Tubulointerstitial Diseases - Nichols Flashcards
What are the various forms of tubulointerstitial disease?
acute tubular necrosis
peylonephritis
interstitial nephritis
cystic disease
What is the relationship between acute kidney injury and acute tubular necrosis?
ATN is a subset of AKI (the worst kind)
What is the relationship between acute tubular necrosis and ischemia?
Ischemic ATN is a subset of ATN (probably around 75% of ATN)
What are the gross pathologies of ATN?
enlarged kidneys (up to 30% over normal) pale cortex (frequently reduced blood flow) congested medulla, espicially at the cortico-medullary junction
Why do you sometimes see bleeding, hemorrhages in ATN?
there can be reperfusion to the area
What portion of the renal tubules are most vulnerable to acute ischemic necrosis and why?
the TALH and the proximal straight tubule;
both of these areas are high in active transport but located in the outer medulla. as such, they already receive less blood flow than the parts of the nephron in the cortex. so they are at increased risk of acute ischemic necrosis. this is the area that gets extremely congested in ATN
What is the histologic finding of ATN at an early ischemic state?
blebbing of the luminal side cell membranes (looks kinda fuzzy and strands througout the lumen)
diffuse edema of tubular cells (vacuolization of cytoplasm)
Loss of brush borders, flattening of epithelium and necrosis and sloughing
What types of casts are typically seen in ATN?
muddy brown casts, that are pigmented, brownish and coarsely granular
The apoptotic renal tubular epithelial cells are most likely to have decreased cytoplasmic activity of what?
BCL2
What can be seen in ATN from rhabdomyolysis?
condensed, darker cells in the cell, this is myoglobin from rhabdomyolysis
What is seen histologically upon ethylene glycol poisoning?
vacuoliztation and calcium oxalate. looks like fragments, like a fan
Why is reversible ATN not considered an oxymoron?
at the level of the pt, it’s reversible. just not on the individual cell levels
Potassium over what is a medical emergency?
over 7 mmol/L
What is the immediate tx for potassium levels of 7 mmol.L
IV CALCIUM GLUCONATE (antagonizes membrane depolarization and protects against cardiac arrhythmiass
IV Insulin + Glucose (drives potassium from bloodstream into cells)
Wht is seen on gross pathology in acute pyelonephritis?
dark red congestion and areas of light tan suppurative inflammation, some with necrosis, some coalescing into abscesses
Acute pyelonephritis is characteristically abscessing because it produces?
liquefactive necrosis
What would microscopy should in renal abscesses?
severe acute inflammation and necrosis, but not liquefaction.
What type of debris is found in the breakdown of dead cells that make the stains so blue?
nucleic acids, and breakdown of especially neutrophils
When pyelonephritis has exteneded all the way ou tto the capsule, what can be seen?
scarrinb visible on the cortical surface ie blunted calyx
What are the two ways the pyelonephritis can occur?
infection ascending from the bladder or infection arriving via the bloodstream
What is the most common hematogenous infection in pyelonephritis?
staph
what is the most common acscneding infection in pyelonephritis?
e coli
What is the relationshpi between Acute Interstitial nephritis and drug reactions?
ain due to drug rxns are a subset of AIN. over 75% of ain cases. but most drug reactions do not cause interstitial nephritis
What is seen on histology in interstitial nephritis?
edema, lymphocytes, macrophages, neutrophils and eosinophils
who is at risk for analgesic nephropathy?
elderly fmelaes, due to long term combination analgesic use
What mutations can lead to autosomal dominant polycystic kidney disease?
polycystin-1 or 2
what is the pathology of autosomal dominant polycytisc kidney disease?
slowly expanding cysts compress normal tissue, causing ischemic atrophy. leading to ciliopathy, defective mechanosensing of urine flow, dysregulatino of cell adhesion
In childhood what is the common cystic kidney diseaes type?
autosomal recessive, with numerous small cysts replacing normal tissue during fetal life, due to mutation sin fibrocystin.
why does autosomal recessive polycystic kidey disease lead to immediate untreatable respiratory failure at birth?
you have pulmonary hypolasia because “breathing” amniotic fluid goes through kidneys. so lungs don’t develop
What is the most common genetic cause of esrd in children?
nephronophthisis - medullary cystic disease complex. small kidneys with numerou ssmall cysts at the corticomedullary junction and chronic tubulo-interstitial nephritis and fibrosis
