Ch 16: Kidney- Diseases of Tubules and Interstitium, Transplant, and Tumors Flashcards Preview

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Flashcards in Ch 16: Kidney- Diseases of Tubules and Interstitium, Transplant, and Tumors Deck (16)
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Differentiate between ARF and AKI

acute renal failure suggests an acute, severe decrease in renal function that leads to increased serum creatinine (prerenal, intrarenal, or post renal)

acute kidney injury is another name for intrarenal ARF, and is further categorized by the part of the kidney affected (glomerular, vessels, or interstitium)


Acute tubular necrosis is defined as impaired tubular epithelial function. What are two etiologies of ATN? How do their presentations differ? What is a common clinical finding in both etiologies?

Ischemic: focal injury to PT and thick limbs of LOH of outer medulla. histology includes flattened epithelium (brush borders are lost in "epithelial simplification"). necrosis is subtle
Nephrotoxic: more extensive widespread necrosis of tubular epithelium, with PT most susceptible.

Urinalysis will show "dirty brown" granular casts cell debris rich is cytochrome pigments are sloughed off of the epithelium


How can you differentiate between types of ARF based on BUN:Cr, and FeNa?

prerenal: BUN:Cr >15 / FeNa 500

intrarenal: BUN:Cr <15/ FeNa > 2% (tubular function not intact). kidney loses ability to concentrate urine (Uosm < 500)

postrenal: BUN:Cr >15 / FeNa < 1%, Uosm > 500)


What is the most common organism to cause pyelonephritis? What do they use for attachment? What are common findings of acute pyelonephritis?

E. coli (uropathogenic).
They use adhesions on fimbria (pili) for attachment (encoded by PAP gene).
Common findings include: small white abscesses, on subcapsular and cut surfaces, neutrophilic infiltrate, bactiuria, fever, flank pain, leukocytosis, WBC casts. Common is diabetics. Typically ascending infection increased in risk by reflux (from a short intravesicular ureter or enhanced during micturition)


What a defining feature of chronic pyelonephritis from acute pyelonephritis? What are two etiologies?

chronic features a broad depressed area of cortical fibrosis and atrophy overlying a dilated calyx (caliectasis).
vesicureteral reflux: seen in scarring at both poles
obstruction of the urinary tract: ex BPH or cervical carcinoma)


What is thyroidization, and in which disease does it occur?

occurs in chronic pyelonephritis. it is when atrophy of tubule epithelium is "pinched off," creating eosinophilic, proteinaceous hyaline casts in the urine. The resulting tubules resemble thyroid follicles


If an kidney specimen were to be described as a yellow gross appearance or nodular lesions...what type of cells may make up these nodules? What would this type of pyelonephritis be called?

xanthoma cells: lipid laden foamy macrophages
This is called Xanthogranulomatous pyelonephritis. It is uncommon, and caused by a variety of pathogens such as e coli, klebsiella, proteus.


What is the histological hallmark of drug induced (acute) hypersensitivity tubulointerstitial nephritis? What are some potential causes? What is the clinical presentation and prognosis like?

Histology features eosinophilic infiltration, with T cells...consistent with a type IV cell mediated immune reaction.
Potential causes include NSAIDs, penicillin, and diuretics.
Clinical presentation: oliguria, fever, rash. Without treatment, may progress rapidly to renal papillary necrosis...with treatment and removal of harmful agent, it can resolve completely


A severe case of pyelonephritis can lead to what condition?

papillary necrosis: this region can form dystrophic calcifications, stay in the papillary region or be sloughed off. This is also the pathologic feature associated with analgesic nephropathy, as well as sickle cell disease (cells sickle in vasa racta and occlude lamina, leading to medulla nd papillary infacts/necrosis)


You have a patient that has a history of gout. What is the likely cause of kidney pathology seen in this patient? What other etiologies could cause this pathology?

Urate nephropathy. This could also present followoing chemotherapy for leukemia. The diagnostic feature includes "gouty tophus," an accumulation of inflammatory cells around urate crystals.


What are the different compositions/etiologies of nephrolithiasis? Which is the most common? Which will give you "staghorn" calculi? Common presentation of nephrolithiasis?

Calcium oxalate or Ca phosphate is the most common (phosphate more common in England, oxalate in US). Both are generally idopathic.

Ammonium Mg phosphate are caused by infection by "urea splitting organisms" such as proteus or providencia. They typically fill the pelvis and calyx to forma cast called a "staghorn calculi"

Uric acid stones are seen in gout patients, are yellow, hard, and radiolucent. Treat with hydration and alkalinazation of urine.

Cysteine: rare, seen in kids with hereditary cysteinuria. This may also have staghorn! (so if pt is a kid with staghorn, most likely cysteine stone)

Passage of a stone causes extreme flank pain (renal colic)


What are the two manifestations of an obstruction of the urinary tract? Which will cause dilation of the collecting system? How might the tract become obstructed?

Renal dysfunction (obstructive nephropathy) or hydroneprhosis (dilation of the collecting system)

Hydronephrosis: first dilation of the collecting ducts, followed by dilation of the DCT and PT

Tract may be obstructed from anything that presses on the tract: malignancy in the region that presses on the tract, or from BPH


Describe the different types of transplantation rejection, and which antigens are involved in each.

hyperacute: immediate binding of antibodies to ABO antigens on endothelial cells, causing severe irreversible injury

acute humoral rejection: HLA antigens are involved...complement is activated and neutrophils are present. severe cases may present with necrotizing arteritis

acute cellular rejection: HLA antigens are involved...most common form, characterized by infiltration of T lymphoctes and macrophages

chronic humoral rejection: similar to acute, with a longer progression (go figure)


Which renal tumor is strongly associated with tuberous sclerosis? What tissues are involved in this tumor?

Angiomyolipoma: hamartoma of blood vessels, smooth muscle, and adipose tissue (name gives it away!)


Your patient is an infant that presents with hypertension, a large unilateral flank mass, and hematuria. There is increased renin secretion. On biopsy, what would you find your patient's tumor to be comprised of?

This is Wilms Tumor. Biopsy would show blastema (immature kidney mesenchyme, resembling normal fetal tissue). Most cases are sporadic and unilateral. However, some may be associated with syndromes such as WAGF syndrome, Denys-Drash syndrome, or Beckwith-Wiedemann syndrome


Most common primary cancer of the kidney? How does it present? Loss of what gene is associated with this cancer, and therefore which hereditary condition is it associated with?

Renal cell carcinoma. Presents with a classic triad of hematuria (most common), flank pain, and a palpable mass.

Loss of VHL tumor suppressor gene leads to increased IGF-1 and increased HIF...this leads to increased VEGF and PDGF. This is therefore associated with Von Hippel Lindau disease: aut dom disorder that increases risk for hemangioblastoma of cerebellum and RCC.

Clear cell renal carcinoma is the most common type (cells have abundant clear cytoplasm)