Renal Pathology 4 Flashcards
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
what are some causes of ischemic ATI?
microscopic polyangiitis, HUS, TTP, decreased effective circulating blood volume (hypovolemic shock)
what are some endogenous agents that could cause nephrotoxic ATI?
myoglobin, hemoglobin, monoclonal light chains, bile/bilirubin
what are some exogenous agents that could cause nephrotoxic ATI?
gentamicin, radiographic contrast agents, poisons (mercury), and organic solvents (carbon tetrachloride)
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
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
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
what are the 3 phases of ATI?
1) initiation phase 2) maintenance phase 3) recovery phase
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
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
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
the prognosis of ATI depends on what?
the magnitude and duration of the injury
what is tubulointerstitial nephritis?
a group of renal diseases that involves inflammatory injuries of the tubules and interstitium
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 do the infectious organisms get to the kidneys in cases of pyelonephritis?
hematogenous infection or ascending infection
what agents are most likely to cause hematogenous infection of acute pyelonephritis?
staphylococcus aures and E. coli
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
