Kidneys II - Tubulointerstitials, Congenital, Adenomas

Question 1

What are the characteristics of acute tubular necrosis?

Answer 1

multiple etiologies

major cause of acute renal failure

usu reversible (can reconstruct itself to restore functionality- labile)

Question 2

What are the two broad categories of acute tubular necrosis?

Answer 2

ischemic (patchy necrosis)

nephrotoxic (segmental e.g. proximal convoluted tubule)

Question 3

Where do we see ischemic ATN?

Answer 3

scattered along length of PCT and loops of Henle - does NOT afect just one focal segment

Question 4

What are some causes for ischemic ATN?

Answer 4

1) thrombus/embolus
2) massive exsanguinations (GSW, trauma, etc)
3) hypovolemia/shock (blood being shunted away from kidneys)

Question 5

Where do we see nephrotoxic ATN?

Answer 5

tend to be segmental, or more focal, particularly within PCT

Question 6

What is unique to nephrotoxic ATN?

Answer 6

sudden onset, which results in coagulative necrosis of renal tubular epithelium

Question 7

What is this?

Answer 7

ATN

key feature here: cortical pallow (esp. in ischemic subtype)

Question 8

What is this?

Answer 8

cortical necrosis of ATN- see fibrosis, scarring, and contraction

Question 9

What’s the treatment for ATN?

Answer 9

vasopressin - to get BP back up and regulate fluid volumes,

make sure kidneys are perfused

dialysis

Question 10

What are some characteristics of acute pyelonephritis?

Answer 10

bacterial infection (usu gram neg)

ascending or hematogenous routes

associated with urine stasis, obstruction, retrograde flow (cystitis to pyelonephritis)

patchy interstitial suppurative inflammation (microabscesses)

Question 11

Does acute pyelonephritis start as cortical disease?

Answer 11

NO! as the disease worsens, it can affect the cortex

Question 12

What is this?

Answer 12

pyuria = pus in urine (so PMNs and RBCs)

NOT pathognomonic

seen in acute pyelonephritis

Question 13

What is another key feature of acute pyelonephritis?

Answer 13

WBC casts - indicative of inflammation/infection

can potentially have 2 different kinds - renal tubular or epithelial casts

Question 14

Where do the WBC cast originate from?

Answer 14

ONLY renal tubule​- so this means it CANNOT be a lower UTI (has to originate in the kidney itself)

Question 15

What is shown here?

Answer 15

acute pyelonephritis - enlarged and swollen

microabscesses: tiny yellow dots scattered throughout cortex and medulla (CLASSIC sign of inflammation)

Question 16

What happens to microabscesses?

Answer 16

will become dropout areas - no longer able to perform renal functions

Question 17

What is the cause of the flank pain seen in acute pyelonephritis?

Answer 17

stretching of the kidney’s capsule due to the enlargement of the organ secondary to inflammatory mediators and infiltrates

Question 18

What is shown here?

Answer 18

chronic pyelonephritis

note the grossly scarred kidneys

Question 19

What causes chronic pyelonephritis?

Answer 19

interstitial fibrosis and atrophy of tubules due to multiple bouts of acute pyelonephritis

Question 20

toxins or drugs inducing acute immunologic (hypersensitivity) reaction in the interstitium - resulting in interstitial inflammation with predominantly _?_

progression?

Answer 20

Interstitial nephritis

eosinophils ; papillary necrosis

Question 21

What is seen histologically in TID - Interstitial Necrosis?

Answer 21

1. tubules separated (should be back-to-back)
2. interstitium full of inflammatory cells
3. normal glomeruli
4. eosinophils!

Question 22

What is this?

Answer 22

papillary necrosis - yellowish-softening coagulative necrosis of medullary pyramid papillae

Question 23

What is this?

What happens when sloughs off?

Answer 23

papillary necrosis!

1. get acute onset of anuria (bc the tubes get blocked)- lose ability to concentrate urine

Question 24

What are the causes of papillary necrosis?

Answer 24

1. acute pyelonephritis
2. interstitial nephritis
3. diabetic nephropathy
4. sickle cell disease
5. nephrotoxity drugs

Question 25

How does hypertension lead to renovascular disease (RVD)?

Answer 25

hypertension-\> medial thickening-\> progress decrease in perfusion of renal cortex -\> atrophy \*long standing hypertension is **leading cause for dialysis and transplant**\*

Question 26

How does **benign nephrosclerosis** lead to RVD?

Answer 26

renal ischemia leads to symmetrically **atrophic kidneys** -\> **glomerular dropout** -\> **tubular dropout** \*chronically can be **fatal** becomes too shrunken over time\*

Question 27

How does **accelerated nephrosclerosis** (malignant HTN) lead to **RVD**?

Answer 27

**Medical emergency!** sudden rise of BP to extreme high levels -\> **_intimal endothelial_ changes and necrosis** of endothelium of small arterioles

Question 28

1. characterized by thrombosis in capillaries and arterioles throughout body 2. hemolytic anemia 3. thrombocytopenia 4. renal failure (cause of mortality)

Answer 28

microangipathy

Question 29

How is **renal artery stenosis** associated with RVD?

Answer 29

(acquired through atherosclerosis or congenital) ## Footnote **Goldblatt kidney**: constriction of renal a. causes ischemia and release of renin leading to HTN

Question 30

How is **thrombotic microangiopathic disorders** related to RVD?

Answer 30

group of disorders caused by **activation of intrinsic coagulation system** **fibrin threads** produced -\> clogged kidney's microvasculature -\> **ischemia** "wire through cheese" analogy: fibrin threads slice RBCs -\> **hemolytic anemia**

Question 31

Microangiopathies are NOT diagnosed with?

Answer 31

kidney biopsy!

Question 32

Examples of microangiopathy?

Answer 32

HUS, thrombotic thrombocytopenia purpura, eclampsia and pre-eclampsia, lupus, malignant hypertension, DIC, etc

Question 33

What's the underlying pathophysiology of microangiopathy?

Answer 33

triggering of **coagulation system** =\> thromboses in microvasculature throughout body -\> fibrin monomers -\> hemolyic anemia

Question 34

How do infarcts present in RVD?

Answer 34

embolic, peripheral, wedge shaped, coagulation necrosis, clinically silent (bc significant functional reserve)

Question 35

What is this? How is it manifested at birth? over time? palpable? mode inheritance?

Answer 35

**adult polycystic disease** ## Footnote 1. present but functional 2. cysts grow and put pressure causing **pressure atrophy** of underlying renal tissue -\> **renal insufficiency and possible microhematuria** 3. yes! 4. **autosomal dominany**

Question 36

What is this? fetus manifestation? cause? mode of inheritance?

Answer 36

**Cystic Dysplasia (pediatrics)** ## Footnote 1. **survive in utero** bc of mom's kidneys but **lethal after birth** 2. failure of normal embryonic development 3. autosomal recessive

Question 37

What is this? cause? clincal presentation? diagnosis? treatment?

Answer 37

**Simple Cyst** ## Footnote 1. acquired 2. **usu asymptomatic** bc kidneys normal function; **rupturing**= fluid into retroperitoneal space causing pain and irritation that subsides over couple of days 3. US or CT 4. rarely need treatment

Question 38

1. most often derived from **renal _tubular epithelial cells_ that fail to produce tubules or nephron structures** 2. localized lesion under 1.5cm metastasis?

Answer 38

**adenoma** as grow \>2cm -\> **rates of metastatic disease rise** (so debate if truly benign or renal cell CA in waiting)

Question 39

1. relatively common 2. usu **eccentric** (at one pole or the other- NOT homogenous); usu. **slow growing** 3. solid, large, lobulated mass beneath capsule; **zones of necrosis and hemorrhage**; 4. distant metasis (usu. silent for a while bc located in **retroperitonium**, but signs from **metastic lesions**); _where invades?_

Answer 39

**renal cell carcinoma** (aka **clear cell tumor** or **hypernephroma)** predilection to invade **renal vein** -\> sending tumor emboli **into circulation** -\> metastases

Question 40

1. **pediatric tumor** of embryonal appearing tissue (one of the most common **intra-abdominal peds tumors**)-\> large globular masses; **more homogenous** 2. often genetics (not always) 3. uni/bilateral treat? histo?

Answer 40

**Wilm's tumor** can be curative with chemo histo: spindle cell and mesenchymal-like cell (blue cell)

Question 41

1. **papillary tumors** composed of ? 2. cauliflower appearance that can occur anywhere there is __ epithelium

Answer 41

**translational cell carcinoma** transitional - duh

Question 42

Obstruction of kidneys results in? Two types?

Answer 42

**anuria** ## Footnote 1. acute = dull flank pain 2. extrinsic = intermittent-\> colicky pain

Question 43

1. buildup of fluid in kidneys as result of obstruction of renal outflow tract 2. dilation of ureters ABOVE the obstruction - _cysts? how to determine?_ 3. _one possible cause?_

Answer 43

**hydronephrosis** 1. not cystic! the dilations are CONNECTED (cysts don't connect) 2. **congenital urethral outlet stricture**

Question 44

1. pyelonephritis (_define_) + hydronephrosis 2. can cause bladder distension if obstruction is in lower urinary tract leading to ? because? 3. an **ascending infection** (cystitis -\> ureritis -\> pyelonephritis) 4. grossly dilated ureters; destroyed kidneys filled with purulent, granular exudate and necrotic debris

Answer 44

**Pyonephritis** ## Footnote 1. Kidney infection **2. vesicoureteral reflux**: reflux of fluid from bladder back into ureters and renal pelvis bc **ureterovesicl junction failed to remain closed**