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Renal 2 > Robbins, Chapter 20, Lecture II - tubulointerstitial diseases > Flashcards

Robbins, Chapter 20, Lecture II - tubulointerstitial diseases Flashcards

1
Q

What am I?
Hearing loss, eye problems (corneal atrophy, lens dislocation), nephritis (micro or macro hematuria and frequently with red cell casts)
Type 4 collagen disorder.

EM=ALTERNATING thickening and thinning of BM, frayed/basket woven/moth eaten

A

Alport Syndrome

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2
Q

What hereditary nephritis is X-linked?

A

Alport Syndrome

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3
Q

80% of patinents with family history of hematuria or recurrent hematuria during childhood have one of __what__ disorders?
Defect in type 4 collegen synthesis

A

Hereditary Nephritis

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4
Q

What are the two types of Hereditary Nephritis?

Which has good prognosis?

A

Alport Syndrome

Thin Basement Membrane Disease - good prognosis

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5
Q

What am I?
Disease onset at birth, symptoms do not occur until later in life.
Earliest sign is microscopic hematuria detected between 5-20 years. Overt kidney failure between 20-50 years.

A

Alport Syndrome

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6
Q 
Thinning of glom BM confirms dx of what?
Asymptomatic hematuria.  
Type 4 collagen mutation.
Most are heterozygous for defective gene >> carriers.
Homozygotes resemble AR Alport
A

Thin Basement Membrane Disease

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7
Q

The following are secondary renal diseases.
Diabetic nephropathy
SLE
Hep C - cryobulinemia (MPGN I)
HIV Nephropathy: FSGN
Do they present with Nephrotic Syndrome or Acute Nephritic Syndrome?

A

Nephrotic Syndrome

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8
Q

The following are secondary renal diseases.
SLE
BActerial endocarditis - Acute PRoliferative GN
Goodpasture Syndrome: RPGN
HSP: IgA Neph
Do they present with Nephrotic Syndrome or Acute Nephritic Syndrome?

A

Acute Nephritic Syndrome

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9
Q

What are the consequences of the two major processes play key pathophysiologic roles as diabetic glomerular lesions develop?
Processes:
1. Metabolic defect linked to hyperglycemia
2. Hemodynamic effects associated with glomerular hypertrophy
Consequences: ?

A
  1. Advanced glycosylation end products

2. contribute to development of glomeruloSCLEROSIS

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10
Q

What am I? (Based on morphology)

  • Capillary BM thickening
  • Diffuse mesangial sclerosis - increased mesangial matrix (which then becomes nodular and acellular&raquo_space;)
  • NODULAR GLOMERULOSCLEROSIS
A

Diabetic Nephropathy/Glomerulosclerosis

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11
Q

Clinical course of what?
Systemic HTN&raquo_space; microalbuminuria and elevated GFR&raquo_space; overt PROTEINURIA&raquo_space; ESRF

What can reverse this?

A

Diabetic Nephropathy/Glomerulosclerosis

Pancreatic transplant can reverse glomerulopathy associated with Type 1 DM

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12
Q

Is (End Stage Diabetic) NEPHROSCLEROSIS a large or small vessels disease?

A

small vessel

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13
Q

SLE has immune complex deposition of subendothelial or subepithelial dense deposits? (seen on IF)
What do you see on LM?

A 
IF = desposits in SubENDOthelium (and mesangium)
LM = "wire loops"
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14
Q

What am I?
Systemic, IgA DEPOSITION IN RENAL MESANGIUM.
Rash on extensor surfaces of arms and legs - lesions contain necrotizing vasculitis with microhemorrhage.
Onset CHILDREN, 3-8yo with excellent prognosis.
Onset often follow respiratory infection.

A

Henoch-Shonlein Purpura

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15
Q

What am I?
Associated with Multiple Myeloma that produces lytic bone lesions and patients often develop infections with encapsulated bacteria.
Congo Red Positive and Apple Green Polarized Light
Light chain ___ deposited in areas of areas of large bloodflow = INCREASED SERUM PROTEIN LEVELS.
Death due to uremia.
EM = massive BM without deposits
Urinalysis = heavy proteinuria

A

(amyloid light chain)

Amyloidosis

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16
Q

What am I?
No Congo Red Positive and Apple Green Polarized Light
IF = IgG and C3

A

Fibrillary Glomerulonephritis

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17
Q

What am I?
Associated with HepC
IgG-IgM compelxes induce vasculitis and membranous GN

A

Essential mixed cryoglobulinemia

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18
Q

What type of tubulointerstitial disease?
Dirty brown casts in urine, following ischemia
Pathogenesis - ischemia or toxins
Definition - damage to tubular epithelial cells and acutely diminished renal function

A

Acute Tubular Necrosis

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19
Q

What type of tubulointerstitial disease?
Eosinophilia, rash, fever
Pathogenesis - inflammation
Definition - eosinophilia

A

Tubulointerstitial fibrosis

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20
Q

What are the two ways that Acute Tubular Necrosis can occur? What part of the nephron does most necrosis occur in each type? Where do casts occur?

A

(1) Ischemic ATN - PCT, PST, Ascending LoH are all PATCHY
(2) Nephrotoxic ATN - PCT and PST are CONTINUOUS while AscLoH is Patchy

Casts along all patchy parts not necrosed - DCT, CD

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21
Q

Necrotic tubular epithelial cells detach and slough off into tubular lumen - what do these casts cause?

A

Obstruction of flow!

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22
Q

Clinical course of ATI (3 stages)? What is the largest clinical issue at each stage

A

(1) Initiation - 36 hours oliguria and rise in BUN
(2) Maintenance - severe oliguric crisis with evidence of uremia. HYPERKALEMIA is the major issue.
(3) Recovery - in a few weeks, initial POLYURIA as water balance is restored. HYPOKALEMIA is clinical problem.

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23
Q

What classifies an oliguric crisis?

A

40-400mL/day

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24
Q

What is (Primary) Tubulointerstitial Nephritis caused by?

A

A group of renal diseases that tend to be insidious, generally characterized by azotemia and inability to concentrate urine (resulting in polyuria).

25
Q

(Gram-negative) E Coli, Proteus, Klebsiella, enterobacter for fecal flora cause what?
Upper or lower infection more common? What sex and age range?

A

UTI
Lower UTI more common
F>M, 0-40yo

26
Q

What predisposing anatomic defect usually presents in pyelonephritis?
Is pyelonephritis normally an ascending or descending infection from where? What does scarring look like?

A 
Vesicoureteral reflux (bacteria gains access to ureters from bladder) and association with subsequent intrarenal reflux (each contraction of the bladder = pushes bacteria up >> ASCENDING to kidney from bladder).
Polar scarring phenomenon.
27
Q

What am I? (morphology)
PATCHY INTERSTITIAL SUPPARATIVE INFLAMMATION, *WBC casts on urinalysis, TUBULAR NECROSIS.
In diabetics you see papillary necrosis.
ALWAYS shows FIBROSIS of the underlying renal pelvis and calyces

A

Acute Pyelonephritis

28
Q

What am I? (clinical)
Patient comes in SICK with fever, malaise, sudden onset flank pain as costovertebral angle, etc.
POLYOMAVIRUS.
Adult women, due to shorter urethra
Males younger than 1yo - congenital defect
Males older than 40yo - CATHETERIZATION and prostate obstruction

A

Acute pyelonephritis

29
Q

Papillary necrosis in acute pyelonephritis:
What three settings?
Male to Female ratio for each.
Length of time for necrosis.
Calcification affects how much of papillae
Color and location of necrosis.

A
  • *See table!!!
    (1) DM - F(1:3), 10 years, PALE GRAY necrosis limited to papillae
    (2) Analgesic nephropathy (abuse) - F(1:5), 7years, frequent calcification in almost all papillae affected, differnt necrotic stages, RED-BROWN necrotic papilla sloughed INTO CALYX
    (3) Obstruction - MALES(9:1), frequent calcification and infection
30
Q

What am I?
CORTICOMEDULLARY SCARRING OVERLYING DILATED, BLUNTED, OR DEFORMED CALYX.
Caused by recurrent ascending infections, obstructive uropathy, XANTHOGRANULOMATOUS (proteus infection)

A

Chronic pyelonephritis

31
Q

What can xanthogranulomatous mimic?

A

RCC

32
Q

Inreased scarring in chronic polynephritis can lead to what?

A

FSGS

33
Q

What am I?
Fever, rash, eosinophilia, acute renal failure (increased SrCr and oliguria) 2-40 days after exposure to: NSAIDS, synthetic penicillins, or other drugs.
Morphology - see pronounced edema in interstitum and eosinophils/neuts

A

(Drug associated) Tubulointerstitial Nephritis

34
Q

What am I?
Small vessel, Hyaline Sclerosis of renal arterioles and small arteries associated with AGING, DM, and HTN.
Sclerosis is due to medial and intimal thickening due to hemodynamic changes. Causes ISCHEMIA of kidney parenchyma.

A

Benign Nephrosclerosis

35
Q

What am I?
Morphology - small kidneys with leathery appearance
Clinical - proteinuria, decreased GFR.
What do you have to be careful to look for in african Americans with HTN or Diabetic nephropathy that’s NOT NORMALLY PRESENT?

A

Benign Nephrosclerosis

Renal insufficiency

36
Q

In Malignant HTN, what do ischemic kidneys result in elevation of in plasma? This causes abnormal amount of what? What does this ultimately cause?

A

Renin increased causes abnormal amount of vasoconstriction»exacerbation HTN.
Ultimately causes FIBRINOID NECROSIS and HYPERPLASTIC ARTERIOLITIS, ischemic atrophy, infarct

37
Q

What are “flea bitten” indicative of?

A

Renal hemorrhage, gross manifestation of Malignant HTN

38
Q

What BP classifies as Malignant HTN/medical emergency?

What other clinical features?

A

200/120

Papilledema, Retinal hemorrhage, ENCEPHALOPATHY, CV abnormalities, early symptoms due to increased ICP

39
Q

How is HTN due to large (UNILATERAL) renal artery stenosis cured?

A

Surgery

40
Q

What are the two most common morphologic etiologies of large vessel disease?
Hint: (1) where do plaques originate (2) strong of beaded appearance

A
  1. Most common - ATHEROSCLEROSIS - plaques at ORIGIN OF RENAL ARTERY
  2. FIBROMUSCULAR DYSPLASIA of the RENAL ARTERY- most commonly in younger women
41
Q

What are the two thrombotic microangiopathies?

A

TTP - therombocytopenia, microangiopathic hemolytic anemia, thrombosis
HUS - TTP without neuro symptoms, WITH renal failure

42
Q

What am I?

Pathogenesis of endothelial injury and activation or from platelette aggregation.

A

Hemolytic Uremic Syndrome / Thrombotic Thrombocytopenic Purpura

43
Q

What am I?
Adults who are older younger than 40. F>M
Pentad of symptoms - Fever, NEURO SYMPTOMS, microangiopathic hemolytic anemia, thrombocytopenia (dcreased platelets), renal failure in 50%.
Relapsing and remitting.
Deficient in ADAMTS13.

A

Classic TTP

44
Q

What am I?
CHILREN and older adults. Associated with SHIGA-like toxin of E. coli O157:H7. Diarrhea positive, prodrome followed by sudden onset of bleeding, severe oliguria, heamturia, neuro changes, HTN.
Long term prognosis?

A

Typical HUS

Poor

45
Q

What am I?
ADULT.
NON-DIARRHEAL, inherited mutation of protein that regulates complement (what % have this?).
SLE/antiphospholipid syndrome, PREGNANCY ASSOCIATED (uncomplicated pregnancy followed by renal failure 3 mo later), systemic sclerosis, chemo, Wegner’s/scleroderma/HTN

A

Atypical HUS

More than 50% have inherited mutations of proteins that regulate complement.

46
Q

What makes TTP different from Atypical HUS?

A

TTP MUST HAVE ADAMTS13 deficiency.

TTP has neuro symptoms, but atypical HUS can too.

47
Q

What does ADAMS13 protein do? What disease is it associated with?

A

Protease that cleaves vWF to decrease clotting. vWF accumulates in TTP due to deficiency in ADAMS13 because of presnce of autoantbodies that inhibit ADAMTS13 funciton.

48
Q

What is elevated in Atherosclerotic Ischemic Renal Disease? A decrease in this (if ACE or ARB are given) will result in what?

A

ANGII

increased RBF but decreased GFR = actue renal failure

49
Q

Atheroembolic Renal Disease result from emboli from what location?

A

Proximal to renal artery

50
Q

Whath am I?

Flank pain, abd pain, hematuria, arrhythmia, nausea/vomiting, oliguria, anuria, arterial HTN.

A

Atheroembolic Renal Disease

51
Q

Renal infarcts are dangerous because the kidney has what? White or red and what shape infarct?

A

has “end organ” vascular supply with a lack of colalteral circulation.
Infarcts are white and wedge-shaped.

52
Q

What do the following result in?
Mural thrombosis on the left side of the heart (most common).
Less frequent causes - vegetative endocarditis, aortic aneurysms, aortic atherosclerosis

A

EMBOLISMS that result in RENAL INFARCT

53
Q

What am I?

Hematuria, hyposthenuria (DILUTE URINE), patchy papillary necrosis, 30% have sub-nephrotic range proteinuria.

A

Sickle Cell Neuropathy

54
Q

What does sickling (due to Sickle Cell Neuropathy) in the vasa recta decrease?

A

Decreases concentrating ability and increase thrombosis

55
Q

What am I?
Follow malignant HTN, obstetric emergency, Septic Shock surgery.
Ischemia and necrosis limited to CORTEX (gom and tubules?)&raquo_space; white infarcts.
THROMBOSIS of glom and renal artery, hemorrhage may be present.
Systemic hypoperfusion and hypoxia

A

Diffuse Cortical Necrosis

56
Q

???

What are the only two things that affect the calyces?

A

CPN - reflux nephropathy and chronic obstructive pyelonephritis

57
Q

Causes of hematuria: SCHITTT

A 
Stones (Nephrolithesis)
Congenital Abnormalities (of the bladder)
Hematologic abnormalities
Infection
Trauma
Tumor
TB
58
Q

What am I?
Hyalizing arteriolar sclerosis, increasing susceptibility to pyelonephritis and PAPILLARY NECROSIS&raquo_space; causing TUBULAR LESIONS and RBC in urine.

A

Diabetic Nephropathy

59
Q

Membranous glom associated with what adenocarcinoma?

A

Lung

Renal 2 (12 decks)

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