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GU > Lecture 5: CKD Part 2 > Flashcards

Lecture 5: CKD Part 2 Flashcards

1
Q

What are the characteristics of nephritic syndrome?

A
  • Urine sediment with hematuria, +/- casts
  • Proteinuria < 3g/d
  • Inflammation/Immune mediated

NephrItic = Inflammation

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2
Q

What are the characteristics of nephrotic syndrome?

A
  • Bland urine sediment
  • Proteinuria > 3g/d
  • Hyperlipidemia

NephrOtic = PrOtein

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3
Q

What are the primary causes of nephritic syndrome?

A
  • Immune complex deposition GN
  • Pauci-immune GN
  • Anti-GBM GN
  • C3 GN
  • Monoclonal Ig GN
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4
Q

What are the causes of immune complex GN?

A
  • IgA nephropathy (Berger’s disease)
  • Infections (Streptococcal)
  • Lupus nephritis
  • Endocarditis
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5
Q

What is goodpasture’s syndrome?

A

Anti-GBM GN + pulmonary involvement.

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6
Q

What causes C3 GN?

A

Abnormalities in the ALTERNATIVE complement pathway.

WIll present with only C3 abnormality. C3+C4 = immune complex.

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7
Q

What causes monoclonal Ig-mediated GN?

A

Monoclonal gammopathies (MM, MGUS)

MGUS = Monoclonal gammopathy of unknown significance.

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8
Q

What causes Pauci-immune GN?

A

Cell-mediated autoimmune processes

Tested via ANCAs

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9
Q

What are the primary signs seen in GN?

A
  1. Edema (periorbital or testicular)
  2. HTN
  3. Gross hematuria
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10
Q

What lab findings are associated with GN?

A
  • Increase in Serum Cr over time.
  • UA: hematuria, moderate proteinuria < 3g/d
  • Urine sediment: RBCs, WBCs, RBC casts.

Usually dysmorphic RBCs.

RBC cast presence = heavy glomerular bleeding and/or tubular stasis.

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11
Q

What tests are associated with each GN?

A
  • Complement: low C3 = C3. Low C3+C4 = immune-complex. (except Berger’s)
  • ASO titer: recent streptococcal infection
  • anti-GBM antibodies = anti-GBM
  • P-ANCA + C-ANCA = Pauci-immune GN
  • SPEP: monoclonal gammopathies
  • Inflammatory markers: ESR, CRP, ANA
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12
Q

When do we do a renal biopsy in regards to GN?

A

We can do it to reveal the inflammation pattern if there is no bleeding disorder or uncontrolled HTN.

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13
Q

What are the primary treatment options for GN?

A
  • Manage HTN/Edema
  • ACEi/ARB for antiproteinuric therapy
  • Immunosuppressants: High corticosteroids or cytotoxic agents.
  • Plasma exchange: Goodpasture’s or Pauci-immune
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14
Q

What is the primary cause of postinfectious GN?

A

GABHS

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15
Q

What S/S are seen in postinfectious GN?

A

Hematuria all the way to nephritic syndrome.

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16
Q

What serum tests would be best to help diagnose postinfectious GN?

A

ASO titers or complement levels.

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17
Q

What would a biopsy of postinfectious GN usually show?

A

Humps of immune complex deposits.

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18
Q

How do we treat postinfectious GN?

A
  • AntiHTNs
  • Salt restriction
  • Diuretics

Steroids show no improvement in mortality.

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19
Q

What is the prognosis of postinfectious GN in a child? Adult?

A
  • In a child, it generally resolves.
  • In an adult, it generally turns into CKD.
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20
Q

What is the most common glomerular disease worldwide?

A

IgA nephropathy, aka Berger’s disease

MC in males, specifically children or young adults.

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21
Q

What is the hallmark symptom of IgA nephropathy?

A

Episode of gross hematuria w/ mucosal viral infection.

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22
Q

How do ASO and complement levels appear in IgA nephropathy?

A

Both appear normal.

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23
Q

What is considered low risk IgA nephropathy and the treatment?

A
  • No HTN
  • Normal GFR
  • Minimal proteinuria
  • Yearly monitoring only.
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24
Q

What is considered high-risk IgA nephropathy and the treatment?

A
  • Proteinuria > 1g/d
  • Decreased GFR
  • HTN
  • ACE/ARB is indicated!
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25
Q

What is the most common systemic vasculitis in childhood?

A

Henoch-Schonlein Purpura

small vessel-vasculitis

Associated with IgA deposition in vessel walls.
Usually incited by a GABHS infection.
More common in males and children.

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26
Q

What are the S/S of henoch-schonlein purpura?

A
  • Palpable purpura in lower extremities and buttocks.
  • Arthralgias
  • Abdominal symptoms
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27
Q

What do serum tests and urine tests look like for henoch-schonlein purpura?

A
  • Serum: normal complement. No confirming test.
  • Urine: Hematuria with some proteinuria
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28
Q

What is the treatment for henoch-schonlein purpura?

A

Supportive only

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29
Q

What is the #1 cause of nephrotic syndrome in the US?

A

DM

Must be > 3g/day for proteinuria.

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30
Q

What are the main S/S of nephrotic syndrome?

A
  • Peripheral edema
  • Dyspnea
  • Pleural effusions
  • Ascites
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31
Q

How does UA and sediment appear for nephrotic syndrome?

A
  • Proteinuria > 3g/d
  • Oval fat bodies if HLD is present.
  • Grape clusters in light microscopy
  • Maltese crosses in polarized light
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32
Q

How do labs generally appear for nephrotic syndrome?

A
  • Hypoalbuminemia < 3g/dL
  • Hypoproteinemia < 6g/dL
  • HLD > 50% of nephrotic patients
  • Elevated ESR
  • Vitamin deficiencies
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33
Q

When is renal biopsy done in a new-onset nephrotic syndrome patient?

A

If idiopathic/no precipitating obvious cause like DM.

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34
Q

What is the treatment for nephrotic syndrome?

A
  • ACE/ARB for moderate loss.
  • Dietary protein restriction for mild.
  • Dietary protein INCREASE for severe (> 10g/d loss)
  • Thiazide/loop diuretics
  • Salt restriction
  • HLD treatment/exercise
  • Anticoagulation if albumin < 2 g/dL
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35
Q

How does nephrotic syndrome affect children?

A

Usually full-blown, requiring corticosteroids.

Usually minimal change disease is MC in children.

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36
Q

What is the primary manifestation of primary nephrotic syndrome in adults?

A

Membranous nephropathy due to immune complex deposition.

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37
Q

What are the S/S of membranous nephropathy in adults?

A
  • Edema
  • Frothy urine
  • Hypercoagulability risk

Also the S/S of minimal change disease

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38
Q

What is the treatment for membranous nephropathy?

A
  • Transplant
  • ACE/ARB
  • Immunosuppressive agents
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39
Q

What is amyloidosis?

A
  • Secondary Nephrotic syndrome
  • Extracellular deposition of amyloid protein
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40
Q

What characterizes amyloidosis?

A
  • Proteinuria
  • Decreased GFR
  • Nephrotic syndrome
  • Chronic inflammation
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41
Q

What is the treatment for amyloidosis?

A

Managing underlying disease

Very limited options

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42
Q

What is the MCC of secondary nephrotic syndrome and the MC of ESRD in the US?

A

Diabetic nephropathy

Usually 10 years post DM-onset.

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43
Q

What test should we order for suspected diabetic nephropathy?

A

Urine Microalbumin.

44
Q

How does early diabetic nephropathy usually present?

A
  • Hyperfiltration with increased GFR.
  • No microalbuminemia yet.
45
Q

What is the usual acute tubulointerstitial disease?

A

Acute interstitial nephritis

46
Q

What are predominant pathologies for chronic tubulointerstitial disease?

A
  • Interstitial fibrosis
  • Tubular atrophy
47
Q

What is the MCC of chronic tubulointerstitial disease?

A
  • Obstructive uropathy, due to obstruction of the urinary tract.
48
Q

What childhood condition is the 2nd most common cause of chronic tubulointerstitial disease?

A
  • Vesicouretal reflux
  • Retrograde flow of urine while voiding
49
Q

What is analgesic nephropathy?

A

Ingestion of analgesics > 1g/d for 3+ years.

50
Q

What are the usual causes of obstructive uropathy?

A
  • Enlarged prostate
  • Renal calculi
  • Cancer
  • Retroperitoneal fibrosis or mass
51
Q

What are the usual S/S associated with obstructive uropathy?

A
  • Hydronephrosis
  • Pain
  • Bladder distension
  • HTN
  • Urine output variation

All of these vary in severity and presence.

52
Q

How does UA and Serum CR usually present for obstructive uropathy?

A
  • UA: normal, maybe hematuria or pyuria.
  • Serum Cr: elevated
53
Q

What are the preferred imaging studies for obstructive uropathy?

A
  1. US
  2. CT w/o contrast (for suspected stone)

All CKD pts to r/o obstruction.
All AKI pts with unknown etiologies.

54
Q

What is the primary treatment for obstructive uropathy?

A

Relieving the obstruction ASAP, as nephron damage is permanent.

Does not restore renal function if large # of nephrons are damaged.

Prolonged destruction will lead to tubular damage.
Long-standing will lead to renal scarring.

55
Q

What is the cause of vesicouretal reflux?

A
  • Incompetent or misplaced vesicouretal sphincter.
  • Inflammation and scarring.
56
Q

How does a kid with vesicouretal reflux typically present?

A
  • Recurrent UTIs
  • In adults, it varies (men tend not to, women have multiple common etiologies for recurrent UTI)
57
Q

What do labs and UA typically look like with someone with vesicouretal reflux?

A
  • Labs: varying elevations in BUN:Cr
  • UA: mild-mod proteinuria.
58
Q

What is the standard diagnostic test for vesicouretal reflux?

A

Voiding cystourethrogram

Contrast in bladder. Pt then voids while being XRAYed

59
Q

What should US show for someone with vesicouretal reflux?

A
  • Asymmetric small kidneys
  • Irregular outlines
  • Thin cortices

Not really visible until Grade III.

60
Q

What is the treatment for vesicouretal reflux?

A
  1. Maintain sterile urine in childhood
  2. Surgical reimplantation of ureters (high-grade persistent for children)
  3. HTN control via ACE/ARB

Surgery not indicated in ADOLESCENTS OR ADULTS.

61
Q

How often is analgesic use generally in analgesic nephropathy?

A

More than 1g/d for 3+ years

Most associated with phenacetin, a banned substance since 1983.

62
Q

What typically happens in analgesic nephropathy?

A
  • Tubulointerstitial inflammation
  • Papillary necrosis.

Analgesics concentrate 10x more in renal papillae.

63
Q

What does UA look like for analgesic nephropathy?

A
  • Hematuria
  • Proteinuria
  • Polyuria
  • Pyuria
  • Sloughed papillae
64
Q

What diagnostic tests are used for analgesic nephropathy?

A
  • CT: small, scarring w/ papillary calcifications.
  • IVP: Ring shadow/golfball on a tee

IVP is not as preferred due to risk of contrast nephropathy.
IVP= IV pyelogram

65
Q

What is the treatment for analgesic nephropathy?

A

Stopping analgesic use.

66
Q

What are the clinical findings associated with autoimmune interstitial nephritis?

A
  • Polyuria with decreased urine osmolality
  • Volume depletion w/ salt wasting
  • Hyperkalemia
  • Hyperchloremic metabolic acidosis
67
Q

What is the treatment for autoimmune interstitial nephritis?

A

Treatment of underlying autoimmune condition.

68
Q

What is nephrocalcinosis and what does it result in?

A
  • Deposition of calcium in renal parenchyma and tubules
  • AKI/CKD/normal
  • Generally no progression to ESRD.
69
Q

What is the MCC of nephrocalcinosis?

A

Increased urinary calcium excretion.

70
Q

What conditions increase the risk of nephrocalcinosis?

A
  • Hyperparathyroidism
  • Vit D therapy
  • Loop diuretics
  • Anything that causes hypercalcemia, hyperphosphatemia, or increased excretion of Ca/P/oxalate in urine.
71
Q

What is the modality of choice for imaging nephrocalcinosis?

A

US

72
Q

For a single/solitary renal cyst, where are most found and how does a patient present?

A
  • Renal cortex
  • Usually benign unless appearing after dialysis (adenocarcinoma potential)
73
Q

What are the two types of medullary cystic kidney disease?

A
  • Childhood: juvenile nephronophthisis (recessive)
  • Adult: dominant
74
Q

How does MCKD typically present physiologically?

Medullary cystic kidney disease

A

Multiple small renal cysts at corticomedullary junction and in the medulla.

Can lead to interstitial inflammation/glomerular sclerosis.

75
Q

What are the S/S of MCKD?

A
  • Polyuria, pallor, lethargy, salt-wasting
  • HTN later
  • Hyperuricemia
  • Growth restriction if juvenile
76
Q

What is the treatment for MCKD?

A
  • Adequate salt/water intake.
  • No therapy to stopping progression
  • Allopurinol for hyperuricemia

No ACE/ARB ):

77
Q

What are the two genes that contribute to autosomal dominant polycystic kidney disease? (ADPKD)

A
  • ADPKD-1: 85% of pts and more SEVERE.
  • ADPKD-2: 15% of pts and slower progression and later onset.

Overall, 90% are inherited.

78
Q

What are the S/S + common historical risk factors for ADPKD?

A
  • Abdominal/flank pain
  • Hx of UTI/nephrolithiasis
  • Hx of HTN
  • FMHx of PKD
79
Q

How does ADPKD present on exam?

A

Large kidneys that are sometimes palpable.

80
Q

How does UA present on ADPKD?

A
  • Micro/macro hematuria
  • Mild proteinuria
81
Q

What confirms ADPKD?

A

US can confirm.
1. Age < 30: 2+ renal cysts
2. Age 30-59: 2+ cysts in each kidney
3. Age 60: 4+ cysts in each kidney

Can also seen hepatic or splenic cysts.

82
Q

For the pain and hematuria symptoms of ADPKD, what is the treatment?

A
  • Pain: analgesics, rest, decompression
  • Hematuria: Rest/hydration.

If hematuria is persistent: renal cell carcinoma should be considered.

83
Q

How is HTN in ADPKD treated?

A
  • ACE/ARB
  • Cyst decompression
84
Q

Where are aneurysms most likely to be in a patient with ADPKD?

A

Cerebral aneurysms within the circle of Willis.

Not recommended to perform arteriogram.

85
Q

If a cyst gets infected in a patient with ADPKD, what is the treatment?

A
  • ABX w/cystic penetration, generally IV + long-term oral.

Need cultures and CT to check for infection.

86
Q

What are the benefits of a vasopressin receptor antagonist and octreotide in ADPKD?

A
  • Slowing kidney volume change
  • Lower rate of progression in ADPKD.
  • Octreotide: decreased cyst growth, no improvement in function.
  • Tolvaptan: V2, which slows renal decline and recommended based on mayo criteria.
87
Q

What is the criteria to be recommended tolvaptan for ADPKD?

A

GFR > 25 and 1 + risk marker:

  • Mayo Class 1C, 1D, 1E
  • Age <=55 and eGFR < 65
  • Kidney length > 16.5cm and age < 50
  • PROPKD > 6
88
Q

Avoiding what substance may help with ADPKD?

A

Caffeine

89
Q

Which tolvapatan formulation is recommended for ADPKD?

A

Jynarque specifically.

Samsca is for hyponatremia.

90
Q

What are the primary SE with tolvaptan and the BBW?

A
  • SE: Hypernatremia or liver enzyme elevation.
  • BBW: Need to be inpatient so serum sodium can be monitored.

CIs: Liver disease or CYP3A4 inhibitor use.

91
Q

What characterizes autosomal recessive PKD?

A

Enlarged kidneys with small cysts on COLLECTING tubules only.

Very rare.

Generally only presents with HTN.

92
Q

What is the usual cause of death for neonates born with autosomal recessive PKD?

A

Pulmonary hypoplasia

Will also result in ESRD by age 10 in 1/3 of pts.

93
Q

How is autosomal recessive PKD diagnosed?

A
  • US showing large, echogenic kidneys.
  • Absence of cysts in parents can help distinguish.
94
Q

How do we treat/manage ARPKD?

A
  • HTN management
  • Dialysis/kidney transplant
95
Q

What is the main cause of renal artery stenosis?

A

Atherosclerotic occlusive disease.

Usually in pts > 45 with a hx.

96
Q

What are the S/S of RAS?

A
  • HTN
  • Pulmonary edema (if HTN uncontrolled)
  • AKI after starting an ACE
  • Abdominal bruits
97
Q

What is the preferred imaging modality for RAS?

A
  • Doppler US showing asymmetric kidneys (unilateral RAS) or small, hyperechoic kidneys (bilateral RAS)
  • Gold standard: renal artery angiography
  • MRA: excellent but pricey

Use CTA if obese, gassy, or inability to lie supine.

98
Q

How do we treat RAS?

A
  • Medical management with antiHTNs.
  • Surgical management: angioplasty or surgical bypass.

Angioplasty doesn’t affect disease progression.

99
Q

What is the primary cause of nephrosclerosis?

A

HTN nephropathy

100
Q

What are the primary risk factors for nephrosclerosis?

A
  • African-American 5x more likely
  • Age, smoking, hypercholesterolemia
  • Long-standing uncontrolled HTN
101
Q

What is the treatment for nephrosclerosis?

A

Manage HTN via thiazides or ACE/ARBs

102
Q

What is the pathophysiology of cholesterol atheroembolic disease?

A

Emboli to kidney from cholesterol crystals.

103
Q

What are the primary risk factors for cholesterol atheroembolic disease?

A
  • Male
  • DM
  • HTN
  • Ischemic cardiac disease
104
Q

What are the S/S of cholesterol atheroembolic disease?

A
  • Worsening HTN/renal function
  • Embolic disease (fever, abd pain, wt loss)
  • Livedo reticularis or localized gangrene
105
Q

How do labs typically present in cholesterol atheroembolic disease?

A
  • Increased Cr
  • Eosinophilia
  • Elevated ESR
  • Low complement
106
Q

How do we definitively diagnose cholesterol atheroembolic disease?

A

Kidney biopsy

107
Q

What are the treatment options for cholesterol atheroembolic disease?

A
  • Statins
  • Steroids (controversial)
  • Supportive tx

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