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Med 2 > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

What are the different roles of the kidneys in the body?

A
  1. Filtration of toxins, metabolic waste products and excess iron
  2. Regulate plasma osmolarity (water, solutes and electrolytes)
  3. Acid-base balance
  4. Produce erythropoietin
  5. Production of renin
  6. Convert Vitamin D to its active form
  7. Urine production and excretion.
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2
Q

What vertebral level are the kidneys found?

A

T12 to L3
Left tends to be T12 to L2
Right L1 to L3

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3
Q

Describe the internal structure of the kidney

A

Outer cortex
Inner medulla
Outer cortex invaginates as renal columens between triangular sections of medulla know as renal pyramids
Pyramids inferior most portion known as renal papilla
Drains into minor Calyx, to major calyx to renal pelvis to the ureter.

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4
Q

What are the different parts of the nephron?

A

Afferent arteriole
Efferent arteriole
Glomerulus
Bowmans capsule
PCT
Loop of Henle
DCT
Collecting duct

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5
Q

What are the three main functional units of the nephron and what do they do?

A

Renal corpuscle = filtration
Renal tubule = absorption and ion secretion
Collecting duct = final reabsorption of water and urine storage.

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6
Q

What is the process of glomerular filtration?

A

Ultrafiltration of blood due to blood pressure gradient.
Across three barriers - endothelial cell of glomerular capillaries, g basement membrane and epithelial cells of Bowmans capsule (podocytes)
Small solutes pass through by passive diffusion (no energy requirement at this stage)

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7
Q

What is the glomerular filtration rate v eGFR

A

GFR = The volume of glomerular filtrate formed per minute by the kidneys.
eGFR = an equation using creatinine, age and gender to estimate kidney function.

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8
Q

What is the basic function of the PCT?

A

Re-absorption by passive or active transport (Na+ SGLT2) - water often follows by osmotic pressure.
Regulated by hormones
Toxins and some drugs are excreted here

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9
Q

What is the PCT responsible for re-absorbing?

A

65% water, Na+, K+, Cl-
100% of glucose and amino acids
Up to 90% of bicarbonate.

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10
Q

What substances does the PCT secrete?

A

Organic acids and bases - bile salts, catecholamines
Hydrogen ions - in exchange for Bicarb.
Drugs/toxins - dopamine, morphine via H+/OC exchanger on apical side driven by Na+/H+ antiporter.

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11
Q

Give a summary of renal cell carcinoma.

A

Most common primary renal malignancy
Originates from PCT
Mutations on chromosome 3
Can invade the renal vein and metastasis to lungs and bones.

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12
Q

What is acute tubular necrosis of the kidney?

A

Ischemia caused by reduced renal blood flow (e.g sepsis)
Death of tubular cells (PCT)
Urinalysis - muddy brown casts
Need to treat the underlying cause

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13
Q

How do SGLT inhibitors affect the PCT?

A

e.g gliflozins
Used in T2DM or as diuretics, slow CVD/CKD progression
Inhibit SGLT2 transporters - more glucose excreted, less sodium and water re-absorbed.

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14
Q

What is the role of the descending limb of the loop of Henle?

A

Permeable to water, not solutes
Water flows from filtrate to interstitial fluid passively via aquaporin channels.
Osmolarity increases as limb ascends - driven by the counter current multiplier system.

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15
Q

What is the role of the ascending (thin) limb of the loop of Henle?

A

Permeable to solutes, not water.
Osmolarity peaks at the bottom as the loop ascends
As filtrates ascend, Na+ and Cl- exit via ion channels - ENaC channels and Cl- channels. Some paracellular in the thin portion
Further up Na+ is actively transported out and Cl- follows through NKCC2 channels in the thick portion.

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16
Q

What is the overall affect of the action of the Loop of Henle?

A

Removal of Na+ whilst retaining water in the tubules -> hypotonic solution arriving at the DCT
Pumping Na+ into the interstitial space -> hyperosmotic environment in the kidney medulla
Some paracellular reasbsoprtion of magnesium, calcium, sodium and potassium.

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17
Q

What is the main mechanism of action of loop diuretics?

A

For example: Furosemide - inhibits NKCC2 transporters in the thick ascending limb.
Stopes Na+, K+ and Cl- re-absoprtion
Reduces Na+ conc in renal medulla - dec water re-absoprtion

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18
Q

What electrolyte abnormalities are common from loop diuretics?

A

Hyponatremia
Hypokalaemia.

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19
Q

What is the role of the early distal convoluted tubule?

A

Responsible for absoprtion of ions and is impermeable to water.
Movement of these ions occurs via active transport.
Macula densa cells are sensory epithelium, involved in tubuloglomerular feedback - to regulate the glomerular filtration rate.

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20
Q

What is the role of thiazide diuretics?

A

Inhibits the NCC symptomter (sodium-chloride co-transporter)
Decrease re-absoprtion of sodium - decrease re-absoprtion of water.

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21
Q

What is the role of principle cells in the late DCT and collecting ducts?

A

Majority of tubular cells
Active uptake of Na+ and K+ excretion

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22
Q

What is the main role of intercalated cells in the late DCT and collecting ducts?

A

Acid-base balance by controlling levels of H+/HCO3-

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23
Q

What is the main role of the collecting ducts in the nephron?

A

Re-absoprtion of water, regulated by ADH, which acts to increase the number of aquaporin 2 channels to allow more re-absoprtion of water.

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23
Q
A
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24
Q

What is the basic pathology of diabetes insipidus?

A

Lack of production (cranial) or response (nephrogenic) to ADH
Leads to less water re-absorption from the filtrate -> polyuria and polydipsia.

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25
Q

What is the basic pathophysiology of SIADH?

A

Increased ADH secretion -> increased aquaporin 2 expression
Increase water reabsorption and more concentrated urine
Dilution of blood causes euvolaemic hyponatremia
Aldosterone secretion in reduce in response to fluid retention -> resulting in further reduction of sodium re-absoprtion in the kidney.

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26
Q

How is creatinine interpreted in U&Es for kidney function?

A

A waste product of muscle metabolism, excreted entirely by the kidney.
Serum levels reflect the kidenys ability to filter creatinine from the blood.
Often used to calculate eGFR
Note levels can be innacurate in individuals with higher muscle mass, obesity and limb amputees.

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27
Q

How is urea used to interpret results in U&Es?

A

A waste product of protein breakdown, produced in the liver and predominantly excreted by the kidneys.
Can be raised due to renal dysfunction, dehydration and upper GI bleeding.

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28
Q

What might an isolated raise in urea indicate?

A

Rises in dehydration
ADH released due to intravascular volume depletion = inc urea and water re-absorption in collecting ducts = leads to higher levels.

Raised in GI bleed = protein breakdown of blood components.

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29
Q

Why is sodium useful in interpretation of U&Es?

A

Main determinant of plasma osmolarity - related to hydration status
Regulated by ADH and other homeostatic mechanisms.
Primarily neurological and related to the severity of derangement and rate of change.

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30
Q

Why is potassium levels important in U&E interpretation?

A

Normally stored intracellular and excreted by the kdienys
Derangement cause myocardial instability and risk of fatal arryhtmias.

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31
Q

What is the normal urine output for a human?

A

1ml/kg/hour

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32
Q

What medications should be held in the acute setting in a patient with an AKI?

A

NSAIDS
ACEinhibitors/ ARBS
Diuretics
Metformin

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33
Q

Define AK

A

A sudden decline in renal excretory funcation over hours or days that results in failure to maintain fluid, electrolyte and acid-base balance.

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34
Q

What is the KDIGO definition of a AKI?

A

Increase in SCr>3.0 mg/dL within 48hrs
Increase in SCr >1.5x baseline over 7d
Urine output <0.5ml/kg/h for 6 hours
Only one is needed.

35
Q

How do you stage AKI by creatinine?

A

Stage 1 - from 1.5 to 2x baseline or >0.3mg?dl
Stage 2 - up to 2.9x baseline
Stage 3 - more than 3x baseline or >4mg/dL or requires dialysis.

36
Q

How do you stage AKI by urine output?

A

All <0.5ml/kg/hr
Stage 1 - in 6-12hrs
Stage 2 - greater than 12hrs
Stage 3 - greater than 24hrs or anuria in 12 hrs.

37
Q

What are the different categories of causes of an AKI?

A

Pre-renal - dec perfusion (most common in 30-50% of cases)
Renal - intrinsic disease
Post-renal - Urinary tract obstruction

38
Q

What are the pre-renal causes of a AKI?

A

Reduced renal perfusion
1. Absolute hypovolemia - haemorrhage, V&D, over-diuresis
2. Low effective arterial blood volume = heart failure, third spacing, sepsis
3. Anatomical - renal artery stenosis
4. Drugs - NSAIDs, ACEinhibitos, diuretics.

39
Q

What are the intra-renal causes of an AKI?

A
  1. Acute tubular necrosis
  2. Acute interstitial nephritis - drug enduced, infection or immune mediated.
  3. glomerular disease - nephrotic and nephritic syndromes
  4. Intra-tubular obstruction
  5. Malignant HTN
40
Q

What are some common causes of post-renal AKI?

A

Ureterus - retroperitoneal fibrosis
Bladder cancer
Prostate hyperplasia/cancer
Urethral stricture

41
Q

What are the different factors affecting the diameter of the afferent and efferent arteriole?

A

Catecholamines - constrict afferent via alpha 1
Angiotensin 2 - constrict afferent and efferent (greater on eff at low conc)
ANP - dilate afferent and constrict efferent
Prostaglandins and dopamine - dilate afferent and efferent.

42
Q

What nephrotoxic medication alter the GFR?
How?

A

ACEi, ARBs, cyclosporin, NSAIDs, tacrolimus
Alters the vascular tone.

43
Q

What nephrotoxic medication has tubular cell toxicity?
How?

A

Aminoglycosides such as gentamicin
Amphotericin B
Cisplatin
Toxic to epithelial cells (PCT)

44
Q

What nephrotoxic drugs cause interstitial nephritis?

A

NSAIDS
Rifampicin
PPIs
Cause inflammation of insterticitium.

45
Q

What nephrotoxic drugs cause crystal nephropathy?

A

Aciclovir
Ampicillin
Form insoluble crystals.

46
Q

Describe why ACEi and ARBs can be useful in CKD but not in AKI**

A

Angiotensin 2 cause vasoconstriction of efferent arteriole through RAAS system = inc GFR
In CKD - ACEi and ARBs - stop this process - prevent hyperfilitration/inc pressure in glomerulus slowing progression of CKD
In AKI - ACEi and ARBs - preventing RAAS - leads to inability to increase GFR in response to hypoperfusion, must stop drugs to improve GFR

47
Q

What are the key clinical features of an AKI?

A

Asymptomatic or non-specific - fatigue, nausea, confusion
Hours-days
May be acutely unwell
Lower urinary tract symptoms

History: PMH (renal disease), DH, recent contrast imaging, input/output

48
Q

What are the signs looked for in a fluid assessment?

A

Hypo - dry mucous membranes, reduced skin turgor, tachycardia and hypotension
Hyper - HTN, pulmonary oedema, peripheral oedema, elevated JVP

49
Q

What are the signs of ureaemia?

A

Ecchymosis (platelet dysfunction)
Encephalopathy - asterixis, confusion, seixures.

50
Q

What is key sign of post-renal obstruction?

A

Palpable or tender distended bladder.

51
Q

What are some key bedside investigations for AKI?

A

Urine dipstick
Urine output measurement
Urine microscopy and culture

52
Q

What are some key bloods for AKI?

A

U+Es LFTs
FBC CRP
VBG

53
Q

When might a renal biopsy be taken in an AKI?

A

Suspected intra-renal AKI

54
Q

What imaging might be done for an AKI?

A

Post-void bladder scan
US-KUB
CT-KUB (non-contrast)
CT-urogram (contrast)
CT-triphasic (kidneys)

55
Q

What is the general management of an AKI?

A

Address drugs
Boost BP
Calculate fluid balance
Dip urine
Exclude obstruction

ABCDE

56
Q

What targeted management might be used for an AKI?

A

Diuretics in volume overload
Immunosuppression in AIN/Rapidly progressive glomerulonephritis
Bladder catheterisation, nephrostomy or ureteric stent insertion depending on the site of obstructive cause.

57
Q

What are some common complications of an AKI?

A

Fluid overload
Electrolyte imbalance
Acid-base disorders (Metabolic acidosis)
End organ complications of uraemia
Chronic kidney disease and end-stage renal disease
Death.

58
Q

What are the indications for renal replacement therapy (dialysis)?

A

AEIOU
Acidosis
Electrolyte imbalances
Ingestion or overdose
Overload
Uremia

59
Q

What when ingested or overdosed requires dialysis?

A

Isoniazide + isopropyl alcohol
Salicylates
Theophylline
Uremia
Methanol and metformin
Barbiturates
Lithium
Ethanol and ethylene glycol
Depakote and dabigatran.

60
Q

Define CKD

A

Abnormal kidney function or structure present for more than 3 months, with subsequent implications for health.
Typically occurs when more than half the nephrons damaged.

61
Q

What are the common causes of CKD?

A

Diabetes and vascular disease - most common
Glomerular disease
Nephrotoxic drugs
Obstructive/reflux nephropathy
Multi-system disease with renal involvement
Hereditary kidney disease.

62
Q

How does damage to the nephrons leads to CKD?

A

When half nephrons are damaged:
1. Hyperfiltration at glomeruli = proteinuria
2. Activation of RAAS = increase systemic and renal blood pressure
3. Increase in capillary pressure and inflammatory mediators -> chronic inflammation and reduced filtration ability of glomerulus = dec GFR.

63
Q

What are the risk factors for CKD?

A

Age >50yrs
Male
History of renal disease/AKI
Diabetes mellitus and cardiovascular disease
Obesity with metabolic syndrome
Gout
Smoking
Black/Hispanic ethnicity

64
Q

What is required for the diagnosis of CKD?

A

Must be three months or more
Stage 1/2 = requires additional evidence or renal disease - proteinuria, electrolyte abnormalities, structural abnormalitieites, history ot kidney transplant
Stage 3-5 = eGFR alone.
Often use GFR and albuminuria to classify.

65
Q

How is CKD classified using GFR and albuminuria?

A
66
Q

What are some common markers for CKD?

A

Albuminuria >30mg/24hrs
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
Histology abnormalities
Structural abnormalities on imaging
History of kidney transplantation
GFR <60

67
Q

What are the common symptoms of CKD?

A

Generally symptomatic until stage 4/5
Symptoms - fatigue, nausea, cramps, restless legs, bone pain, pruritisis, abnormal urine output, fluid overload, coma/seizures, sexual dysfunction
Due to high urea levels

68
Q

What are the common clinical findings of CKD?

A

Ammonia smelling breath
Pallor (aenmia)
Congitive impairement
Hypertension
Volume disturbance
Peripheral neuropathy
Microvascular disease = retinopathy, palpable bladder

Normally found incidentally - HTN, haematuria. protein uria and dec eGFR and raised creatinine

69
Q

What is proteinuria be definition?

A

Urinary albumin: creatinine >3mg/mmol

70
Q

What bedside investigations should be done for CKD?

A

Urine dipstick and protein
Blood pressure
Capillary blood glucose
ECG

71
Q

What bloods should be done for CKD?

A

U&Es
FBC
LFT inc albumin
Bone profile for electrolytes
Serum PTH
Lipid profile
HbA1c
Myeloma screen

72
Q

What auto-antibodies should be tested for in CKD?

A

ANCA
ANA
Serum complement is suspecting secondary glomerular disease.

73
Q

What imaging should be done for CKD?

A

Plain abdo x-ray
US-KUB
CT or MRI.

74
Q

What is the typical management for CKD?

A

Lifestyle - weight, exercise, smoking, alcohol and diet restriction
Co-mobs - glycaemic control, BP
Immunisations - influenza and pneumococcus
Avoidance of nephrotoxic medications
Assess for cardiovascular risk factors + primary prevention

75
Q

How should CKD be monitored?

A

FBC and iron studies - anaemia
Serum calcium/phosphate/PTH - renal bone disease
U&Es plus urine protein (eGFR and albuminuria)

76
Q

When is renal replacement therapy often used for CKD?

A

When eGFR reaches 5-10ml/min/1/73^2
End-stage CKD

77
Q

What are the benefits of kidney transplant in CKD patients?

A

Best long term outcomes
Removes need for dialysis, reduce renal complications, improve QoL
Can be from cadaveric or live donors

78
Q

How is a good tip for identifying a transplanted kidney on abdo examination?

A

Original kidney is left in situ
Transplanted kideny can be felt in the iliac fossa.

79
Q

How to prevent graft rejection in kideny transplant?

A

INduction and maintenance immunosuppression to prevent graft rejection.

80
Q

What are the common complications of CKD?

A

A WET BED
Acid base balance - metabolic acidosis
Water removal - pulmonary oedema due to fluid overload
Erythropoiesis -> Aneami of CKD
Toxin removal -> uremic encephalopathy due to accumulation of toxins
Blood pressure control -> salt and water overload and hypertension
Electrolyte - imbalance -> hyperK+
Vitamin D -> renal bone disease -> secondary hyperparathryoidism.

81
Q

How do SLGT in the nephron contribute to glucose re-absoprtion?

A

SGLT2 - reabsorb 90%, high capacity low sensitivity
SGLT1 - reabsorb 10%, low capacity and high sensitivity.

82
Q

Where is glucose-6-phosphate found?

A

Liver
The cortex of the kidney
Intestinal epithelium

83
Q

What is the relationship between insulin and the kidney?

A

Insulin is metabolised by the kideny
Increased insulin suppresses gluconeogenesis in the kidney and enhances glucose re-uptake.

84
Q

What is the relationship between hyperglycaemia and the kidney?

A

Diabetic nephropathy
Hyperglycaemia promotes
1. protein kinase C and growth factors -> tuberstitial injury
2. Acceleration of RAAS -> hypertension -> glomerular damage
3. Advanced glycation end production -> overproduction of mesangial cell matrix -> glomerular damage
Leading to proteinuria and nephron loss.

85
Q
A

Med 2 (22 decks)

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