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Lecture 5: CKD Part 2 Flashcards

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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
What is the most common systemic vasculitis in childhood?
Henoch-Schonlein Purpura | small vessel-vasculitis ## Footnote Associated with IgA deposition in vessel walls. Usually incited by a GABHS infection. More common in males and children.
26
What are the S/S of henoch-schonlein purpura?
* Palpable purpura in lower extremities and buttocks. * Arthralgias * Abdominal symptoms
27
What do serum tests and urine tests look like for henoch-schonlein purpura?
* Serum: normal complement. No confirming test. * Urine: Hematuria with some proteinuria
28
What is the treatment for henoch-schonlein purpura?
Supportive only
29
What is the #1 cause of nephrotic syndrome in the US?
DM | Must be > 3g/day for proteinuria.
30
What are the main S/S of nephrotic syndrome?
* Peripheral edema * Dyspnea * Pleural effusions * Ascites
31
How does UA and sediment appear for nephrotic syndrome?
* Proteinuria > 3g/d * Oval fat bodies if HLD is present. * Grape clusters in light microscopy * Maltese crosses in polarized light
32
How do labs generally appear for nephrotic syndrome?
* Hypoalbuminemia < 3g/dL * Hypoproteinemia < 6g/dL * HLD > 50% of nephrotic patients * Elevated ESR * Vitamin deficiencies
33
When is renal biopsy done in a new-onset nephrotic syndrome patient?
If idiopathic/no precipitating obvious cause like DM.
34
What is the treatment for nephrotic syndrome?
* 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
35
How does nephrotic syndrome affect children?
Usually full-blown, requiring corticosteroids. | Usually minimal change disease is MC in children.
36
What is the primary manifestation of primary nephrotic syndrome in adults?
Membranous nephropathy due to immune complex deposition.
37
What are the S/S of membranous nephropathy in adults?
* Edema * Frothy urine * Hypercoagulability risk | Also the S/S of minimal change disease
38
What is the treatment for membranous nephropathy?
* Transplant * ACE/ARB * Immunosuppressive agents
39
What is amyloidosis?
* Secondary Nephrotic syndrome * Extracellular deposition of amyloid protein
40
What characterizes amyloidosis?
* Proteinuria * Decreased GFR * Nephrotic syndrome * Chronic inflammation
41
What is the treatment for amyloidosis?
Managing underlying disease | Very limited options
42
What is the MCC of secondary nephrotic syndrome and the MC of ESRD in the US?
Diabetic nephropathy | Usually 10 years post DM-onset.
43
What test should we order for suspected diabetic nephropathy?
Urine Microalbumin.
44
How does early diabetic nephropathy usually present?
* Hyperfiltration with increased GFR. * No microalbuminemia yet.
45
What is the usual acute tubulointerstitial disease?
Acute interstitial nephritis
46
What are predominant pathologies for chronic tubulointerstitial disease?
* Interstitial fibrosis * Tubular atrophy
47
What is the MCC of chronic tubulointerstitial disease?
* Obstructive uropathy, due to obstruction of the urinary tract.
48
What childhood condition is the 2nd most common cause of chronic tubulointerstitial disease?
* Vesicouretal reflux * Retrograde flow of urine while voiding
49
What is analgesic nephropathy?
Ingestion of analgesics > 1g/d for 3+ years.
50
What are the usual causes of obstructive uropathy?
* Enlarged prostate * Renal calculi * Cancer * Retroperitoneal fibrosis or mass
51
What are the usual S/S associated with obstructive uropathy?
* Hydronephrosis * Pain * Bladder distension * HTN * Urine output variation | All of these vary in severity and presence.
52
How does UA and Serum CR usually present for obstructive uropathy?
* UA: normal, maybe hematuria or pyuria. * Serum Cr: elevated
53
What are the preferred imaging studies for obstructive uropathy?
1. US 2. CT w/o contrast (for suspected stone) ## Footnote All CKD pts to r/o obstruction. All AKI pts with unknown etiologies.
54
What is the primary treatment for obstructive uropathy?
Relieving the obstruction ASAP, as nephron damage is permanent. | Does not restore renal function if large # of nephrons are damaged. ## Footnote Prolonged destruction will lead to tubular damage. Long-standing will lead to renal scarring.
55
What is the cause of vesicouretal reflux?
* Incompetent or misplaced vesicouretal sphincter. * Inflammation and scarring.
56
How does a kid with vesicouretal reflux typically present?
* Recurrent UTIs * In adults, it varies (men tend not to, women have multiple common etiologies for recurrent UTI)
57
What do labs and UA typically look like with someone with vesicouretal reflux?
* Labs: varying elevations in BUN:Cr * UA: mild-mod proteinuria.
58
What is the standard diagnostic test for vesicouretal reflux?
Voiding cystourethrogram | Contrast in bladder. Pt then voids while being XRAYed
59
What should US show for someone with vesicouretal reflux?
* Asymmetric small kidneys * Irregular outlines * Thin cortices | Not really visible until Grade III.
60
What is the treatment for vesicouretal reflux?
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
How often is analgesic use generally in analgesic nephropathy?
More than 1g/d for 3+ years ## Footnote Most associated with phenacetin, a banned substance since 1983.
62
What typically happens in analgesic nephropathy?
* Tubulointerstitial inflammation * Papillary necrosis. | Analgesics concentrate 10x more in renal papillae.
63
What does UA look like for analgesic nephropathy?
* Hematuria * Proteinuria * Polyuria * Pyuria * Sloughed papillae
64
What diagnostic tests are used for analgesic nephropathy?
* 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
What is the treatment for analgesic nephropathy?
Stopping analgesic use.
66
What are the clinical findings associated with autoimmune interstitial nephritis?
* Polyuria with decreased urine osmolality * Volume depletion w/ salt wasting * Hyperkalemia * Hyperchloremic metabolic acidosis
67
What is the treatment for autoimmune interstitial nephritis?
Treatment of underlying autoimmune condition.
68
What is nephrocalcinosis and what does it result in?
* Deposition of calcium in renal parenchyma and tubules * AKI/CKD/normal * Generally no progression to ESRD.
69
What is the MCC of nephrocalcinosis?
Increased urinary calcium excretion.
70
What conditions increase the risk of nephrocalcinosis?
* Hyperparathyroidism * Vit D therapy * Loop diuretics * Anything that causes hypercalcemia, hyperphosphatemia, or increased excretion of Ca/P/oxalate in urine.
71
What is the modality of choice for imaging nephrocalcinosis?
US
72
For a single/solitary renal cyst, where are most found and how does a patient present?
* Renal cortex * Usually benign unless appearing after dialysis (adenocarcinoma potential)
73
What are the two types of medullary cystic kidney disease?
* Childhood: juvenile nephronophthisis (recessive) * Adult: dominant
74
How does MCKD typically present physiologically? | Medullary cystic kidney disease
Multiple small renal cysts at corticomedullary junction and in the medulla. | Can lead to interstitial inflammation/glomerular sclerosis.
75
What are the S/S of MCKD?
* Polyuria, pallor, lethargy, salt-wasting * HTN later * Hyperuricemia * Growth restriction if juvenile
76
What is the treatment for MCKD?
* Adequate salt/water intake. * No therapy to stopping progression * Allopurinol for hyperuricemia | No ACE/ARB ):
77
What are the two genes that contribute to autosomal dominant polycystic kidney disease? (ADPKD)
* ADPKD-1: 85% of pts and more SEVERE. * ADPKD-2: 15% of pts and slower progression and later onset. | Overall, 90% are inherited.
78
What are the S/S + common historical risk factors for ADPKD?
* Abdominal/flank pain * Hx of UTI/nephrolithiasis * Hx of HTN * FMHx of PKD
79
How does ADPKD present on exam?
Large kidneys that are sometimes palpable.
80
How does UA present on ADPKD?
* Micro/macro hematuria * Mild proteinuria
81
What confirms ADPKD?
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
For the pain and hematuria symptoms of ADPKD, what is the treatment?
* Pain: analgesics, rest, decompression * Hematuria: Rest/hydration. | If hematuria is persistent: renal cell carcinoma should be considered.
83
How is HTN in ADPKD treated?
* ACE/ARB * Cyst decompression
84
Where are aneurysms most likely to be in a patient with ADPKD?
Cerebral aneurysms within the circle of Willis. ## Footnote Not recommended to perform arteriogram.
85
If a cyst gets infected in a patient with ADPKD, what is the treatment?
* ABX w/cystic penetration, generally IV + long-term oral. | Need cultures and CT to check for infection.
86
What are the benefits of a vasopressin receptor antagonist and octreotide in ADPKD?
* 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
What is the criteria to be recommended tolvaptan for ADPKD?
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
Avoiding what substance may help with ADPKD?
Caffeine
89
Which tolvapatan formulation is recommended for ADPKD?
Jynarque specifically. ## Footnote Samsca is for hyponatremia.
90
What are the primary SE with tolvaptan and the BBW?
* 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
What characterizes autosomal recessive PKD?
Enlarged kidneys with small cysts on COLLECTING tubules only. | Very rare. ## Footnote Generally only presents with HTN.
92
What is the usual cause of death for neonates born with autosomal recessive PKD?
Pulmonary hypoplasia | Will also result in ESRD by age 10 in 1/3 of pts.
93
How is autosomal recessive PKD diagnosed?
* US showing large, echogenic kidneys. * Absence of cysts in parents can help distinguish.
94
How do we treat/manage ARPKD?
* HTN management * Dialysis/kidney transplant
95
What is the main cause of renal artery stenosis?
Atherosclerotic occlusive disease. | Usually in pts > 45 with a hx.
96
What are the S/S of RAS?
* HTN * Pulmonary edema (if HTN uncontrolled) * AKI after starting an ACE * Abdominal bruits
97
What is the preferred imaging modality for RAS?
* 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
How do we treat RAS?
* Medical management with antiHTNs. * Surgical management: angioplasty or surgical bypass. | Angioplasty doesn't affect disease progression.
99
What is the primary cause of nephrosclerosis?
HTN nephropathy
100
What are the primary risk factors for nephrosclerosis?
* African-American 5x more likely * Age, smoking, hypercholesterolemia * Long-standing uncontrolled HTN
101
What is the treatment for nephrosclerosis?
Manage HTN via thiazides or ACE/ARBs
102
What is the pathophysiology of cholesterol atheroembolic disease?
Emboli to kidney from cholesterol crystals.
103
What are the primary risk factors for cholesterol atheroembolic disease?
* Male * DM * HTN * Ischemic cardiac disease
104
What are the S/S of cholesterol atheroembolic disease?
* Worsening HTN/renal function * Embolic disease (fever, abd pain, wt loss) * Livedo reticularis or localized gangrene
105
How do labs typically present in cholesterol atheroembolic disease?
* Increased Cr * Eosinophilia * Elevated ESR * Low complement
106
How do we definitively diagnose cholesterol atheroembolic disease?
Kidney biopsy
107
What are the treatment options for cholesterol atheroembolic disease?
* Statins * Steroids (controversial) * Supportive tx

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