Chapter 20: The Kidney Flashcards
(73 cards)
1
Q
What is the most common and 2nd most common causes of Chronic Renal Failure (CRF) and End-Stage Renal Disease (ESRD)?
A
- Diabetes = MOST common
- High BP = second most common
2
Q
What is the single most important question to ask a patient suspected of having renal disease?
Why?
A
- - “Have you had this before?”
- Hx of disease can imply a significantly worse prognosis or chronicity
3
Q
What is the average size of the kidney?
A
- 120-150 grams and continues to grow until late teens/early 20s
- Length: 10-12 cm
- Width: 6cm
4
Q
How is the hilar area of the kidney different from the parenchyma?
A
Hilar, ureter and urinary bladder are lined by transitional cell epithelium
5
Q
Why is the right kidney lower than the left?
A
Liver pushes it down
6
Q
Where is the kidney located?
A
Renal angle: between the lower border of the 12th rib and lateral border of the erector spinae muscle.
7
Q
If a patient comes in with kidney pain, what is its distribution?
A
Starts from renal angle and radiates forward (anterior) towards the groin.
8
Q
How are the kidneys attached?
A
- Fascial plane, renal artery and vein, ureter and mesentary.
- There are NO suspensory ligments.
9
Q
But what about the splenorenal ligament, is that a suspensory ligament that holds the kidney in place?
A
No
10
Q
Do all small tumors form a mass?
A
NOOOO.
11
Q
What is creatinine and in kidney dysfunctions, it is ↑ or ↓ ?
What about BUN levels?
A
-
Creatnine is a breakdown product of muscle metabolism. Usually, it is excreted NL.
- If kidney dysfunction:
- ↑ serum creatinine and BUN (blood urea nitrogen)
-
↓ urine creatinine and BUN
*
- If kidney dysfunction:
12
Q
When is a renal biopsy performed?
A
Because of the invasivness, there must be DEFINITE indications of a kidney dysfunction.
13
Q
What is always performed with a renal biopsy?
A
UA
14
Q
Kidney diseases often result in edema.
What causes generalized edema vs localized edema?
A
- Generalized edema: Heart, kidney and liver failure
- Localized: only lung failure
15
Q
Renal diseases can be catagorized based on what 4 compartments of the kidneys?
A
- Glomeruli (often immunologically mediated)
- Tubules (often toxic/infectious inury)
- Interstitium
- Blood vessels
16
Q
In the kidneys,
- DM is mainly a __________ disease.
- Systemic HTN is mainly a _________ disease.
A
- DM= glomerular disease
- HTN= tubulointestinal disease (d/t vascular damage)
17
Q
Glomerular disorders are though to be due to what?
A
Immunologic diseases (primary or secondary)
18
Q
What is responsible for the long-term complications in diabetics?
A
Persistant hyperglycemia (glucotoxicity)
19
Q
Azotemia
A
↑ BUN & ↑ creatinine d/t a ↓ in GFR
20
Q
Pre-renal Azotemia
A
Azotremia d/t hypoperfusion of the kindeys (d/thypotension, shock, CHF, or cirrhosis of liver) W/O damage of the parenchyma
21
Q
Post-renal azotemia
A
Azotremia d/t urine outflow is obstructed after leaving the kidney (distal to calyces and renal pelvis). If the obstruction is removed, azotemia is corrected.
22
Q
Uremia
A
Azotremia + other clinical findings and signs like: metabolic, hematologic, endo, GI, neuro and CV effects
23
Q
If Puttoff says uremia, what is the condition of the patient?
A
They are in chronic kidney diasease (CKD, same as chronic renal failure)
24
Q
How does a patient with uremia progress and present?
How do we dx in children?
A
- Pt has nonspecific sx, which become chronic and worse overtime as the disease worsens.
- Dx in children is hard because of the non-specific sx.
25
**Azotremia** is often seen in _________ syndromes
**_Nephritic_** syndromes
26
**Know the difference between nephrotic and nephritic syndromes**
27
What is the **NL GFR?**
**90-120 mL/min**/1.73m2
Older ppl will lower GFR bc it varies w age.
28
What is **acute kidney injury (AKI)/acute renal failure?**
## Footnote
**Severe cases show?**
**Reversible?**
* **Rapid decline of GFR** due to glomerular, interstitial, vascular or acute tubular injury (ATN).
* **Severe cases** will show: **oliguria** or **anuria**
* **Reversible**, or can progress to CKD.
29
Injury to what morphological structure of the kidney is the most common cause of **Acute Kidney Injury?**
**Acute tubular injury (ATN)**
30
What is **Chronic Kidney Disease (CKD/Chronic Renal Failure)?**
Mild/severe cases show?
Reversible?
**Azotremia -\> uremia**
* **Persistantly ↓ GFR t**hat is **less than 60 mL/min**/1.73 m2 for **at least 3 months** and/or **persistent albuminuria.**
* **Mild cases** = **clinically silent**
* **Severe cases=** **uremia**
* **Generally, _irreversible_**
31
**CKD** affects _____ of all adults in the US.
**11%**
32
What is **end-stage renal disease?**
**Less than 5%** of NL GFR and the **end stage of uremia.**
33
What is **rapidly progressive glomerulonephritis (RPGN)?**
**Nephritic syndrome** with **rapid decline (days-weeks) in GFR**, indicating severe glomerular injury.
* **Can manifest as:** acute nephritis, proteinemia and acute renal failure
34
**Glomerular disease** is often associated with what 4 main systemic disorders?
**1. SLE**
**2. Diabetes**
**3. Amyloidosis**
**4. Vasculitis**
35
What clinical renal diseases are characterstic of **tubulointestinal diseases?**
* **1. UTI**
* **2. Urinary tract obstruction**
* **3. Renal tumors**
**Renal tubular defects** and **acute renal failure** can be both glomerular and tubulointestinal.
36
What clinical renal diseases are characteristic of **glomerular diseases?**
**1. Nephrotic/nephritic syndromes**
**2. Asymptomatic hematuria/proteinuria**
**3. CRF**
**Renal tubular defects** and **acute renal failure** can be both glomerular and tubulointestinal.
Renal tubular defects and acute renal failure can be both glomerular and tubulointestinal.
37
What are **isolated urinary abnormalities?**
**Glomerular hematuria** and or **subnephrotic proteinuria**
38
What is the **renal corpsucle?**
**Glomerulus and Bowmans capsule (urinary space)**, which captures the glomerular filtrate and sends it into the tubular system.
39
Which cells of the glomerulus are contractile, phagocytic, capable of proliferation, and l**aying down both matrix and collagen?**
**Mesangial cells**
40
What is a **diffuse vs. focal glomeruopathy?**
- **Diffuse** = affects ALL of the glomeruli in kidney (more than 50%)
- **Focal** = not all glomeruli are affected; others are NL (less than 50%)
41
What is **segmental vs. global glomerulopathy?**
* **Segmental**: only PORTIONS of affected glomeruli are damaged
* **Global**: the entire glomerulus is affected.
42
Once any renal disease destroys nephrons and **↓ GFR to 30-50% of the normal rate**, what happens?
Progression to **ESRF** occurs at a steady rate. The 2 major histological fxs are
* **1. FSGS (focal segmental glomerulosclerosis)**
* **2. Tubulointerstitial fibrosis**
43
What can cause **progressive glomerular injury?**
**Primary** or **secondary** glomerular injury
44
Progressive injury is due to a cycle of glomerular and nephron loss, followed by what?
Compensatory changes that will further cause injury and glomerulosclerosis and eventually, end-stage renal disease.
45
What is the principal glomerular manifestation of **progressive glomerular injury**?
**Focal segmental glomerulosclerosis**, eventually leading to global glomerular involvement and glomerular obsolencence.
46
The **extent of damage to ___________ is MOST correlated** to worsening renal function?
**Tubulointerstitial damage,**
rather than the severity of glomerular injury
47
What is the pathological response of the **glomerulus** to injury?
What do we see in **acute** vs **chronic injury**?
1. **Hypercellularity** of
* **-Endothelial** and **mesengial cells**
* **-Inflammatory cells (leukocytes)**
* **-Proliferation of epithelial cells & inflammatory cells** =\> plasma proteins leaks into space =\> **+ coagulation factors** =\> form **crescents**
2. **BM thickening** and **deposits**
3. **Hyalinosis** (injury of endothelium) and **sclerosis** (deposition of ECM)
* **Acute**: hypercellularity and crescents
* **Chronic**: BM thickening, hyalonisis and sclerosis
48
What can be used to visualize **thickening of the capillary wall?**
**Light microscopy** with **PAS staining**
49
What does **electron microscopy** show for **basement membrane thickening?**
**Subendothelial/subepithelial deposits** of immune complexes, fibrin, amyloid and increased synthesis of BM components.
50
What morphological change to the glomerulus is characterized by the **accumulation of homogenous/eosinophilic material** under **light microscopy** and is typically the **end result of many forms of glomerular injury?**
**Hyalinosis**
51
**Chronic glomerular responses** to injury include what 3 morphological changes?
1. **- Basement membrane thickening**
2. **- Hyalinosis**
3. **- Sclerosis**
52
**Glomerular injury is mostly d/t _immune mechanisms._**
## Footnote
How can Ab cause injury?
* 1. **Ab react in glomerulus & \*\*\*\***
* bind to **fixed intrinsic antigens =\> immune complex**
* bind to **planted antigens =\> immune complex**
* **Can be exogenous (drugs, infections)**
* **Endogenous (DNA, immunoglobulins, immune complexes)**
* 2. Circulating **Ab-Ag complex** in glomerulus
* Endogenous
* Exogenous
53
The **major cause** of **glomerulonephritis** is what?
_**In situ** immune complex formation_
54
What diseases are caused by **in-situ formation of immune complexes?**
1. Anti-GBM nephrititis
2. Membranous glomerulonephropathy
3. Post-strep glomerulonephritis
....
55
In the **Heymann model of glomerulonephritis** (experimental counterpart oto membranous nephropathy), Abs reacts to what Ag?
This Ag is normally found where?
**Megalin**, normally found in epithelial cell (podocyte) foot processes
56
Which Ag underlies most cases of primary human **_membranous nephropathy?_**
**M-type phospholipase A2 receptor (PLA2R)**
57
**In _membranous nephropathy_, Ab binding to PLA2R in glomerular _epithelial_ _cell membranes_** =\> leads compliment activation =\> immune complex forms where on the BM?
Characteristic BM appearance on **light microscopy?**
- **SUBepithelial part** of BM
- **THICKENED BM** appearance on light microscopy
58
what is the pattern of immune deposition seen in **membranous nephropathy** (in-situ immune complex deposition) with **immunofluorescence**,?
## Footnote
**Reflects what?**
* **GRANULAR** pattern
* **d/t VERY localized antigen-AB interaction.**
59
What is the antigen associated with **anti-GBM nephritis**?
**NC1 domain of type 4 collagen Ag**
60
What characteristic pattern seen with **immunofluorescence** in diseases caused by **Abs directed against NL glomerular BM components** (i.e., anti-GBM)?
**Diffuse linear** pattern bc Abs bind to intrinsic Ags along the entire legnth of GBM
61
Often **anti-GBM Abs** cross react with other BM's, especially where?
What **syndrome** does this occur in?
- **Lung alveoli,** forming lesions in lung and kidney
## Footnote
**- Goodpasture syndrome**
62
What kind of glomerular damage occurs due to **anti-GBM Abs?**
Leading to which clinical syndrome?
- Causes **severe _necrotizing**_ and _**crescentic_ glomerular damage**
- Leading to r**apidly progressive glomerulonephritis (RPGN)**
63
**_EXOGENOUS_** Ags from which bacteria/viruses create **_circulating immune complexes_** leading to **glomerulonephritis**?
What are endogenous sources?
* **- Streptococcal proteins**
* **- Surface Ag of _HBV_ and viral antigens of _HCV_**
* **- Ags of T_reponema pallidum_ and P_lasmodium falciparum_**
## Footnote
**Endogenous: SLE, IgA nephropathy**
64
How do **highly cationic Ags** vs. **highly anionic Ags** vs. **neutral Ags** differ in where they **deposit** and **form immune-complexes form** in the glomerulus?
- **Cationic (+)** --\> **cross the GBM** and form in **subepithelial deposits**
- **Anionic (-)** --\> **dont cross GBM** and form **subendothelially deposits**
- **Neutral charge** --\> tend to accumulate in the **mesangium**
65
**Immune complexes** deposited in which locations of the glomerulus are more likely to be involved in an inflammatory response due to be accessible to the circulation?
- **Subendothelial** portions of capillaries
- **Mesangial** locations
66
**_Immune complexes can form deposits:_**
1. Subepithelial area (1)
2. Epimembranous (2)
3. Subendothelial area (3)
4. Mesengial area (4)
**Which nephropathies are most likely in each area?**
**1. Subepithelial humps (1)**
* Acute glomerulonephritis
**2. Epimembranous deposits (2)**
* Membranous nephropathy
**3. Subendothelial deposits (3)**
* lupus nephritis
* membranoproliferative glomerulonephritis
4. Mesenangial area (4)
* IgA nephropathy
67
Which coagulation factor may act as the stimulus for **crescent formation** associated w/ glomerular injury?
**Thrombin**
68
What is the most frequent clinical presentation of **Focal Segmental Glomerulosclerosis?**
1. **Nephrotic syndrome**
2. **- Nonnephrotic proteinuria**
69
Most common type of glomerular injury causing **nephritic syndrome?**
**Immunologically** mediated
70
What is the difference betwene **primary** and **secondary glomerulonephritis?**
* ***_primary_*** *glomerulonephritis* == disorders in which the kidney is the only/ predominant organ involved
* ***_secondary_*** *glomerulonephritis* == when the glomerulus is affected by systemic immunologic diseases such as _SLE_, _vascular disorders such as HTN_, or m_etabolic diseases such as Fabry disease_
* glomerular diseases are often associated with systemic disorders (e.g. _diabetes mellitu_s, _SLE_, _vasculitis_, and _amyloidosis_)
71
**\_\_\_\_\_\_\_\_** are important for the maintenance of **glomerular barrier function**
**visceral epithelial cells (i.e. podocytes);**
separated from the endothelial cells by BM
72
* Diff types of glomerulopathies are characterized by one or more of four tissue changes.
* If **acute** vs **chronic**, what changes do we see?
* **acute** glomerular response to injury == **hypercellularity** and formation of **crescents** (if severe)
* **chronic** glomerular responses to injury ==**BM thickening**, **hyalinosis**, and **sclerosis**
73
