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Renal Physiology Flashcards

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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.
In dct

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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

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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24
What is the basic pathophysiology of SIADH?
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.
25
How is creatinine interpreted in U&Es for kidney function?
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.
26
How is urea used to interpret results in U&Es?
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.
27
What might an isolated raise in urea indicate?
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.
28
Why is sodium useful in interpretation of U&Es?
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.
29
Why is potassium levels important in U&E interpretation?
Normally stored intracellular and excreted by the kdienys Derangement cause myocardial instability and risk of fatal arryhtmias.
30
What is the normal urine output for a human?
1ml/kg/hour
31
What medications should be held in the acute setting in a patient with an AKI?
NSAIDS ACEinhibitors/ ARBS Diuretics Metformin
32
Define AKI
A sudden decline in renal excretory funcation over hours or days that results in failure to maintain fluid, electrolyte and acid-base balance.
33
What is the KDIGO definition of a AKI?
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.
34
How do you stage AKI by creatinine?
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.
35
How do you stage AKI by urine output?
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.
36
What are the different categories of causes of an AKI?
Pre-renal - dec perfusion (most common in 30-50% of cases) Renal - intrinsic disease Post-renal - Urinary tract obstruction
37
What are the pre-renal causes of a AKI?
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.
38
What are the intra-renal causes of an AKI?
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
39
What are some common causes of post-renal AKI?
Ureterus - retroperitoneal fibrosis Bladder cancer Prostate hyperplasia/cancer Urethral stricture
40
What are the different factors affecting the diameter of the afferent and efferent arteriole?
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.
41
What nephrotoxic medication alter the GFR? How?
ACEi, ARBs, cyclosporin, NSAIDs, tacrolimus Alters the vascular tone.
42
What nephrotoxic medication has tubular cell toxicity? How?
Aminoglycosides such as gentamicin Amphotericin B Cisplatin Toxic to epithelial cells (PCT)
43
What nephrotoxic drugs cause interstitial nephritis?
NSAIDS Rifampicin PPIs Cause inflammation of insterticitium.
44
What nephrotoxic drugs cause crystal nephropathy?
Aciclovir Ampicillin Form insoluble crystals.
45
Describe why ACEi and ARBs can be useful in CKD but not in AKI**
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
46
What are the key clinical features of an AKI?
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
47
What are the signs looked for in a fluid assessment?
Hypo - dry mucous membranes, reduced skin turgor, tachycardia and hypotension Hyper - HTN, pulmonary oedema, peripheral oedema, elevated JVP
48
What are the signs of ureaemia?
Ecchymosis (platelet dysfunction) Encephalopathy - asterixis, confusion, seixures.
49
What is key sign of post-renal obstruction?
Palpable or tender distended bladder.
50
What are some key bedside investigations for AKI?
Urine dipstick Urine output measurement Urine microscopy and culture
51
What are some key bloods for AKI?
U+Es LFTs FBC CRP VBG
52
When might a renal biopsy be taken in an AKI?
Suspected intra-renal AKI
53
What imaging might be done for an AKI?
Post-void bladder scan US-KUB CT-KUB (non-contrast) CT-urogram (contrast) CT-triphasic (kidneys)
54
What is the general management of an AKI?
Address drugs Boost BP Calculate fluid balance Dip urine Exclude obstruction ABCDE
55
What targeted management might be used for an AKI?
Diuretics in volume overload Immunosuppression in AIN/Rapidly progressive glomerulonephritis Bladder catheterisation, nephrostomy or ureteric stent insertion depending on the site of obstructive cause.
56
What are some common complications of an AKI?
Fluid overload Electrolyte imbalance Acid-base disorders (Metabolic acidosis) End organ complications of uraemia Chronic kidney disease and end-stage renal disease Death.
57
What are the indications for renal replacement therapy (dialysis)?
AEIOU Acidosis Electrolyte imbalances Ingestion or overdose Overload Uremia
58
What when ingested or overdosed requires dialysis?
Isoniazide + isopropyl alcohol Salicylates Theophylline Uremia Methanol and metformin Barbiturates Lithium Ethanol and ethylene glycol Depakote and dabigatran.
59
Define CKD
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.
60
What are the common causes of CKD?
Diabetes and vascular disease - most common Glomerular disease Nephrotoxic drugs Obstructive/reflux nephropathy Multi-system disease with renal involvement Hereditary kidney disease.
61
How does damage to the nephrons leads to CKD?
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.
62
What are the risk factors for CKD?
Age >50yrs Male History of renal disease/AKI Diabetes mellitus and cardiovascular disease Obesity with metabolic syndrome Gout Smoking Black/Hispanic ethnicity
63
What is required for the diagnosis of CKD?
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.
64
How is CKD classified using GFR and albuminuria?
65
What are some common markers for CKD?
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
66
What are the common symptoms of CKD?
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
67
What are the common clinical findings of CKD?
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
68
What is proteinuria be definition?
Urinary albumin: creatinine >3mg/mmol
69
What bedside investigations should be done for CKD?
Urine dipstick and protein Blood pressure Capillary blood glucose ECG
70
What bloods should be done for CKD?
U&Es FBC LFT inc albumin Bone profile for electrolytes Serum PTH Lipid profile HbA1c Myeloma screen
71
What auto-antibodies should be tested for in CKD?
ANCA ANA Serum complement is suspecting secondary glomerular disease.
72
What imaging should be done for CKD?
Plain abdo x-ray US-KUB CT or MRI.
73
What is the typical management for CKD?
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
74
How should CKD be monitored?
FBC and iron studies - anaemia Serum calcium/phosphate/PTH - renal bone disease U&Es plus urine protein (eGFR and albuminuria)
75
When is renal replacement therapy often used for CKD?
When eGFR reaches 5-10ml/min/1/73^2 End-stage CKD
76
What are the benefits of kidney transplant in CKD patients?
Best long term outcomes Removes need for dialysis, reduce renal complications, improve QoL Can be from cadaveric or live donors
77
How is a good tip for identifying a transplanted kidney on abdo examination?
Original kidney is left in situ Transplanted kideny can be felt in the iliac fossa.
78
How to prevent graft rejection in kideny transplant?
INduction and maintenance immunosuppression to prevent graft rejection.
79
What are the common complications of CKD?
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.
80
How do SLGT in the nephron contribute to glucose re-absoprtion?
SGLT2 - reabsorb 90%, high capacity low sensitivity SGLT1 - reabsorb 10%, low capacity and high sensitivity.
81
Where is glucose-6-phosphate found?
Liver The cortex of the kidney Intestinal epithelium
82
What is the relationship between insulin and the kidney?
Insulin is metabolised by the kideny Increased insulin suppresses gluconeogenesis in the kidney and enhances glucose re-uptake.
83
What is the relationship between hyperglycaemia and the kidney?
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.

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