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Genitourinary > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Glomerular diseases: _______ is a condition of abnormally elevated nitrogen in the blood (elevated BUN and Creatinine). It is associated with insufficient/dysfunctional filtering of the blood by the kidneys (decreased GFR) and can lead to uremia and acute injury if uncontrolled.

A

Azotemia

Types:
1. Intrinsic (damage to vascular/tubular component leads to dec. reabsorption; infection/disease)

  1. Pre-renal (dec. perfusion)
  2. Post-renal (bilateral urinary outflow obstruction or rupture)
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2
Q

Glomerular diseases: There are 3 main types of azotemia:

  1. Intrinsic
  2. Pre-renal (heart failure; hypoperfusion)
  3. Post-renal azotemia (obstruction; ureter, stone, prostate)

What additional work up/labs should be performed to determine the type of azotemia?

A
  1. Intrinsic
    - Specific gravity: < 1.01
    - Urine osmolarity: <400
    - BUN;Cr: <20
    - FE of Na2+: >1
  2. Pre-renal:
    - specific gravity: > 1.02
    - urine osmolarity: >500
    - BUN;Cr: > 20
    - FE of Na2+: <1
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3
Q

Glomerular diseases: ______ is a condition of increased urea in the blood. It is a clinical term associated with systemic manifestations.

It can occur from systemic metabolic and endocrine changes including:

  1. Heart (fibrinous/uremic pericarditis)
  2. Peripheral neuropathy
  3. Ulcers, esophagitis
A

Uremia

Other examples:

  1. Neuromuscular
    - -myopathy, encephalopathy
  2. Skin
    - -pruritus (itching)
    - -uremic frost (chronic failure)
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4
Q

Glomerular disease: Low ionized blood calcium stimulates the parathyroid gland to release PTH. PTH begins removing the calcium from your bones to restore the blood calcium level.

How does this occur? What are the other functions of PTH?

A
  1. Phosphate Trashing hormone
    - -inc. phosphate excretion
    - -inhibits HCO3- reabsorption
  2. Calcium release from bone
    - osteoclasts
  3. Stimulates calcitriol formation and calcium reabsorption in DCT
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5
Q

Glomerular diseases: Renal osteodystrophy refers to an alteration of bone morphology in patients with chronic kidney disease. Early indicators include high phosphorus, or high PTH levels.

What are examples of osteodystrophy associated with chronic renal disease?

A
  1. osteitis fibrosa cystica
    - -secodary hyperparathyroidism
  2. osteomalacia
    - -vit. D deficiency
  3. osteoporosis
    - -loss of bone mass
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6
Q

Glomerular disease: Healthy kidneys activate Vitamin D (calcitriol) which help maintain normal PTH levels as well as allows absorption of calcium from

A

the gut

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7
Q

Glomerular disease: Waxy casts can be seen in patients with

A

end-stage renal disease or chronic renal failure

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8
Q

Glomerular disease: A patient presents with complaints of acute onset hematuria.

Other features include:

  1. red cell casts on urinalysis
  2. decreased GFR
  3. mild proteinuria
  4. HTN

You suspect

A

Nephritic syndrome

*e.g. acute post-streptococcal glomerulonephritis

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9
Q

Glomerular disease: Nephrotic syndrome is seen with glomerular disease.

It is associated with heavy proteinuria (_______), hypoalbuminemia (______grams), peripheral edema and hyperlipidemia.

A
  1. Proteinuria > 3.5 g/day
  2. Hypoalbuminemia <3g/day)
  3. Edema (loss of oncotic)
  4. Hyperlipidemia (liver supplies fat to blood)
  5. Lipiduria ((fatty cast)
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10
Q

Glomerular disease: Acute kidney injury leads to a rapid decline in GFR (hours to days).

It may be due to glomerular, interstitial, vascular, or tubular injury.

What is the hallmark of acute kidney injury?

A

Oliguria (dec. urine)

*Inc. BUN; Cr > 15

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11
Q

Glomerular diseases: Chronic kidney disease is when there is renal disease > 3 mos.

It causes persistent decline in GFR and increased _________.

It is often due to HTN and diabetes.

A

Increased albuminuria

microalbumin in the urine

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12
Q

Glomerular diseass: GFR < 5% indicates

A

End stage renal disease

*Dialysis

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13
Q

Glomerular diseases: Which of the following is a function of the kidney?

a. EPO production
b. Production of Active Vit. D
c. Renin secretion
d. Prostaglandins

A

All of the above

  1. EPO
    - -respond to hypoxia
    - -from peritubular capillary interstitial cells
  2. Vitamin D (1, 25 OH2-D)
    - -hydroxylation
    - -conversion in PT
  3. Renin
    - -JG cells
    - -response to dec. pressure on afferent side and sympathetic (b1)
  4. Prostaglandins
    - -vasodilate afferents
    - -inh. by NSAIDS (analgesic effects)
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14
Q

Glomerular diseases: Glomerular diseases are often characterized by an issue with _____

A

Filtration

*immune complexes

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15
Q

Glomerular diseases: Glomerular diseases can be divided based on their histologic findings:

  1. ________ (portion of a glomerulus)
  2. ____ (all of a glomerulus)
  3. ____: Some glomeruli involved
  4. ______ (all of almost all of the glomeruli)
A
  1. Segmental
  2. Global
  3. Focal
  4. DIffuse
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16
Q

Glomerular diseases: The following are common responses to glomerular injury:

  1. Hypercellularity
  2. Basememnt membrane thickening
  3. Hyalinosis
  4. Sclerosis

Hypercellularity and Basement Membrane thickening are seen at what stage of glomerular injury?

A

Acute

  1. Hypercellularity
    - Mesangial/Endothelial
    - -Inflammatory/crescent form
    * hyperplasia
  2. Basement membrane thickening
    - -immune complexes/fibrin deposits
    - -inc. protein deposits (diabetes)
    - -membrane prolif.
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17
Q

Glomerular diseases: The following are common responses to glomerular injury:

  1. Hypercellularity
  2. Basememnt membrane thickening
  3. Hyalinosis
  4. Sclerosis

Hyalinosis and Sclerosis are seen at what stage of glomerular injury?

A

CHronic

  1. Hyalinosis
    - –capillary damage
  2. Sclerosis
    - -ECM matrix deposition
    - -diabetic glomerulosclerosis
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18
Q

Glomerular diseases: THe following are diagnostic methods for determining glomerular disease:

  1. H&E
  2. PAS
  3. Trichrome
  4. Silver stain
  5. Immunofluourscence (IF)
  6. Electron Microscopy

Explain what each of these look for

A
  1. PAS:
    - -bm and mesangium
  2. Trichrome:
    - -fibrosis
  3. Silver:
    - -bm
  4. IF
    - -Ig types
    - -presence/absence of complement
    - -pattern of deposition
  5. EM
    - -location of deposits
    - -bm
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19
Q

Glomerular diseases: Many glomerular diseases are immune (Ab) mediated.

There are 2 possible types seen on immunofluourescence:

  1. ______: forms in the glomerular tissue. It occurs due to an Ab against a fixed intrinsic tissue antigen (e.g. basement membrane component).
  2. Deposition of circulating immune complexes (auto-immune)
A
  1. In situ (linear)
    * *Type IV collagen MC Ag
  2. Circulating (autoimmune; granular)
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20
Q

Glomerular diseases: Membranous glomerulopathy is thickening of the glomerular basement membrane. What is the proposed cause for this?

A

In situ Ab complex against Phospholipase A2 receptor (PLA2R)

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21
Q

Glomerular diseases: Anti-glomerular basement membrane disease is the 2nd most common glomerular disease caused by In situ Ab complex against intrinsic tissue antigens.

Explain anti-glomerular basement membrane disease

A

Antigen: Type IV collagen

Disease: Goodpasteur syndrome (if involves kidney and lung)

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22
Q

Glomerular diseases: Planted antibody complexes are complexes that are NOT inherent in the glomerulus. What are examples of planted antibody complexes?

A

DNA (autoimmune), Nuclear proteins, Bacterial/viral products (HIV)

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23
Q

Glomerular diseases: Diseases involving circulating Ab-complexes are known as immune-complex mediated glomerulonephritis.

True/False: The antigen may be endogenous (Lupus -DNA; IgA nephropathy) or Exogenous (microbial - strep proteins; HCV or HBV)

A

True

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24
Q

Glomerular disease: Most mechanisms of glomerular injury are immune-mediated. They may occur in response to a local inflammatory reaction (nephritic).

List examples of mechanisms of glomerular injury?

A
  1. Antibodies
  2. Complement
    - -dense deposit disease
    - -C5-C9 (MAC complex)
  3. Cell-mediated immunity
    - -T cells/macros
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25
Q

Glomerular diseases: How does complement play a role in glomerulonephritis?

A
  1. C5a - chemoattracs neutrophils
  2. C5b-C9 - MAC complex
    (activates mesangial and epithelial cells = release proteases)
  • -produce free radical intermediates
  • -produce proteases
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26
Q

Glomerlar diseases: Podocyte disruption is the MC cause of Nephrotic glomerular injury. Podocytes have have limited capacity for replication and repair. Issues with filtration can arise as a result of loss of slit diaphragm integrity and impairment of the charge barrier.

What diseases can nephrotic type glomerular injury be seen in?

A

Focal Segmental glomerulosclerosis (FSGS), Minimal change disease, Membranous nephropathy, amyloidosis, diabetic glomerulonephropathy

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27
Q

Nephritic: A patient presents with the following labs:

  1. Hematuria
  2. RBC casts in urine on microscopy
  3. Proteinuria < 3.5 g/day
  4. Dec. GFR
  5. Inc. BUN; Cr
  6. HTN, edema

These features most likely correlate with _____ syndrome.

A

Nephritic syndrome

Associated with:
–inflammatory changes in glomeruli (leukocytes, hyperplasia of glomerular cells)

NOTE: sufficient injury to glomerular capillaries results in RBC and protein spillage into the urine

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28
Q

Nephritic: Nephritic manifestations may:

a. rapidly develop, but cause reversible renal insufficiency
b. progress rapidly with renal failure that resolves ONLY with aggressive treatment
c. persist for years and slowly proceed to renal failure

A

ALL

a. acute glomerulonephritis
b. rapidly progressive glomerulonephritis
c. chronic glomerulonephritis

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29
Q

Nephritic: What is the only means of definitive diagnosis of nephritic vs. nephrotic glomerular diseases?

A

Renal biopsy

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30
Q

Nephritic: The most common nephritic diseases fit under 3 main categories:

  1. Anti-GBM
  2. Immune-complex
  3. Pauci-immune (ANCA-related)

Explain

A
  1. Anti-GBM (in situ)
    - -Goodpasteur
    - -Type 1
  2. Immune complex (circulating)
    - -Type 2
  3. Pauci
    –Type 3
    –No Ig or C3 deposits
    (granulomatosis w/ polyangiitis - PR3-ANCA/c-ANCA)
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31
Q

Nephritic: A 7 year old boy presents to the clinic with his mother. His mother complains he has had fever and malaise. She states he has recently recovered from strep throat, but now has cola colored urine. You note periorbital edema on observation. In addition to his hematuria, he also suffers from HTN and oliguria.

Biopsy reveals hypercellular, inflamed glomeruli.

EM shows “starry sky granular appearance with subepithelial humps and “lumpy bumpy” features.

Labs reveal

  1. dec. complement
  2. dec. C3 levels
  3. anti-DNAse and + ASO titers

You suspect?

A

Post-strep glomerulonephritis

–2-4 wks after group A strep (B-hemolytic; pharyngeal or impetigo)

  • nephrogenic strains: M protein virulence factor
  • IgG, IgM, C3 on GBM and mesangium

NOTE: circulating immune complexes – deposit and activate complement (granular on EM)

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32
Q

Nephritis: A 7 year old male presents to the clinic with fever, malaise and peri-orbital edema. His mother reports dark, smoky, cola colored urine in small amounts (oliguria). He is hypertensive.

PMH is significant for Strep pharyngitis

Labs:

  • -anti-DNAse B titers
  • -Positive ASO
  • -Dec. total complement levels
  • -low C3

You suspect Post-strep glomerulonephritis. How is it Diagnosed? Tx?

A

Post-strep glomerulonephritis presents in children after infection (typically with Group A strep).

Diagnosis:

  • *Biopsy (hypercellular, inflamed glomeruli)
  • -immune complex deposition (granular IF)
  • -subepithelial “humps” on EM

Treatment:

  • -supportive care
  • -rarely progresses to renal failure (kids)
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33
Q

Nephritic: Nephritic syndrome begins abruptly with oliguria, hematuria, facial edema and HTN.

What do you expect the plasma C3 levels to look like during acute syndrome? What features persist after several weeks?

A
  1. Plasma C3 lower during acute syndrome
    - -resolve 1-2 wks
  2. Hematuria and Proteinuria persist for months
    - -after nephritis resolves

NOTE: Patients have abnormal urinary sediment for years

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34
Q

Nephritic: Rapidly progressing glomerulonephritis (RPGN) is a pattern of severe glomerular injury and rapid renal failure (days to weeks). It tends to have poor prognosis due to rapid deterioration of renal function.

It is characterized by the presence of crescents on biopsy. These crescents consist of ____ and _____ with glomerular parietal cells, monocytes and macrophages.

A

(fibrin and plasma proteins (C3b)

Diseases:

  • -may occur from post-strep glomerulonephritis (adults only)
  • -Goodpasture (type II HSR)
  • -Granulomatosis with polyangitis (Wegener; PR3-Anca)
  • -Microscopic polyangiitis (MPO ANCA)
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35
Q

Nephritic: The following features (on the renal biopsy) describe what disease?

  1. Linear and smooth IF pattern (IgG and C3 on GBM)
  2. hypercellularity
  3. Crescents
  4. Fibrin deposition in glomeruli
  5. No deposits viewed on EM
A

Rapidly progressing glomerulonephritis

*No deposits on EM, but may show disruption of basement membrane

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36
Q

Nephritic: A 22 year old male presents with cough, dyspnea and hemoptysis. He complains of hematuria and oliguria. Patient is hypertensive. Labs reveal anti-GBM abs and mild proteinuria.

You Goodpasture syndrome, a type ______ HSR that results from Abs against the glomerular and alveolar basement membranes. These Abs induce glomerulonephritis by binding in situ to the basement membrane and activating complement.

A

Type II HSR

  • -bind in situ (linear pattern)
  • -activate complement and recruit inflammatory cells (PMN’s)

*peak ages 20-40y/o males

Tx: Plasmapharesis

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37
Q

Nephritic: Rapidly progressing glomerulonephritis may be caused by ANCA-associated autoimmune disorders (Pauci-immune glomerulonephritis). These disorders include:

  1. Granulomatosis w/ polyangiitis/Wegener (PR3-ANCA/c-ANCA)
  2. Microscopic polyangiitis (MPO-ANCA/p-ANCA)

In both disorders, anti-neutrophil cytoplasmic Abs (ANCAs) bind directly to leukocytes, engaging ______ and inducing inflammation.

A

Fc receptors

–engages Fc receptors (ANCA bound antigen)

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38
Q

Nephritic: A 34 year old male presents to the clinic with complaints of flank pain, low grade fever, and episodic flare ups of hematuria. Symptoms are concurrent with an URI (or GI infection).

Labs reveal:
-Entrapped circulating immune complexes (activate complement)
LM: Mesangial proliferation
EM: Mesangial immune complex deposits
IF: IgA based immune complex deposits in the mesangium

A

IgA nephropathy (berger)

  • MC type of glomerulonephritis
  • *renal pathology of Henoch Schonlein purpura

Features:

  • -recurrent episodic gross hematuria w/ RBCs casts.
  • -flares, URI’s or gastroenteritis

NOTE: Not to be confused with Buerger (thromboangiitis obliterans)

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39
Q

Nephritic and Nephrotic: A 5 year old presents to the clinic with his dad. The father complains his son started having abdominal pain following an upper respiratory infection. He also states that his son complains of tenderness at the joints (arthralgia), and he pees blood (hematuria).

You note purpuric skin lesions on the child’s buttocks and extensor surfaces.

Biopsy:
-IgA, IgG, C3 deposits in mesangial region

What is the most likely abnormality?

A

Henoch-Shconlein purpura

due to: small vessel vasculitis

follows: URI

Biopsy:
-IgA, IgG, C3 deposits in mesangial region

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40
Q

Nephritic or Nephrotic: Membranoproliferative glomerulonephritis is a pattern of immune-mediated disease that affects the mesangium and the basement membrane portions of the glomerulus.

It has two types:

  1. Type I
  2. Type II

Which of the former is associated with HBV and HCV?

A

Type I

-immune complexes of IgG and complement

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41
Q

Nephritic and Nephrotic: Type I MPGN is associated with immune complexes (IgG and complement). It can be due to HCV or HBV infection.

The following are clinical/lab findings of Type I:

  1. Large, Hypercellular glomeruli
  2. Lobulated appearance
  3. Granular “tram track” pattern on IF

True/False - The lobulated appearance is a result of mesangial/epithelial proliferation and deposition of subENDOthelial immune complexes.

A

True

Immunoflourescence: Granular

  • -“tram track”
  • -splitting of GBM (mesangial cells extend into capillary loop)

NOTE: Hypercellular and capillary wall thickening

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42
Q

Nephritic or Nephrotic: True/False - Eliminating the associated condition (bacterial endocarditis or osteomyelitis) may cause the glomerulonephritis to resolve, suggesting a causal relationship between the two.

A

True

  • Acute = resolve
  • type I MPGN: persistent, indolent w/ chronic antigenemia
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43
Q

Nephritic or Nephrotic: Type I MPGN can occur at any age, but is most frequent in older children and young adults.

It is more common in underdeveloped countries where chronic infections are more prevalent. In patients with MPGN type 1, what do you expect to see with regard to C3 levels?

A

Low C3 levels

–deposit as subendothelial deposits (dec. in plasma)

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44
Q

Nephritic or Nephrotic: MPGN type 2 (dense deposit disease) has pathognomonic electron dense transformation of GBM’s and extensive complement deposition.

What factor is associated with this disease and its progression?

A

C3 nephritic factor

-IgG autoAb = stabilizes C3 convertase (inc. complement; dec. C3 levels)

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45
Q

Nephrotic or Nephritic: The following would be found on biopsy of what disorder?

  • -bands of capillary wall staining
  • -coarse granular and linear mesangial staining C3
  • No IgG
A

MPGN type 2

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46
Q

Nephrotic or Nephritic: Systemic Lupus erythematosis (SLE) is an autoimmune disease w/ generalized dysregulation and hyperactivity of B cells. It involves production of autoantibodies to nuclear and non-nuclear antigens, including DNA, RNA, nucleoproteins and phospholipids.

What is the MC complication of SLE?

A

Nephritis

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47
Q

Nephrotic and Nephritic: Diffuse proliferative glomerulonephritis (DPMN) is a type of glomerulonephritis associated with SLE.

What are its features?

A
  1. “Wire looping” on LM
  2. Subendothelial and Mesangial deposits
    - -IgG
    - -NO C3
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48
Q

Nephrotic and Nephritic: _______ is a type of hereditary hematuria that is associated with a mutation in type IV collagen (MC alpha COL4A5). This causes thinning of the glomerular basement membrane. It is most commonly X-linked dominant.

Patients present with gross hematuria, sensorineural hearing loss and eye abnormalities

A

Alport syndrome

  • -thin bm lesion
  • -familial
  • -no progression to renal failure

NOTE: mutation in alpha subunit (COL4A5 MC)

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49
Q

Nephrotic and Nephritic: A patient presents with nerve deafness, lens dislocation and posterior cataracts. He reports blood in his urine with no additional symptoms (asymptomatic hematuria).

Biopsy reveals “basketweave” thickening and thinning of bm

A

Alport syndrome

-Biopsy:
“basketweave” thickening and thinning of bm

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50
Q

Diuretics: These diuretics act by inhibiting NaCl in the DCT. They also increase Ca2+ reabsorption (dec. kidney stones).

They are considered the BEST anti-HTN diuretic.

A

Thiazides

  • hydrochlorothiazide
  • chlorthalidone
  • indipamide
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51
Q

Diuretics: What are the clinical uses for Thiazides?

A
  1. HTN
  2. Edema (heart failure)
  3. Nephrolithiasis (dec. urine Ca2+)
  4. Nephrogenic diabetes insidpidus (Inc. Na2+/water excretion)
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52
Q

Diuretics: These are the most efficacious diuretics. They act by inducing renal prostaglandins. They are also used to treat HTN, but have minimal chronic effects.

A

Loop diuretics

  • furosemide
  • Bumetanide
  • Ethacrynic acid (NOT sulfonamide)
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53
Q

Diuretics: When are Loop diuretics most often used?

A
  1. Edema
  2. HTN
  3. Hyperkalemia (to Inc. K+ excretion)
  4. Acute Renal failure (Inc. K+ excretion; Inc. Urinary flow)
  5. Anion overdose (dec. reabsorption of Br, Fl, I)
  6. Hypercalcemia
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54
Q

Diuretics: This class of diuretics increases Na excretion and decreases K+ secretion. They are often used for patients suffering from hypokalemia.

A

K+ sparing

  • Spironolactone (antagonist of aldosterone receptor)
  • Triamterene/Amiloride (inhibit Na flux at luminal membrane)
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55
Q

Diuretics: When are K+ sparing diuretics most often used?

A
  1. Hypokalemia
  2. Heart failure (spironolactone)
  3. Hyperaldosteronism (inhibit excess mineral corticoids due to 2o hyperaldosteronism)
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56
Q

Diuretics: These diuretics function to draw water into the plasma from interstitial and cellular sites. They are clinically used in acute renal failure and to reduce intracranial and intraocular pressure.

A

Osmotic diuretics

  1. Mannitol
    - -acute renal failure
    - -reduce intracranial pressure
  2. Glycerol
    - -reduce intraocular pressure
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57
Q

Diuretics: These drugs block sodium bicarbonate reabsorption, increasing diuresis.

A

Carbonic anhydrase inhibitors

  • -Acetazolamide
  • -Dorzolamide
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58
Q

Diuretics: Adverse effects of these drugs include:

  1. HypOkalemia
  2. Potentiate Loop diuretics
  3. NOT for normal pregnancy (use in HTN patients)
A

Thiazides

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59
Q

DIuretics: Adverse effects of these drugs include:

  1. Ototoxicity (high dose I.V.)
  2. Hearing impairment
  3. Increased blood cholesterol
  4. Uric acid (gout)
A

Loop diuretics

  1. Bumetanide
    - -hearing impairment
    - -Hypersensitivity rxns
  2. Ethacrynic acid
    - -most ototoxic
    - -good for patients with HSR to other drugs
  3. Furosemide
    - -inc. blood cholesterol
    - -gout
  4. Torsemide
    - -HSR
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60
Q

DIuretics: Adverse effects of these drugs include:

  1. Gynecomastia
  2. Kidney stones
A

K+ sparing

  1. Spironolactone
    - -Gynecomastia (tumorigenic)
  2. Triamterene
    - -kdiney stones
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61
Q

DIuretics: Adverse effects of these drugs include:

  1. nausea, vomiting, pulmonary congestion, edema
A

Osmotic diuretics

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62
Q

Nephrotic syndrome: Nephrotic syndrome occurs due to podocyte disruption that affects the glomerular filtration charge barrier.

It results in massive proteinuria >3.5 g/day. What are other findings of nephrotic syndrome?

A
  1. Hypoalbuminemia (<3 g/100ml)
  2. Hyperlipidemia
  3. Edema
  4. Frothy urine with fatty casts

NOTE: May be primary (direct podocyte sclerosis/damage) or secondary (secondary process that injures porodcytes; diabetes)

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63
Q

Nephrotic syndrome: What is an alternative to 24-hour urine collection with regard to testing for nephrotic syndrome?

A

Protein to creatinine ratio (random urine specimen)

  • correlates closely with daily protein
  • limit in patients whose daily Cr production varies from 1000mg
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64
Q

Nephrotic: What are common findings on urinalysis that can aid in diagnosis of nephrotic syndrome?

A
  1. Nephrotic sediment
    - -lipiduria
    - -fatty casts
    - -oval fat body
    - -Maltese cross (cholesterol)
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65
Q

Nephrotic: In nephrotic syndrome, plasma proteins are lost in the urine (leading to hypoalbuminemia). This is due to loss of _______ and dec _______.

A

Loss of oncotic pressure

Decreases GFR = Inc. Aldosterone

Ultimately: Inc. water and Na retention (edema)

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66
Q

Nephrotic:

  1. Nephrotic syndrome is often associated with a hypercoagulable state (e.g. thromboembolism) due to loss of ________ in the urine.
  2. It is also associated with increased infection due to loss of ____ in the urine and soft tissue compromise (edema).
A
  1. Loss of at-III

2. Loss of Igs

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67
Q

Nephrotic: The following are glomerular disease associated with nephrotic syndrome:

  1. Focal segmental glomerulosclerosis
  2. Minimal change disease
  3. Membranous glomerulopathy
  4. Amyloidosis
  5. Diabetic glomerulopathy

Which of the former are predominantly seen in kids? Which have good response to steroids?

A

Kids:

  • -minimal change disease
  • (good response)

Adults:

  • Focal segmental (African Americans)
  • Membranous (Caucasians)
  • Amyloidosis
  • Diabetic
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68
Q

Nephrotic: Focal segmental glomerulosclerosis is a common cause of nephrotic syndrome in African American adults.

It has an overall poor prognosis due to progression to chronic renal failure. What are common clinical findings?

A

*vary based on patterns of injury

  1. Asymptomatic proteinuria (insidious onset)
    - -progress to nephrotic syndrome
  2. HTN
  3. Progressive decline in renal function
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69
Q

Nephrotic: What is the prognosis for Focal segmental glomerulosclerosis?

A
  • poor prognosis (due to progressive decline in renal function)
  • end stage renal disease
  • recur in transplanted kidneys

NOTE: HIV and collapsing FSGS = worst

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70
Q

Nephrotic: Focal segmental glomerlosclerosis tends to have variable to poor response to corticosteroid therapy.

ACEs and ARBs may be used for certain patients. Who would benefit from this treatment?

A

Patients w/ FSGS due to Obesity or reduced renal mass

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71
Q

Nephrotic: You receive the following lab and biopsy report for a patient you suspect has nephrotic syndrome:

  1. Microscopic hematuria
  2. Segmental sclerosis and adjacent adhesion
  3. IF w/ IgM and C3 in sclerotic segments
  4. Collapsing glomeruli (HIV nephropathy; Heroin)

Based on your findings, what type of nephrotic syndrome do you suspect this patient has?

A

focal segmental glomerulosclerosis

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72
Q

Nephrotic: The most common cause of nephrotic syndrome in children. It is often idiopathic, but may be triggered by recent infection, immunization or immune stimulus.

It is characterized by:

  1. normal appearing glomeruli (maybe lipids in PCT cells)
  2. Negative IF
    (no immune deposits)
  3. Effacement of foot processes on EM
A

Minimal change disease

-puffy, weight gain, ill-feeling, frothy urine

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73
Q

Nephrotic: Minimal change disease is believed to be immune-related due to its tendency for remission after treating with corticosteroids.

What is believed to cause the heavy proteinuria?

A
  • loss of polyanionic sites on GBM and podocytes (lose normal charge of GBM)
  • anionic proteins (albumin) easily pass through capillary walls

NOTE: Selective proteinuria (albumin > globulins)

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74
Q

Nephrotic: A patient diagnosed with minimal change glomerulopathy develops azotemia.

What does this mean?

A

Incorrect diagnosis

–FSGS or drug complication (induced interstitial nephritis)

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75
Q

Nephrotic: Membranous glomerulopathy is the most common cause of nephrotic syndrome in Caucasian adults. It has poor corticosteroid response, but is less likely than FSGS to progress to chronic renal failure.

It is most often idiopathic, but it can also be associated with what disorders?

A
  1. Primary Disease:
    - -Ab to phospholipase A2 receptor
  2. Secondary:
    - -NSAIDS, penicillamine
    - -HBV, HCV
    - -Systemic Lupus
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76
Q

Nephrotic: A patient’s renal biopsy reveals the following:

  1. LM: diffuse capillary and GBM thickening
  2. IF: granular
    - -immune complex/C3 deposits
  3. EM:
    - -spike and dome appearance w/ subendothelial deposits
    - -foot process effacement

What is the expected prognosis for this patient?

A

Membranous glomerulopathy

–tends to have variable clinical response. Some patients show spontaneous remission, while others may have persistent proteinuria or progress to end-stage renal disease.

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77
Q

Nephrotic: A patient presents with the following:

  1. Proteinuria >6g/day
  2. Extensive glomerular sclerosis
  3. Chronic tubulointerstitial disease

You suspect nephrotic syndrome. What type correlates best with the above findings?

A

Membranous glomerulopathy

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78
Q

Nephrotic: Membranous glomerulopathy is a highly variable disease with a poor prognosis (except in children, who have higher rate of permanent remission).

Some patients may receive treatment. How is it treated?

A
  1. Corticosteroids
    - -variable response
  2. Corticosteroids and/or immunosuppressive drugs
    - -patients with progressive renal failure
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79
Q

Nephrotic: ______ is associated with chronic diseases (myeloma, RA) but most commonly involves the kidney with systemic disease.

It is detecte via biopsy. Biopsy with apple-green birefringence with polarized Congo red would reveal deposits within the mesangium.

A

Amyloidosis

  • abnormal protein folding
  • amyloid deposits
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80
Q

Nephrotic: The number one cause of chronic kidney failure in the U.S.

Presentation includes:

  1. glomerulonephritis
  2. proteinuria
  3. dec. GFR
  4. HTN
A

Diabetic glomerulonephropathy

81
Q

Nephrotic: Early, mild diabetic glomerulosclerosis typically presents with low levels of asymptomatic albuminuria (microalbuminuria). However, as the disease progresses, proteinuria becomes more severe and reach the nephrotic range.

What is the best test to detect renal damage from diabetes?

A

Random urine albumin (microalbumin)

ALternative: urine albumin creatinine ratio (urine ACR)

NOTE: baseline CMP, BMP

82
Q

Nephrotic: Diabetes mellitus patients with glomerulosclerosis also present with diabetic vasculopathy of the small vessels.

What is the cause of this?

A

non-enzymatic glycosylation of the CBM in the microvasculature

  • high circulating glucose (abnormal metabolic state)
  • thickening of basement membrane
83
Q

Nephrotic: What are other clinical/lab findings associated with diabetic glomerulonephropathy?

a. Inc. oxidative injury
b. Excessive matrix production – podocyte injury
c. Mesangial expansion
d. GBM thickening

A

All of the above

–Increased permeability

84
Q

Nephrotic: How does GFR differ in early diabetes compared to late stage?

A

GFR increased in early stage (dec. in late)

  • glomerular hypertrophy
  • inc. renal size

NOTE: intraglom. HTN and glomerular hypetrophy may contribute to dev. of diabetic nephropathy

85
Q

Nephrotic: True/False - Hyperfiltration is a significant contributing factor to diabetic glomerulosclerosis?

A

True

-leads to intraglomerular HTN and glomerular scarring

86
Q

Nephrotic: You are asked to analyze a biopsy of a patient’s kidney.

You note:

  1. GBM thickening
  2. Inc. mesangial matrix (EM)
  3. Kimmelstiel-Wilson nodules (well-defined)
  4. Sclerosis

What do you suspect?

A

Diabetic glomerulosclerosis (glomerulonephropathy)

*Kimmelsteil-Wilson nodules “Christmas balls”

87
Q

Nephrotic: Nearly all forms of acute glomerulonephritis or other glomerular disease can progress to chronic glomerulonephritis.

It presents with renal failure, uremia, and eventual death w/out intervention.

What is a characteristic of chronic glomerulonephritis?

A

Glomerular and tubulointerstitial fibrosis

  • dec. GFR
  • -uremia (retain uremic toxin)

Net result: CKD

88
Q

Electrolytes: TBW is managed by

  1. Physical factors
  2. Humoral factors

Give examples of each

A
  1. Physical
    - -peritubular hydrostatic pressure
    - -oncotic pressure
    - -effective osmolarity
  2. Humoral
    - -aldosterone, Ang II (thirst), ADH
    - -catechols, prostaglandins
89
Q

Electrolytes: Sodium is the major extracellular cation. Plasma sodium is a good reflection of intravascular volume status.

What is the main source of energy for Na2+ reabsorption at all nephron segments?

A

Na/K+ ATPase

  • basolateral
  • 3 Na out; 2 K in

NOTE: low intracell. Na conc. and negative cellular potential = inc. passive diffusion of Na into the cell through the luminal membrane

90
Q

Electrolytes: Na2+ reabsorption in the proximal tubule is accompanies by secretion of what?

A

H+

–Na/H exchanger (NHE3)

91
Q

Electrolytes: In the Thick ascending limb, Na2+ entry occurs along with entry of what ions?

A

NKCC

–K, 2Cl

92
Q

Electrolytes: Describe Na2+ transport in the DCT and CCD

A
  1. DCT
    –Na in with Cl-
    (NCCT)
  2. CCD
    –Na2+ in via channel
    (ENaC)
93
Q

Electrolytes: Isotonic fluids include normal saline and whole blood.

True/False: The majority of isotonic fluid should remain in the intravascular space so long as there are not anatomic or physiologic abnormalities.

A

True

94
Q

Electrolytes: What two compounds are the main determinants of osmotic gradients?

A

Na and glucose

*both extracellular

NOTE: Total Body sodium is responsible for clinical signs of volume depletion

95
Q

Electrolytes: Water shifts between the ECF and ICF compartments by osmosis. Thus, there must be an osmotic gradient between the compartments for water to move from a point of low solute concentration to high solute concentration.

Explain which way water will shift in a hyponatremic state. What about a hypernatremic state?

A
  1. Hypernatremic state (or hyperglycemia)
    - -water moves from ICF to ECF
    (a. k.a. hyperosmolar ECF)
  2. Hyponatremic
    –water moves from ECF into ICF
    (high volume in ECF)
96
Q

Electrolytes: Third space fluid loss describes abnormal accumulation of fluid into interstitial space, body cavities or even joints. It may occur from burns, edema and surgery.

Why are labs unreliable following surgery?

A

–2/3 of administered IV fluid moves out of the intravascular space into the soft tissues

–resolves over time (fluid returns to intravascular space)

–electrolyte deficits tend to follow this process unpredictably

97
Q

Obstruction: ______ describes obstruction of urinary flow at ANY level of the urinary tract.

It may be acute or chronic; partial or complete; unilateral or bilateral

A

Obstructive uropathy

–if uncorrected, predisoposal to UTI, urosepsis, chronic renal failure

98
Q

Obstruction: Distension of the renal calyces and pelvis with urine due to obstruction of urinary flow.

Full recovery is expected if it is corrected in the acute phase. If prolonged, pressure atrophy will occur.

A

Hydronephrosis

99
Q

Obstruction: Hydronephrosis in children is usually due to a congenital abnormality:

  1. _______: due to narrowed/kinked ureter at connection with the kidney.
  2. ______: abnormal insertion of the ureter into the bladder
  3. _______: reflux of urine from the bladder back into the ureter
  4. ______: small flaps of tissue within the post. urethra can obstruct flow
A
  1. Ureteropelvic junction obstruction
  2. Ureterovesical junction obstruction
  3. Vesico-ureteral reflux
  4. Urethral valves
100
Q

Obstruction: The most common cause of hydronephrosis in kids is ureteropelvic junctional obstruction. It is due to narrowing of the junction b/t the ureter and the kidney.

This most often occurs from _________

A

Stenosis of the Proximal ureter

–abnormal layer of SM cells or fibrous tissue (replace SM cels)

–sometimes due to abberrant or accessory artery (extrinsic compression)

101
Q

Obstruction: Adults may have strictures with similar effects to hydronephrosis of ureteropelvic jxnal obstruction. However, it is most often caused by

A

-previous surgery (scarring) or inflammatory process (endometriosis, neoplasm)

(extrinsic compression in adults)

102
Q

Obstructing: Urethral valves are membranous folds within the lumen of the posterior urethra that can cause obstructon.

Obstruction is often accompanied by:

  • hydronephrosis
  • diminished urine stream
  • UTI
  • renal failure

Obstruction via posterior urethral valves is most common seen in what patients?

A

Male newborns

103
Q

Obstruction: Hydronephrosis in adults is usually acquired.

Which of the following could contribute to adult hydronephrosis?

a. renal calculi
b. E. coli infection
c. prostatic hypertrophy/carcinoma
d. urethral stricture (post injury)

A

Answer: A, C, D

  • renal calculi
  • prostatic hypertrophy/cancer
  • urethral stricture
  • retroperitoneal/pelvic tumors (cervical/lymphoma)
104
Q

Obstruction: On gross, hydronephrosis appears with dilated anatomy upstream to the obstruction.

This obstruction can occur anywhere from the renal pelvis to the urethral meatus.

What are other gross features? How is it best treated?

A

Gross:

  • dilated anatomy
  • azotemia
  • loss of renal parenchyma
  • thin rim of renal cortex

Treatment: Relieve obstruction

105
Q

Obstruction: True/False - Patients with hydronephrosis are at increased risk of tubular dysfunction and renal insufficiency.

As damage progresses and the kidney becomes non-functional, these patients may become pre-disposed to ongoing urinary tract infections.

A

True

*due to urine stasis

106
Q

Obstruction: The common clinical features associated with hydronephrosis are Pain and Azotemia.

What are the causes for these clinical presentations?

A
  1. Pain
    - -inc. hydrostatic pressure
    - -distension of collecting system (renal capsule)
  2. Flank pain
    –only w/ micturition
    (vesiculoureteral reflux)
  3. Azotemia (post-renal)
    - -inc. BUN;Cr
    - -suggests bilateral obstruction (or unilat. if 1 functioning kidney)
    - -oliguria or anuria
107
Q

Obstruction: What are the most common causes for obstructions occurring ABOVE the bladder?

a. calculus
b. tumor (e.g. urothelial carcinoma)
c. blood clots
d. sloughed papillae

A

Answer: All of the above

Note: sloughed papillae = renal papillary necrosis (bilateral due to predisposing systemic factors)

108
Q

Obstruction: Obstructive lesions in the ureter most often cause ________ compression.

Common causes of ureteral compression include:

  1. Peri-ureteral inflammation/fibrosis (endometriosis)
  2. Pregnancy (enlarging uterus)
  3. Tumor compression of ureter (cervical cancer; rectal, prostate)
A

Extrinsic compression

109
Q

Obstruction: Bladder obstruction may occur from:

  1. Calculi
  2. Tumors (obstruct ureter entrance)
  3. Functional (neurogenic)

The bladder can malfunction due to a neurologic disorder. What are examples?

A
  1. Brain
    - -stroke, tumors
  2. Spinal cord injury
    - -car accident
    - -myelomeningocele
  3. Peripheral nerve injury
110
Q

Obstruction: Prostatic enlargement can lead to urethral compression.

What are common etiologies?

A
  1. Nodular hyperplasia (benign prostatic hyperplasia)
  2. Carcinoma
  3. Inflammation
111
Q

Obstruction: Obstruction of the urethra may be due to the presence of strictures or due to urethral neoplasms (rare).

What are common causes of urethral strictures?

A
  1. Inflammation
    - -gonoccocal urethritis
    - -trauma

–scar tissue that reduces the caliber of the urethral lumen

112
Q

Obstruction: Urolithiasis (kidney stones) is the most common cause of urinary tract obstruction in adults. It has the highest incidence in middle-aged caucasian men. Prevalence tends to increase with age.

What are causes of urolithiasis?

A

Environmental and occupational

  • -lack of access to water
  • -hot environment (southeast U.S.)
113
Q

Obstruction: Urolithiasis is associated with increased Calcium absorption and delivery to the kidney, with subsequent increase in its urinary excretion.

What is a major risk factor for stone formation?

A

Dehydration

–dec. urine volume

–mechanism: supersaturation (inc. urine conc. of stones constituents)

114
Q

Obstruction: Calcium oxalate is the most common type of crystal involved in urolithiasis.

What are risk factors associated with calcium oxalate-type stones?

A
  • -high urine Ca2+
  • -high urine oxalate
  • -low urine citrate
  • -pH = no effect

**envelope or dumbbell shape

115
Q

Obstruction: Calcium phosphate is another type of crystal involved in urolithiasis.

What are risk factors associated with calcium phosphate?

A
  • -inc. urine calcium
  • -inc. urine PO4
  • -dec. urine citrate
  • -high pH > 6.5
116
Q

Obstruction: Kidney stones formed from uric acid occur as a result of what kind of diet?

A

High meat diet

  • -higher uric acid excretion
  • -low urine pH

NOTE: Radiolucent, rhomboid or rosette

117
Q

Obstruction: _______ crystals are typically due to a genetic defect with decreases reabsorption of cystine in the kidney.

A

Cystine crystals

  • -cystinuria
  • -low urine pH (less soluble)

NOTE: hexagonal shaped

118
Q

Obstruction: Struvite crystals are commonly seen in patients suffering from

A

UTI

–urease + bacteria (proteus, klebsiella)

NOTE: staghorn calculi (deer antlers)

119
Q

Obstruction: Calcium oxalate stones arise from

  1. Icreased GI absorption of calcium and increased bone turnover (inc. PTH).
  2. Oxalate
  3. Low urine citrate excretion

What causes increased urine oxalate?

A
  1. Dietary
    - -spinach (MC)
  2. Vitamin C metabolism
  3. leum (Crohn disease) –fat binds Ca2+ and stops it binding oxalate
    - -inc. free oxalate
  4. Primary hyperoxaluria
    - -AR
    - -inc. oxalate from liver
120
Q

Obstruction: Calcium oxalate stones arise from

  1. Increased GI absorption of calcium and increased bone turnover (inc. PTH).
  2. Oxalate
  3. dec. urine citrate excretion

Normally, urinary citrate complexes with calicum, and inhibits stone formation. What causes dec. urine citrate excretion?

A

Metabolic acidosis – decreases citrate excretion by inc. reabsorption

121
Q

Obstruction: Uric acid stones are formed by increased urinary excretion of uric acid.

Uric acid is associated with increased cell turnover or cell lysis (purine catabolism).

What are etiologies for inc. uric acid stones?

A
  1. Lesch Nyhan (HGPRT deficiency)
  2. Diet rich in purines
    - -fish, red meat, Arby’s
  3. Inc. tissue breakdown –tumor lysis syndrome
  4. Low urine pH
    - -non-ionized uric acid (less soluble)
122
Q

Obstruction: Struvite stones are formed by urease producing bacteria via their conversion of urea to _______ producing alkaline urine and subsequently causing formation of struvites.

A

NH3

  • -staghorn calculi
  • -pH >7.2

–rapid growth, recur

123
Q

Obstruction: A 34 year old male presents complaining of severe flank pain on his right side (unilateral). He complains of pain radiating to his upper thigh. He states he has had nausea, vomiting, and is peeing blood. He claims he cannot find a comfortable position to sit or sleep.

What is your suspicion? How do you diagnose?

A

Urolithiasis

–pain may radiate anteriorly (if stone is in upper part of ureter) OR in ipsilateral groin (if stone in lower ureter)

“renal colic” - waves of sharp, intense pain

Diagnosis:

  1. Helical CT w/out contrast
    - -high sensitivity
  2. Strain urine (collect stone)
    - -Tx depends on stone
124
Q

Obstruction: The most effective method for prevention of ALL types of kidney stones is urine dilution (2L/day).

Other methods for prevention include alkalinization. What stones would alkalinization work for and how?

A

Uric acid or Cystein stones

Methods:
–inc. food rich in alkali (fruits)

–dec. acid (animal protein)

–K+ citrate = metabolized to HCO3- in liver

125
Q

Obstruction: Prevention of the development of calcium oxalate stones involves:

  1. Dec. Calcium excretion
  2. Dec. oxalate excretion
  3. Inc. urine citrate

Describe how these can be accomplished

A
  1. Dec. Calcium excretion
    - -Thiazide diuretic (reabsorbs calcium)
    - -restrict dietary sodium (enhances calcium out)
  2. Dec. oxalate
    - -avoid Vit. C supplements
    - -dec. spinach, rubarb, potatoes
  3. Increase urine citrate
    - -inhibits calcium stones
    - -eat fruits (alkaline)
126
Q

Obstruction: Prevention of the development of uric acid stones includes

  1. reduce consumption of purine-containing foods
  2. Alkalinize urine
  3. Xanthine oxidase inhibitors (allopurinol, febuxostat)

What is the purpose of the xanthine oxidase inhibitors?

A

decrease formation of uric acid

127
Q

Obstruction: How can you prevent

  1. Struvite stones
  2. Cysteine stones
A
  1. Struvite
    - -prevent UTI
  2. Cysteine
    - -alkalinize (K+ citrate)
128
Q

Obstruction: Kidney stones <4mm are likely to pass spontaneously.

Larger stones require intervention. What are treatments for urolithiasis?

A
  1. Hydration
  2. Analgesics
    - -opiates, NSAIDS (ketorolac IV)
  3. Pain management
  4. Surgery
    - ureteral stent
    - percutaneous nephrostomy
    - extracorporeal shock
    - open surgical resection
129
Q

Electrolytes: There are three possible mechanisms for the development of hyponatremia:

  1. Hypertonic loss
  2. Gain of plain water or free water
  3. Hypotonic gain

Give examples of each.

A
  1. Hypertonic loss (loss of electrolytes)
    - -diuretics, 21 OH deficiency, Addison’s

*volume depletion

  1. Gain of free water
    - -SIADH, inc. drinking
  2. Hypotonic gain
    - -RHF, cirrhosis, intake of hypotonic salt, nephrotic syndrome (lose albumin)

*volume excess (Starling forces)

130
Q

Electrolytes: What are possible methods for treating hyponatremia?

A
  • isotonic fluids (I.V)
  • hypertonic saline (rapid correction)

NOTE: Caution with hypertonic saline, can lead to central pontine myelinosis

131
Q

Electrolytes: Rapid correction with hypertonic saline should be performed with caution due to risk of fluid shifts.

This can lead to Central pontine myelinolysis (especially in at-risk patients including malnutrition, liver disease, and chronic alcoholics).

What happens in central pontine myelinolysis?

A

Focal demyelination of central basis pontis

Sx:

  • -Confusion, delirium, hallucinations, tremor, balance issues, problems swallowing, slurred speech
  • -Weakness in the face, arms, or legs, usually affecting both sides of the body.

NOTE: Neurological disorder that most frequently occurs after too rapid medical correction of sodium deficiency (hyponatremia). The rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells.

132
Q

Electrolytes: SIADH is a syndrome of increased ADH leading to increased retention of water. This creates a dilute state in the body with Hyponatremia (<120 mEq), hyperconcentrated urine, and the inability to excrete water. In addition, cerebral edema may develop leading to neurologic dysfunction.

What are potential causes for SIADH?

A
  1. Pulmonary dysfunction
    - -TB
  2. Ectopic ADH
    * *small cell carcinoma (salt and pepper chromatin)
  3. Drugs (inc. ADH type)
  4. CNS (infections, trauma)
  5. Drugs (haloperidol, SSRI, anti-depressants)
133
Q

Electrolytes: Addison disease is due to autoimmune destruction of the renal cortex.

It is marked by hypertonic loss of sodium, leading to hyponatremia.

What are findings of Addison (with regard to electrolyte balance)?

A
  1. Hyponatremia
  2. Hyperkalemia
  3. Metabolic acidosis (normal anion gap)
134
Q

Electrolytes: Potassium is secreted, reabsorbed and excreted.

List the sites of reabsorption and secretion. List the mechanisms by which K+ is reabsorbed/secreted at each site.

A
  1. Proximal tubule
    - -paracellular (solvent drag)
  2. TAL
    - -paracellular (K+ gradient)
  3. CCD
    a. reabsorption: H+/K+ anti-porter (alpha cells)
    b. secretion: K+ channels apical (principle cells)
  4. IMCD
    a. reabsorption:
  5. Na/K+ ATPase
135
Q

Electrolytes: Hyperkalemia occurs when serum K+ >5.5 mEq.

Clinically causes include:

  1. RBC hemolysis
  2. Acidosis
  3. Renal failure
  4. Spironolactone (K+ sparing)

Hyperkalemia can affect muscle, leading to absent deep tendon reflexes and also have major effects on the heart, producing ventricular dysrhythmia. What is a sign of hyperkalemia on an ECG?

A

Peaked T-waves (inc. repolarization)

  • -high hyperkalemia (7-8 mEq)
  • -inc. Creatinine
136
Q

Electrolytes: Hypokalemia occurs when serum K+ <3.5

Common causes include:

  1. Thiazide/Loop diuretics
  2. Mannitol
  3. Diarrhea
  4. Alkalosis
  5. Primary aldosteronism

What are clinical findings of hypokalemia?

A
  1. Muscle weakness (changed membrane potential)
  2. Fatigue
  3. Polyuria (severe hypokalemia; Nephrogenic DI)
    - -refractory to ADH
  4. Rhabdomyolisis
    –muscle rupture due to dec. ATP
    (hypokalemia inhibits insulin = dec. glycogenesis)
  5. U-waves on ECG (V2)
137
Q

Electrolytes: Hypertonic plasma may be caused by

  1. Hypernatremia/Hyperglycemia (glucose, vomiting, diarrhea)
  2. ICF contraction (diabetes insidpidus, bleeding)
  3. ECF expansion (antibiotics, inc. sodium bicarbonate)

Vomiting leads to hypernatremia due to loss of ______. It does not get reabsorbed into the duodenum, leading to decreased acid and increased HCO3-.

A

Loss of gastric acid (HCl)

(also loss of Na and K+)

Clinical:

  • hypovolemia
  • metabolic alkalosis
  • hypokalemia
  • dilutional hyponatremia
138
Q

Electrolytes: Diabetes insipidus presents in patients who have a lack of ADH effects. There are two main types:

  1. ________: Kidneys don’t produce ADH due to posterior pituitray defect.
  2. ________: Kidneys do not respont to ADH
A
  1. Central
  2. Nephrogenic
    - -typically associated with Lithium (inc. insensitivity)
139
Q

Electrolytes: Secretory diarrhea is a self-limiting type of diarrhea that results in isotonic loss of fluid.

It is most often due to infection (viral, bacterial) with endogenous mechanisms inducing diarrhea. Examples of this include Cholera and E.coli and tumors. Describe the mechanisms by which these cause isotonic fluid loss.

A

Isotonic loss: ECF changes (only) with gains/losses of Na and H2O

E.coli and Cholera toxin:
—Increased excretion of Na, K+ and HCO3- followed by large amounts of water (isoosmotic)

Tumors:
–Secrete VIP which increase the secretion of ions followed by water

140
Q

Electrolytes: Exogenous osmotic diarrhea results from poor absorption of carbohydrates (lactose, sorbitol) or from high dose sodium phosphate (Na citrate laxatives).

What happens to the electrolyte balance in this type of diarrhea?

A
  • hypotonic loss (electrolyte poor)

- hypernatremia may be seen if poor responst to thirst

141
Q

Electrolytes: A loss of large volumes of water and electrolytes (diarrhea) can result in volume depletion.

Typically, it presents as normo-natremic. However, in certain cases, it may present as hyponatremia. What can lead to hyponatremia?

A

Ingestion of excessive quantities of water following diarrhea

—dilutes plasma Na2+

142
Q

Electrolytes: Diarrhea nromally induces metabolic acidosis due to increased secretion of HCO3-.

It may lead to a normal anion gap or high anion gap.

Describe the situations that would lead to the latter and the former.

A
  1. Normal anion gap
    - -hyperchloremic
    - -loss of large volumes
  2. High anion gap
    –lactic acidosis
    (hypovolemic shock; severe volume depletion)
143
Q

Electrolytes: Two common causes of hyperchloremic (normal anion gap) metabolic acidosis and hypokalemia are diarrhea and proximal or distal tubule renal tubular acidosis (RTA).

True/False - While diarrhea leads to increased K+ loss in the stool, renal tubular acidosis causes K+ loss from the kidneys.

A

True

144
Q

Electrolytes: Renal tubular acidosis is typically associated with a normal anion gap [(hyperchloremic) metabolic acidosis] that is due to a defect in either renal
excretion of acid (H⁺), reabsorption of bicarbonate (HCO₃⁻) or both.

There are 3 main types of renal tubular acidosis:

  1. type 1 (classic distal renal tubular acidosis)
  2. type 2 (proximal renal tubular acidosis)
  3. type 4 (hyperkalemic distal renal tubular acidosis)

What is seen in type 1?

A
  • Impaired renal excretion of acid in distal tubule

- hypokalemia

145
Q

Electrolytes: Renal tubular acidosis is typically associated with a normal anion gap [(hyperchloremic) metabolic acidosis] that is due to a defect in either renal
excretion of acid (H⁺), reabsorption of bicarbonate (HCO₃⁻) or both.

There are 3 main types of renal tubular acidosis:

  1. type 1 (classic distal renal tubular acidosis)
  2. type 2 (proximal renal tubular acidosis)
  3. type 4 (hyperkalemic distal renal tubular acidosis)

What is seen in type 2?

A
  • Impaired HCO3- reabsorption in proximal tubule
  • hypokalemia

**MC in kids w/ Fanconi syndrome

146
Q

Electrolytes: Renal tubular acidosis is typically associated with a normal anion gap [(hyperchloremic) metabolic acidosis] that is due to a defect in either renal
excretion of acid (H⁺), reabsorption of bicarbonate (HCO₃⁻) or both.

There are 3 main types of renal tubular acidosis:

  1. type 1 (classic distal renal tubular acidosis)
  2. type 2 (proximal renal tubular acidosis)
  3. type 4 (hyperkalemic distal renal tubular acidosis)

What is seen in type 4?

A

–impaired transport of distal tubule = impaired transport of electrolytes (Na, Cl, K)

–Hyperkalemia

Causes:
—hypoaldosteronism or inadequate renal response to aldosterone

147
Q

Vascular Disorders: Disorders associated with ANCA related vasculitis include

  1. Granulomatosis with polyangiitis
    (necrotizing granulomatous inflammation)
  2. Upper and lower respiratory tract (large cavitary lesions; saddle nose)
  3. Churg-Strauss syndrome
    (eosinophilia and asthma)
  4. Microscopic polyangiitis
    (no asthma or granulomatous inflammation)

What is a common histological feature of these disorders?

A

Fibrinoid necrosis

148
Q

Vascular: Nephrosclerosis, hardening of the walls of the smalle arteris and arterioles, (e.g. benign nephrosclerosis) may occur as a result of aging or HTN.
It typically affects both kidneys (bilateral).

What are histologic features of nephrosclerosis?

A
  1. Medial thickening of the small arteries
  2. Progressive luminal narowing
  3. Hyaline arteriosclerosis
  4. Interstitial fibrosis
  5. Tubular atrophy and cast formation
  6. Glomerulosclerosis
  7. Collagen deposition in Bowman’s space
149
Q

Vascular: Patients with benign HTN can develop progressive renal failure which may lead to end stage renal disease.

In what population is it more common to see more aggressive “benign” nephrosclerosis? What are common lab findings indicating this?

A

African Americans

*MC cause of end stage renal disease

Labs:

  • mild proteinuria
  • hematuria
  • azotemia (elevate BUN)
150
Q

Vascular: Which of the following is a common gross findings of Nephrosclerosis?

a. renal cell hyperplasia
b. fine, granular cortical sufaces
c. coarse scars
d. thinned cortex (cut section)

A

B-D

  1. atrophic kidney (smaller size)
  2. fine, granular cortical surfaces
  3. coarse scars
  4. thinned cortex in cut section
151
Q

Vascular: _______ is a form of arteriosclerosis characterized by hardening of the arterioles and loss of SM cells.

It is typically seen in the kidneys and the brain and often accompanies nephrosclerosis.

A

Hyaline arteriolosclerosis

–progressive loss of nephrons – renal atrophy

Seen in:

  • elderly (normotensive)
  • diabetes mellitus
  • HTN
152
Q

Vascular: _____ is the most insignificant form of arteriolosclerosis because it does not lead to arterial lumen narrowing.

It is most often seen in older patients and has no clinical consequence

A

Medial calcific sclerosis

(Monckeberg)

*MC sites: calcified muscular arteries in pelvis, neck, breast

153
Q

Vascular: _______ (accelerated HTN) is uncommon, but when present can cause significant kidney damage.

It may complicate HUS, TTP, or scleroderma, and may also be seen in > 130 diastolic.

A

Malignant HTN

–medical emergency

Histologic:

  • -fibrinoid necrosis
  • -hyaline arteriolosclerosis
154
Q

Vascular: What are common clinical issues associated with malignant HTN?

A
  • papilledema
  • -retinopathy
  • -encephalopathy (HTN)
155
Q

Vascular: Malignant HTN is proposed to occur from high blood pressure + microvascular constriction. This leads to endothelial injury as blood hits the narrowed vessels.

Plasma components may also leak into the injured arteriolar walls causing ___1___, into the intima leading to __2___, OR into the subendothelial zone of glomerular capillaries.

A
  1. Fibrinoid necrosis
    - -injury + platelets
  2. Edematous intimal thickening
  3. Subendothelial zone - consolidating glomeruli
    * Thrombosis also occurs
156
Q

Vascular: An uncommon (secondary) cause of HTN that is due to any cause of decreased blood flow to the kidney.

It is often associated with inc. renin synthesis from the ischemic kidney (JG cells; hyper-renemic)

A

Renal artery stenosis

  • MC due to atheromatous plaque
  • associated w/ HTN unresponsive to meds
  • curable if lumen is restored (surgery)
157
Q

Vascular: A 48 year old female presents to the clinic complaining her hypertension meds no longer help. On PE you note:

  1. systolic and diastolic bruit present (upper quadrant supine and costovertebral angle sitting)
  2. elevated plasma or renal vein renin
  3. Inc. Ang II and aldosterone

Based on these findings, what do you suspect? What are common causes?

A

Renal artery stenosis

  • MC atherosclerosis
  • 2nd MC fibromuscular dysplasia

NOTE: May be responsive to ACE inhibitor or ARBs

158
Q

Vascular: In renal artery stenosis, there are 3 possible types of lesions that may be seen:

  1. Medial fibroplasia
  2. Perimedial hyperplasia (outer media)
  3. Medial hyperplasia

Which of these is the most common? How is it ID’d?

A

Medial fibroplasia

-aneurysms w/ alternating areas of stenosis and dilation
string of beads

159
Q

Vascular: A 64 year old male presents to the clinic complaining of nausea and vomiting. He states he has seen blood in his urine. He also states he has had flank pain for the past 2 days.

Labs reveal proteinuria > 3.5g.

Past medical history includes diagnosis of renal cell carcinoma.

What do you suspect?

A

Renal vein thrombosis

  • associated with renal cell carcinoma and nephrotic syndrome
  • proteinuria (nephrotic) main sign
160
Q

Vascular: True/False - Atherosclerosis can damage the kidney via diminished blood flow or CO.

For example, atheromatous debris may embolize into intra-renal arteries and glomerular capillaries leading to acute renal failure.

A

True

  • risk during angiographic procedures
  • debris can elicit foreign body rxn = inc. fibrosis
161
Q

Vascular: Renal infarcts are often caused by obstruction of the ______ or ______ due to embolus.

It presents with sudden onset of flank pain and hematuria, though, small infarcts may be asymptomatic.

A

obstruct interlobar or arcuate arteries

Sources:

  • -mural thrombi (MI, a-fib)
  • -infected valves (bacterial endocarditis)

–complicated atherosclerotic plaques in the aorta

162
Q

Vascular: Renal infarcts can feature coagulative necrosis with what type of inflammatory cells?

A

Eosinophils

  • -loss of nuclei
  • -inflammatory infiltrat
163
Q

Vascular: ______ are diverse insults that lead to excessive activation of platelets.

On peripheral smear:

  • -thrombocytopenia (due to inc. clots)
  • -schistocytes (hemolytic anemia)

On Microscope:

  • microvascular occlusion
  • platelet-fibrin thrombi
A

Thrombotic microangiopathy

–(-) Coomb

–HUS, TTP
(microangiopathic hemolytic anemia)

164
Q

Vascular: Thrombotic microangiopathies are caused either by HUS or TTP.

____ is caused by endothelial damage due to invasion of plasma constituents into arterial intima, walls, and the subendothelial zone of glomerular capillaries.

A

HUS

–narrowing vessels = ischemia

–thrombosis (focal ischemic necrosis)

165
Q

Vascular: Thrombotic microangiopathies are caused either by HUS or TTP.

_____ is due to a genetic/acquired deficiency of a metalloprotease that normally cleaves vWF multimers on endothelial cells.

Lack of this protease leads to uncleaved multimers, increased platelet aggregation and microvascular thrombosis.

A

TTP (ADAMST13)

166
Q

Vascular: What are common causes of HUS?

A

Typical: E. Coli (O157:H7; Shiga)

Atypical: mutated complement regulatory proteins

167
Q

Vascular: Symptoms of TTP include:

  1. Fever
  2. Neurologic symptoms
  3. Microangiopathic hemolytic anemia
  4. Thrombocytopenia
  5. Renal failure

If untreated, TTP has a high mortality. However, it is markedly reduced with treatment. How is it treated?

A

plasma exchange (plasmapheresis).

168
Q

Vascular: Renal pathology of TTP/HUS is similar to that of malignant hypertensive nephropathy in that is has what histologic features?

a. fibrinoid necrosis
b. edematous intimal expansion (arterial)
c. glomerular consolidation, necrosis or congestion
d. vascular platelet-rich thrombi in glomeruli

A

All of the above

169
Q

Vascular: Nephropathy is the MC solid organ manifestation of sickle cell disease.

Low oxygen tension will be seen in the medulla due to sickling of RBC’s and subsequent occlusion of the ______ lumen.

A

Vasa recta occlusion

170
Q

Vascular: Due to occlusion of the vasa recta lumen, sickle cell nephropathy can present with the following pathologic findings:

  • infarcts (medulla; papilla)
  • papillary necrosis
  • ischemic scarring (medulla)
  • focal tubular loss
  • atrophy
  • glomerular congesion

What are lab findings of Sickle cell nephropathy?

A
  1. Hematuria (trait and disease)
  2. Proteinuria
  3. Loss of urine conc. ability
    - -1.010 SG
  4. Pyelonephritis
  5. FSGS or MPGN - nephrotic syndrome
171
Q

Vascular: Cortical necrosis is widespread injury resulting in anuria.

It can complicate hypovolemic or endotoxic shock. It may be seen with acute renal artery obstruction.

What is a classic example of a situation with diffuse cortical necrosis?

A

-placental abruption

(separates from decidual layer of endometrium)

Gross:
–diffuse pale yellow necrosis in cortex

NOTE: may also be seen in septic shock or extensive surgery

172
Q

Tubular/Interstitial: Acute tubular injury is associated with acute renal failure +/- evidence of necrosis of _______ (inflammation, ischemia)

A

tubular epithelial cells

173
Q

Tubular/Interstitial: Acute renal failure is associated with acute rise in serum creatinine and BUN.

It is classified as

  1. pre-renal
  2. renal (intra-renal; acute renal failure)
  3. post-renal

What is the most common cause for intrarenal injury (acute renal failure)?

A

Ischemica acute tubular injury

174
Q

Tubular/Interstitial: Acute renal failure is reversible because it is often caused by prolonged ischemia or nephrotoxic agents.

What are examples? What can be caused by both?

A

-Mismatched blood transfusion, severe hemolysis or SK muscle injury

Both: ABO incompatibility (hemolytic transfusion)

175
Q

Tubular/Interstitial: Which part of the nephron is most vulnerable to ischemia? Which is most vulnerable to toxic injury?

A
  1. Ischemia
    –PST and Ascending limb
    (patchy)
  2. Toxic
    –PCT
    (widespread)
176
Q

Tubular/Interstitial: Ischemic (acute) tubular injury manifests as ___1___ at multiple points with large __2___ areas in between.

It primarily affects the straight portion of the PT and the ascending thick limb.

A
  1. necrosis
  2. skip areas

Critical event: tubular epithelial cell injury

177
Q

Tubular/Interstitial: Nephrotoxic (acute) tubular injury is most obvious in the PCT.

It is most often caused by which of the following?

a. aminoglycosides
b. radiocontrast agents
c. IgG deposition
d. ethylene glycol

A

A, B, D

  • aminoglyco
  • radiocontrast
  • ethylene glycol (Ca2+ oxalate; vacuolar)
  • Mercuric Cl- (calcification)
  • Carbon tetrachloride (fatty changes)
178
Q

Tubular/Interstitial: In acute tubular injury, necrosis and sloughing of epithelial cells results in cast formation (which can be seen in the urine).

The presence of casts leads to obstruction and increased intra-luminal pressure.

What affect does this have on glomerular filtration?

A
  • reduces GFR
  • also see dec. glomerular capillary filtration pressure
  • fluid back-leak
179
Q

Tubular/Interstitium: Acute tubular injury presents with

  1. focal glomerular necrosis
  2. Skip areas (ischemic)
  3. Rupture of basement membranes (ischemic)

Cast formation also occurs. What are common casts seen?

A
  1. eosinophilic hyaline casts
  2. Pigmented granular casts
  3. “dirty brown” casts and renal epithelial cells (UA microscopy)
  4. Calcium oxalate crystals (ethylene glycol)
180
Q

Tubules/Interstitium: In the case of ethylene glycol poisoning, what could we expect to see on histo/biopsy/UA?

A
  1. Histo
    - vacuolar appearance
    - -diffuse tubular changes
  2. UA
    - -oxalate crystals
181
Q

Tubules/Interstitium: Acute tubular injury occurs in three stages:

  1. Initiation phase (up to 36 hours)
  2. Maintenance phase (days 2-6)
  3. Recovery phase (diuretic)

During the initiation phase, we see a slight decline in ______ accompanied with “ill” feeling (sluggish, somnolence w/ malaise)

A

dec. urine output

182
Q

Tubules/Interstitium: Acute tubular injury occurs in three stages:

  1. Initiation phase (up to 36 hours)
  2. Maintenance phase (days 2-6)
  3. Recovery phase (diuretic)

This occurs during the maintenance phase, characterized by sustained dec. urine output, Inc. BUN, Hyperkalemia, and metabolic acidosis

A

Oliguric crisis

  • dec. urine output
  • inc. BUN
  • Inc. K+
  • Metab. acidosis

*NOT present in everyone

183
Q

Tubules/Interstitium: Acute tubular injury occurs in three stages:

  1. Initiation phase (up to 36 hours)
  2. Maintenance phase (days 2-6)
  3. Recovery phase (diuretic)

During the recovery phase, there is increased vulnerability to ____

A

Infection

–concern for hypokalemia (due to rapid increase in urine volume - 3L/day)

*loss of large amts. of Na, water, K+

184
Q

Tubular/Interstial: Prognosis for acute tubular injury depends on the severity of the damage.

However, complete re-establishment of normal renal architecture and function is possible.

When do we see higher mortality?

A

sepsis and extensive burns

NOTE: nephrotoxic better prognosis
–subtle tubular impairment may persist

185
Q

Tubular/Interstitial: Tubulointerstitial nephritis is inflammatory injury in the ABSENCE of nephrotic or nephritic syndrome.

It is most manifests as dysfunction in

A

-urine concentration ability

Clinical:

  • salt wasting
  • polyuria
  • polydipsia
  • inability to excrete acids (metabolic acidosis)
186
Q

Tubular/Interstitial:

  1. Acute tubulointerstitial nephrritis is marked by edema and what cells?
  2. Chronic interstitial nephritis is marked by fibrosis and what cells?
A
  1. Acute
    - edema, granulocytes
  2. Chronic
    - -fibrosis
    - -mononuclear (lymphocytes)
187
Q

Tubular/Interstitial: Tubulointerstitial nephritis may be caused by drugs or toxins.

There are 3 MOA’s associated:

  1. Interstitial immunologic rxn
    (hypersensitivity)
  2. Acute tubular injury
  3. Sub-clinical, insidious cumulative injury
    - -analgesic

Where do NSAIDS fall?

A

All 3mechanisms

188
Q

Drugs/toxins can induce tubulointerstitial nephritis via activation of cell-mediated (T-cell) immune response.

The antigen could be:

  1. drug itself (hapten)
  2. drug bound to tissue
  3. drug metabolit
  4. tissue alteration due to drug

What are the most commonly implicated drugs?

A

NSAIDs, Diuretics (thiazides), antibiotics (B-lactam - penicillins), RIfampin

NOTE: Histologic - eosinophils and T-cell infiltrates

189
Q

Tubular/Interstitial: Drug/toxin induced tubulointerstitial nephritis typically presents with acute renal failure ~2 weeks after taking the drug.

What would be seen on UA lab?

a. erythrocytes, eosinophils, leukocytes
b. leukocytes casts
c. glucosuria
d. aminoaciduria

A

All of the above

  • -sodium wasting
  • -renal tubular acidosis

Clinical:
–fever, rash, allergic symptoms (eosinophilia)

Prognosis:
–full recovery if discontinue drug

190
Q

Tubular/Interstitial: NSAIDS can cause acute kidney injury by decreasing vasodilatory _____.

May present as an analgesic nephropathy, causing hypersensitivity or cell mediated immune reaction. Less commonly, it presents as minimal change disease/membranous nephropathy.

A

dec. vasodilatory prostaglandins (prostacyclin; PGE2)

191
Q

Tubular/Interstitial: Analgesic nephropathy results from chronic over-consumption of painkillers.

It is typically cumulative (2kg of analgesic combinations: aspirin + phenacetin or acetaminophen). What is the basis for developing analgesic nephropathy?

A

-direct nephrotoxicity or ischemic damage (drug-induced vascular changes)

  • Acetaminophen - inc. risk
  • Phenactin - banned
192
Q

Tubular/Interstitial: Common clinical features of this disorder include:

  1. distal tubular acidosis
  2. can’t concentrate urine
  3. yellow, necrotic papillary tips that slough off (into renal pelvis)
  4. dystrophic calcification

What are these findings most often associated with?

A

Analgesic nephropathy

–colic (papillary tip passage)

–progress to renal failure – end stage renal disease

NOTE: MC in females; sickle cell; acute pyelnephritis

193
Q

Tubules/Interstitium: Presence of uric acid crystals in the collecting ducts.

It occurs in the setting of chemotherapy (purine catabolism)

A

Acute uric acid nephropathy

–pre-treat w/ allopurinol (xanthine ox inhibitor)

194
Q

Tubules/Interstitium: Presence of monosodium urate crystals in acidic distal tubules and CDs.

It appears with Tophus formation in the medulla w/ giant cell reaction.

A

Chronic urate nephropathy

*lead poisoning (dec. uric acid excretion)

195
Q

Tubules/Interstitium: True/False - With regard to nephrolithiasis (kidney stones), uric acid represents a less common cause. Calcium oxalate is more common.

A

True

196
Q

Any cause of hypercalcemia causes nephrocalcinosis, including:

  • hyperparathyroidism
  • multiple myeloma
  • Vit. D intox
  • metastatic cancer
  • milk-alkali syndrome

What are clinical signs?

A
  1. passage of urinary stones
  2. can’t concentrate urine (polyuria)
    - renal failure
  3. relative ADH resistance
  4. inc. free water diuresis (polyuria, polydipsia)

NOTE: similar to central diabetes insipidus

197
Q

Tubular/Interstitial: Seen in myeloma patients as a result of Bence Jones proteinuria and cast nephropathy.

It is MC associated with AL type of amyloidosis.

A

Light chain cast nephropathy

–light chain deposition (glomerulus; tubular bm)

–hypercalcemia (nephrocalcinosis)

NOTE: acute w/ dehydration, nephrotoxic antibiotics, concomitant acute infection

198
Q

Some immunoglobulin light chains are directly toxic to renal epithelial cells.

True/False: Bence-Jones proteins combine with urinary glycoprotein (Tamm-Horsfall) to form tubular casts, which can lead to lumen obstruction and inflammation.

A

True

199
Q

A 12 year old male presents to the clinic after a routine analysis is positive for microscopic hematuria. The patient denies urinary symptoms including gross hematuria, urgency, frequency or dysuria. The patient was recently diagnosed with sensorineural hearing and fitted with cochlear implants. His two maternal uncles were also diagnosed with hearing impairments as teenagers.

The patient has no additional past medical history and has met all other developmental milestones. Physical exam is notable for anterior lenticonus.

You suspect

A

Alport syndrome

*Type IV collagen

Genitourinary (2 decks)

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