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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
What is the histology of Acute interstitial infectious nephritis
disappearance of the brush border in prox tubule lymphocyte invasion eosinophils around veins tubulitis
26
What is Eosinophiluira (Hansel's stain) consisten with?
AIN | Atheroembolic AKI - AIN
27
What is a Gallium stain? What is stained, what isnt stained?
binds to areas of inflammation/rapid cell division Interstitial nephritis = stains ATN = no stain
28
What are signs of ATN, AKI
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
29
What is the most common cause of acute kidney injury?
Acute Tubular Injury/Necrosis
30
What are 3 causes of ATN?
1. Ischemia 2. Sepsis 3. Nephrotoxins
31
What are some examples of Nephrotoxins
``` Synthetic cannabinoids Hetastarch (hyperoncotic fluid resuscitation) Mannitol IVIG CONTRAST!! ```
32
What are the two stages of ATN?
1. Tubular injury - vasoconstriction, debris, fluid leak into interstitiom, injury, ischemia, toxins 2. Blood flow disturbance - endothelial cell injury, Vasoconstriction
33
What is the Dx of ATN
Muddy brown urine casts FENA >2%/FEUr Fluid challenge - Volume depleted and not CHF, Hepatorenal
34
What is the management of ATN
Dialysis
35
What are 8 general causes of Tubulointerstitial Nephropathy?
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
What are 4 features of Chronic TIN?
1. Atrophy of tubular cells 2. Tubular Dilation 3. Mononuclear cell infiltration 4. interstitial fibrosis
37
What 3 things are the cellular infiltrate composed of in chronic TIN
1. lymphocytes 2. macrophages 3. B cells
38
What does chronic interstitial nephritis look like on a histology slide?
tubules are gone
39
What are 3 prominent clinical manifestations of Chronic Interstitial Nephritis?
1. Insidious onset (decrease GFR) 2. Tubular proteinuria mainly composed of LMW protein (<1g/day) 3. Inactive urinary sediment etc: 4. Proximal tubular dysfunction (Fanconi, renal tubular acidosis) 5. Distal tubular dysfunction 6. Salt-wasting syndrome 7. salt-sensitive hypertension
40
What are the two features of Myeloma Kidney?
1. excess MONOCLONAL Ig (Light Chains) | 2. bone destruction
41
How do light chains cause renal damage?
1. Light chains filtered through - cause PCT damage 2. attach to Tamm-Horsfall = "CAST NEPHROPATHY" 3. LC Glomerular Disease = LC deposit in GBM
42
What is the clinical presentation of LCGD?
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
What are lab changes that suggest myeloma?
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
What is a risk of Immune paresis?
Increased infection risk
45
What are 3 prerenal causes of renal injury?
1. Hypercalcemia (polyuria, hypotension, fever) 2. NSAIDS (Oliguria, hyperkalemia) 3. Hyperviscosity (IgA, IgG3) - Mental changes, tumor lysis
46
What are 2 Renal causes of renal injury?
1. Proximal tubular injury from LC, Uric Acid, Casts (Fanconi) 2. Glomerular disease (LCDD, amyloid) - proteinuria, crystalluria, nephrotic, proteinuria, hematuria
47
What is a post-renal cause of renal injury?
Calculi (Colic)
48
What are 3 histological findings of Renal Disease with Multiple myeloma (by descending prevalence)
1. Myeloma kidney (cast) - 30%-50% 2. Interstitial nephritis/fibrosis w/o cast - 20-30% 3. Amyloidosis - 10%
49
What is the Tx for Myeloma Nephropathy? (hypercalcemia, LC, Supportive)
1. hypercalcemia - BISPHOSPHONATE 2. LC - Steroid, proteasome inhibitor 3. supportive - Dialysis
50
What are two general categories for causes of Chronic pyelonephritis
1. chronic obstruction | 2. chronic reflux-associated
51
What is Chronic pyelonephritis? (3 things)
1. interstitial inflammation 2. scarring of renal parenchyma 3. scarring of pelvicalyceal system
52
What are examples of chronic obstruction causes of chronic pyelonephritis
1. recurrent acute inflammations 2. stones 3. ureteral obstruction 4. prostate 5. obstruction of the urethra
53
What is an example of a chronic reflux-associated cause of chronic pyelonephritis
vesicoureteral reflux
54
What are 3 ways to investigate vesicoureteral reflux?
1. Voiding cystourethrography 2. Ultrasound 3. DMSA (visual tubular scarring)
55
What cause Vesicoureteral reflux?
failure of the flap covering the ureter in the bladder
56
What is the appearance/histology of a scarred kidney from chronic pyelonephritis?
1. hypertrophy of interlobular blood vessels | 2. eosinophilic material in tubule
57
What is DMSA used to Dx?
Acute nephritis
58
What is the Tx for Vesicoureteral reflux?
1. antimicrobial prophylaxis | 2 Surgical reimplantation of ureter
59
What ion imbalance is TI disease in Sarcoidosis related to?
hypercalcemia - hypercalciuria from: Hyperabsorption Increase VitD activation (inc prod of 1-alpha-hydroxylase)
60
Describe Sarcoidosis TI disease
chronic Granulomatous intersitial nephritis
61
What does Sarcoidosis Ti disease (Granulomatous interstitial nephritis) look like histologically?
Giant Multinucleated cells surrounded by mononuclear infiltrate, fibrosis
62
What is the Biopsy like in Granulomatous interstitial nephritis disease?
normal glomeruli interstitial infiltration = Mononuclear cells, NONCASEATING granuloms in insterstitium tubular injury
63
What is the DDX of Granulomatous interstitial nephritis
``` sarcoidosis drug induced TB, mycobacterium Wegeners, brucellosis, histoplasmosis CROHN's ```
64
What can hypercalcemia in Sarcoidosis lead to?
Nephrolithiasis Nephrocalcinosis (seen in pts with CKD) Polyuria
65
What is the treatment of Sarcoidosis
Glucocorticoids - recovery depends on extent of fibrosis
66
What 3 things do Hyperuricemia/Hyperuricosuria cause?
Renal lesions from crystallization of uric acid: 1. Acute urate nephropathy 2. Chronic urate nephropathy 3. Uric acid nepholithiasis
67
What is tumor lysis syndrome?
``` Oncologic emergency Tumor cells release intracellular contents: high K, UR, PO4 low Ca risk for CARDIAC ARRHYTHMIAS ```
68
What is phosphate Nephropathy? What does it commonly result in?
Under recognized cause of acute and chronic renal failure | commonly results in: hyperphosphatemia, hyperphosphaturia, transient hypocalcemia
69
What does phosphate nephropathy look like histologically?
Van kossa stain: | Abundant calcium phosphate deposits in the DCT, collecting ducts
70
What are risk factors for phosphate Nephropathy
``` Excessive OSPS dosing AKD or CKD renal transplant age HTN ACEI, ARB, diuretic or NSAID use abnormal bowel motility ```
71
What is Fanconi syndrome
found in children with renal rickets, glycosuria, hypophosphatemia PCT: global dysfxn: exretion of AA, Glucose, Phosphate, Bicarb, UA
72
What are the clinical problems of Fanconi Syndrome?
``` Acidosis Dehydration (eletrolyte impalance) RICKETS OSTEOMALACIA growth failure ```
73
What are causes of Fanconi Syndrome?
``` Inherited (younger pts) Acquired causes: 1. drugs (CISPLATIN, IFOSFAMIDE) 2. Dysproteinemias 3. Heavy Metal (LEAD) ```

Nephrology (13 decks)

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