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Year 1: Patho/Pharm > Kidney Patho > Flashcards

Kidney Patho Flashcards

1
Q

Definition
Acute Kidney Injury (AKI)

A

Acute onset (hours to days)

3 types
1. pre-renal
2. intra-renal
3. post-renal

Increase in serum creatinine
Decrease urinary output
OR
BOTH

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2
Q

Definition
Oligouria

A

urinary output < / = 30cc/hour

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3
Q

Definition
Azotemia

A

Increased serum creatinine
Increase serum blood urea nitrogen (BUN)
BUN:Cr ratio > 20:1

*inability kidney to filter waste products (nitrogenous waste)

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4
Q

Definition
Uremia

A

Systemic signs and symptoms resulting from loss of kidney function (inability filter waste)

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5
Q

3 categories of acute kidney injury

A
  1. pre-renal
    - before the kidney
    - blood volume
    - cardiac output
    - obstruction blood flow
  2. intra-renal
    - inside the kidney
  3. post-renal
    - after the kidney
    - obstruction of urine flow
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6
Q

Pre-renal AKI
Definition

A

Trigger –> decrease renal blood flow –> decrease glomerular perfusion, filtration

Triggers include
1. obstruction
2. decrease blood volume - hemorrhage, dehydration, third spacing
3. decrease cardiac output
4. decrease renal blood flow

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7
Q

Urinalysis and serum indicators
Pre-renal AKI

A

Decrease renal blood flow sensed by juxtaglomerular cells

Release renin and activation RAAS compensation
Reabsorption sodium, water, urea
- BUN:Cr > 20:1

Oliguria (< 30ml/hour)

High urine osmolality > 500mOsm/kg
- aldosterone promotes water reabsorption

Decreased excreted sodium
- FEna = Na excreted / Na filtered < 1%

Decrease glomerular filtration
increase creatinine, increase BUN

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8
Q

Most common cause of pre-renal AKI

A

sepsis

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9
Q

Compensatory systems
Decreased renal blood flow

A
  1. SNS
    - NE and E released
    - vasoconstriction
  2. HPA axis
    - Cortisol release
    - vasoconstriction
  3. ADH
    - anti-diuretic hormone release
    - reabsorption water
  4. RAAS pathway
    - vasoconstriction
    - retention sodium and water
    - reabsorption urea
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10
Q

Drugs that potentiate pre-renal AKI

A

Vasoactive medications
- dopamine
- ACE inhibitors
- ARBs

NSAIDS & Radioactive contrast dyes
- decrease blood flow to kidney

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11
Q

Definition
Intra-renal AKI

A

INtra-renal AKI
- intrinsic
- direct damage to the renal parenchyma
- results in nephron dysfunction

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12
Q

Causes of Intra-renal AKI

A
  1. Glomerulus: Glomerulonephritis
  2. Tubules: acute tubular necrosis
  3. Vasculature: infarct, thrombosis (pre-renal progresses to intra-renal)
  4. interstitial disease: infection, tumors (acute nephritis)
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13
Q

Most common cause of intra-renal AKI

A

Acute tubular necrosis (ATN)

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14
Q

Glomerulonephritis
Definition

A

Injury to the glomerulus

Leads to inflammation of the glomerular capillaries and destruction of the glomerular membrane

Acute or chronic

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15
Q

Nephrotic Syndrome
Definition

A

Results from injury to the glomerulus

Unable to prevent filtration of proteins

Results in >/= 3.5g / day of protein in urine

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16
Q

Pathophysiology
Acute Tubular Necrosis

A
  1. Injury: nephrotoxins
  2. Ischemia

Nephrotoxins
- direct damage to tubular epithelial cells

Ischemia
- Lack of blood supply

Tubular epithelial cell dysfunction

  1. Cannot reabsorb
    - High urine sodium (> 30mmol/L)
    - High FEna (Na excreted / Na filtered) > 1 %
    - Low urine osmolality (<400mOsM/L)
    - Low urine specific gravity (1.010-1.012)
    - Low BUN:Cr ratio < 15:1
  2. Cannot secrete
    - hyperkalemia
    - metabolic acidosis (cannot secrete H+ ions)
  3. Increase Tubular pressure = decrease GFR
  • necrotic cells slough off
  • plug the tubule
  • formation brown casts in urine
  • tubule opposes filtration pressure in artery
  • decrease GFR
  • increase serum creatinine, increase serum urea (azotemia)
  • decrease urinary output (oliguria)
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17
Q

Factors required for reversible intra-renal AKI

A
  1. ischemia is not prolonged
  2. basement membrane is present
  3. tubular epithelial cells regenerate
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18
Q

Definition
Post-Renal AKI

A

Obstruction of urinary flow
Backs up into the renal pelvis
increase intra-tubular pressure
Decreases filtration

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19
Q

Causes of Post-Renal AKI

A

tumour
stones
trauma
strictures
prostate
neurogenic bladder

*< 5% of AKI

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20
Q

4 stages to the clinical course of AKI

A
  1. Initiation (onset)
    - oligouria
    - increase Cr
    - increase BUN
    -*reversible before damage at this stage
  2. Extension
    - ischemia
    - inflammation
  3. maintenance phase (oliguric phase)
    - initiation event resolved
    - injury established by extension phase (ischemia, inflammation)
    - 10-14 days (healing inflammation)
    - longer duration is poor prognosis
  4. recovery phase (polyuria)
    - most recovery within 3 weeks, can take up to 1 year for full recovery of function
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21
Q

Clinical Signs and Symptoms
Oliguric phase (maintenance phase) AKI

A

Oligouria
- decrease U/O
- normal SG (cannot reabsorb water)
- high urine sodium (cannot reabsorb sodium)
- low urine osmolality (cannot reabsorb water)
- BUN:Cr < 15:1
- FEna > 1%

Urinalysis
- RBC, protein (damage glomerular membrane)
- brown casts (tubular necrosis)
- WBC (inflammation)

FVO
- decrease GF = fluid retention
- edema, hypertension, heart failure
- pulmonary edema, crackles
- bounding pulses, jugular venous distention

metabolic acidosis
- tubules cannot excrete H+
- tubules cannot reabsorb HCO3-
- decrease pH

hyponatremia
- tubules cannot reabsorb sodium
- sodium excrete in urine
- hyponatremia serum

hyperkalemia
- tubules cannot excrete potassium
- hyperkalemia in serum
- cardiac dyrhythmias

hypocalcemia, hyperphosphatemia
- kidney cannot activate vitamin D
- cannot absorb calcium in GI
- PTH released increase bone reabsorption - increase phosphate in blood

Azotemia and neurological symptoms
- increase waste, creatinine, BUN
- fatigue, stupor, coma, confusion

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22
Q

Clinical Signs and Symptoms
Recovery (polyuric) phase

A

Kidney able to excrete waste (unable to concentrate urine)

result is polyuria > / = 3-5 L / day urine

Recovery function 1-3 weeks , up to 1 year

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23
Q

Risk in Recovery phase

A

dehydration
hypovolemia
electrolyte imbalances

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24
Q

Management of AKI

A

Hospital admission

  1. electrolytes
    - monitor and manage sodium, potassium, calcium, phosphate
  2. fluid
    - monitor fluid volume overload / dehydration
    - replacement / diuretics / dialysis
  3. blood pressure and cardiac output = kidney perfusion
  4. dietary changes
    - fluid volume restrictions
    - sodium or potassium restrictions or supplements
    - increase protein
  5. dialysis
    - acidosis, FVO, hyperkalemia
  6. medication renal dose adjustments
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25
Q

Prevention of AKI

A

Renal dose adjustments for medications and age

Fluid to wash out nephrotoxic medications

Maintaining renal perfusion
- treating infections (sepsis)
- hydration and prevention dehydration
- monitoring fluids post operatively, trauma, burns
- maintaining healthy blood pressure and cardiac output
- maintaining normoglycemia
- maintaining healthy liver

Immediate treatment of urinary obstructions
- BPH, tumours, stones

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26
Q

Definition
Chronic Kidney Disease

A

Also known as
- renal insufficiency
- chronic renal failure

chronic, irreversible loss of kidney function
- nephron destruction

change in structure or function present for > 3 months

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27
Q

Classification
Chronic Kidney disease

A
  1. GFR
  2. Albuminuria

GFR

Stage 1, normal, > 90ml/min
stage 2, mild, 60-89ml/min
stage 3, moderate, 30-59ml/min
stage 4, severe, 15-29ml/min
stage 5, end stage renal disease < 15ml/min

albuminuria

stage 1, mild, < 3mg/mmol
stage 2, moderate, 3-30mg/mmol
stage 3, severe, > 30mg/mmol

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28
Q

Definition
Glomerular filtration rate

A

Amount of blood filtered in mL per minute by the glomerular membrane = number functioning nephrons = kidney function

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29
Q

Factors that affect GFR

A

Age
sex
height
weight
*serum creatinine

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30
Q

Over-estimation GFR

A

kidney actively secretes creatinine in addition to creatinine that is filtered at the glomerulus

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31
Q

Clinical ways to assess albuminuria

A

Urinalysis
- albumin
- creatinine

24 hour urinalysis
- albumin
- creatinine

POCT
- albumin dipstick

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32
Q

Who should be screened for CKD?

A

Anyone who has risk factors for CKD
- smoking
- diabetes
- hypertension
- hyperglycaemia
- physically inactive

Screen
1. GFR
2. albuminuria

earlier diagnosis = slow progression

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33
Q

Nephropathy secondary to Diabetes Mellitus
Pathophysiology
Clinical signs

A
  1. Hyperglycemia
  2. Inflammation -> scaring -> dysfunction glomerular filtration membrane/tubular dysfunction

hyperglycaemia –> oxidative radicals –> microvascular damage, glomerular filtration membrane damage, epithelial cell damage

glucose -> free radicals -> inflammation -> scaring/fibrosis -> decreased filtration, decreased tubular reabsorption, proteinuria, waste/FVO

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34
Q

Nephropathy secondary to hypertension

A
  1. HTN
  2. renal artery stenosis
  3. ischemia -> inflammation -> scarring/dysfunction (glomerular filtration membrane, tubular epithelium)

Hypertension –> microvascular damage –> renal artery stenosis –> decreased renal blood flow –> ischemia –> inflammation –> scarring/fibrosis –> damage and reduce glomerular filtration –> ischemia tubular epithelium –> dysfunction

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35
Q

What percentage of kidney function do you see clinical signs and symptoms of CKD manifest?

A

25% kidney function

36
Q

Clinical manifestations all body systems
Chronic Kidney Disease (CKD)

A

Neuro
- confusion, fatigue, HA, sleep disturbances, encephalopathy

Eyes
- retinopathy

Cardiac
- dysrhythmias (hiperkalemia)
- HF
- HTN
- uremic pericarditis
- CAD (dyslipidemia)

Pumonary
- edema (FVO)
- uremic pleurites

GI
- uremic gastritis
- ulcers, hemorrhages
- N/V/anorexia

Integumentary
- urochromes (yellow skin, brown/white nails)
- pruitis uremia
- ecchymosis (loss of clotting factors)
- pale (loss of EPO, RBC, anemia)

MSK
- weakness, numbness, tingling
- fractures
- electrolyte disturbances (hyponatremia, hyperkalemia, hypocalcemia, hyperphsophatemia)

Metabolic
- hyperglycemia
- dyslipidemia

Haematological
- bleeding (loss of platelets, clotting factors)
- infection (loss of blood cells, immunoglobulins)
- decreased response to vaccination
- anemia

Endocrine
- dysmenorrhea, infertility
- loss of libido

37
Q

Diagnosis
CKD

A
  1. history
  2. clinical signs and symptoms
  3. GFR and albuminuria (stage of kidney disease)
  4. urinalysis (casts, RBC, WBC, protein)
  5. imaging (US, CT, etc.)
38
Q

Pharmacological Management
Supportive management CKD

A

Management: HTN
- ACEi (IPRIL) and ARBs (SARTAN)
- renal protective
- slow eGFR decline, slow microalbuminuria
*not effective for end stage

Management: Dyslipidemia

Management: Glucose

Dietary modifications
- plant based proteins
- weight loss (not end stage)
- protein restriction ( not old people )

Vaccinations
- infection risk

Blood products
- anemia

Dialysis
- acidosis
- hyperkalemia
- FVO
- waste products

39
Q

3 functions of the kidney

A
  1. water and electrolyte balance
  2. acid-base balance
  3. remove waste
  4. hormones (EPO, activation vitamin D)
40
Q

pre-renal AKI
Absolute loss of fluid examples

A

blood loss
trauma
surgery
diarrhea
vomiting
diabetes mellitus uncontrolled
burns
diuretics

41
Q

pre-renal AKI
relative fluid loss examples

A

Hypotension
decreased cardiac output
heart failure

DIstributive shock
sepsis
ascites

42
Q

pre-renal AKI
renal artery hypo perfusion examples

A

Emboli
tumour
stenosis
Vasoactive medications
- dopamine
- epinephrine
- NSAIDS
- ARBs
- ACE inhibitors

43
Q

Pre-Renal AKI
BUN:Cr Ratio

A

Normal BUN: Cr ratio 20:1

pre-renal AKI
> 20:1

  • decrease waste filtration
  • urea follows sodium
44
Q

Example nephrotoxins that cause
intra-renal AKI

A

aminoglycosides
NSAIDS
heavy metals - lead
ethylene glycol - antifreeze
radiocontrast dyes
myoglobulin
uric acid waste (tumour lysis syndrome)

45
Q

Glomerular filtration membrane anatomy

A

3 layers of cells

  1. endothelial layer (fenestrations)
  2. basement membrane (selectively permeable, negative charge, pores)
  3. epithelial layer (podocytes, filtration slits)
46
Q

Clinical Signs and Symptoms
Early post-renal AKI

A

Intra tubular pressure decreases glomerular filtration
- increase serum creatinine, BUN
- oligouria
- increase absorption sodium, water, urea
- FEna < 1%
- urine osmolality > 500mOsM/L

47
Q

Clinical Signs and sympotms
Late post-renal AKI

A

Back pressure destroys the tubular epithelial cells
mimics intra-renal AKI

  • high urine sodium
  • low urine osmolality
  • FENa > 1%
  • BUN:Cr < 15:1
  • high urine sodium concentration > 30mmol/L
48
Q

End of recovery phase
AKI

A

marked by normalization acid-base balance, electrolytes, fluids

49
Q

Goal of treatment
AKI

A
  1. Remove mechanism of injury

Supportive care to keep patient alive during recovery and correct imbalances

  1. correct fluid volume
  2. correct electrolyte imbalances
  3. correct acid-base imbalances
  4. monitor and correct HTN, dyslipidemia, hyperglycaemia
  5. monitor and correct infection, immunosuppression, anemia
  6. diet changes and supplementation
  7. renal replacement therapy / dialysis
50
Q

Goal Treatment
CKI

A

Correct fluid volume, acid-base, electrolyte imbalances
Correct HTN, dyslipidemia, hyperglycemia
Correct anemia, infection, immunocompromised
protein restriction (exception old, end stage)
weight loss (exception old, end stage)
Dialysis (end stage)
Avoid nephrotoxins

51
Q

Nephrotic syndrome
Clinical manifestations

A
  1. Proteinuria > 3.5 g per day
    - loss of albumin (hypoalbuminuria), edema; loss of immunoglobulins (infection); loss of WBC (infection); loss of clotting factors (bleeding) and anti-thrombin (clots)
  2. lipiduria
    - fat floating on urine “foamy”
  3. hematuria
    - RBC found in urine
    - dark brown, tea coloured
  4. Edema
    - third spacing, decreased oncotic pressure
    - increase RAAS and ADH
  5. Dyslipidemia
    - increase TG, LDL, cholesterol
52
Q

Nephritic syndrome
Clinical manifestations

A

Proteinuria < 3.5g per day
*most common cause is post-infectious glomerulonephritis

53
Q

Types of Glomerulonephritis

A
  1. acute vs. chronic
  2. immune vs. non immune
  3. primary vs. secondary

primary
- direct injury to the glomerulus
- trauma, infection, type II-IV hypersensitivity reactions, clots

secondary
- diabetes mellitus, hypertension etc.

54
Q

Pathophysiology
Glomerulonephritis

A
  1. Immune mediated OR 2. non-immune mediated –> injury to the glomerulus –> inflammation
  • deposition inflammatory mediators, auto-immune complexes, complement
  • proliferation mesangial cells and endothelial cells –> decrease renal blood flow –> decrease GFR
  • inflammation damages epithelial cells (filtration slits) and basement membrane (negative charge) –> loss of selective filtration –> proteinuria, hematuria
  • inflammation –> fibrosis –> scaring –> decrease GFR

Result:
oligouria
azotemia (increase creatinine, increase urea)

55
Q

Post-infectious glomerulonephritis
Clinical symptoms

A

Prior infection that has since cleared
- staphylococcus
- streptococcus
- HBV/HCV
- varicella virus

Type III hypersensivity reaction (IgM/IgG) deposit in the glomerular membrane –> mesangial proliferation –> decrease RBF –> decrease GFR

Most common cause of nephritic syndrome
proteinuria < 3.5g per day

56
Q

Explain how creatinine and eGFR are related

A

estimated GFR = 24 urine creatinine clearance (calculation compared to plasma creatinine)

Creatinine
- filtered = excreted in urine (not reabsorbed)
- slightly overestimated (some secreted)
- reflect kidney function (functional nephrons)
- muscles produce at stable rate (false rhabdomyolysis, malnutrition)
- calculation affected by (age, height, weight, gender)

57
Q

Intact nephron hypothesis
What is it
What stage of CKD

A

Stage 2 CKD
Mild
GFR 60-89mL/min
surviving nephrons compensate for loss of nephrons - hyperfunction, hypertrophy - maintain normal fluid balance, electrolytes, acid-base balance

58
Q

Uremic Syndrome
What is it
What stage of CKD or % kidney function

A

Systemic signs occur at 25% kidney function
Normal eGFR 90mL/min
Moderate eGFR 30mL/min (stage 3) clinical signs and symptoms appear

Uremic syndrome (stage 5)

59
Q

Anatomy
Nephron

A

Renal corpuscle
- bowman’s capsule
- glomerulus
- mesangial cells (macrophages, vasoconstriction afferent arteriole)

Renal tubules
- proximal convoluted tubule
- loop of henle
- distal tubule

60
Q

Renal tubules
Cells and Function

A

Proximal tubule
- brush boarder cells
- microvilli increase SA for reabsorption
- high mitochondria for active transport

Distal tubule

  • Intercalated cells - H+ excretion, HCO3- absorption (acid base balance)
  • Principle cells - sodium and potassium balance, (influenced by macula densa - sodium sensing cells, and aldosterone)
61
Q

Glomerulus
Cells and function

A

Mesangial cells
- vasoconstriction of glomerulus capillaries (smooth muscle cell function)
- phagocytosis and release of inflammatory cytokines (monocyte function)

Juxtaglomerular cells
- located around afferent arteriole
- sense decrease in renal blood flow
- release renin in response to beta 1 adrenergic stimulation

Macula densa cells
- located between the afferent and efferent arteriole
- sodium sensing cells of the distal convoluted tubule

62
Q

Natriuretic peptides
Function

A

ANP - atrial natiuretic peptide
BNP
release from overstretch of cardiomyocytes
prevention sodium/water reabsorption by kidney
increase diuresis

CNP
released by vascular endothelium from stretch
increase vasodilation afferent arteriole
icnrease GFR
increase diuresis

Renal natriuretic peptide
released by collecting duct stretch
increase vasodilation afferent arteriole
increase diuresis

63
Q

Hormones produced by the kidney

A

EPO
- erythropoetin
- juxtaglomerular complex
- sensation hypoxia –> stimulation RBC production

RNP
- renal natriuretic peptide
- released by collecting duct
- increase diuresis

Vitamin D3 activation
- 1,25 dihydroxyvitamin D
- allows for calcium reabsorption

Renin
- release day juxtaglomerular cells in response to low blood flow
- angiotensinogen -> angiotensin I
- angiotensin I –> angiotensin II (ACE)
- Aldosterone

  • vasoconstriction
  • vascular/cardiac remodeling
  • sodium and water reabsorption
64
Q

5 functions of the kidneys

A
  1. Fluid balance, blood pressure
  2. acid-base balance
  3. hormones, aldosterone, renin (RAAS), vitamin D (active), urodilantin (diuretic)
  4. excretion waste (urine)
65
Q

Anatomy:
Location of the Kidney

A

T12-L3
retroperitoneal cavity
R kidney lower than L kidney (liver displaces)

66
Q

Definition Nephron
Measurement of nephron function

A

Nephron - functional unit of the kidney
Glomerular filtration rate = number of functioning nephrons

  1. Creatinine (muscle waste product)
  2. Cystatin C (early kidney damage marker)
  3. BUN (blood urea nitrogen)
67
Q

Components of the
Renal Corpuscle

A

Bowman’s Capsule
Glomerular capillaries
Mesangial Cells (release cytokines, vasoconstriction to maintain RBF, phagocytosis)

68
Q

3 Layers of the glomerular filtration membrane

A
  1. Endothelial cells
  2. Basement membrane (anionic charge, repels protein)
  3. Epithelial cells (filtration slits)

Selectively permeable
1. size
2. charge
3. hydrostatic pressure, oncotic pressure

69
Q

Components of the
Juxtaglomerular apparatus

A
  1. Juxtaglomerular cells (produce renin, afferent arteriole)
  2. Macula densa (sodium sensing cells, between afferent/efferent arteriole)
70
Q

Components of the
Nephron

A
  1. Proximal convoluted tubule
  2. Descending loop of henle (thick, thin)
  3. Ascending loop of henle (thin, thick)
  4. distal convoluted tubule
  5. collecting duct
71
Q

Function and cells
Proximal convoluted tubule

A

Function
- production of primary urine
- reabsorption of solutes

Brush boarder cells
- microvilli, increase SA, reabsorption
- Active reabsorption sodium, secretion hydrogen (Na/H pump)
- water and urea passively reabsorbed (follow sodium)
- cuboidal epithelial cells

72
Q

FUnction and cells
Descending loop of henle

A

Function
- concentration and dilution of urine

Cuboidal epithelial cells (THICK)
- active reabsorption sodium
- water passively follows

Squamous epithelial cells (THIN)
- no transport

73
Q

Function and cells
Ascending loop of henle

A

Impermeable to water
Active transport sodium reabsorption

74
Q

Function and cells
Distal convoluted tubule

A

Function
- Acid base balance
- blood pressure

Principle cells
- production aldosterone
- Na/K pump
- reabsorption sodium, excretion potassium

Intercalated cells
- excretion hydrogen
- reabsorption potassium (H/K pump)
- reabsorption bicarbonate

75
Q

Function
Collecting duct

A

Function
- reabsorption / excretion water
- Aquaporins insert via ADH signal

76
Q

Ureter
Anatomy, cell type
Function
Referred pain location

A

Cell: smooth muscle, involuntary
Function: connection renal pelvis to bladder, drain urine ; peristaltic contractions
Referred pain: umbilicus (upper ureter), vulva/penis (lower ureter)

77
Q

Bladder
Anatomy
Function

A

Anatomy

  1. detrusor
  2. trigone
  3. internal spincter (all smooth muscle, involuntary)

and external spincters (voluntary, SNS, skeletal muscle)

Function

  1. Micturition reflex (involuntary, PNS, mechanoreceptors stretch 300cc)
78
Q

Regulation of renal blood flow (RBF)

A
  1. Autoregulation
  2. Hormones
  3. Nervous system

Autoregulation
- mesangial cells
- maintain GFR regardless of fluctuation blood pressure (normal range)

Hormones
1. RAAS
2. natriuretic peptides
3. sympathetic nervous system (SNS)

RAAS
- renin released by juxtaglomerular cells (low BP, SNS)
- angiotensin II (vasoconstriction systemic, vasoconstriction efferent arteriole, release ADH posterior pituitary)
- aldosterone (reabsorption sodium, water)

Natriuretic peptides
1. urodilantin
- collecting ducts, release in response to stretch
2. ANP (aortic/carotid), BNP (ventricles), CNP (vascular endothelium)
- released in response to stretch
- vasodilation afferent arteriole
- increase GFR and urination

SNS
- Release NE and E
- bind to beta adrenergic receptors on juxtaglomerular cells, release renin
- activation of the RAAS pathway

79
Q

Stimuli that increases renin release

A
  1. hypovolemia (detected at afferent arteriole, low RBF)
  2. activation SNS and release of NE / E binding beta adrenergic receptors
  3. prostaglandins (decrease renal blood flow)
  4. low sodium at collecting duct
80
Q

Define Net filtration pressure

A
  1. hydrostatic pressure
  2. oncotic pressure
    inside and outside the bowman capsule
    determines direction of filtrate
81
Q

Diseases which decrease GFR

A

Increased Bowman capsule hydrostatic pressure
- tumours
- strictures
- stones

Increased plasma oncotic pressure
- dehydration
- vomitting
- diarrhea
- loss of water, blood becomes high concentration

Loss of glomerular membrane
- diabetes
- sepsis

82
Q

Renal hormones

A
  1. Vitamin D
    - activates vitamin D (1, 25 dihydroxyvitamin D)
    - absorption calcium, excertion phsophate (GI and kidney)
    - bone health
    - CKD osteoporosis
  2. erythropoetin (EPO)
    - bone marrow formation RBC
    - CKD anemia
83
Q

Function plasma creatinine concentration

A

serial measurments
differentiate chronic vs. acute kidney injury

84
Q

Cystatin C function

A

early detection of decreased GFR

85
Q

Urine chemistry

A

Bilirubin = dark orange
urobilinogen = RBC hemolysis
ketones = fat metabolism
glucose = hyperglycemia
sodium - increase or decrease with disease
potassium - increase or decrease with disease
protein - glomerular dysfunction, should be negative

86
Q

Microscopic urine

A
  1. bacteria
  2. RBC
  3. WBC
  4. crystals (stones)
  5. Fat (nephrosis)
  6. casts
87
Q
A

Year 1: Patho/Pharm (39 decks)

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