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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
ATN toxin type is associated with...
-**Aminoglycosides**,contrats dyes,cisplation,anti-freeze, myoglobin,uric-acid,Lead poison....
26
Biopsy and location wise, how do you differentiate ischemia and toxin mediated ATN?
-Ischemia:*dscontinous *damage/Damages areas high in energy consumption **(PCT and Asc Loop of Henle**) -Toxin:*continous* damage/ Damages first encountered area--**>PCT.**
27
What are the stages in ATN and what do you see?
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**
28
Diagnosis and decribe what you see..(3)
-ATN -Blockage on tubule lumen (WHY?) -**Muddy brown CAST (granular cast)-**->necrosis of epi cells, -**Epi cell flattening**
29
Lead posoning presentation?
-Inhb Ferrochelatase-->incr protoporphirin +Microcytic anemia+Basophilic stippling on Blood smear.
30
Causes of Interstitial nephritis (8)
**-Drugs 5P's** (Pee-*Diuretics-Thiazide and Furosemide.*/*Pencillin and Chephalosporins* /Rimfampin/PPI (Omeprazole)/P*ain-free (NSAIDS*) and Sulfa drugs) -*Infections:***Acute and Chronic Pyelonephritis** -*Toxins*:**Analgesic** *-Metabolic:***Light chains cast Nephropathy (M.M**), **Urate Nephropathy**, **Nephrocalcinosis**, **Transplant rejection. **
31
# Diagnosis Inflamation of Renal interstitium and tubules relating drug use. -Presentation is malaise,fever rash
-Interstitial Nephritis.
32
What mechanism of damage does Interstitial nephritis involve?
-Type 1 or 4 Hypersensitivity reaction. -Drugs will act as a hapten-->triggering of Imm system.
33
Urianalysis of Interstitial Nephritis relating drugs and what should the history include + presentation?
-Elavated BUN/creatinine, **sterile pyuria**, **EOSINPHILS**,WBC cast -**History of drug use. ** -T**RIAD:Fever,malaise, rash**-->Hypersensitivity reaction.
34
# Differentiate Acute vs. Chronic Interstilial Nephritis
-Eosinphils in Acute-Lymphocytes (mononuclear cells) in Chronic.
35
Complications of Acute Pyelonephritis(2) Presentation Where does it affect?
-Perinephric abscess,Renal Papillary Necrosis, Chronic Pyelonephritis LM:**coagulative necrosis. ** -Fever,malaise,nausea/vomiting,costoverterbral angle tenderness -Invades interstitium-->spares glomerulus and vessels
36
Diagnosis
-Acute Puelonephritis (abscess)
37
Chronic Pyelonephritis gross description? -How do you describe if you see eosinphilic cast?
-**Blunted Calyces and Papilla** -Scarring of same areas. -**Flattening of upper and lower papillae.** **Thyrozydation.**
38
Why blunting of specific lower and upper papillae in chronic pyelonephritis?
-They are compound papillae.
39
2 types of Chronic Pyelonephritis and how to differentiate?
-**Obstructive:hydronephrosis, scarring everywhere, thin cortex** -**Reflux:**scarring in upper and lower papillaes
40
What is Xantogranulomatous Pyelonephritis? What microbe is it associated with and what do you see in Biopsy?
-Ass with Chronic pyelonephritis that has nodules that **mimmic tumor**-->ass with **Proteus Mirabilis infections.** -On biopsy you see **Foamy macrophages**.
41
What pre-disposing conditions will cause NSAID Nephropathy?
- **Hypovolemia or setting of renal disease. ** - Giving NSAIDS in this situations will cause NSAID Nephropathy.
42
What drugs cause **Analgesic Nephroptahy** and what complications (2) they have?
-Acetaminophen (Tylenol)+Apsirin everyday for varoius yr's. -Transitional Urinary Tract Cancer + Renal Papillary Necrosis.
43
Causes of Papillary Necrosis?(4)
-N**SAIDS, Acute Pyelonephritis, Diabetus Mellitus,Sickle cell dis or trait. **
44
How to differentiate between Diabetic and Analgesic Renal Papillary Necrosis?
-Diabetic:all cells are in similar stage of damage -Analgesic:cells are at diff stage Both cause oxidative damage.
45
What do you see microscopally in Analgesic Nephroptahy?
-**Papillary necrosis + Dysmorphic Calcification.**
46
Where does you analgesic concentrate in kideny?
**Medulla**
47
Where do you see Fibrinoid Necrosis?
-Some **Vasculitis, Hyper-acute rejection, and Malignant Hypertension. **
48
Tumor Lysis syndrome presentation -Blood work?
-**Hyperkalemia,Hyperphosphatemia,Hypocalcemia, Hyperuricemia.** -arrythmias,peaked T waves, seizures, muscle weakness, Tetany, Acute kideny Injury. ****
49
# DIAGNOSIS Patient has Leukemia/Lymphoma ands gets his first chemotherapy treatment and develops muscle weakness, arrythmias and seizures?
-Tumor Lysis Syndrome (High cell turnover)
50
**Uric Nephropathy is ass with?
Tumor Lysis Syndrome.
51
How to we prevent Tumor Lysis Syndrome?
-**Allopurinol.Agrresive Hydrated,Rasburicase**(inhb allantoin formation)
52
Why **Rasburicase** is better than Allopurinol for tretament of prevention of Tumor Lysis Syndrome?
-Prevents Xanthine from precipitating. -Lower uric acid levels faster
53
What are the 3 test you do for diagnosing a plasma dyscracia disease and why?
-**Serum Protein Electrophoresis**--> elevated Ig production (M spike) -**24hr. Urianalyses:** Light chain Ig that gets filtered. -**Bones marrow biopsy** (confirmation):
54
Multiple Myeloma pathogenesis:
-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
Complications of Multiple Myeloma?
-Primary amyloidosis-->Renal injury **(Ligth Chain Nephropathy)** -incr risk of infection.
56
Renal Tubular Acidosis types and what they ALL have in common?
-*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
58
Type 1 RTA defective Transporters?
-**H+ ATPase ** -**H+/K+ ATPase also affected (reabsp K+)** -Both on **alpha intercalated cells. **
59
What is associated with Type 1 RTA..(4) -Complications (2)
-**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
# What drug ? Mood stabilizer for **bipolar disorder**; treats acute** manic episodes** and prevents relapse. Adverse effect
Lithium. -Diabetus Insipidus** (Amiloride)**
61
Type 2 RTA pathogenesis..
-**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
Associated events with Type 2 RTA? (3)
-Everything that excretes HCO-3 -**Acetozolamide, Topiramate (Carbonic Anhydraze Inhb.) -Faucconi syndrome (disorder with PCT reabsp.)..** -**Multiple Myeloma (Light Chain Nephropathy)**
63
Why urine pH is acidic in Type 2 RTA?
-Because as you decr H+ in lumen of tubules you reabsp. more HCO-3-->causing a acidic urine.
64
# Diagnosis glycosuria,aminoaciduria,phosphouria,and uric acid on urine.
-**Faucconi syndrome(defective PCT)**
65
Type 4 RTA pathogenesis
Defc in aldosterone or alsodterone sensitivity. -Non-functional aldosterone-->**NO H+ nor K+ excretion**-->metabolic acidosis and Hyperkalemia. -Collecting tubules.
66
Disorders associated with Type 4 RTA? (4)
-Spironolactone chronic use -Addison disease -Diabethic nepgropathy. -ACHE inhb., ARB,Aloskiren
67
# Location of pathology of each RTA Type 1 Type 2 Type 4
-ALPHA intercalted cell -PCT - collecting tubules (aldosterone recep)
68
# Diagnosis normal anion Gap metabolic acidosis **urine pH >5.5 ** **Hypokalemia **
Type 1 RTA **-ATPase mutation**,R.A, SJorgen syndrome, **Lithium**
69
# Diagnosis RTA Normal Gap Metabolic Acidosis Hyperkalemia urine pH<5.5
Type 4 RTA -pH <5.5 because HCO-3 starts to get reabsp. -Spironolactone, Addison disease, Diabetic Nephropathy.
70
Normal Anion Gap Metabolic Acidosis urine pH <5.5 Hypokalemia
Type 2 RTA -Hypokalemia due to activation of RAAS by HCO-3 by osmotic diuresis-->mild hypovolemia.
71
Hyperkalemia RTA. Think off
TYPE 4 RTA
72
Hypokalemia RTA, what do you see next?
-Type 1 and 2-->you look at pH -pH>5.5-->Type 1 -ph<5.5-->Type 2
73
Hyperacute Transplant rejection pathogenesis
-type 2 hypersensitivity, preformed antibodies towards donar graft. -Within minutes.
74
-Excessive endothelial injury-->**Thrombosis-->Fibrinoid necrosis due to ischemia -After transplantation
-Hyper-acute transplant rejection.
75
Acute Transplant rejection pathogenesis
-Type 4 Hypersensitivity -Humoral (antibodies) and Cellular response-->CD8+ and CD4+-->they acts against donor MHC.
76
# 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. **
-**Hyperacute**
77
Chronic Graft Rejection
-**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
-Thrombosis -Interstitial inflamation -Arteriolosclerosis (smooth muscle proliferation)
79
Nephrocalcinosis
-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
Ass disease with nephrocalcinosis
-PTH tumor, excess vit. D, sarcoidosis, renal osteodystrophy, mil-alki syndrome.
81
post rena AKI long term gross app(2)
-Dilation pelvis and kidney and tubules atrophy

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