Renal Tubular and Interstitial Diseases Flashcards

1
Q

Definition of AKI

A

Loss of renal function over hours or days

Clinically as retention of nitrogenous waste products (rising creatinine and urea)

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2
Q

Causes of AKI in hospital setting

A

ATN

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3
Q

ATN

A

Most common cause of AKI in hospitalized

Ischemia or exposure to substance directly toxic to tubular epithelial cells

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4
Q

Types of nephrotoxic injury

Ischemic injury

A

Aminoglycosides
IV contrast media…other random medicines..also .ethylene glycol

Endogenous - myoglobin from rhabdomyolysis

Ischemic - spetic, burns, homrrhage, prolonged dehydration, CHF

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5
Q

Most susceptible areas of injury of the PCT

A

S3 segment and TALH (thick ascending loop of Henle)

High tubular energy requirement (ATP)
Decreased O2 supply
Minimal glycolytic machinery

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6
Q

Pathology of ATN…early

A

Loss of apical brush borders

Blebbing of atypical cytoplams into lumen with eventual loss

Vacuoolization of cytoplasm

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7
Q

Pathology of ATN

A

Luminal ectasia

Epithelial simplification from loss of cytoplasm

Granular casts (of cellular debris and Tamm-Horsfall prtoein)

With renal tubular epithelial casts

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8
Q

ATN regnerative phase

A

Mitotic figures

increased N/C ratio

Prominent nucleoli

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9
Q

U/A of ATN

A

Tubular epithelial cells
Tubular epithelial casts
Granular casts “muddy brown”
Multiple granular casts

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10
Q

GFR and ATN

A

DECREASED because

Vasoconstriction - AA via increased NaCl and flow to the macula densa

Tubular obstruction - casts and cell debris

Denuded tubular epithelium - back leak of filtrate to the interstitium

Direct toxocity to glomerular vasculature

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11
Q

FENa

A

Frctional excretion of Na

Urinary (Na)/plasma (Na) *GFR

U(na)P(cr)/(PnaUcr)

When conserving Na, would be below 1%…in ATN, over 1-2%

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12
Q

ATN clincal

A

Sustained decrease in urine output

some do NOT have oliguria

Sodium and H2O overload - hypervolemia

Elevated BUN, creatinine, K+

Acidosis

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13
Q

ATN management

A

Prevention is key**

Na, H2O, and K restriction

Diuretics will not alter the outcome but will assist in management

Close assement of dosing

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14
Q

ATN recovery phase

A

Steady increase in urine volume…solute diuresis, eliminating the accumulated Na and water…decreased ability of kindye to concentrate (loss of medullary osmolarity and ADH)

Hypokalemia

BUN and cr return to normal

More infections

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15
Q

Atn outcome

A

Prognosis depends on clinical setting

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16
Q

Contrast neprhopathy

A

Renal vascular constriction caused by high osmolarity, endothelin and adenosine

12-24 hours after constrat

Non-oliguric and function reutnr in 5-7 days

Pts with diabetic nephropathy at higher risk

17
Q

Contrast nephropathy managmeent

A

Prevention

Risk./benefit

Acetylcysteine not provem

Fluids - bicarb or normal saline…just hydrate them

18
Q

Aminoglycoside toxicity

A

Accumulates in proximal tubular cells

Intracellular concentrations arem uch higher than plasam

5-7 days after initiating tx

Decreased istal ADH sensitivity, fanconi syndrome, hypomagnesemia

NON-oliguric

19
Q

Drug associated AIN

A

INvolvement of kidney by immunologic response to medication

T-cell mediated or AB mediated

Acute renal fialure within 1-2 weeks of drug expoure

Also maybe to systemic AI ds of malignant neoplasms

Allergic reaction

20
Q

Drug induced AIN

A

Fever, rash, eosinophilia

Mild flank pain

AKI

Leukocyturia with eosinophiluria

US - normal or enlarged kindey and increased cortical echogenecity

21
Q

Acute pyelonephritis

A

Acute bacterial infection with suppurative inflammation

Most by ascending urinary tract infection (E coli)

Minority from hematogenous from Stpah

Does NOT cause AKI unless bilateral, septic, dehydrated or has one kidney

22
Q

Acute pyelonpehritis urinalysis

A

WBCs and bacteria are nonspecific that could be found in cystitis

WBC casts are specific and localized to renal parenchyma

23
Q

COmplications of acute pyeloneprhitis

A

Papillary necrosis - diabetics

24
Q

Acute pyeloneprhtiis clinical

A

Fever, chills, severe unilateral flank pain, dysuria, urgency

Urine and blood culture

25
Q

Papillary necoriss

A

Diabetes
Analgesic neprhopathy
Sickle cell
Obstruction

26
Q

Tubular obstruction

A

Myeloma kindey - any patient with unexplained renal fialure and bland urinary sediment

Oxalate - ehtylene glycol

27
Q

Light chain cast neprhopathy

A

Lymphoplasmacytic disorders (MM)

Light chain casts (B-J) - brittle and fractured

TEC damage

28
Q

Rhabdomyolysis and AKI

A

Pt usually found down (myositis, drug)

AKI from pigment crystals in tubules…direct toxicity and also vasoconstriction

VOlume depletion increases greatly the risk for AKI-seomtimes IV fluid is initiated after earthquakes

Low calcium, High phosphorus and K

Positive blood by dipstikc but no RBCs

29
Q

Bile cast neprhpathy

A

Veyr high bilirbuin

30
Q

CIN

A

Tubular atrophy, macrophage, and lymphocytic infiltration and interstitial fibrosis

Lithium, analgesics
Hypercalcemia 
Sarcoidosis
Atherosceloritc vascular disease
CHronic pyeloneprhtois
Cystic diseases
31
Q

When to suspect CIN

A

Pyuria with negative urine culture

Changes in K and H+ out of proportion to change of decreased GFR

POlyuria (decreased conc ability)

Low BP

Known reason for CIN

32
Q

Path of analgesic neprhopathy

A

Primary is medullary iscehmia

Acetaminophindecreases cellular glutathione and subsequent gen of oxidavtive

Aspirin inhibits prostaglandin and decrease vasodilatory

Chronic cortical tubulointersittial neprhitis and pap necorsis

Uroepi malig risk

33
Q

ANalagesic outcome

A

Withdraw drug

Progressive impairment can lead to ESRD

Can lead to uroepithelial carcinoma

34
Q

Chronic pyeloneprhitis

A

Cortical scarrring and atrophy with reflux neprhopathy or bstruction and associated recurrent infection

Present iwht proteinura, HTN< and renal insuff

35
Q

CIN US

A

Small and shrunken kidney

36
Q

CIN micro

A

Interstitla fibrosis and chronic inflam infiltrate in fibrotic areas predominialy lymphocytic