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Nephrology > Renal Tubular Disease > Flashcards

Renal Tubular Disease Flashcards

1
Q

What is the incidence of Tubulo-Interstitial Disease in AKI & CKD cases? what can it progress to?

A

10%-15%

ESRD

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2
Q

What are the 4 functions of the Interstitium?

A
  1. Structural support of Tubules, vasculature
  2. Conduit for solute and oxygen transfer
  3. Production of cytokines
  4. Hormone production
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3
Q

What are the 3 hormonal functions of the interstitium?

A
  1. prostaglandins
  2. erythropoeitin
  3. 1-OH-hydroxylation of vitD
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4
Q

How do NSAIDS worsen CKD?

A

NSAIDS inhibit prostaglandin production (reduce kidney perfusion, reduce GFR)

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5
Q

What are the two categories of TI Diseases?

A
  1. Infectious

2. Drug-induced

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6
Q

What is the 3 step progression of tubulointerstitial injury?

A
  1. Glomerular related events
  2. Interstitial inflammation
  3. Interstitial fibrosis and scarring
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7
Q

What happens during glomerular injury of TIN?

A

hemodynamic changes
proteinuria induced tubular cell activation/damage
-apoptosis
cytokines - activation of complement

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8
Q

What happens during the interstitial inflammation of TIN?

A

caused by T-cells (CD4>CD8)

in the ABSENCE of antibody deposition

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9
Q

What type of AIN is there Abs against TBM?

A

Rifampin-induced AIN

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10
Q

What happens during the interstitial fibrosis and scarring of TIN?

A

progressive sclerosis

HYPOXIA

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11
Q

What happens during Acute allergic interstitial nephritis

A

Acute rise in creatinine from offending agent

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12
Q

What is the clinical triad of Acute allergic interstitial nephritis?

A
  1. Rash-maculopapular
  2. fever
  3. eosinophilia
    flank/back pain from renal swelling
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13
Q

What is the most important long term predictor of any renal disease?

A

Stability of the interstitium

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14
Q

What are clinical features of AIN?

A
  1. minimal HTN
  2. early loss of concentrating ability
  3. Early osteomalacia
  4. non AG metabolic acidosis
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15
Q

What happens to the interstitium during Drug associated AIN?

A
  1. interstitial edema
  2. cellular infiltrate (majority: CD4 Tcells)
  3. TUBULITIS (tubule infiltration by Tcells)
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16
Q

What are the drugs associated with Drug associated AIN?

A
  1. Abx(penicillin, methicillin, cephalosporins, sulfonamides, rifampin, vancomycin, cipro)
  2. NSAIDS
  3. Diuretcs
  4. PPI
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17
Q

What is the most common penicillin involved with DAAIN? what are Sx? how is it managed?

A

Methicillin - Triad, oliguric renal failure

Tx: steroid responsive, remove offending agent

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18
Q

What is the onset of NSAID associated AIN? Sx? Biopsy?

A

onset: 2 weeks to 18 months
Sx: triad is uncommon
Biopsy: minimcal change or membranous patter or interstitial granuloma formation

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19
Q

What is the onset of PPI associated AIN? how fast is progression? Tx?

A

onset: 10 weeks
FIBROSIS often develops after 7 days
Tx: early steroids (lower response)

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20
Q

What 3 situations do you do a biopsy in AIN?

A
  1. pts with drug related AIN and do not recover after drug cessation/steroids
  2. advanced Renal Failure
  3. HIGH GRADE PROTEINURIA
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21
Q

What does Acute Interstitial Nephritis show in light microscopy?

A

loss of normal TI architecture
dense cellular infiltrate
tubular distortion

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22
Q

What does light microscopy show is AIN is not treated in time?

A

PAPILLARY SCLEROSIS

fibrosis + edema = blue trichrome stain

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23
Q

What may cause incomplete recovery from AIN after steroids/drug cessation?

A

NSAID induced AIN
persistent oliguric AKI >3 weeks
age, too much damage, preexsiting renal damage

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24
Q

What are the 3 most common causes of Interstitial infection nephritis?

A

B-hemolytic streptococci
Leishmania
EBV, measles
(pyelonephritis)

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25
Q

What is the histology of Acute interstitial infectious nephritis

A

disappearance of the brush border in prox tubule
lymphocyte invasion
eosinophils around veins
tubulitis

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26
Q

What is Eosinophiluira (Hansel’s stain) consisten with?

A

AIN

Atheroembolic AKI - AIN

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27
Q

What is a Gallium stain? What is stained, what isnt stained?

A

binds to areas of inflammation/rapid cell division
Interstitial nephritis = stains
ATN = no stain

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28
Q

What are signs of ATN, AKI

A
  1. rise in serum Cr (0.3mg/dl over 48 hours)
    and/or
    1.5x baseline within a week
  2. Urine volume <0.5ml/kg/hr for 6 hours
    <400mL/day
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29
Q

What is the most common cause of acute kidney injury?

A

Acute Tubular Injury/Necrosis

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30
Q

What are 3 causes of ATN?

A
  1. Ischemia
  2. Sepsis
  3. Nephrotoxins
31
Q

What are some examples of Nephrotoxins

A 
Synthetic cannabinoids
Hetastarch (hyperoncotic fluid resuscitation)
Mannitol
IVIG
CONTRAST!!
32
Q

What are the two stages of ATN?

A
  1. Tubular injury - vasoconstriction, debris, fluid leak into interstitiom, injury, ischemia, toxins
  2. Blood flow disturbance - endothelial cell injury, Vasoconstriction
33
Q

What is the Dx of ATN

A

Muddy brown urine casts
FENA >2%/FEUr
Fluid challenge - Volume depleted and not CHF, Hepatorenal

34
Q

What is the management of ATN

A

Dialysis

35
Q

What are 8 general causes of Tubulointerstitial Nephropathy?

A
  1. Immune mediated (SLE, sarcoidosis, wegener’s)
  2. Hematologic (Multiple myeloma, Light chain disease)
  3. Drugs (Analgesics, Chinese herbs)
  4. Toxins
  5. Metabolic disorder (hyper-uricemia,calcemia,phosph)
  6. Hereditary (pckd)
  7. Infection
  8. Misc (Balkan, VUR, OBSTRUCTION)
36
Q

What are 4 features of Chronic TIN?

A
  1. Atrophy of tubular cells
  2. Tubular Dilation
  3. Mononuclear cell infiltration
  4. interstitial fibrosis
37
Q

What 3 things are the cellular infiltrate composed of in chronic TIN

A
  1. lymphocytes
  2. macrophages
  3. B cells
38
Q

What does chronic interstitial nephritis look like on a histology slide?

A

tubules are gone

39
Q

What are 3 prominent clinical manifestations of Chronic Interstitial Nephritis?

A
  1. Insidious onset (decrease GFR)
  2. Tubular proteinuria mainly composed of LMW protein (<1g/day)
  3. Inactive urinary sediment

etc:

  1. Proximal tubular dysfunction (Fanconi, renal tubular acidosis)
  2. Distal tubular dysfunction
  3. Salt-wasting syndrome
  4. salt-sensitive hypertension
40
Q

What are the two features of Myeloma Kidney?

A
  1. excess MONOCLONAL Ig (Light Chains)

2. bone destruction

41
Q

How do light chains cause renal damage?

A
  1. Light chains filtered through - cause PCT damage
  2. attach to Tamm-Horsfall = “CAST NEPHROPATHY”
  3. LC Glomerular Disease = LC deposit in GBM
42
Q

What is the clinical presentation of LCGD?

A

Markedly increased Urinary total protein
Dipstick negative (trace positive)
Presence of LC (BENCE JONES PROTEINS)

Constitutional symptoms (fatigue, weight loss)
skeletal pain (back pain)
normal sized kidneys, bland urine
43
Q

What are lab changes that suggest myeloma?

A
  1. Elevated ionized calcium
  2. Lytic bone lesions
  3. Immune paresis (reduction in levels of other Ig classes)
  4. Abnormal serum Free Ligh Chain ratio
  5. significant cytopenias
44
Q

What is a risk of Immune paresis?

A

Increased infection risk

45
Q

What are 3 prerenal causes of renal injury?

A
  1. Hypercalcemia (polyuria, hypotension, fever)
  2. NSAIDS (Oliguria, hyperkalemia)
  3. Hyperviscosity (IgA, IgG3) - Mental changes, tumor lysis
46
Q

What are 2 Renal causes of renal injury?

A
  1. Proximal tubular injury from LC, Uric Acid, Casts (Fanconi)
  2. Glomerular disease (LCDD, amyloid) - proteinuria, crystalluria, nephrotic, proteinuria, hematuria
47
Q

What is a post-renal cause of renal injury?

A

Calculi (Colic)

48
Q

What are 3 histological findings of Renal Disease with Multiple myeloma (by descending prevalence)

A
  1. Myeloma kidney (cast) - 30%-50%
  2. Interstitial nephritis/fibrosis w/o cast - 20-30%
  3. Amyloidosis - 10%
49
Q

What is the Tx for Myeloma Nephropathy? (hypercalcemia, LC, Supportive)

A
  1. hypercalcemia - BISPHOSPHONATE
  2. LC - Steroid, proteasome inhibitor
  3. supportive - Dialysis
50
Q

What are two general categories for causes of Chronic pyelonephritis

A
  1. chronic obstruction

2. chronic reflux-associated

51
Q

What is Chronic pyelonephritis? (3 things)

A
  1. interstitial inflammation
  2. scarring of renal parenchyma
  3. scarring of pelvicalyceal system
52
Q

What are examples of chronic obstruction causes of chronic pyelonephritis

A
  1. recurrent acute inflammations
  2. stones
  3. ureteral obstruction
  4. prostate
  5. obstruction of the urethra
53
Q

What is an example of a chronic reflux-associated cause of chronic pyelonephritis

A

vesicoureteral reflux

54
Q

What are 3 ways to investigate vesicoureteral reflux?

A
  1. Voiding cystourethrography
  2. Ultrasound
  3. DMSA (visual tubular scarring)
55
Q

What cause Vesicoureteral reflux?

A

failure of the flap covering the ureter in the bladder

56
Q

What is the appearance/histology of a scarred kidney from chronic pyelonephritis?

A
  1. hypertrophy of interlobular blood vessels

2. eosinophilic material in tubule

57
Q

What is DMSA used to Dx?

A

Acute nephritis

58
Q

What is the Tx for Vesicoureteral reflux?

A
  1. antimicrobial prophylaxis

2 Surgical reimplantation of ureter

59
Q

What ion imbalance is TI disease in Sarcoidosis related to?

A

hypercalcemia - hypercalciuria
from:
Hyperabsorption
Increase VitD activation (inc prod of 1-alpha-hydroxylase)

60
Q

Describe Sarcoidosis TI disease

A

chronic Granulomatous intersitial nephritis

61
Q

What does Sarcoidosis Ti disease (Granulomatous interstitial nephritis) look like histologically?

A

Giant Multinucleated cells surrounded by mononuclear infiltrate, fibrosis

62
Q

What is the Biopsy like in Granulomatous interstitial nephritis disease?

A

normal glomeruli
interstitial infiltration = Mononuclear cells,
NONCASEATING granuloms in insterstitium
tubular injury

63
Q

What is the DDX of Granulomatous interstitial nephritis

A 
sarcoidosis
drug induced
TB, mycobacterium
Wegeners,
brucellosis,
histoplasmosis
CROHN's
64
Q

What can hypercalcemia in Sarcoidosis lead to?

A

Nephrolithiasis
Nephrocalcinosis (seen in pts with CKD)
Polyuria

65
Q

What is the treatment of Sarcoidosis

A

Glucocorticoids - recovery depends on extent of fibrosis

66
Q

What 3 things do Hyperuricemia/Hyperuricosuria cause?

A

Renal lesions from crystallization of uric acid:

  1. Acute urate nephropathy
  2. Chronic urate nephropathy
  3. Uric acid nepholithiasis
67
Q

What is tumor lysis syndrome?

A 
Oncologic emergency
Tumor cells release intracellular contents:
high K, UR, PO4
low Ca
risk for CARDIAC ARRHYTHMIAS
68
Q

What is phosphate Nephropathy? What does it commonly result in?

A

Under recognized cause of acute and chronic renal failure

commonly results in: hyperphosphatemia, hyperphosphaturia, transient hypocalcemia

69
Q

What does phosphate nephropathy look like histologically?

A

Van kossa stain:

Abundant calcium phosphate deposits in the DCT, collecting ducts

70
Q

What are risk factors for phosphate Nephropathy

A 
Excessive OSPS dosing
AKD or CKD
renal transplant
age
HTN
ACEI, ARB, diuretic or NSAID use
abnormal bowel motility
71
Q

What is Fanconi syndrome

A

found in children with renal rickets, glycosuria, hypophosphatemia

PCT: global dysfxn: exretion of AA, Glucose, Phosphate, Bicarb, UA

72
Q

What are the clinical problems of Fanconi Syndrome?

A 
Acidosis
Dehydration (eletrolyte impalance)
RICKETS
OSTEOMALACIA
growth failure
73
Q

What are causes of Fanconi Syndrome?

A 
Inherited (younger pts)
Acquired causes:
1. drugs (CISPLATIN, IFOSFAMIDE)
2. Dysproteinemias
3. Heavy Metal (LEAD)

Nephrology (13 decks)

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