Chapter 20.2 Tubular and Intersitial Diseases Flashcards
(70 cards)
1
Q
What is acute renal failure (acute kidney injury)??
A
- Acute decline in renal function (fall in GFR => ↑ BUN/Cr) that is usually reversible.
- Often, results in tubular necrosis.
2
Q
What are 2 major causes of acute renal failure (acute kidney injury)?
Which is the most common?
A
- Acute Tubular Injury/Necrosis
- Poor renal perfusion
- Most common: acute tubular injury
3
Q
Most common cause of acute renal failure/AKI is
A
Acute tubular injury
-due to acute pyelonephritis
4
Q
- What is damaged in acute tubular injury?
A
tubular epithelial cells
5
Q
What are the 2 most common causes of Acute Tubular Injury?
A
- Ischemia of the kidneys
- Dierct toxic injury of tubules (drugs/ toxins)
6
Q
How does the pattern of tubular damage in the proximal tubule and ascending loop of henle seen in acute tubular injury differ between ischemic and toxic sources?
A
- Both see same amount of casts in same areas, but different patterns of necrosis.
-
Ischemia causes
- Patchy necrosis in proximal tubule and TALoH
- Toxic injury causes
- Continuous necrosis in proximal tubule & patchy necrosis in TALoH
- Both have epithelial casts that occlude the lumen of TALoH (patchy) => DCT => CD
7
Q
Why are tubular epithelial cells particularly vulnerable to ischemia?
A
- Increased SA for reabsorption
- High NRG requirements because many mT and need O2
8
Q
- How will toxicities affect proximal epithelial cells?
A
- widespread injury, resuling in swelling and vacuolization
9
Q
In ATI, what occurs to necrotic tubular epithelial cells over time?
Leads to?
A
Die, slough into lumen of tubule and obstruct urine flow, forming granular casts in tubules that are muddy brown.
10
Q
Can proximal epithelial cells regenerate?
A
Yes, as long as the BM is intact
11
Q
How does ischemic ATI cause necrosis of tubular cells?
A
- Ischemic ATI => vasoconstriction => decrease in GFR and necrosis of tubular cells
- Vasoconstriction occurs due to loss of tubular cell polarity: Na/K ATPase moves from BL side => luminal side of tubular epithelial cell, pumping Na+ into the urine
- Na+ is sensed by macula densa => triggering vasoconstriction
- => decrease in GFR
12
Q
Ischemic ATI occurs in what situations?
A
- hypovolemia, cardiogenic shock, massive bleeding
13
Q
- Toxic ATI is caused by what drugs and toxins?
A
- Ethylene glycol (anti-freeze)
- Aminoglycosides
- Heavy medals (e.g. lead)
- Myoglobinuria from crush injury
- Radiocontrast dye
- Urate (e.g. tumor lysis syndrome
14
Q
What are the 3 stages of the clinical course of AKI/ARF due to ATI and major electrolyte/lab findings in each stage?
Which stage is marked by an increases susceptibility to infection?
A
-
Initiation– Injury occurs
- Lasts 36 hrs, we see a slight decline or pee (oliguria)
- Maintenance
- Low urine output with uremic features
- Hyperkalemia
- Metabolic acidosis
- Recovery (depends on duration and nature)
- High urine output: polyuria (3L/day) => loss of water, Na, K, hypokalemia
- muscle problems
- Susceptible to infection
15
Q
What is the prognosis of ATI dependent on?
How likely are these pts to survive?
A
- Magnitude and duration of injury
- Recovery is typical, some may need dialysis
16
Q
What is Tubulointerstitial Nephritis
A
- Group of renal diseases that cause inflammation of renal tubules and interstitium.
17
Q
- Tubulointerstitial Nephritis is generally characterized by what 2 things?
A
- Insidious onset
- Azotemia due to decrease GFR, making it difficult to concentrate urine (polyuria and nocturia)
18
Q
- What are the clinical hallmarks of Tubulointerstitial Nephritis that distinguish it from Glomerular diseases?
A
- NO nephritic or nephrotic syndrome
- Defects in tubular function –> defect in concentrating urine = polyuria and nocturia
- Salt wasting
- Dimished ability to excrete acids (metabolic acidosis)
19
Q
- What causes tubulointestinal nephritis?
A
- 1. Infection: acute, chronic, other
- 2. Toxins
- 3. Metabolic diseases
- 4. Physical factors (chronic obstruction)
- 5. Neoplasm (Bence-Jones proteins)
- 6. Immunological reactions
- 7. Vasular diseases
- 8. Other
20
Q
Acute Tubulointerstitial Nephritis has what 3 characteristics?
A
- Rapid onset
- Characterized by
- interstitial edema
- leukocytic infiltration in tubules and interstitium
- Tubular injury
21
Q
Chronic Tubulointerstitial Nephritis has what 3 characteristics?
A
- mononuclear leukocytes
- interstitial fibrosis
- lots of tubular atrophy
22
Q
- How can we tell if it is acute/chronic tubulointerstitial nephritis ?
A
- If edema is present with eosinophils/neutrophils => acute
- If fibrosis and tubular atrophy => chronic
23
Q
What is a UTI?
A
- An infection anywhere along the urinary tract from urethra => renal cortex.
- Can cause tubulointestitial nephritis
24
Q
85% of UTIs due to what?
A
Enteric bacteria (e.coli)
25
What are the most common causes of **UTIs**?
**Gram (-) rods:**
* **1. E.coli**
* 2. Proteus
* 3. Klebsiella or Enterobacter
* 4. streptococcus faecalis
* 5. staph
26
What bacteria causes UTIs and produces **urease**, which can cause **struvite kidney stones?**
**Proetus mirabilis**
27
Most **UTIs** are ________ infections.
**Ascending,** from a lower urinary tract infection: urethra =\> cystitis =\> pyelonephritis
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* **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ i**s what allows bacteria to gain access to ureters, while **stasis** makes it easier
* **Vesicoureteral Reflux (VUR)**
* **Congenital: malformed or incompetent valve**
* **Acquired: atony of bladder**
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What is the I**ntrarenal Reflux?**
* **Infected bladder urine d/t VUR** =\> renal pelvis and deep into the renal parenchyma through via tips of the papillae
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* **Absence of VUR** cause what types of infections?
**Lower UTI (cystitis and urethertiis):** infection remains localized to the bladder.
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What is the source of infections in **UTI** and who are they more common in?
* **Patients fecal flora**
* **Women** bc shorter urethra
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What type of UTIs do we most commonly see in clinical practice?
**Lower UTIs**
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What is **cystitis**?
What is it mainly due to?
* Infection and inflammation of the LUT (**bladder mucosa)**
* 95% due to **bacteria** (e.coli)
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**Cystitis** is a lower urinary tract that causes what symptoms?
pain with urination (**dysuria**), **frequency**/**urgency**, **suprapubic pain**, **NO** systemic symptoms (no fevers, chills, sweats)
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**Pyelonephritis** is an infection of the
**kidneys**; tubules, interstitium, renal pelvis
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Most common cause of clinical **pyelonephritis** arises from what?
**Ascending infection** from the bladder
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Who is most likely to get **pyelonephritis**?
Patient with a **predisposing anatomic defect: VUR** and **intrarenal reflex**
38
What are 2 of the common predisposing medical conditions for **Pyelonephritis**?
**1. DM**
**2. Pregnant people**
39
What is the **vesicoureteral reflux?**
1. **Incompetence of the vesicoureteral valve** that causes urine to reflux from bladder =\> ureter =\> kidney
40
How can **vesicoureteal reflu**x be acquired in both children and adults?
- Children --\> congenital defect (most common) when the intravesical protion of the ureter does not NTR the bladder oliquelym causing a backflow of piss.
- Adults --\> obstruction, often due to prostatic hypertrophy
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**Vesicoureteral reflux** can be diagnosed via a \_\_\_\_\_\_\_\_\_\_\_\_\_\_.
* What will we see
* **Voiding cystourethrogram.**
* **Hydronephrosis** (Dilated ureter)
42
Although ascending infection is the most common route of bacteria entering the kidney, they may also do so **hematogenously**, which is most often occurs in what clinical setting?
**Sepsis**
43
**Acute Pyelonephritis** is acute bacterial infection of the kidney that is almost always the result of
**[ascending cystitis infection + predisposing anatomic defect** [vesicoureteral junction or obstruction of bladder outlet].
44
What is a **viral pathogen** causing **pyelonephritis** in **kidney allografts** often leading to the development of **nephropathy/allograft failure?**
**Polyomavirus**
45
**Drug and toxin-induced tubulointersitial nephritis** is the SECOND most common cause of what?
**AKI (acute renal failure)**
46
**Acute pyelonephritis** is most common in who?
**Females** from **infancy** to age **40**
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What are sx of **acute pyelonephritis?**
1. Sudden onset **CVA tenderness**
2. **SYSTEMIC SIGNS – fever and malaise** (whereas with cystitis there are no systemic signs)
3. **WBC Casts**
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Which has **systemic signs**: cystitis or acute pyelonephritis?
**acute pyelonephritis**
49
What are the morphological hallmarks of **Acute Pyelonephritis?**
Is the **glomerulus** affected?
1. **Patchy interstitial suppurative inflammation**
2. **Aggregates of neutrophils (WBC) in tubules**
3. **Neutrophilic tubulitis**
4. **Tubular necrosis**
5. Glomerulus is **NOT** affected
50
Grossly, what does **acute pyelonephritis** look like?
**multiple foci** of areas of y**ellow-greyish-white acute inflammation (liquefactive necrosis, pus)** & **abscesses**
51
What complications are assocaited with **Acute Pyelonephritis?**
1. **Papillary Necrosis**
2. **Pyonephrosis:** pus accumulation in pelvis, calyx, ureter that obstructs kidney
3. **Perinephric abcess**
52
What is **Chronic Pyelonephritis?**
**chronic tubuloiterstitial inflammation** and **renal scarring** with of the **_calyces_**, **_pelvis_** and **_parenchyma_**.
53
What are hallmarks of **Chronic Pyelonephritis?**
1. **Corticomedullary scaring** with **blunted/deformed calyce**s and flattened papilla in _upper/lower poles_
2. Interstitial **fibrosis** and **atrophy** of tubules
3. H**yaline arteriosclerosis**
4. **Thyroidiization of the kidney**: tubules contain eosinophil-protein materal and look like thyroid follicles
54
VUR w/chronic pyelonephritis à
**polar cortical scarring**
55
**Xanthogranulomatous Pyelonephritis** is a rare form of chronic pyelonephritis associated with \_\_\_\_\_\_
**proteus**
56
**Xanthogranulomatous pyelonephritis** is a rare form of chronic pyelonephritis characterized by the accumulation of what?
Associated with what infection?
The large, yellowish orange nodules may be clinically confused with?
* accumulation of **foamy macrophages** w/ plasma cells, lymphocytes, PMN leukocytes, giant cells
* Proteus infection
* Renal cell carcinoma
*
57
**Chronic Pyelonephritis** may develop into ?
**FSGS =\> ESRD**
58
**Papillary necrosis** is a complication of **acute pyelonephritis** most often seen in which 4 patients/settings?
* **1) Diabetics**
* **2) Analgesic Nephropathy**
* **3) Urinary tract obstruction**
* **4) Sickle Cell Disease**
59
What is **papillary necrosis?**
* **Coagulative necrosis** of renal papillae.
* Sloughing off of the tissue causes **gross hematuria** that is often **painless**; **renal function is often NL.**
60
What is the M:F ratio for **papillary necrosis** associated with **diabetes mellitus**?
Time course?
How do the papillae appear and are they calcified?
* F
* 10 years
* **Pale, greyish necrosis** of ONLY papilla
61
What is the M:F ratio for p**apillary necrosis associated with Analgesic Nephropathy (NSAIDS)?**
Time course of abuse?
How does the necrosis appear on the papillae, how diffuse is the necrosis and is there calcification?
* F
* 7 years
* **Red-brown necrotic** papilla sloughed into calyces with **frequent calcification**
62
Which gender has a higher incidence of **papillary necrosis as a result of obstruction?**
Are calcifications rare or frequent?
* **Males**
* **Frequent**
63
Only what 2 entities causing renal damage affect the **calyces**,making **pelvocalyceal** damage an important diagnostic clue?
**1) Chronic pyelonephritis**
**2) Analgesic nephropathy**
64
What is **Acute (Drug-Induced) TubuloInterstitial Nephritis?**
* **Hypersensitivity _Type I and 4 reaction_** to a number of drugs that cause **tubulitis** and **acute renal failure**
65
**_TUBULOINTERSTITIAL NEPHRITIS CAUSED BY DRUGS (ALLERGIC NEPHRITIS)_**
## Footnote
Why is it clinically important to recognize **drug-induced acute interstitial nephritis?**
**Withdrawl** of the offending **drug** is followd by recovery, which may take several months
66
Does **Acute (Drug-Induced) TubuloInterstitial Nephritis** depend on the dose?
**_NO_**
67
How do drugs cause **Acute (Drug-Induced) TubuloInterstitial Nephritis?**
* **Drugs acts as a hapten** until concentrated in the tubules to be excreted in urine.
* Then, they activate **IgE** and **T/B/Plasma cells** in the localized area
68
* What are patients with **analgesic nephropathy** more likely to develop?
* **Urothelial carcinoma** of the renal pelvis
69
NSAIDs have been shown to cause what 2 renal syndromes developing concurrently?
**- Acute interstitial nephritis**
**- Minimal change disease**
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