ICL 1.9: Tubulointerstitial Disease Flashcards
a 25 year old male present to the ER after a car accident. He is hypotensive, diaphoretic and oliguric (low urine).
cause of oliguria?
acute tubular necrosis
this is the most important and most common cause of acute renal failure!!!
there’s ischemic damage to the kidney leading to ischemic damage to the nephron
what are the two major types of acute tubular necrosis?
- toxic
- ischemic
they both have the same clinical picture but just different morphologies –> they both lead to sudden damage to tubular epithelial cells
what are the phases of acute tubular necrosis?
- oliguria for 10-12 days
water + salt + potassium overload
hyperkalemia can lead to muscle weakness and bradycardia
urinalysis will show tubular cell casts (muddy brown casts*) and RBCs
there can also be metabolic acidosis
- polyuria after 10-12 days = increased volume of urine
decreased Na + K + Cl due to their loss in the urine
- recovery on the 17th day due to regeneration of the renal concentrating ability
what are the complications of acute tubular necrosis?
- cardiovascular = congestion, HTN and arrhythmias
2. CNS = lethargy, somnolence, twitching and seizures due to Na changes
which parts of the nephron are effected in acute tubular necrosis?
toxic is mostly in PCT while ischemic can effect PCT and loop of Henle
toxic is continuous while ischemic skips areas of the nephron
the distribution of the areas of necrosis is more segmental with ischemic injuries
toxic injuries result in more diffuse proximal tubular injury
what is the etiology of toxic acute tubular necrosis?
- heavy metals: mercury, lead, gold, arsenic*
- organic solvents: chloroform, carbon tetrachloride
- antibacterial: polymyxin, neomycin, sulfa
- mushrooms
- pesticides
- ethylene glycol (antifreeze)*
characteristics of the toxic damage is necrosis which is most prominent in the PCT!
what are the gross changes seen in toxic injuries result in acute tubular necrosis?
- pale, swollen kidney
2. edema
what are the microscopic changes seen in toxic injuries result in acute tubular necrosis?
necrosis is obvious and is associated with an intact basement membrane in toxic tubular necrosis
BM isn’t ruptured!
describe the acute tubular necrosis seen with ischemic injury?
- focal at multiple points with skip areas in between
- there is rupture of the basement membrane = tubulorhexis
- occlusion of the lumina by casts
- both proximal and distal tubules involved
what are the causes of ischemic tubular necrosis?
renal vasoconstriction and the factors behind it
they include dehydration which leads to hypovolemia and shock
what are the typical clinical situations associated with ischemic acute tubular necrosis?
- mismatched blood transfusion with massive hemolysis
- crush injury
- burns
- hemolysis
- gram negative septicemia* with DIC and pooling of blood in peripheral capillaries leading to poor perfusion of capillaries
a 15 year old girl presents with a skin rash and elevated creatinine after recovering from a sore throat.
UA: eosinophiluria
diagnosis?
pathogenesis?
acute interstitial nephritis due to hypersensitivity to drugs
she was fine but had a sore throat and then after she gets a skin rash and elevated creatinine which means kidney damage
she has eosinophils in the urine which occur when there’s a hypersensitivity reaction or parasites
she probably got antibiotics for sore throat and had an allergic reaction to it
a 65 year old lady with a 20 year history of Rheumatoid arthritis presents with elevated BUN and creatinine & mild hematuria.
diagnosis?
pathogenesis?
chronic interstitial nephritis from long term NSAID use!
associated with NSAID therapy – NSAIDs inhibit prostaglandins which leads to ischemia of the kidney and chronic inflammation = chronic interstitial nephritis
20 year history of RA is chronic
she’s 65 so she could have other issues….other issues that could lead to increase in BUN and creatinine could be HTN and CHF but she doesn’t have either of those so what is it…
did she get GOLD therapy for RA? she wouldn’t have hematuria and she’d be nephrotic with 4+ protein in the urine and edema which she doesn’t have either
people with RA take NSAIDs which lead to chronic interstitial nephritis!
what is acute interstitial nephritis?
inflammation of tubules and interstitium that causes acute renal failure without signs of nephrotic/nephritic syndromes
most often caused by hypersensitivity type I reaction to drugs/antibiotics but can also be caused by infections or systemic illnesses
associated with urinary tract infection treated with antibiotics
you’d see:
1. eosinophilia
- eosinophils in kidney and urine
- elevated IgE
- can sometimes see WBC casts without symptoms of cystitis = “sterile pyuria”
- fever, rash, malaise after exposure to a trigger
what is chronic interstitial nephritis?
mononuclear cells causing fibrosis and atrophy of tubules; often asymptomatic since it’s chronic and renal failure is identified incidentally
most often caused by chronic NSAID use or could also be phenacetin use; improves when you discontinue drug use
with aspirin you’d see decreased prostaglandins and ischemia
with phenacetin you’d see a direct toxic effect
both would result in papillary necrosis* and interstitial lymphocytes –> the ischemia causes papillary necrosis so then the kidney tries to expel the dead tissue which can cause pain!
