• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

Card Range To Study



Play button


Play button




Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

76 Cards in this Set

  • Front
  • Back
What are the clinical features of acute kidney injury?
acute kidney failure, with oliguria or anuria
What is the pathogenesis of ischemic AKI?
ischemia, proximal tubule is most seriously affected as it consumes the most energy
What is the most common cause of acute renal failure?
ischemic AKI
What is the pathogenesis of toxic AKI?
toxins cause direct tubular injury with resultant necrosis
What does toxic AKI look like in histo?
necrotic cells or sloughed epithelial cells within the lumen, hyaline and granular casts in distal nephron segments
What causes toxic AKI?
casts of hemoglobin/myoglobin, mercury, ethylene glycol, radio contrast, aminoglycosides
What does ischemic AKI look like?
regenerative changes, loss of proximal tubule brush border, tubule dilation, flattening of the epithelium
What is the prognosis of AKI?
recovery is common, mortality increased when part of multiorgan failure
What is obstructive uropathy?
structural or functional abnormality in urinary tract that blocks the normal outflow of urine
What is the clinical presentation of unilateral renal obstruction?
can be clinically silent unless there is a kidney stone
How does bilateral urinary tract obstruction present?
impaired urinary concentrating ability, polyuria, polydipsia
How does obstruction of the bladder outlet present?
micturition difficulties
What casues urinary tract obstruction in kids?
congenital anomalies, posterior urethral valves, ureteropelvic junction malformation
What causes urinary tract obstruction in adults?
kidney stones
What causes urinary tract obstruction in older men?
What cause intrarenal urinary tract obstructions?
deposits in tubule, stones, tumors, sloughed papillary tissue wihtin the renal pelvis
What causes intrinsic extrarenal urinary tract obstruction?
stones, tumors in ureter, ureteropelvic junction obstruction
What causes extrinsic extrarenal urinary tract obstruction?
neoplasms, inflammatory lesions of retroperitoneum
What can cause urethral obstruction?
strictures, posterior urethral valves
What causes prostate obstruction?
BPH, carcinoma
What causes urinary bladder obstruction?
carcinoma, neurogenic bladder
What is hydronephrosis?
dilation of the pelvis and calyces, thinning of overlying parenchyma
What is the earliest morphologic change of obstructive nephropathy?
dilation of the tubules, esp collecting ducts
What is the course of obstructive nephropathy?
dilation of the tubules, esp collecting ducts
Bowman's space may become enlarged, periglomerular fibrosis
interstitial mononculear inflammation, atrophy of proximal tubules, worsening interstitial fibrosis, can have superimposed pyelonephrosis
What is a cystitis?
bacterial infection of lower urinary tract
What is pyelonephritis?
infection of upper urinary tract
What is the pathogenesis of acute pyelonephritis?
ascending from cystitis or blood-borne seeding the kidney
What is the pathogenesis of UTI in males and kids?
anatomic or functional efect preventing normal emptying/urinary flow
What pathogen causes mostt UTIs?
E coli
What other pathogens cause UTI?
Staph faecalis, Staph albus, Klebsiella, Proteus
What does Proteus mirabilis infection cause?
urea splitting, staghorn calculi in pelvicaliceal system, can perpetuate infection
How does acute cystitits present?
urgency with pyuria
How does acute pyelonephritis present?
flank tenderness, pain, fever, pyuria, acute renal failure if bilateral
What is the prognosis of acute UTI?
excellent in uncomplicated acute
What is the prognosis of chronic pyelonephritis?
from repeated bouts, can be congenital or calculi, can develop chronic kidney disease and uremia
What does acute pyelonephritis look like?
plugs of neutrophils in tubular lamina and surrounding interstitium, tubular injury, abscess formation
What does chronic pyelonephritis look like?
broad-based scars, jig-saw pattern of interstitial fibrosis, tubular atrophy, interstitial mononuclear inflammatory cells with intervening spared areas
glomeruli are spared until late
What is acute interstitial nephritis?
interstitial inflammation and edema
Waht is chronic intersittial nephritis?
insidious onset, fibrosis
What are the clinical features of acute interstitial nephritis?
oliguric kidney failure, features of hypersensitivity reaction: fever, rash, peripheral eosinophilia
What do you see in urinalysis of acute intersitital nephritis?
hematuria, pyuria, white cell casts, can have eosionphiluria
What is NSAID-related AIN?
Na retention/edema, hyperkalemia, decline in renal function/acute kidney failure, interstitial nephritis, with nephrotic syndrome
What is the pathogenesis of NSAID-related AIN?
inhibition of vasodilating renal PGs resulting in renal hypoperfusion
podocyte effacement, nephrotic range proteinuria
AIN and minimal change-like lesion
What is the pathogenesis of AIN?
hypersensitivity reaction/immunologic injury from drugs, infections, systemic immunologic disorders
What drugs cause AIN?
sulfa drugs, methicillin, beta-lactam antibiotics, rifampin, thiazides, furosemide, NSAIDs
What is the prognosis of AIN?
glmerular and tubulointersitital abnormalities reversible on discontinuation of drugs,
NSAID related injury reversible within days with discontinuation of offending agent
What is the pathology of AIN?
edematous interstitium, increased space between tubules, interstitial inflammation, lymphocytes, eosinophils, can invade tubular epithelium, tubules show injury or degenerative changes/necrosis
non-necrotizing granulomatous inflammation
What is the prognosis of AIN?
typically reversible, may require dialysis
What causes papillary necrosis?
diabetes, sickle cell, analgesic abuse nephropathy, obstruction
What are the clinical features of chronic intersitital nephritis?
insidious decline in renal function, aminoaciduria, glycosuria, renal tubular acidosis, decreased urinary concentrating ability, mild proteinuria
What can cause chronic interstitial nephritis?
crystal deposition, analgesics, Sjogren syndrome, sarcoidosis, multiple myeloma causing light chain nephropathy
What is the pathogenesis of CIN?
deposits that precipitate in tubules, ongoing immunological injury
What is the pathology of CIN?
inflammation with tubule injury in absence of proportional glomerular/vascular disease, interstitial fibrosis, tubular atrophy, also specific deposits
What is the prognosis of CIN?
fibrosis is irreversible, can improve renal function and prevent ESRD if contributing factors are removed and aggravating factors are controlled
What is the clinical presentation of hyperacute rejection?
0 - 3 days after transplant, typically while still in OR, patient is swollen, acute rise in serum creatinine
What is the pathogenesis of hyperacute rejection?
preformed antibodies, esp ABO or HLA, seldom seen because of matching
antibodies bind to antigens on vascular endothelial cells, complexes fix complement, activates neutrophils, active coagulation cascade
What is the pathology of hyperacute rejection?
widespread thrombosis wiht extensive ischemic injury, necrotizing vasculitis, influx of neutrophils in arteries and peritubular capillaries, thrombosis of blood vessels and ischemic necrosis, C4d in peritubular capillaries
When does accelerated acute rejection present?
3-7 days
What is the clinical presentation of accelearated acute rejection?
fever and tenderness over graft site
What si the pathogenesis of accelerated acute rejection?
humoral mechanisms, de novo antibodies or induction of amnestic response
What is the pathology of accelearated acute rejection?
similar to hyperacute with arterial and capillary thrombosis, infiltration of neutrophils in arteries and peritubular capillaries, ischemic injury, C4d positive in peritubular capillaries
When does acute rejection occur?
more than 7 days after transplant, usually within first several months
How does acute rejection present?
abruptly increased creatinine, graft tenderness
What is the pathogenesis of acute rejection?
humoral and cellular (CD4 and CD8)
acute cellular or acute vascular
vascular is due to humoral mechanisms (ABs to HLA-Class I antigens), C4d is present in most cases with humora mechanisms
What is the pathogenesis of acute cellular rejection?
lymphocytic interstitial infiltrate and lymphocytes invading tubular epithelium
What is the pathogenesis of acute vascular rejection?
lymphocytes under endothelium of arteries
What is pathogenesis of severe acute vascular rejection?
full thickness infiltration of inflammatory cells in arterial walls, transmural necrosis
Waht ist he prognosis for acute cellular rejection?
responds well to increased anti-rejection therapy
What is the prognosis for vascular rejection?
needs more aggressive therapy, less responsive to treatment
What is chronic allograft nephropathy?
scarring of renal graft
What causes chronic allograft nephropathy?
preexisting disease in donor, recurrent/de novo disease, preceding acute rejection, scarring due to drug toxicity
What does chronic allograft nephropathy look like?
interstitial, vascular and glomerular scarring, arteries show concentric fibrointimal thickening of arteries
What is the prognosis of chronic allograft nephropathy?
inexorable decline, can lose the graft
What is calcineurin inhibitor nephrotoxicity?
acute or chornic nephrotoxicity, in kdineys from patients on CNI after receiving other transplants
What is the pathogenesis of calcineurin inhibitor nephrotoxicity?
CNI is toxic to renal cells, induces vasoconstriction, casues concentric arteriole hyalinosis, due to vascular smooth muscle cell necrosis
What does chronic CNI toxicity look like?
pattern of scarring in which fibrotic tubulointerstitial areas are interspersed with more normal regions,s triped fibrosis, prolonged vasoconstrction along medullary rays