Renal 1118 Disease Of Renal Tubules And Interstitium

Front 1

What are the clinical features of acute kidney injury?

Back 1

acute kidney failure, with oliguria or anuria

Front 2

What is the pathogenesis of ischemic AKI?

Back 2

ischemia, proximal tubule is most seriously affected as it consumes the most energy

Front 3

What is the most common cause of acute renal failure?

Back 3

ischemic AKI

Front 4

What is the pathogenesis of toxic AKI?

Back 4

toxins cause direct tubular injury with resultant necrosis

Front 5

What does toxic AKI look like in histo?

Back 5

necrotic cells or sloughed epithelial cells within the lumen, hyaline and granular casts in distal nephron segments

Front 6

What causes toxic AKI?

Back 6

casts of hemoglobin/myoglobin, mercury, ethylene glycol, radio contrast, aminoglycosides

Front 7

What does ischemic AKI look like?

Back 7

regenerative changes, loss of proximal tubule brush border, tubule dilation, flattening of the epithelium

Front 8

What is the prognosis of AKI?

Back 8

recovery is common, mortality increased when part of multiorgan failure

Front 9

What is obstructive uropathy?

Back 9

structural or functional abnormality in urinary tract that blocks the normal outflow of urine

Front 10

What is the clinical presentation of unilateral renal obstruction?

Back 10

can be clinically silent unless there is a kidney stone

Front 11

How does bilateral urinary tract obstruction present?

Back 11

impaired urinary concentrating ability, polyuria, polydipsia

Front 12

How does obstruction of the bladder outlet present?

Back 12

micturition difficulties

Front 13

What casues urinary tract obstruction in kids?

Back 13

congenital anomalies, posterior urethral valves, ureteropelvic junction malformation

Front 14

What causes urinary tract obstruction in adults?

Back 14

kidney stones

Front 15

What causes urinary tract obstruction in older men?

Back 15

BPH

Front 16

What cause intrarenal urinary tract obstructions?

Back 16

deposits in tubule, stones, tumors, sloughed papillary tissue wihtin the renal pelvis

Front 17

What causes intrinsic extrarenal urinary tract obstruction?

Back 17

stones, tumors in ureter, ureteropelvic junction obstruction

Front 18

What causes extrinsic extrarenal urinary tract obstruction?

Back 18

neoplasms, inflammatory lesions of retroperitoneum

Front 19

What can cause urethral obstruction?

Back 19

strictures, posterior urethral valves

Front 20

What causes prostate obstruction?

Back 20

BPH, carcinoma

Front 21

What causes urinary bladder obstruction?

Back 21

carcinoma, neurogenic bladder

Front 22

What is hydronephrosis?

Back 22

dilation of the pelvis and calyces, thinning of overlying parenchyma

Front 23

What is the earliest morphologic change of obstructive nephropathy?

Back 23

dilation of the tubules, esp collecting ducts

Front 24

What is the course of obstructive nephropathy?

Back 24

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

Front 25

What is a cystitis?

Back 25

bacterial infection of lower urinary tract

Front 26

What is pyelonephritis?

Back 26

infection of upper urinary tract

Front 27

What is the pathogenesis of acute pyelonephritis?

Back 27

ascending from cystitis or blood-borne seeding the kidney

Front 28

What is the pathogenesis of UTI in males and kids?

Back 28

anatomic or functional efect preventing normal emptying/urinary flow

Front 29

What pathogen causes mostt UTIs?

Back 29

E coli

Front 30

What other pathogens cause UTI?

Back 30

Staph faecalis, Staph albus, Klebsiella, Proteus

Front 31

What does Proteus mirabilis infection cause?

Back 31

urea splitting, staghorn calculi in pelvicaliceal system, can perpetuate infection

Front 32

How does acute cystitits present?

Back 32

urgency with pyuria

Front 33

How does acute pyelonephritis present?

Back 33

flank tenderness, pain, fever, pyuria, acute renal failure if bilateral

Front 34

What is the prognosis of acute UTI?

Back 34

excellent in uncomplicated acute

Front 35

What is the prognosis of chronic pyelonephritis?

Back 35

from repeated bouts, can be congenital or calculi, can develop chronic kidney disease and uremia

Front 36

What does acute pyelonephritis look like?

Back 36

plugs of neutrophils in tubular lamina and surrounding interstitium, tubular injury, abscess formation

Front 37

What does chronic pyelonephritis look like?

Back 37

broad-based scars, jig-saw pattern of interstitial fibrosis, tubular atrophy, interstitial mononuclear inflammatory cells with intervening spared areas
glomeruli are spared until late

Front 38

What is acute interstitial nephritis?

Back 38

interstitial inflammation and edema

Front 39

Waht is chronic intersittial nephritis?

Back 39

insidious onset, fibrosis

Front 40

What are the clinical features of acute interstitial nephritis?

Back 40

oliguric kidney failure, features of hypersensitivity reaction: fever, rash, peripheral eosinophilia

Front 41

What do you see in urinalysis of acute intersitital nephritis?

Back 41

hematuria, pyuria, white cell casts, can have eosionphiluria

Front 42

What is NSAID-related AIN?

Back 42

Na retention/edema, hyperkalemia, decline in renal function/acute kidney failure, interstitial nephritis, with nephrotic syndrome

Front 43

What is the pathogenesis of NSAID-related AIN?

Back 43

inhibition of vasodilating renal PGs resulting in renal hypoperfusion
podocyte effacement, nephrotic range proteinuria
AIN and minimal change-like lesion

Front 44

What is the pathogenesis of AIN?

Back 44

hypersensitivity reaction/immunologic injury from drugs, infections, systemic immunologic disorders

Front 45

What drugs cause AIN?

Back 45

sulfa drugs, methicillin, beta-lactam antibiotics, rifampin, thiazides, furosemide, NSAIDs

Front 46

What is the prognosis of AIN?

Back 46

glmerular and tubulointersitital abnormalities reversible on discontinuation of drugs,
NSAID related injury reversible within days with discontinuation of offending agent

Front 47

What is the pathology of AIN?

Back 47

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

Front 48

What is the prognosis of AIN?

Back 48

typically reversible, may require dialysis

Front 49

What causes papillary necrosis?

Back 49

diabetes, sickle cell, analgesic abuse nephropathy, obstruction

Front 50

What are the clinical features of chronic intersitital nephritis?

Back 50

insidious decline in renal function, aminoaciduria, glycosuria, renal tubular acidosis, decreased urinary concentrating ability, mild proteinuria

Front 51

What can cause chronic interstitial nephritis?

Back 51

crystal deposition, analgesics, Sjogren syndrome, sarcoidosis, multiple myeloma causing light chain nephropathy

Front 52

What is the pathogenesis of CIN?

Back 52

deposits that precipitate in tubules, ongoing immunological injury

Front 53

What is the pathology of CIN?

Back 53

inflammation with tubule injury in absence of proportional glomerular/vascular disease, interstitial fibrosis, tubular atrophy, also specific deposits

Front 54

What is the prognosis of CIN?

Back 54

fibrosis is irreversible, can improve renal function and prevent ESRD if contributing factors are removed and aggravating factors are controlled

Front 55

What is the clinical presentation of hyperacute rejection?

Back 55

0 - 3 days after transplant, typically while still in OR, patient is swollen, acute rise in serum creatinine

Front 56

What is the pathogenesis of hyperacute rejection?

Back 56

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

Front 57

What is the pathology of hyperacute rejection?

Back 57

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

Front 58

When does accelerated acute rejection present?

Back 58

3-7 days

Front 59

What is the clinical presentation of accelearated acute rejection?

Back 59

fever and tenderness over graft site

Front 60

What si the pathogenesis of accelerated acute rejection?

Back 60

humoral mechanisms, de novo antibodies or induction of amnestic response

Front 61

What is the pathology of accelearated acute rejection?

Back 61

similar to hyperacute with arterial and capillary thrombosis, infiltration of neutrophils in arteries and peritubular capillaries, ischemic injury, C4d positive in peritubular capillaries

Front 62

When does acute rejection occur?

Back 62

more than 7 days after transplant, usually within first several months

Front 63

How does acute rejection present?

Back 63

abruptly increased creatinine, graft tenderness

Front 64

What is the pathogenesis of acute rejection?

Back 64

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

Front 65

What is the pathogenesis of acute cellular rejection?

Back 65

lymphocytic interstitial infiltrate and lymphocytes invading tubular epithelium

Front 66

What is the pathogenesis of acute vascular rejection?

Back 66

lymphocytes under endothelium of arteries

Front 67

What is pathogenesis of severe acute vascular rejection?

Back 67

full thickness infiltration of inflammatory cells in arterial walls, transmural necrosis

Front 68

Waht ist he prognosis for acute cellular rejection?

Back 68

responds well to increased anti-rejection therapy

Front 69

What is the prognosis for vascular rejection?

Back 69

needs more aggressive therapy, less responsive to treatment

Front 70

What is chronic allograft nephropathy?

Back 70

scarring of renal graft

Front 71

What causes chronic allograft nephropathy?

Back 71

preexisting disease in donor, recurrent/de novo disease, preceding acute rejection, scarring due to drug toxicity

Front 72

What does chronic allograft nephropathy look like?

Back 72

interstitial, vascular and glomerular scarring, arteries show concentric fibrointimal thickening of arteries

Front 73

What is the prognosis of chronic allograft nephropathy?

Back 73

inexorable decline, can lose the graft

Front 74

What is calcineurin inhibitor nephrotoxicity?

Back 74

acute or chornic nephrotoxicity, in kdineys from patients on CNI after receiving other transplants

Front 75

What is the pathogenesis of calcineurin inhibitor nephrotoxicity?

Back 75

CNI is toxic to renal cells, induces vasoconstriction, casues concentric arteriole hyalinosis, due to vascular smooth muscle cell necrosis

Front 76

What does chronic CNI toxicity look like?

Back 76

pattern of scarring in which fibrotic tubulointerstitial areas are interspersed with more normal regions,s triped fibrosis, prolonged vasoconstrction along medullary rays