Renal Pathology 4 Flashcards by erin flaherty

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?

ischemic ATI and Nephrotoxic ATI

How well did you know this?

Not at all

Perfectly

what are some causes of ischemic ATI?

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

How well did you know this?

Not at all

Perfectly

what are some endogenous agents that could cause nephrotoxic ATI?

myoglobin, hemoglobin, monoclonal light chains, bile/bilirubin

How well did you know this?

Not at all

Perfectly

what are some exogenous agents that could cause nephrotoxic ATI?

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

what is considered to be pathognomonic of ATI?

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

How well did you know this?

Not at all

Perfectly

what are the 3 phases of ATI?

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

the prognosis of ATI depends on what?

the magnitude and duration of the injury

How well did you know this?

Not at all

Perfectly

what is tubulointerstitial nephritis?

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

hematogenous infection or ascending infection

How well did you know this?

Not at all

Perfectly

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

staphylococcus aures and E. coli

How well did you know this?

Not at all

Perfectly

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

E. coli, proteus, and enterobacter

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

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

how can you treat uncomplicated E. coli cystitis?

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

what is a viral pathogen causing pyelonephritis in kidney allografts?

polyomavirus

who is at risk of viral acute pyelonephritis?

kidney transplant recipients on immunosuppression

how is viral acute pyelonephritis characterized?

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

what are 3 complications of acute pyelonephritis?

papillary necrosis, pyonephrosis, and perinephric abscess

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

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

how does papillary necrosis look on microscopic examination?

characteristic ischemic coagulative necrosis with preservation of outlines of tubules

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

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

what is perinephric abscess?

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

what is chronic pyelonephritis?

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

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

pelvocalyceal damage

staghorn calculus is associated with infection of what organism?

proteus mirabilis- a gram negative facultative aerobe

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

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

how do you treat a complicated UTI?

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

how do you treat an acute uncomplicated case of pyelonephritis?

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

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

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

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

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

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

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

How does proteus mirabilis grow on the blood agar plates?

in successive waves (swarming)

what are patients undergoing chemotherapy at risk of getting?

tumor lysis syndrome--> acute uric acid nephropathy

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

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

what mutations are associated with ADTKD?

MUC1, UMOD, REN, HNF1-beta

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

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