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PBL Y2 S4 > Case 7- Chronic kidney disease > Flashcards

Case 7- Chronic kidney disease Flashcards

1
Q

What are the 4 main functions of the kidney?

A
  • Maintenance of extracellular fluid volume, primarily through regulating Na+ (water follows)
  • Excretion of metabolic waste: inc urea and creatinine
  • Acid-base balance
  • endocrine; hormone secretoin
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2
Q

What is the endocrine function of the kidney?

A
  • RAAS: renin produced by the kidney, involved in production of Ang II and regulates BP
  • Erythropoietin: RBC production and regulation
  • Vitamin D: calcium regulation
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3
Q

What 2 processes does the process of concentrating urine rely on?

A
  • Counter current multiplier: in the Loop of Henle
  • Counter current exchanger: vasa recta
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4
Q

How do the ascending and descending limb vary in their permeability?

A

Descending= impermeable to NaCl = only H2O reabsorbed
Ascending= impermeable to water, only NaCl reabsorbed

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5
Q

What is the max gradient possible between tubular fluid and surrounding interstitial fluid?

A

200 mOsm/Kg

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6
Q

Compare the osmolalities of very dilute urine and the max concentrated urine

A

Very dilute= 100
Max concentration= 1200

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7
Q

How does the osmolality of tubular fluid change throughout the nephron?

A

End of PCT= isotonic
bottom of Loop of Henle= hypertonic
Before DCT= hypotonic
(then altered to suit hydration needs)

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8
Q

What does reabsorption throughout the PCT rely on?

A

Electrochemical gradient from Na+/K+ ATPase.

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9
Q

What does the PCT reabsorb?

A
  • Na+ via SGLT2 (some by SGLT1) and then K+/Na+ ATPase
  • Glucose via SGLT2 (some by SGLT1) and then GLUT2
  • HCO3-
  • Citrate
  • Amino acids
  • K+ (paracellular route)
  • H2O (paracellular route)
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10
Q

What is responsible for Na+ absorption in the PCT?

A

NHE-3 = Na+/H+ exchanger on the apical membrane

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11
Q

What does the PCT excrete?

A

Bile salts

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12
Q

What is reabsorbed in the thin ascending limb and how?

A

Na+ = passively via ENaC
Cl- = passively by Cl- channels

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13
Q

What is reabsorbed/ excreted in the thick ascending limb and how?

A

Active process; Na+/K+ ATPase sets gradient:
- NKCC2 on apical side, reabsorbs Na+, K+ and 2Cl-

K+ is excreted (recycled) by ROMK2 (passive), as it has built up from NKCC2

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14
Q

What is reabsorbed in the early DCT?

A

Na+, Cl- and Ca2+ (impermeable to water):
- NCC: reabsorbs Na+ with Cl- (apical)
- TRPV5 reabsorbs Ca2+ (apical)
- NCX1: Na+/ Ca2+ exchanger reabsorbs Ca2+ for Na+ (basolateral)
- PMCA1b (Ca2+ ATPase pump) on basolateral side
- Na+ reabsorbed via Na/K+ ATPase

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15
Q

What are the 2 types of cells present in the late DCT and early CD? Give their net effect / function

A

Principal cells (bulk): uptake of Na+ into blood and extrude K+ in urine via ROMK1/3

Intercalated cells: involved in acid base balance:
- Type A = use H+ ATPase and H+/K+ ATPase to secrete H+ into urine
- Type B= secrete HCO3- and reabsorb H+

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16
Q

What are the effects of aldosterone on resorption in the collecting duct?

A

Increases ENaC = more resorption of Na+ (so water can follow)
Stimulates ROMK1/3 opening

Reverses the basolateral K+ channel, so K+ can be excreted (resorbed into cell, then leaves apical side via ROMK1/3)

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17
Q

What transporter in the CD is stimulated with a high plasma K+?

A

Cl-/ K+ co-transporter (in principal cell)

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18
Q

Why doesn’t aldosterone itself cause water retention?

A

If ADH isnt present, then we cannot absorb water as there are no AQP2’s present. Aldosterone only causes water retention indirectly by creating an osmotic gradient

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19
Q

What do the intercalated cells in the collecting duct help protect against? How do they do so?

A

Help protect against hypokalaemia and acidosis:
- If low plasma K+ is detected then H+/K+ ATPases are activated to reabsorb K+
- if acidosis is detected, then H+ ATPases are activated to excrete H+

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20
Q

Describe the permeability of the late DCT and CD to water, how can it vary?

A

Impermeable to water in the absence of ADH. When ADH is present, it binds to V2 receptors = insertion of AQP2 on apical membrane. Water can leave urine and enter the cell, then leave via AQP3/4 basolaterally (always there)

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21
Q

What AQP channels are present in the thick descending limb?

A

AQP1

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22
Q

How is K+ distributed in the body? Give the concentrations

A
  • Most in cells (intracellular)= 98%, concentration 150-160mmol/L
  • Remaining in ECF= 2%, at 4-5 mmol/L
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23
Q

How does hypo/hyperkalaemia affect depolarisation?

A

Hypokalaemia= hyperdepolarisatoin
Hyperkalaemia= depolarisation

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24
Q

Where is most of K+ reabsorbed?

A

PCT, then Loop of Henle (remaining amount is variable in CD/ late DCT)

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25
Q

What non-modifable factor determines concentration of urine?

A

Length of loop of Henle; if longer = more concentrated urine

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26
Q

What is the counter current exchanger?

A

Vasa recta surrounding the nephron has blood moving in the opposite direction to tubular fluid. As blood comes out the glomerulus, it is around 300. Then Na+ is taken up from tubular fluid. As it descends, blood osmolality is increased to 1200 (same as urine). As it ascends, it reabsorbs water.
(opposite to the tubular fluid mechanism)

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27
Q

How does diabetes cause polydipsia?

A
  • high glucose, exceeds Tm (transport maximum), so glucose remains in the tubular fluid.
  • glucose is osmotically active, so can attract water
  • Glucose is in the tubular fluid and osmolality is high (1200), so encourages water to remain in the tubular fluid
  • Osmotic diuresis and dehydration
  • Detected by the hypothalamus = release of Ang II = thirst centre to drink more
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28
Q

Following head trauma, a patient develops central diabetes inspidus which is associated with a reduction in vasopressin secretion. The osmolality of a spot urine sample is expected to be…?

A

100, as this is what urine concentration is at DCT (before affected by ADH)

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29
Q

What is the distribution of Mg2+ and Ca2+ in the body?

A

99% of Ca2+ in bone, 1% in ECF
50% of Mg2+ in bone, 50% in ECF

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30
Q

How are Ca2+ and Mg2+ affected by osteoblasts/ osteoclasts?

A

Both Ca2+ and Mg2+ can be moved into the bone (from ECF) by osteoblasts
They can be moved out of bone into ECF via osteoclasts

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31
Q

How does Ca2+ affect depolarisation threshold?

A

Hypercalcaemia = raises depolarisation threshold
Hypocalcaemia = lowers depolarisation threshold

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32
Q

How does Mg2+ affect heart rate?

A

Hypermagnesaemia = lowers HR
Hypomagnesaemia = raises HR

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33
Q

How is Mg2+ and Ca2+ reabsorbed by the kidney?

A

Predominantly PCT and Loop of Henle (around 90% of both) via paraellular routes, then more selective reabsorption in DCT (remaining)

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34
Q

How is Ca2+ reabsorbed by the DCT?

A
  • Enters via TRPV5, then bound to calbindin-D28K
  • Transported to basolateral side and can exit by NCX1 (exchanged with Na+) or by PMCA1b (ATPase; pumped against concentration gradient)
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35
Q

What stimulates resorption of Ca2+?

A

TRPV5 is opened by:
- Parathyroid hormone, vitamin D and sex hormones (bind to receptors on basolateral side)
- Klotho from tubular fluid, can bind to it directly

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36
Q

How is Mg2+ reabsorbed by the kidney?

A

TRPM6 on apical side (so takes up Mg2+ from the urine into the cell). It is driven by an electrochemical gradient

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37
Q

What can stimulate Mg2+ absorption?

A

Epidermal growth factor

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38
Q

What is the average renal blood flow?

A

1L/min (around 20% of Q)

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39
Q

What achieves the filtration barrier of the kidneys?

A
  • Podocytes on the epithelium: have foot processes (pedicles), stops larger molecules leaving the blood into tubular fluid.
  • Endothelium: fenestrated
  • Cells of the basement membrane have a negative charge; repels negatively charged ions
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40
Q

What type of blood vessels line the glomerulus?

A

Fenestrated capillaries

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41
Q

How does the PCT balance pH?

A

NHE-3 brings in a Na+ for H+ (goes into blood)
To balance the Na+, this transporter is linked to a Cl- transporter (Cl- is exchange with anion, i.e. HCO3-) so Cl- also enters

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42
Q

What transporter in the PCT is responsible for the regulation of cell volume?

A

NHE-1, on basolateral side = pumps Na+ into cell and H+ into blood.
If cell is shrinking, it takes up Na+ so water can follow

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43
Q

What is the transport maximum (Tm) of glucose in the kidneys? At what glucose level is this exceeded?

A

1.25 mmol/min
Exceeded when plasma glucose >10 mmol/L

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44
Q

A diabetic patient with a low GFR and high plasma glucose has a filtered glucose rate of 0.48 mmol/L. Why might their dipstick urinalysis be positive for glucose if this doesnt exceed Tm?

A
  • Have lost functioning nephrons, so the GFR isnt reflective of the single nephron GFR (likely to be higher)
  • Low global GFR = build up of uraemic toxins (from urea - as not excreting it) = damage remaining nephrons. Splay increases
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45
Q

What is ‘splay’ and what is it caused by?

A

Splay is the concentration difference between a substance’s maximum renal reabsorption (i.e. Tm of glucose) vs. appearance (i.e. presence of glucose) in the urine
This is due to variation in the functioning of individual nephrons

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46
Q

How much glucose is produced by the kidney (as a % of body’s production)? Where is it produced?

A

20% glucose is produced by gluconeogenesis in the cortex, i.e. from lactate, pyruvate, oxaloacetate

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47
Q

How is the kidney’s production of glucose affected by diabetes?

A

300% increase in gluconeogenesis in the kidneys.

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48
Q

What factors do equations used to estimate GFR based on serum creatinine concentration take into account?

A

Age, sex, ethnicity

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49
Q

What is GFR? Give the average value

A

125ml/min; the volume of plasma filtered by the glomerulus per minute

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50
Q

Give the average total volume of plasma filtered at the glomerulus per day

A

125ml/min x 60 x 24 = 180L/d

51
Q

What does the 3 layers of the glomerular basement membrane possess to aid filtration?

A

Has a middle layer with type IV collagen and laminins, then the outer layers both have heparin sulfate (glycan) which has a negative charge. This helps repel plasma proteins, i.e. albumin, as they have a negative charge.

52
Q

What is the role of Mesangial cells?

A
  • Phagocytose macromolecles that pass through
  • Have contractile ability to control blood flow through the glomerulus
  • Stimulate juxtaglomerular cells to secrete renin
53
Q

How does the Bowman’s capsule structure control filtration?

A

Has podocytes; filtration slits between these allow substances of under 25-30nm to pass
After this is nephrin proteins, which have to be <7-9nm to pass

54
Q

What are the 3 main contributing factors to GFR?

A
  • Net filtration pressures
  • Surface area
  • Permeability of glomerulus
55
Q

What are the 3 contributors to net filtration pressure?

A
  • Glomerular hydrostatic pressure: i.e. pressure of blood that favours filtration (main force)
  • Glomerular oncotic pressure: pressure of proteins which opposes filtration
  • Bowman’s capsule hydrostatic pressure: opposes filtration
56
Q

What are the normal values for pressures that contribute to overall net filtration pressure? (give the average NFP)

A

Glomerular hydrostatic= 55mHg
glomerular oncotic pressure= 30mmHg
Capsular hydrostatic= 15mmHg

NFP= 55 - (30+15) = 10mmHg

57
Q

What alters glomerular hydrostatic pressure?

A

Blood pressure: high BP = higher hydrostatic pressure

58
Q

What could alter glomerular hydrostatic pressure?

A

More proteins present in the blood, i.e. multiple myeloma

59
Q

What could alter capsular hydrostatic pressure?

A

Kidney calculi

60
Q

What is the filtration coefficient?

A

Product of the glomerular membrane’s permeability to water and the surface area of the membrane

61
Q

How do you calculate renal clearance by the kidneys?

A

UV / P
U= Urinary concentration of X
V= urine volume per unit time
P= plasma concentration of X

62
Q

What is autoregulation? How does it work?

A

Maintains renal blood flow and GFR despite changes in systemic pressure. If renal artery pressure increases, there is a corresponding increase in resistance to flow by the AFFerent arteriole (it constricts), but efferent remains the same.
This means glomerular capillary pressure stays constant = renal BF and GFR are maintained

63
Q

What are the 2 mechanisms responsible for autoregulation?

A

Myogenic: vascular SM cell responds to stretch by vasoconstricting (reflex), thus if resistance increases, pressure is maintained
Tubuloglomerular feedback: DCT monitors what is going through it and regulates vasoconstriction/dilation as necessary

64
Q

Where is the macula densa found?

A

DCT

65
Q

How does the kidney respond to an increase in arterial pressure?

A
  • Increases glomerular pressure and renal plasma flow = raised GFR
  • Increased plasma colloid osmotic pressure (as proteins are dissolved in less fluid) attempts to decrease GFR (minor effect)
  • more fluid enters PCT, which increases reabsorption in the PCT and LOH to counteract this (glomerulotubular feedback)
  • Macula densa in DCT detects high flow rate, releases a transmitter (thought to be adenosine)
  • Afferent arteriole constricts (adenosine binds to AT1 receptor)
  • Pre-glomerular resistance increases
    = GFR is lowered
66
Q

How does the kidney respond to a lowered arterial pressure?

A

Same detection mechanisms (but opposite), however prostaglandin E2 is released instead. This causes efferent arteriole to constrict = raise glomerular pressure and GFR

67
Q

What factors would make an ideal marker for GFR?

A
  • Must be freely filtered (i.e not affected by size or charge barrier)
  • Not reabsorbed in the PCT
  • Not secreted in the DCT
  • Excreted in the urine
68
Q

What can be used as a marker for GFR? Give their disadvantages

A
  • Creatinine = affected by diet, gender, age, ethnicity
  • Insulin= not endogenous, needs to be infused into blood
  • Cystatin C= currently in trials, also affected by age, gender and ethnicity
69
Q

What comprises the juxtaglomerular apparatus?

A
  • Macula densa
  • JG cells (modified SM)
  • Mesangial cells
70
Q

What is ACR used to measure?

A

glomerular damage, as it helps decide if a patient is in a state of proteinuria

71
Q

How is pH calculated? What is it normally in arterial blood?

A

pH = -log10 [H+]

Normally 7.4

72
Q

What is the Henderson-Hasselbauch equation?

A

pH = pK + log10 [HCO3-]/[CO2]

Works out pH using concentration of HCO3- and Co2

73
Q

What is pK?

A

Constant at 6.1

74
Q

Compare respiratory/ metabolic acidosis/ alkalosis

A

Respiratory acidosis: increased CO2, if lungs cant compensate the kidneys excrete acid
Respiratory alkalosis: low CO2, i.e. hyperventilation or altitude
Metabolic acidosis: low HCO3-
Metabolic alkalosis: high HCO3-

75
Q

What values of CO2 (mmHg) and HCO3- (mM) would maintain pH at 7.4?

A

CO2= 40mmHg
HCO3-= 24mM

76
Q

What are the 3 mechanisms for buffering H+?

A
  • Resorption of filtered HCO3-
  • Excretion of H+ as titratable acid (TA)
  • Excretion of H+ as NH4 (ammonium)
77
Q

How is HCO3- reabsorbed into the blood?

A
  • H+ secreted across the apical membrane reacts with HCO3- to form CO2 and H2O via carbonic anhydrase IV
  • CO2 diffuses into cell, reacts with H2O to form HCO3- and H+ via CA II
  • HCO3- can leave via basolateral membrane into blood
78
Q

How is H+ excreted as ‘titratable acid’?

A
  • In the blood H+ reacts with to HCO3- to form H2O and CO2
  • CO2 enters and reacts via CA II to form H+ and HCO3-
  • HCO3- leaves basolaterally to neutralise blood, H+ goes into urine
  • H+ binds to HPO4- to form H2PO4-
79
Q

How is H+ excreted as NH4-?

A

Glutamine metabolism releases OH- and NH4-. The OH- reacts with CO2 to form HCO3-, released into blood
NH4- dissociates into NH3 and H+, can freely diffuse into tubular fluid
Recombines= excreted as acid

80
Q

Where are the carbonic anhydrases relevant to the kidney found?

A

CA II = soluble so in cytoplasm
CA IV = bound to membrane (extracellualr)

81
Q

Where is HCO3- reabsorbed throughout the kidney?

A

Most in the PCT (80%)
Small amounts in thick ascending limb (10%), DCT (6%) and CD (4%)

82
Q

How much ammonium and titratable acid needs to be secreted each day? Where is this mainly?

A

Ammonium: 40 mmol, mainly PCT

TA: 30mmol, mainly PCT, some CD and then small in DCT

83
Q

What are the 4 types of renal tubule acidosis?

A

Type 1: distal RTA
Type 2: proximal RTA
Type 3: mix of type 1 and 2
Type 4: hyperkalaemia

84
Q

Which type of renal tubule acidosis occurs with hypoaldosteronism?

A

Type 4- hyperkalaemia

85
Q

The NHE3 and H+ ATPase transporters are unable to work past what pH?

A

NHE3= pH 6
H+ ATPase= pH 4-5

86
Q

Other than NHE3 and H+ ATPase, what transporter is present in the TAL and DCT for acid base balance?

A

AE2: basolateral HCO3- and Cl- exchanger, i.e. reabsorbs HCO3- into blood

87
Q

Type A (alpha) intercalated cells in the DCT and CD have 2 isoforms of specific transporters, name them

A

kAE1 (same as AE2): basolateral HCO3- exchanger with Cl-
V-type H+/K+ ATPase: allows reabsorption of K+ too

88
Q

What channels reabsorb NH4+ in the TAL?

A

NKCC1: ammonium can take place of K+, i.e. Na+, 2Cl- and NH4- is taken up into cell (apical)
ROMK2: apical reabsorption
Can also use Na+/K+ ATPase

89
Q

what is the kNBCe1 transporter responsible for?

A

HCO3- efflux over basolateral membrane: 3 HCO3- transported with Na+ (has electrogenic potential)

90
Q

What happens in type 1 renal tubular acidosis? Can it be treated?

A

Defective H+ secretion in the distal nephron, leads to metabolic acidosis. Can be autosomal dominant or recessive, and is due to multiple mutations: kAE1, V-type H+ ATPase, CAII. Treatable with HCO3-

91
Q

What happens in type 2 renal tubular acidosis? Can it be treated?

A

Autosomal recessive condition where HCO3- reabsorption is impaired (proximal nephron), leads to metabolic acidosis. Associated with mutated kNBCe1 (i.e. 3 HCO3- with Na+)

92
Q

If respiratory or metabolic acidosis is chronic, what changes can it lead to? Why?

A

Increased expression of NHE3 in PCT: in attempt to excrete H+ (exchanges it with Na+)
Increased expression of kNBCe1 in PCT, in attempt to reabsorb more HCO3-

93
Q

If respiratory or metabolic alkalosis is chronic, what changes can it lead to? Why?

A

More type B (beta) intercalated cells in the collecting tubule, as these secrete HCO3- into urine

94
Q

What is the typical first sign of diabetic kidney disease?

A

Persistant leakage of protein

95
Q

How is the filtration barrier affected by diabetic kidney disease?

A
  • Thickening of basement membrane
  • Flattening of podocytes (foot processes)
  • Mesengial cell proliferation and expansion of matrix, leads to sclerosis (nodular -> advanced)
96
Q

What is nephrotic syndrome characterised by?

A

This is a clinical presentation (not a disease itself):
- Massive proteinuria
- Low protein in the blood (including albumin), which leads to…
- Oedema

97
Q

What is a normal protein:creatinine ratio (PCR)? What values might be seen in nephrotic syndrome?

A

<20 mg/mmol
Nephrotic syndrome: >200mg/mmol

98
Q

Why is PCR used for proteinuria assessment, not just the total level of protein?

A

Normalise/ correct it for concentration of the urine, i.e. excrete creatinine a lot

99
Q

PCR is often used for children to assess proteinuria, what test might be used for adults or in diabetes monitoring? Give normal & nephrotic values

A

Albumin: creatinine ratio (ACR):
- >3mg/mmol normal
- >30 mg/mmol nephrotic syndrome

100
Q

What % of diabetics develop diabetic nephropathy?

A

40%

101
Q

Which ethnicity has increased risk for diabetic nephropathy?

A

Indian

102
Q

What are the stages of injury following diabetes leading to DKD?

A

1: Hyperfiltration- i.e. from hyperglycaemia
2: Microalbuminuria
3: Macroalbuminuria
4: Proteinuria: unselective loss of protein
5: Declining renal function

103
Q

How could you treat diabetic nephropathy?

A

-Glycaemic control
- RAAS blockade
- Lipid lowering
- Diuretics
- SGLT2 inhibitors= T2D

104
Q

What drugs may be used to inhibit RAAS for diabetic nephropathy? Give examples

A

ACE-inhibitors= ramipril etc.
Angiotensin II receptor blockers= end in ‘sartan’ i.e. candesartan

105
Q

What type diuretics may be used in diabetic kidney disease? Give their MOA and an example

A

Loop diuretics: inhibit NKCC2 in thick ascending limb to increase excretion of NaCl = more water excreted. Example= furosemide

Thiazide diuretics: inhibit NCC in DCT, so more water excreted. Risk. of hypercalcaemia. Example= indapamide

K+ sparing diuretics: in distal DCT, block ENaC to reduce Na+ reabsorption. Example= amiloride

Aldosterone receptor antagonist: blocks Na+/K+ ATPase and ENaC by reducing aldosterone action. Example= spironolactone

106
Q

What do SGLT2 inhibitors drug names end in?

A

Flozin

107
Q

Why aren’t SGLT2 inhibitors approved for T1D with diabetic kidney disease?

A

Risk of diabetic ketoacidosis

108
Q

What are some options for renal replacement therapy?

A

Peritoneal dialysis: tube into abdomen, linked to hypertonic fluid to allow fluid to enter abdomen, then leaves with waste products
Haemodialysis: access circulation, blood gets cleaned
Surgery

109
Q

What are some advantages of peritoneal dialysis?

A
  • gentle; no anti-coagulation
  • Less likely to cause hypotension or fluid shifts
  • Cheap
  • Immediate use
  • Continuous use
110
Q

What are some advantages/ disadvantages of haemodialysis?

A
  • increased solute clearance (efficient)
  • intermittent; not tolerant when haemodynamically active
  • Need anti coagulation
  • Requires specialist care
  • 4 hour session 3x a week
111
Q

What glucose transporters are present in the early vs late PCT and why?

A

Early PCT: SGLT2 and GLUT2, as these have low affinity and high capacity as there is lots of glucose to reabsorb

Late PCT: SGLT1 and GLUT1, as these have high affinity and low capacity, as there is not much glucose to reabsorb

112
Q

What is the effect of calcitonin on Ca2+ reabsorption?

A

Calcitonin lowers Ca²⁺ reabsorption to try and reduce blood levels of Ca²⁺

i.e. calciTONIN, “tones in” (i.e. lowers) the blood Ca²⁺

113
Q

What is the first line of treatment for hypertension?

A

If patient >55 or of african or afro-carribean origin: Calcium-channel blocker, i.e. amplodipine

If patient is <55 or has type II diabetes (or not of African origin): ARB or ACE-i

114
Q

What are the targets of advanced glycation end-products?

A

Can lead to glycation of basement membrane (endothelial cells), especially in the efferent arteriole = hyaline arteriosclerosis, increased obstruction to blood flow= high GFR = hyperfiltration

115
Q

Name what Na+ transporters are present in each part of the nephron

A

PCT — Na/AA, SGLT, NHE
Loop of Henlé — NKCC2
Early DCT — NCC
Late DCT — ENaC and Na⁺/K⁺-ATPase

116
Q

Where is ADH synthesised/ released from?

A

Synthesised in hypothalamus, released from posterior pituitary

117
Q

What channel do the macular densa cells possess? Why?

A

NKCC2: Allows the macula densa cells to sense the NaCl concentration in the tubular fluid. When the GFR increases = higher flow rate of fluid = higher delivery of NaCl to the macula densa

118
Q

What are the 5 stages of Tervaet classification for diabetic nephropathy? Give what clinical sign may be present

A

Stage I: thickening of GBM
Stage IIA: mild mesengial expansion (i.e. microalbuminuria, ACR >3mg/mmol)
Stage IIB: severe mesengial expansion (i.e. macroalbuminuria, ACR>30mg/mmol)
Stage III: Nodular sclerosis: PCR >200mg/mmol
Stage IV: Advanced diabetic nephropathy = declined renal function

119
Q

What is nephritis syndrome? What is it characterised by?

A

Reduction in kidney function:
- Haematuria
- Proteinuria, but less than nephrotic syndrome

120
Q

What are some physiological effects of acute kidney injuries?

A
  • Water and salt overload = oedema and HTN
  • Excessive retention of K+
  • Metabolic acidosis (unable to secrete H+)
121
Q

How are organ transplants matched?

A

HLA type A, B and C on chromosome 6. Don’t have to fully match, but the less they match the more likely it is to fail. May require lifelong immunosuppression

122
Q

For each of the following conditions, state what may be found in the urine:
- Glomerular disease
- Renal tubular disease
- Tubular dysfunction

A

Glomerular disease= RBC and protein
Renal tubular disease= high H+ ions
Tubular dysfunction= amino acids and glucose

123
Q

What is the most common cause for chronic renal failure?

A

Diabetes: accounts for 30-40% of those needing dialysis
(second most common= hypertension)

PBL Y2 S4 (9 decks)

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