia
  • IgA nephropathy
  • Renal transplant rejection
  • Anti-GBM-Antibody syndrome (Goodpasture syndrome)
  • Sarcoidosis
  • Sjogren Syndrome
  • SLE
80
Q

vary with underlying cause; may have no s/s
Polyuria, decreased urinary concentrating ability
Volume depletion due to salt-wasting
Hyperkalemia
Hyperchloremic metabolic acidosis
what could this dx be?

A

Autoimmune Interstitial Nephritis

81
Q

imaging reveals small, scarred kidneys, what could be the dx

A

Autoimmune Interstitial Nephritis

82
Q

tx for autoimmune interstitial nephritis

A

controlling underlying cause

83
Q

Deposition of calcium in renal parenchyma and tubules
what is the dx

A

Nephrocalcinosis
Can cause AKI, CKD
May also have normal renal function
Most pts do not progress to ESRD

84
Q

cause of nephrocalcinosis

A

Caused by increase in urinary excretion of calcium, phosphate, and/or oxalate
MCC - increased urinary calcium excretion

85
Q

risk for nephrocalcinosis

A

conditions that cause hypercalcemia, hyperphosphatemia, or increased excretion of calcium, phosphate or oxalate in urine
* Hyperparathyroidism
* Vit D therapy
* Loops (in high doses for a long period)
* Numerous other conditions

86
Q

presentation of nephrocalcinosis

s/s, labs, urine

A
  • S/S - asx MC (incidental finding) - May see s/s of underlying cause
  • Labs - possible hypercalcemia, hyperphosphatemia
  • Urine - bland; may have sterile pyuria or hematuria
  • Proteinuria, if present, usually < 500 mg/d
  • 24-hr urine - increased Ca, phosphate, or oxalate
87
Q

imaging of choice for nephrocalcinosis

A

US is modality of choice
Can also be visualized with CT

88
Q

tx for nephrocalcinosis

A

correcting underlying metabolic disorder

89
Q

65-70% (MC) of all renal masses

A

Single or Solitary Renal Cyst

90
Q

where are most Single/Solitary Renal Cyst located?

A

outer cortex, may be in medulla

Often incidental US finding
Renal size usually normal

91
Q

what signs are not present in Single or Solitary Renal Cyst
unlike most other kidney diseases?

A

HTN, signs of ESRD
not present

92
Q

management for single/solitary renal cyst

A
  1. If appears benign on imaging, routine follow up is acceptable management
    * Refer to Bosniak score
    * If develop after onset of dialysis → potential for adenocarcinoma
93
Q

dx Medullary Cystic Kidney Disease during childhood is called what?

A

Juvenile Nephronophthisis

94
Q

which Medullary Cystic Kidney Disease
are recessive and dominant

A
  • Childhood (Juvenile NPH) - autosomal recessive
  • Adult (MCKD) - autosomal dominant
95
Q

Medullary Cystic Kidney Disease
forms where

A

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

96
Q

presentation of medullary cystic kidney disease

A

Polyuria, pallor, lethargy, renal salt wasting
* HTN - later in disease
* Hyperuricemia can be present
* Juvenile NPH - growth restriction, ESRD < 20 yrs
* MCKD - ESRD ages 20-70

97
Q

tx for Medullary Cystic Kidney Disease

A

adequate salt and water intake
No therapy to stop progression
Allopurinol if hyperuricemic
Does not recur in renal transplants

98
Q

prevalence of Autosomal Dominant PKD

A

1 in 400 to 1 in 1000 pts
90% from autosomal dominant inheritance

99
Q

2 genes of Autosomal Dominant PKD

A
  1. ADPKD-1 - 85% of pts - more severe course
  2. ADPKD-2 - 15% of pts - slower progression, later onset in life
100
Q

presentation of Autosomal Dominant PKD

s/s, PE, labs

A

s/s

  • abd or flank pain MC
  • hx of UTI and nephrolithiasis
  • hx of HTN in >50 %
  • Fhx of PKD in 75%

exam - large kidneys, may be palpable

Labs - hematuria (micro / gross), mild proteinuria - H&H tend to be maintained

101
Q

what confirms ADPKD

A

US confirms dx; can use CT if unclear
* Age < 30 - 2+ renal cysts
* Age 30-59 - 2+ cysts in each kidney
* Age 60 + - 4+ cysts in each kidney

102
Q

where else can cysts be found in ADPKD

A

40-50% have hepatic cysts
Cysts also often seen in spleen

103
Q

tx for ADPKD (7)

A
  1. Pain -Bed rest, analgesics, cyst decompression
  2. Hematuria - Bed rest, hydration - resolves in ~ 1 wk
    - Directed tx if sx of nephrolithiasis, UTI
    - recurrent - possible RCC
  3. Nephrolithiasis - Pain control, hydration of 2-3 L/d
  4. HTN - ACE/ARB, Cyst decompression
  5. Cerebral aneurysms - Screening arteriography not recommended
  6. infected cyst - quinolones, TMP-SMZ
    - May need 2 wks of IV tx then long-term oral abx
  7. Avoidance of caffeine and protein
104
Q

pain in ADPKD could be due to what

A

infection, bleeding into cysts, nephrolithiasis

105
Q

hematuria in ADPKD could be due to what?

A

usually due to rupture of cyst
May also be due to kidney stone, UTI

106
Q

what sx is MC in ADPKD (50% of pts at time of dx?)

A

HTN

107
Q

about 20% of pts experience ____ in ADPKD

A

nephrolithiasis

108
Q

10-15% of ADPKD have a cerebral aneurysm in what location?

A

circle of willis

109
Q

pt with ADPKD exhibits flank pain, fever, ↑ WBC
what could this be? what is the work up?

A

infected cyst
CX - blood and urine may be +/-
CT scan - can help diagnose

110
Q

what other complications can be seen in ADPKD

A

mitral valve prolapse, aortic aneurysms, aortic valve disease, colonic diverticula

111
Q

what medication slows rate of change in kidney volume, lower rate of progression, reduces intracellular cyclic AMP

A

Vasopressin receptor antagonists

112
Q

which Vasopressin receptor antagonist decreases cyst growth, has no improvements of kidney function?

A

Ocreotide

113
Q

this Vasopressin V2 Receptor Antagonist slows renal decline

A

Tolvaptan (Jynarque, Samsca)

114
Q

when is Tolvaptan recommended?

A
  1. Recommended for all pts 18+ with GFR of 25+ mL/min and 1+ risk marker:
    * Mayo Class 1C, 1D, 1E
    * Age ≤ 55 years and an eGFR < 65
    * Kidney length > 16.5 cm in patient < 50 y/o
    * PROPKD Score of > 6
115
Q

which Tolvaptan is for ADPKD

A

Jynarque

116
Q

which Tolvaptan is for hypervolemic/euvolemic hyponatremia

A

Samsca

117
Q

dosing for Tolvaptan

A

45 mg in AM, 15 mg 8 hrs later (prior to 4 pm)
* Titrate up every 1-4 wks to max 90 mg AM and 30 mg PM
* Greater reduction in urinary osmolality = greater impairment of cyst growth

118
Q

SE of Tolvaptan

A

thirst/polydipsia, polyuria/nocturia, hypernatremia, increased liver enzymes

119
Q

BBW for Tolvaptan

A

should be initiated and reinitiated in patients only in a hospital where serum sodium can be closely monitored

120
Q

CI of Tolvaptan

A

liver disease, pts on strong CYP3A4 inhibitors, allergy to rx

121
Q

rare
Enlarged kidneys with small cysts on collecting tubules only
what is this dx

A

Autosomal Recessive PKD

122
Q

presentation of Autosomal Recessive PKD

A

varies widely
* Enlarged kidneys (bilateral abdominal masses)
* Impaired urine concentration
* Metabolic acidosis
* HTN common

123
Q

Up to 50% of neonates with ARPKD die from ____

A

pulmonary hypoplasia

Intrauterine kidney disease causes severe oligohydramnios

124
Q

prognosis with ARPKD

A

80% of surviving neonates live to age 10 or longer
* ⅓ will develop ESRD by age 10
* Many pts also develop portal hypertension from periportal fibrosis

125
Q

diagnostics for ARPKD

A

large, echogenic kidneys
* Cysts visible only after birth
* Absence of renal cysts in either parent - helps distinguish ARPKD from ADPKD

126
Q

tx for ARPKD

A

no specific therapy
Management of HTN
Dialysis and kidney transplant

127
Q

renal artery stenosis is MC due to what

A

80-90% due to atherosclerotic occlusive disease
10-15% - fibromuscular dysplasia

128
Q

Suspect what if unexplained HTN in woman < 40

A

Renal Artery Stenosis

129
Q

pts with HTN and RAS MC have what other condition

A

> 45 yrs with atherosclerotic disease hx

130
Q

risk factors of renal artery stenosis

A
  1. atherosclerotic disease
  2. CKD
  3. DM
  4. tobacco use
  5. HTN
131
Q

s/s of RAS?
causes?

A

HTN, abd bruit (refractory or new-onset)
* Pulmonary edema with poorly controlled HTN
* AKI after starting an ACE inhibitor

132
Q

lab findings for RAS

A

elevated BUN/Cr if significant ischemia

133
Q

imaging needed/findings for RAS

describe imaging options

A

US - 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

  • CT angiography - may be less accurate, more expensive than US - Uses IV contrast
  • MRA - excellent but expensive; uses contrast

Renal angiography - gold standard

134
Q

what could lead to a false positive of RAS in imaging?

A

MRA
Turbulent blood flow = false + results

135
Q

tx for RAS

A

medical management, surgery
* Angioplasty - can reduce number of anti-HTN meds; does not change progression of disease
* Surgical bypass - more risks and no superior efficacy to angioplasty

intervention not proven better > meds for HTN, complications

Stenting produces better results than not

136
Q

Hypertensive nephropathy
Sclerosis of arteries and arterioles
Interstitial fibrosis and decreased glomerular tuft

A

Nephrosclerosis
Up to 27% of ESRD pts have HTN as cause of CKD

137
Q

risk factors for nephrosclerosis

A
  • African American race - 5x more common
  • Increased age, smoking, hypercholesterolemia
  • Longstanding uncontrolled HTN
138
Q

tx for nephroscleroisis

A

**management of HTN
**
Most pts require multiple antihypertensives
Thiazide diuretics and ACE/ARB MC

139
Q

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

A

Cholesterol Atheroembolic Disease

140
Q

Cholesterol Atheroembolic Disease often follow ____

the cause of it

A

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

141
Q

risk factors for Cholesterol Atheroembolic Disease

A

male, DM, HTN, ischemic cardiac disease

142
Q

s/s of cholesterol atheroembolic disease

A

Onset usually 1-14 days after inciting event
* worsening HTN and renal function
* < 50% of pts have signs of embolic disease - fever, abdominal pain, wt loss
* livedo reticularis, localized gangrene

143
Q

labs with increased Cr, eosinophilia (60-80%), elevated ESR, low complement
are with what dx

CKD

A

Cholesterol Atheroembolic Disease

144
Q

how to definitively dx of Cholesterol Atheroembolic Disease

A

kidney biopsy

145
Q

tx for Cholesterol Atheroembolic Disease

A

no specific effective therapy
* Statins
* Steroids (controversial)
* Supportive tx

GU: Clin Med IIA (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions