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RENAL > Acute Kidney Injury and Tubulointersticial Disease > Flashcards

Acute Kidney Injury and Tubulointersticial Disease Flashcards

1
Q

Guidelines for Acute Kideny Injury (AKI) (3)

A
  1. Incr in serum creatinine of 0.3mg/dL within 48HR.
  2. Incr serum creatinine of 1.5x the baseline level within 1 week
  3. Urine production of <0.5mL/kg/HR.per 6HR (oliguria)
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2
Q

Normal creatinine values males and females

A

-Males: 0.74-1.3 mg/dL
-Females: 0.5-1 mg/dL

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3
Q

Graph of your AKI

A
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4
Q

Prenal AKI mayor causes

A

-NSAIDS (chronic pain),Burns,Cardiogenic shock, Hemorrages,Diarrhea
-Hypo-albuminuria (Hepato-Renal syndrome)
-HF (Cardio-Renal syndrome)

-All relate Hypo-perfusion.

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5
Q

Pathophysiology of Pre-renal AKI..

A

-Hypoperfusion–>Incr. RAAS system–>Hypertension+reabsp of H2O and Na+(less Na and H2O in urine)–>less H2O in lumen your BUN INCR.
-All this is possible because** tubules are NOT damaged**.

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6
Q

What do you expect in Pre-renal AKI

1.Urine osmolarity: concentrated or Diluted
2.GFR: incre or decr
3.Urine Na+ :incr or decr
4.FE%Na+ :incr or decr
5.serum BUN/Creatinine: incr or decr

A

1.Increase (>500mOsm/Kg)
2.Decr GFR
3.Decr. (<20)
4.Decr (1%)
5.Incr (20:1 ratio)

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7
Q

Why do you NOT see a AKI when only one kidney is affected?

A

-The other kidney will be able to withstand the load.
-Dosent permit increase in creatinine nor oliguria.

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8
Q

Post-Renal AKI associated with…(2)
-Pathophysiology

A

-Obstructions BELOW bladder–>in order to affect both kidneys.
-BPH,Post urethral valve (congenital), advanced stage cervical cancer.

-Backflow–> 1.Damaged Tubules:absp is affected (values as intrarenal)

2.Non-damgaed tubules:absp is FUNCTIONAL (values as Pre-renal)

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9
Q

Intra-Renal AKI sub-divisions(3) ans associations

A

-Vascular–>Vasculitis
-Glomerular-->Glomerulonephritis (RPGN)
-Tubular–>1.Acute Tubular Necrosis-->a)Ischemia and b)Toxins (myoglobin,aminoglycosides,contrast agents, metals,cisplatin)
2.Tubulointerstitial Nephritis (Tubular Acidosis, Pyelonephritis,Drugs)

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10
Q

What are the Toxins associated with Acute Tubular Necrosis in Intra-renal AKI?

A

-Myoglobin,Contrast agents, aminoglycosides,cisplatin,metals,MTX,anti-freeze

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11
Q

Pathophysiology of Intra-Renal AKI…

A

-NO Functional Tubules–>cannot regulate

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12
Q

What do you see in INTRA-RENAL AKI

1.Urine osmolarity: concentrated or Diluted
2.GFR: incre or decr
3.Urine Na+ :incr or decr
4.FE%Na+ :incr or decr
5.serum BUN/Creatinine: incr or decr

A

1.Diluted (<350)
2.-Decr GFR (specially in Acute Tubular Necrosis–>sloughing of cells casuing obstr–>incr glomerular hydrostatic pressure).
3.(>40)
4.(>2%)
5.(<15:1)

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13
Q

How so we differentiate between** Damaged Post renal AKI vs Acute Tubular Necrosis Intra renal AKI**?

A

-POST-RENAL Damaged:urianalysis (nothings)
-Acute Tubular Necrosis: urianalysis you see renal tubular cell cast (muddy brown app)

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14
Q

Acute Glomerulonephritis (Intra renal) present similar to…
WHY?

A

-Pre renal AKI
-Its not affecting Tubules,only the glomerulus

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15
Q

How to diffbetween Pre-renal AKI vs. Acute Glomerulonephritis (Intra-renal)?

A

-Pre-renal:urianalysis normal or Hyaline cast
-Acute Glomerulonephritis:RBC cast or hematuria

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16
Q
A
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17
Q

Can your Pre-renal and Post-renal AKI progress to Intra-renal AKI?

A

-YES
-This is why a patient that suffers a severe burn is given IV fluids immediatly do prevent progression to Intrarenal AKI.

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18
Q

Complications of AKI(3)

A

-Hyperkalemia, metabolic acidosis and hyperurecemia–>serotitis.

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19
Q

Fill the table:

A
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20
Q

What are the 2 main causes of Acute Tubular Necrosis?

A

-Ischemia (any hypovolemia states–>cardiogenic shock, hemorrage, burns, sepsis,NSAIDS)–>how it relates to pre-renal injury progressing to intra-renal injury.
-Toxins (myoglobin–>rhabdomyolysis, so -statins may also cause it, cisplatin,MTX, antifreeze, aminoglycosides, metals (Lead), contrast dyes)

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21
Q

Prognosis of Acute Tubular Necrosis

A

Ischemia–>Poor
Toxins–>Good

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22
Q

Pathophysiology of Acute Tubular Necrosis..

A

-Ischemia (either toxins or ischemia by hypoperfusion)–>3 changes -Na+/K+ ATPase moves from basolateral to apical surface, -Integrins decr. and -Tight junctions also decr.–>NOT being able to reabsp. Na+, therfore incr lumen sodium promoting H2O to follow** and Epi cells are easier tu slough off–>causing lumen obstruction and **DECR GFR **due to backflow.

-The further decr in volume in blood due to H2O excretion will worsen the necrosis.

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23
Q

Why is Acute TubulaR Necrosis considered a Intrinsic AKI?

A

-Obstruction it has on renal tubules.

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24
Q

ATN ischemia associated with..

A

-NSAIDS,cardiogenic shock,Hemmorages,anythings that casues hypoperfusion.
-Same as Pre-renal injury.This is why we sat that pre-renal injuries cause Intrinsic AKI.

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25
Q

ATN toxin type is associated with…

A

-Aminoglycosides,contrats dyes,cisplation,anti-freeze, myoglobin,uric-acid,Lead poison….

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26
Q

Biopsy and location wise, how do you differentiate ischemia and toxin mediated ATN?

A

-Ischemia:dscontinous damage/Damages areas high in energy consumption (PCT and Asc Loop of Henle)
-Toxin:continous damage/ Damages first encountered area–>PCT.

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27
Q

What are the stages in ATN and what do you see?

A

1.Injury:decline urine output
2.Mantainance: INCR BUN/creatinine, oliguria (<400mL/Day),Hyperkalemia–>most comm cause of death due to fatal arrythmias. Last for 3 weeks
3.Recovery: Tubular Re-Epithelization.** HYPOKALEMIA**

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28
Q

Diagnosis and decribe what you see..(3)

A

-ATN
-Blockage on tubule lumen (WHY?)
-Muddy brown CAST (granular cast)-->necrosis of epi cells,
-Epi cell flattening

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29
Q

Lead posoning presentation?

A

-Inhb Ferrochelatase–>incr protoporphirin +Microcytic anemia+Basophilic stippling on Blood smear.

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30
Q

Causes of Interstitial nephritis (8)

A

-Drugs 5P’s (Pee-Diuretics-Thiazide and Furosemide./Pencillin and Chephalosporins /Rimfampin/PPI (Omeprazole)/Pain-free (NSAIDS) and Sulfa drugs)
-Infections:Acute and Chronic Pyelonephritis
-Toxins:Analgesic
-Metabolic:Light chains cast Nephropathy (M.M), Urate Nephropathy, Nephrocalcinosis, **Transplant rejection. **

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31
Q

Diagnosis

Inflamation of Renal interstitium and tubules relating drug use.
-Presentation is malaise,fever rash

A

-Interstitial Nephritis.

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32
Q

What mechanism of damage does Interstitial nephritis involve?

A

-Type 1 or 4 Hypersensitivity reaction.
-Drugs will act as a hapten–>triggering of Imm system.

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33
Q

Urianalysis of Interstitial Nephritis relating drugs and what should the history include + presentation?

A

-Elavated BUN/creatinine, sterile pyuria, EOSINPHILS,WBC cast
-History of drug use. **
-TRIAD:Fever,malaise, rash**–>Hypersensitivity reaction.

34
Q

Differentiate

Acute vs. Chronic Interstilial Nephritis

A

-Eosinphils in Acute-Lymphocytes (mononuclear cells) in Chronic.

35
Q

Complications of Acute Pyelonephritis(2)
Presentation
Where does it affect?

A

-Perinephric abscess,Renal Papillary Necrosis, Chronic Pyelonephritis
LM:**coagulative necrosis. **
-Fever,malaise,nausea/vomiting,costoverterbral angle tenderness
-Invades interstitium–>spares glomerulus and vessels

36
Q

Diagnosis

A

-Acute Puelonephritis (abscess)

37
Q

Chronic Pyelonephritis gross description?
-How do you describe if you see eosinphilic cast?

A

-Blunted Calyces and Papilla
-Scarring of same areas.
-Flattening of upper and lower papillae.

Thyrozydation.

38
Q

Why blunting of specific lower and upper papillae in chronic pyelonephritis?

A

-They are compound papillae.

39
Q

2 types of Chronic Pyelonephritis and how to differentiate?

A

-Obstructive:hydronephrosis, scarring everywhere, thin cortex
-Reflux:scarring in upper and lower papillaes

40
Q

What is Xantogranulomatous Pyelonephritis?
What microbe is it associated with and what do you see in Biopsy?

A

-Ass with Chronic pyelonephritis that has nodules that mimmic tumor–>ass with Proteus Mirabilis infections.
-On biopsy you see Foamy macrophages.

41
Q

What pre-disposing conditions will cause NSAID Nephropathy?

A
  • **Hypovolemia or setting of renal disease. **
  • Giving NSAIDS in this situations will cause NSAID Nephropathy.
42
Q

What drugs cause Analgesic Nephroptahy and what complications (2) they have?

A

-Acetaminophen (Tylenol)+Apsirin everyday for varoius yr’s.
-Transitional Urinary Tract Cancer + Renal Papillary Necrosis.

43
Q

Causes of Papillary Necrosis?(4)

A

-N**SAIDS, Acute Pyelonephritis, Diabetus Mellitus,Sickle cell dis or trait. **

44
Q

How to differentiate between Diabetic and Analgesic Renal Papillary Necrosis?

A

-Diabetic:all cells are in similar stage of damage
-Analgesic:cells are at diff stage

Both cause oxidative damage.

45
Q

What do you see microscopally in Analgesic Nephroptahy?

A

-Papillary necrosis + Dysmorphic Calcification.

46
Q

Where does you analgesic concentrate in kideny?

A

Medulla

47
Q

Where do you see Fibrinoid Necrosis?

A

-Some **Vasculitis, Hyper-acute rejection, and Malignant Hypertension. **

48
Q

Tumor Lysis syndrome presentation
-Blood work?

A

-Hyperkalemia,Hyperphosphatemia,Hypocalcemia,
Hyperuricemia.

-arrythmias,peaked T waves, seizures, muscle weakness, Tetany, Acute kideny Injury. **

49
Q

DIAGNOSIS

Patient has Leukemia/Lymphoma ands gets his first chemotherapy treatment and develops muscle weakness, arrythmias and seizures?

A

-Tumor Lysis Syndrome (High cell turnover)

50
Q

**Uric Nephropathy is ass with?

A

Tumor Lysis Syndrome.

51
Q

How to we prevent Tumor Lysis Syndrome?

A

-Allopurinol.Agrresive Hydrated,Rasburicase(inhb allantoin formation)

52
Q

Why Rasburicase is better than Allopurinol for tretament of prevention of Tumor Lysis Syndrome?

A

-Prevents Xanthine from precipitating.
-Lower uric acid levels faster

53
Q

What are the 3 test you do for diagnosing a plasma dyscracia disease and why?

A

-Serum Protein Electrophoresis–> elevated Ig production (M spike)
-24hr. Urianalyses: Light chain Ig that gets filtered.
-Bones marrow biopsy (confirmation):

54
Q

Multiple Myeloma pathogenesis:

A

-Plasma Cell Dyscracia–>IgG overproduction.
-CRAB:HyperCalcemia, Renal Acute Injury, Anemia and Bones lytic lesions. **
-urine dipstick:usually shows for albumin.
-Blood smear:”Rolex Formation”
-Biopsy: monoclonal plasma cells–>reasson of anemia.
-24HR urine test: Bence Jones Protein=Ig**

55
Q

Complications of Multiple Myeloma?

A

-Primary amyloidosis–>Renal injury (Ligth Chain Nephropathy)
-incr risk of infection.

56
Q

Renal Tubular Acidosis types and what they ALL have in common?

A

-Type 1-cannot secrete H+ from alpha intercalted cells
-Type 2 -not able to reabsp HCO-3 due to decf. of Carbonic Anhydrase in PCT.
-Type 4-aldosterone decf. or aldosterone sensative.

-All have Normal Anion Gap Metabolic Acidosis

57
Q
A
58
Q

Type 1 RTA defective Transporters?

A

-H+ ATPase **
-H+/K+ ATPase also affected (reabsp K+)**
-Both on **alpha intercalated cells. **

59
Q

What is associated with Type 1 RTA..(4)
-Complications (2)

A

-Lithium (mayorly excrted by kidney)
-Genetic mutations
-R.A
-SJorgen Syndrome

-Incr risk of Ca++-Phosphate stones and Hypercalciuria–>fracture–>actions to buffer alkaline urine.
-due to urine pH and bone turnover related to buffering.

60
Q

What drug ?

Mood stabilizer for bipolar disorder; treats acute** manic episodes** and prevents relapse.

Adverse effect

A

Lithium.

-Diabetus Insipidus** (Amiloride)**

61
Q

Type 2 RTA pathogenesis..

A

-PCT cannot reabsp. HCO-3–> metabolic acidosis
-Excess HCO-3 in lumen–>osmotic diuresis–>mild hypovolemia–>RAAS activation->Na+reabsp. and K+ excretion–>Hypokalemia.
-When urine is not acidic–>theres no need to excrete HCO-3–> it will be reabsp.–>Acidic urine

62
Q

Associated events with Type 2 RTA? (3)

A

-Everything that excretes HCO-3
-Acetozolamide, Topiramate (Carbonic Anhydraze Inhb.)
-Faucconi syndrome (disorder with PCT reabsp.)..
-Multiple Myeloma (Light Chain Nephropathy)

63
Q

Why urine pH is acidic in Type 2 RTA?

A

-Because as you decr H+ in lumen of tubules you reabsp. more HCO-3–>causing a acidic urine.

64
Q

Diagnosis

glycosuria,aminoaciduria,phosphouria,and uric acid on urine.

A

-Faucconi syndrome(defective PCT)

65
Q

Type 4 RTA pathogenesis

A

Defc in aldosterone or alsodterone sensitivity.
-Non-functional aldosterone–>NO H+ nor K+ excretion–>metabolic acidosis and Hyperkalemia.
-Collecting tubules.

66
Q

Disorders associated with Type 4 RTA? (4)

A

-Spironolactone chronic use
-Addison disease
-Diabethic nepgropathy.
-ACHE inhb., ARB,Aloskiren

67
Q

Location of pathology of each RTA

Type 1
Type 2
Type 4

A

-ALPHA intercalted cell
-PCT
- collecting tubules (aldosterone recep)

68
Q

Diagnosis

normal anion Gap metabolic acidosis
**urine pH >5.5 **
**Hypokalemia **

A

Type 1 RTA
-ATPase mutation,R.A, SJorgen syndrome, Lithium

69
Q

Diagnosis RTA

Normal Gap Metabolic Acidosis
Hyperkalemia
urine pH<5.5

A

Type 4 RTA
-pH <5.5 because HCO-3 starts to get reabsp.
-Spironolactone, Addison disease, Diabetic Nephropathy.

70
Q

Normal Anion Gap Metabolic Acidosis
urine pH <5.5
Hypokalemia

A

Type 2 RTA
-Hypokalemia due to activation of RAAS by HCO-3 by osmotic diuresis–>mild hypovolemia.

71
Q

Hyperkalemia RTA. Think off

A

TYPE 4 RTA

72
Q

Hypokalemia RTA, what do you see next?

A

-Type 1 and 2–>you look at pH
-pH>5.5–>Type 1
-ph<5.5–>Type 2

73
Q

Hyperacute Transplant rejection pathogenesis

A

-type 2 hypersensitivity, preformed antibodies towards donar graft.
-Within minutes.

74
Q

-Excessive endothelial injury–>**Thrombosis–>Fibrinoid necrosis due to ischemia
-After transplantation

A

-Hyper-acute transplant rejection.

75
Q

Acute Transplant rejection pathogenesis

A

-Type 4 Hypersensitivity
-Humoral (antibodies) and Cellular response–>CD8+ and CD4+–>they acts against donor MHC.

76
Q

Type of Transplant Rejection

-Inflamation of Interstitium and tubules–> you see lymphocytes in interstitium–>vasculitis
-Well prevented with immunosupression since it has **cytokine mediated damage. **

A

-Hyperacute

77
Q

Chronic Graft Rejection

A

-Type 2 and 4 Hypersensitivity.
-CD4+ reacting to recipient APC presenting Donor peptides. (MHC)
-Specific for arteriolosclerosis–>occluding vessels for long times–>damage.
-Proliferation of smooth muscle–>paranchymal atrophy **and interstitial fibrosis.

78
Q
A

-Thrombosis
-Interstitial inflamation
-Arteriolosclerosis (smooth muscle proliferation)

79
Q

Nephrocalcinosis

A

-Presents as Diabetus Insipidus__> NO dysuris, poluris and inability to concentrate urine/;

-Nephrolithiasis
-Tubular defects - poor concentrating
ability (polyuria), salt wasting, and
renal tubular acidosis.

80
Q

Ass disease with nephrocalcinosis

A

-PTH tumor, excess vit. D, sarcoidosis, renal osteodystrophy, mil-alki syndrome.

81
Q

post rena AKI long term gross app(2)

A

-Dilation pelvis and kidney and tubules atrophy

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