Renal Pathology 4 Flashcards

1
Q

ATI is the most common cause of AKI. It can be caused by a variety of conditions. What are the 2 categories for these conditions?

A

ischemic ATI and Nephrotoxic ATI

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2
Q

what are some causes of ischemic ATI?

A

microscopic polyangiitis, HUS, TTP, decreased effective circulating blood volume (hypovolemic shock)

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3
Q

what are some endogenous agents that could cause nephrotoxic ATI?

A

myoglobin, hemoglobin, monoclonal light chains, bile/bilirubin

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4
Q

what are some exogenous agents that could cause nephrotoxic ATI?

A

gentamicin, radiographic contrast agents, poisons (mercury), and organic solvents (carbon tetrachloride)

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5
Q

what are the 2 critical events that occur in both ischemic and nephrotoxic ATI?

A

1) tubular injury and 2) persistent and severe disturbances in blood flow

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6
Q

There are several factors that predispose the tubules to toxic injury. What are some of these factors?

A

increased surface area, active transport systems, high rate of metabolism and O2 consumption, capability for reabsorption and concentration of toxins

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7
Q

what is considered to be pathognomonic of ATI?

A

abundance of the extreme of coarsely granular casts, i.e. “muddy brown” granular casts present in sheets

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8
Q

what are the 3 phases of ATI?

A

1) initiation phase 2) maintenance phase 3) recovery phase

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9
Q

what are the key characteristics of the initiation phase of ATI?

A

lasts about 36 hours; only indication is a slight decline in UO and a rise in BUN

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10
Q

what are the key features of the maintenance phase of ATI?

A

sustained decreases in urine output (40-400mL/day), salt/water overload, rising BUN, hyperkalemia, metabolic acidosis

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11
Q

what are the key features of the recovery phase of ATI?

A

steady increase in urine volume; hypokalemia; vulnerability to infection; bun and creatinine levels begin to return to normal

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12
Q

the prognosis of ATI depends on what?

A

the magnitude and duration of the injury

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13
Q

what is tubulointerstitial nephritis?

A

a group of renal diseases that involves inflammatory injuries of the tubules and interstitium

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14
Q

tubulointerstitial disorders are distinguished clinically from the glomerular diseases by what two hallmarks?

A

1) absence of nephritic or nephrotic syndromes 2) presence of defects in tubular function

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15
Q

how do the infectious organisms get to the kidneys in cases of pyelonephritis?

A

hematogenous infection or ascending infection

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16
Q

what agents are most likely to cause hematogenous infection of acute pyelonephritis?

A

staphylococcus aures and E. coli

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17
Q

what agents are most likely to cause ascending infection of acute pyelonephritis?

A

E. coli, proteus, and enterobacter

18
Q

what are some associations with acute pyelonephritis? (like what could lead to acute pyelonephritis)

A

Urinary tract obstruction, catheterization, vesicoureteral reflux, pregnancy, diabetes, immunosuppression

19
Q

how can you treat uncomplicated E. coli cystitis?

A

a single dose of antibiotic (fosfomycin) or a 3-day course of a TMP/SMZ, or nitrofurantoin

20
Q

what is a viral pathogen causing pyelonephritis in kidney allografts?

A

polyomavirus

21
Q

who is at risk of viral acute pyelonephritis?

A

kidney transplant recipients on immunosuppression

22
Q

how is viral acute pyelonephritis characterized?

A

nuclear enlargement and intranuclear inclusions visible by light microscopy in tubular epithelial cells

23
Q

what are 3 complications of acute pyelonephritis?

A

papillary necrosis, pyonephrosis, and perinephric abscess

24
Q

what is papillary necrosis and who is at most risk for getting this?

A

diabetics, sickle cell disease people, and those with urinary tract obstruction; the tips of the pyramids have areas of gray-white to yellow necrosis

25
Q

how does papillary necrosis look on microscopic examination?

A

characteristic ischemic coagulative necrosis with preservation of outlines of tubules

26
Q

what is pyonephrosis and who is t most risk of getting this?

A

the suppurative exudate is unable to drain and so it fills the renal pelvis, calyces, and ureters with pus; seen when there is total or almost complete obstruction particularly when it is high in the urinary tract

27
Q

what is perinephric abscess?

A

an extension of suppurative inflammation through the renal capsule into the perinephric tissue

28
Q

what is chronic pyelonephritis?

A

a disorder in which chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis

29
Q

what is an important diagnostic tool when trying to diagnose chronic pyelonephritis?

A

pelvocalyceal damage

30
Q

staghorn calculus is associated with infection of what organism?

A

proteus mirabilis- a gram negative facultative aerobe

31
Q

how do you treat an uncomplicated UTI caused by P. mirabilis?

A

empirical treatment involves outpatient treatment with either a 3-day course of TMP/SMZ or an oral fluoroquinolone (ciprofloxacin)

32
Q

how do you treat a complicated UTI?

A

the patient may also be treated outpatient with oral antibiotics for 10-21 days

33
Q

how do you treat an acute uncomplicated case of pyelonephritis?

A

outpatient with fluoroquinolones, although a regimen of 7-14 days is recommended; an alternative would be a one-time dose of ceftriaxone or gentamycin followed by either TMP/SMZ

34
Q

drug- and toxin-induced tubulointerstitial nephritis: toxins and drugs can injure kidneys in at least three ways. What are they?

A

1) they can trigger an interstitial immunologic reaction 2) they can cause ATI 3) they can cause subclinical but cumulative injury to tubules that takes years to result in CKD

35
Q

when does drug-induced acute interstitial nephritis begin and how is it characterized?

A

2-40 days after drug exposure; it is characterized by fever, eosinophilia, rash, and renal abnormalities

36
Q

What is the main difference between chronic pyelonephritis caused by VUR and that caused by obstructive uropathy?

A

that caused by obstructive uropathy leads to diffuse uneven scarring of the kidney secondary to the high pressure backflow

37
Q

How does proteus mirabilis grow on the blood agar plates?

A

in successive waves (swarming)

38
Q

what are patients undergoing chemotherapy at risk of getting?

A

tumor lysis syndrome–> acute uric acid nephropathy

39
Q

besides pyelonephritis, what are the other tubulointerstitial diseases? (5)

A

urate nephropathy, hypercalcemia and nephrocalcinosis, ADTKD, myeloma kidney, bile cast nephropathy

40
Q

what mutations are associated with ADTKD?

A

MUC1, UMOD, REN, HNF1-beta

41
Q

what are the contributing factors of multiple myeloma that lead to kidney damage?

A

bence-jones proteinuria and nephropathy, amyloidosis of AL type, light chain deposition, hypercalcemia and hyperuricemia