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Year 2 - Semester 2 > Renal - Week 2 > Flashcards

Renal - Week 2 Flashcards

1
Q

what makes up the lower urinary tract?

A

the bladder and urethra

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2
Q

how is the ower urinary tract protected?

A

Lower urinary tract is protected by layers of fascia
Protection from pubic rami anteriorly and the iliac wings posteriorly
Peritoneum reflects over the dome of the bladder

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3
Q

describe the makeup of the bladder

A
  • Has transitional epithelium
  • Then lamina propria
  • Then submucosa

Urothelium
• Multilayered epithelium; Apical (umbrella cells)
• Functions include: Barrier, afferent signaling
Lamina propria
• Functional centre’ coordinating urothelium and Detrusor
• Blood vessels, nerve fibres, myofibroblasts
Detrusor muscle
• Smooth muscle arranged in bundles
• Functional syncytium
• Each detrusor cell- 600 microns long by 5 microns

Stroma
• collagen and elastin
• Innervation of muscle: postganglionic parasym.

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4
Q

how is the male detrusor muscle different

A

thicker to work against the resistance caused by the prostate

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5
Q

what are bladder tight junctions involved in

A

play a major role in cell signalling during bladder stretching

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6
Q

describe normal bladder function

A
  • Compliant Reservoir for urine storage
  • Barrier function (GAG layer, tight junctions):
  • Passive passage of urea, Na,K;
  • Resists water passage but not truly waterproof
  • Damage to urothelium plays a role in disease

• Volitional Voiding (muscular function)

  • Bladder pressure remains constant despite increase in volume
  • Bladder is highly compliant
  • Visco-elastic properties (elastin/collagen; detrusor relaxation without change in tension)
  • Bladder filling- sensors detect increase in wall tension
  • Afferent neurons to dorsal horn of sacral spinal cord-
  • sensory/real time data on bladder state relayed to brainstem and higher centres
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7
Q

describe Volitional Micturition/Voiding

A

• voiding is through the spino-bulbar reflex and children who have not been potty trained void through this reflex
• this can be controlled by higher centres through modulation by Pontine Micturition Centre (Barrington’s nucleus) - PONS
• further processing and relaying of signals in Onuf’s nucleus in intermediolateral S2,3,4
• feel full at 250ml and uncomfortable at 500ml
• during voiding
o coordination of
 detrusor contraction
 urethra relaxation
o if this is not coordinated it can lead to voiding difficulties

Micturition: Positive feedback loop (inhibitory controls)
Detrusor contracts  Wall tension rises  Afferent signals to PMC  Efferent signals- increase detrusor contraction

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8
Q

what is the role of neurotransmitters in voiding

A

• Excitatory neurotransmission: Cholinergic (Ach)
• Role for nitric oxide in relaxation of bladder neck/EUS
• GABA and glycine inhibitory neurons
• Bladder activity subject to facilitation and inhibition (higher centres and local reflexes)
o Facilitation = contraction of detrusor & relaxation of sphincter when bladder less than full e.g anxiety states
o Inhibition = allows postponement of voiding

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9
Q

what happens to bladder control in spinal injuries

A
  • Loss of central inhibition
  • Typically reflex voiding through pelvic sympathetic nerves and pudendal nerves
  • The level of the spinal injury can change the clinical picture – different storage and voiding symptoms
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10
Q

what are we interested in, in terms of bladder control

A

We are interested in how often the person urinates, and how much urine the person passes at once
• Bladder responsible for STORAGE of urine
• When the bladder contains c. 300mls (and it is socially convenient) VOIDING is initiated.
• Normal voiding pattern - 300-400mls per void, 4-5 per day (<7)- depending on input
• No urgency or incontinence.
Can use a frequency/volume chart - to show if they have nocturia or frequency issues

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11
Q

what is a bladder diary

A
  • Collected by patient
  • 3 consecutive days
  • NB - Monitors Input as well as Output
  • Most informative chart
  • Frequency
  • Functional capacity
  • Nocturia
  • Also Input diary: detects Hyperhydration / Excessive intake; Effects of caffeine, EtOH; Diurnal Ingestion Patterns & Binges
  • “Wet” (Urinary incontinence) episodes
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12
Q

what are storage LUTS (lower urinary tract symptoms)

A
  • Urgency
  • Frequency
  • Nocturia
  • UI
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13
Q

what are voiding LUTS (lower urinary tract symptoms)

A
  • Hesitancy
  • Poor flow
  • Intermittency
  • Terminal dribbling
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14
Q

describe causes of frequency and nocturia

A

Reflects increased urinary production or decreased storage capacity
• Polyuria: Consider DM/DI, excess fluid intake
• Decreased bladder capacity: reduced compliance, reduced functional capacity, neurogenic bladder, irritation
Nocturia: Nocturnal frequency
• Normal <2x night
• Ageing bladder, BOO, decreased compliance, dietary habits
• Effect of ageing: Renal concentrating ability decreases with age-
• increased renal blood flow at night (lying down) leads to increased urine
• production
• Risk of falls and injury 2x
Nocturnal polyuria:
• Production of more than one third of 24-hour urine output between midnight and 0800

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15
Q

describe poor flow, hesitancy and dribble

A
  • Decreased force of micturition usually secondary to bladder outlet obstruction (BOO – bladder outflow obstruction, urethral stricture) - “Plumbing problem”-
  • May also occur with underactive / hypocontractile bladder (eg Sp cord injury) – “Pump problem”
  • Hesitancy: Delay in start of micturition
  • Intermittency: Involuntary start-stop; Prostatic enlargement
  • Post-void dribble: Release of small amount of urine after micturition
  • Due to release of urine retained in bulbar/prostatic urethra
  • Straining: Use of abdominal muscles to void (Valsalva only normally required at end of voiding)
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16
Q

describe incontinence

A
  • Defined as ‘involuntary loss of urine that is a social or hygienic problem and is objectively demonstrable’
  • URGE INCONTINENCE (UUI)
  • Involuntary loss of urine associated with strong desire to void (detrusor contraction)
  • STRESS INCONTINENCE (SUI)
  • Involuntary loss of urine when intra-abdominal pressure rises without detrusor contraction eg with coughing, sneezing, laughing, straining, exerting
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17
Q

how do we assess bladder control symptoms

A 
•	Take history
–	F/V chart or Bladder diary
–	Examination
•	Urinalysis
•	Special investigations
–	IPSS (International Prostate Symptom Score)
–	Flow rate & PVR (post-void residual vol)
–	Urodynamics
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18
Q

what is the International Prostate Symptom Score (IPSS)

A 
7 questions: 
•	Frequency
•	Nocturia
•	Weak urinary stream
•	Hesitancy
•	Intermittency
•	Incomplete bladder emptying
•	Urgency
Plus quality of life (QoL) / Bother Score question: 0 = Delighted; 6 = Terrible

• Score: 0-7 / 35: Mild symptoms
• 8-19 / 35: Moderate symptoms
20-35 / 35: Severe symptoms

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19
Q

describe Urodynamic Assessment

A

• Pressure transducers
– Bladder
– Rectum
• Pressure from bladder and rectum measured during filling and voiding
• Patient asked to cough periodically
• Subtracting rectal (abdominal) pressure from bladder = detrusor activity

During filling phase, a catheter is placed in the urethra. It has a transducer which measures the pressure and there is another in the rectum measuring abdominal pressure. The intravesicle pressure minus the abdominal pressure gives the detrusor pressure. Fluid is pumped into the bladder. The squiggles are when the patient coughs

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20
Q

what is unstable bladder

A

detrusor overactivity

urination during filling phase but coughing has no effect

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21
Q

what is stress incontinence

A

coughing causes leaks

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22
Q

what is BOO (bladder outflow obstruction)

A
  • No unstable contractions during filling
  • No leak whilst coughing during filling
  • Very high pressure and low flow during voiding
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23
Q

Symptoms of outflow obstruction

A
  • “The bladder is an unreliable witness”
  • Storage symptoms may come first
  • Then voiding (obstructive) symptoms
  • Then decompensation of detrusor
  • Residual urine, chronic retention
  • Bladder failure
  • Renal failure
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24
Q

what is the management of LUTS

A
  • Over-active bladder – Lifestyle, anti-muscarinics (Solifenacin, Fesoterodine, Oxybutynin), selective β-3 adrenoreceptor agonist (Mirabegron), Intradetrusor Botox
  • Stress Incontinence – Pelvic floor exercises, weight loss, surgery (autologous rectus abdominis sling, artificial sphincter)
  • Bladder Outlet Obstruction – Medical therapies: alpha-blockers (Tamsulosin), 5ARI (Finasteride), surgery (TURP, laser prostatectomy)
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25
Q

what is Bartter’s syndrome

A

blocks 2 Cl, Na, K transporter - effects similar to loop diuretics – loss of Na, K, H2O, hypercalcuria

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26
Q

what is Gitelman’s syndrome

A

blocks Cl, Na transporter - effects like thiazide diuretics – loss of Na, K, a more modest amount of water

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27
Q

what is Liddel’s syndrome

A

hyperactive ASC - opposite effect of any diuretic, leads to volume expansion and hypertension - can treat with amiloride

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28
Q

what is Pseudohypoaldosteronism

A

inactive ASC - Na loss, K retention, high aldosterone – like amiloride diuretics - note this is high aldosterone even though it says hypo as the lack of a working ASC means the body acts as if there is little aldosterone even though the body is trying to correct by producing lots

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29
Q

what do inactivating mutations of aquaporins lead to

A

(nephrogenic) Diabetes insipidus - polyuria, polydipsia ( drinking lots)

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30
Q

what is Addison’s disease

A

destruction of adrenal glands - loss of Na, hyperkalaemia, hypovolaemia - less aldosterone -> same renal result as spironolactone

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31
Q

what is Psychogenic polydipsia

A

whole body hypo-osmolarity

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32
Q

what are the components of semen

A
  • Sperm – testis
  • Citric acid, enzymes, acidic proteins – prostate
  • Fructose, basic proteins - seminal vesicle
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33
Q

describe the development of the urinary system

A

Collecting duct comes from one embryological origin, the nephric duct, and the rest of the nephron comes from the metanephrogenic mesenchyme
This is why we think of the nephron as finishing at the distal tubule and the collecting duct as something else

During development, the mesonephros (which becomes the testis and epididymis) and the metanephros (the kidneys in humans) have tubes leading to around the same area of what will become the bladder

As we develop, the tubes from the testis move downwards to where the prostate will be and those from the metanephros enter into the bladder. Women destroy the ducts from the testis obviously

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34
Q

describe renal angenesis

A 
•	Bilateral 
o	no kidneys form
o	rare
o	fatal after birth
o	lack of amniotic fluid causes Potter’s facies 	
	flat nose
	flat chin
	ears against head

• unilateral
o one kidney missing
o common (1 in 500)
o often no clinical implications unless someone removes the working one

supernumerary ureter
• no problem if they both enter bladder but can be ectopic
o this gives a higher chance of UTI

pelvic kidney
• kidney does not move up
• can be an issue in pregnant women where it takes up space for the uterus

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35
Q

describe congenital abnormalities of cloacal development

A

• failure of correct positioning of Rathke and Tourneaux folds results in
o rectovaginal fistula
o Rectoprostatic fistula
o Rectoclocal canal (rectum, vagina and urethra unite inside body)
• In males, incomplete migration of the urethral groove from the base of the penis to the tip results in hypospadias

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36
Q

what endocrine and exocrine functions does the kidney have

A

• Exocrine/excretory functions
o Fluid and electrolyte balance
 Blood pressure/electrolyte fine balance
o Removal of toxins

•	Endocrine functions
o	Blood (anaemia)/bone (renal bone disease)/blood pressure
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37
Q

what is the definition of CKD

A

GFR of less than 60ml/min for >90 days/3 months

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38
Q

what are the causes of CDK

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
  • Cystic kidney disease (APCKD)
  • Renovascular disease
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39
Q

what are the concequences of CKD

A
  • Many problems start early
  • Excretory/endocrine effects
  • Dialysis/transplant/ increased morbidity and mortality
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40
Q

what are the stages of CDK

A
  • 120 – 90 stage 1 -NORMAL
  • 90-60 – stage 2
  • 60-30 – stage 3
  • 30-15 stage 4
  • 15-0 stage 5
  • Also need biopsy or radiologically proven kidney disease for STAGE 1 AND 2
  • For 45 or lower, no need for proof – can be classed as stage 3
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41
Q

what is normal GFR

A

125ml/min/1.73m2 - often rounded down to 120ml/min

42
Q

what are means of working out if a patient has CDK

A

• Serum creatinine – can be very misleading
• Creatinine clearance – (24 hour urine collection)
o May be affected by age/muscle mass/drugs
o Urea and creatinine clearance more accurate
• Isotope GFRs – expensive and time consuming
• Formulae – for estimated GFR (MDRD) or creatinine clearance (cockcroft and gault) - based on creatinine – small errors can cause errors in calculation

43
Q

what is the epidemiology of CDK

A

6,2% of the population has stage 3 CKD or worse

Up to 25% of elderly patients may be expected to have stage 3 CKD or worse

44
Q

what are strategies to halt progression of CKD

A

• Control blood pressure
o RAS inhibition

• Reduce proteinuria
o RAS inhibition

• In diabetes – optimize glycaemic control

• SGLT2 inhibitors - used to treat diabetes
o These can have a significant benefit

45
Q

what happens in high proteinuria

A

diabetes or glomerulonephritis
• Too much protein to take up into lysosomes in cell
• The cells die
• Fibroblasts and macrophages clear away the cell but leave fibrosis

46
Q

what is important to do with drugs in CKD

A

• They have limited kidney function so some drugs can act as toxins – avoid
o NSAIDs/ contrast/ gentamicin
o Phosphate enemas

• Drug dosing
o Many drugs need to be adjusted – lower doses in CKD
 Especially chemotherapy agents
 Many toxic agents will be contraindicated
o If in doubt, check BNF
o Remember - >25% of elderly patients may have CKD

47
Q

what are complications of CKD

A 
•	Hypertension
o	Cause/consequence
o	Causes left ventricular hypertrophy / stroke / end-organ damage – eyes/kidneys
o	BP goals
	“normal” – 130/80
	Diabetes mellitus/proteinuria – 125/75

• Potassium
o Important to measure K in all CKD patients
 Hyperkalaemia is common as GFR declines <25
• may occur at GFR >25 in diabetes
• these patients may also be on ACE inhibitors which can cause hyperkalaemia
• or have a high potassium diet
o decreased GFR leads to lower distal sodium delivery and therefore increasing potassium absorption
o dietary advice
o potassium binders - eaten with food to prevent it being absorbed

• acidosis
o much acidosis in CFR is due to animal protein in food
 inability to acidify urine in CKD
 phosphate/sulphates/other anions – v late
o aim to keep serum bicarbonate >22 - beneficial effect in progression of CKD
o replace with NaHCO3
 can lead to fluid overload

• anaemia
o Hb <12 in males <11 in females
 Generally normochromic normocytic anaemia (anaemia of chronic disease)
o Decreased response of EPO to an hypoxic response and….
 Decreased red cell survival
 Iron deficiency
 Blood loss – dialysis / blood samples / GI
 Aluminium / hyper PTH / B12/folate deficiency

48
Q

describe erythropoietin replacement therapy

A

• All pts with Hb <105 should and adequate iron stores should be on EPO
o Better quality of life/ less dyspnoea / reduced left ventricular hypertrophy
• Target 100-120 range
o Any higher can lead to hypertension or thrombosis
• If poor response to EPO
o Check iron stores / CRP / B12 and folate / PTH / aluminium / malnutrition? / malignancy?

49
Q

what is renal osteodystrophy

A

• High turnover bone disease
o Secondary hyperparathyroidism

• Low turnover bone disease
o Osteomalacia
o Adynamic bone disease
o Aluminium bone disease
• If kidneys aren’t working then vit D levels are reduced
o Cannot uptake calcium – hypocalcaemia
 Soft bones – osteomalacia – rickets in children
o In response to this, PTH increases
 This increases absorption from the gut but also from the bone
 This leads to osteitis fibrosa (secondary hyperparathyroidism)
 Also increases phosphate which needs to be excreted by the kidney – can lead to hyperphosphataemia

50
Q

what is treatment for CKD

A

o Phosphate restrict
 Diet – 0.8-1.0g/kg/day
 Binders – calcium or non-Ca binders

o Vitamin D therapy
 Increases Ca/ decreases P04

o Monitor PTH 6/12
 Keep to 2-3x normal

o Parathyroidectomy may be required

Haemodialysis – in hospital – 4-5 hours
Peritoneal dialysis – 24/7 treament which putting fluid in and draining waste products out – better for independent patients
Transplantation
Conservative care – treat symptoms etc but no dialysis

When do you start dialysis -when creatinine clearance 9-14

51
Q

what are concequences for hyperphosphataemia

A

Vessel calcification (within medial layers as opposed to intimal like CV disease
o Non-compliant vessels
o Systolic hypertension – L ventricular hypertrophy
o Diastolic hypotension – myocardial ischaemia
• Calciphylaxis (nasty ulcers)

52
Q

how are CKD and cardiovascular disease related

A

Increased risk of cardiovascular disease and death from all causes as CKD progresses

53
Q

how are CKD and malnutrition related

A
  • Common in CKD
  • Decreased protein intake
  • Decreased appetite
  • Low albumin – related to inflammation?
  • Malnourished patients do worse on dialysis
  • Diet with 0.6-0.8g/kg/day advised
54
Q

which patients should be admitted (with CKD)

A

• Anyone with a rapid increase in BP or creatinine
• Stage 3 CKD with hypertension/proteinuria/haematuria/ rising creatinine
• Any stage 4/5 CKD who is suitable for treatment
• Late referral patients do considerably worse
o Aneamia/ renal bone disease/ dialysis access

55
Q

what is normal serum sodium?

A

135 – 145 mmol/L

56
Q

whats important to remember about hyponatraemia

A
  • It is the commonest electrolyte abnormality you will see (20-30% of hospital admissions)
  • It can kill
  • It is usually – but not always- caused by an excess of water
57
Q

what percentages of water are men and women?

A

Men 60% water

Women 55% water

58
Q

what bodily compartments do we have

A
  • Intracellular ~ 30 litres
  • Interstitial ~ 9 litres
  • Vascular ~ 3 litres - the compartment which we have direct access to
59
Q

describe insensible losses

A

Water coming out of the kidneys, guts, lungs and skin all come from the vascular space. Lungs and skin are insensible losses – can be up to 0.5 litres of water a day - can increase through fever, sweating and tachypnoea

60
Q

whats important to remember about saline solutions

A

Saline solutions are not isotonic with blood so it is possible to dilute vascular space by giving too much low sodium saline. This can causes organs to swell and those in tight compartments like the brain can be affected leading to confusion

61
Q

what are signs of hypovolaemia

A
  • postural hypotension
  • tachycardia
  • absence of jugular venous pulse at 45 degrees
  • reduced skin turgor/dry mucosae
  • supine hypotension
  • oliguria
  • organ failure
62
Q

what are signs of hypervolaemia

A
  • hypertension
  • tachycardia
  • raised jugular venous pulse at 45 degrees
  • gallop rhythm
  • peripheral and pulmonary oedema - can displace pitting oedema not fat ankles
  • “third space gains” - peritoneal space, joint space etc
  • Organ failure
63
Q

describe hypovolaemic hyponatraemia

A 
•	Includes common conditions
o	Haemorrhage
o	Vomiting
o	Diarrhoea
o	Burns
o	Diuretic states
	Hyperglycaemia
	Hypercalcaemia
o	Sequestration
	Inflammation in a compartment draws water in
o	Misc. renal diseases
o	Heat exposure
o	Addisons disease

o Iatrogenic
 Diuretics
 Stomas/fistulae
 Gastric aspiration

  • Excessive sodium losses, water losses are insufficient to concentrate sodium back up
  • Depends on the volume of water loss and the concentration of sodium therein
64
Q

describe Euvolaemic hyponatraemia

A 
•	Water being evenly distributed
•	Hyponatraemia is dilutional
•	Common causes
o	Hypotonic IV fluids
o	Hypothyroidism – rare
o	SIADH
65
Q

describe hypervolaemic hyponatraemia

A 
•	In which water gains exceed sodium gains
•	3 classic cases
o	Heart failure
o	Liver failure
o	Nephrotic syndrome
66
Q

describe heart failure

A
  • X ray shows enlarged heart
  • Base of lungs opaque from water
  • Veins have lots of water and are visible

• A reduced cardiac output
o Reduced effective circulating volume
o Reduced organ perfusion
o Physiological correcting mechanisms kick in
o Hypovolaemia wins over tonicity
o Renin / angiotensin / aldosterone stimulation
o ADH stimulation

• Correcting mechanisms
o Sodium retention (aldosterone)
o Water retention (aldosterone and ADH)
o Hyponatraemia results from dilution
o Fluid overload worsens LV function
o Hypovolaemia continues to win over hyponatraemia
o Maladaptive response as it starts a vicious cycle

67
Q

describe SIADH - syndrome of inappropriate ADH secretion

A
  • Secretion not suppressed by reduced tonicity
  • Water reabsorption is excessive
  • Sodium diluted
  • Hyponatraemia results
  • Clinically euvolaemic

• Aetiology

o Pituitary hypersecretion
 Neurological
• Meningitis, encephalitis, head injury, stroke

o	Ectopic hypersecretion
	Malignancy
•	Small cell lung cancer (SCLC) , pancreas, bladder,  prostate
	Pulmonary 
•	TB, pneumonia
o	Potentiation of action
	Drugs e.g. 
•	Thiazide diurectics
•	Carbamazepine
•	Amitriptyline
68
Q

describe treatment of hypovolaemia

A 
	Restoration of volume
•	Blood if necessary
•	Crystalloid (0.9% saline)
	Cessation of diuretics
	Steroids for addison’s
69
Q

describe treatment of hypervolaemia

A 
	Diuretics
•	Usually loop diurectics 
o	Furosemide
o	Bumetanide
•	Fluid restriction
•	Treatment of underlying cause
70
Q

describe treatment of euvolaemic hyponatraemia

A 
	Stop IV fluids
	Thyroxine replacemen
	Fluid restriction
•	Down to 500ml/day
	Rarely	
•	Demeclocycline
71
Q

what is calcitriol?

A

the activated form of vitamin D – promotes intestinal absorption of calcium and the renal reabsorption of calcium and phosphate

72
Q

how much kidney function may an 80 year old healthy male have lost

A

50%

73
Q

describe acute renal impairment causes

A

• Pre-renal causes
o Dehydration
o Hypotension

• Renal causes
o Glomerulonephritis
o Drug effects (NSAIDs)

• post-renal causes
o obstruction of the urinary tract

74
Q

what conditions are diuretics indicated in?

A

o heart failure
o renal failure
o liver failure
o hypertension

75
Q

describe ACE inhibitors

A

o Ramipril
o Lisinopril
o Inhibit the enzyme which converts the decapeptide angiotensin I to the octapeptide angiotensin II
o Hypertension and heart disease

Affect the glomerulus

76
Q

describe angiotensin receptor antagonists

A

o Losartan
o Candesartan
o Block the effects of angiotensin II at its receptor
o Hypertension and heart disease

Affect the glomerulus

77
Q

describe SGLT-2 inhibitors

A

o Canagliflozin
o Dapagliflozin
o Inhibit the cotransporter protein which reabsorbs glucose with sodium
o Increase urinary excretion of glucose and are indicated for type II diabetes

Affect the proximal tubule

78
Q

describe uricosuric drugs

A

o Febuxostat
o Probenecid - also prevents penicillin excretion
o Prevent uric acid reabsorption so indicated for gout

Affect the proximal tubule

79
Q

describe PTH analogues

A

o Produced by recombinant DNA technology
o Can be administered to maintain calcium reabsorption

Affects distal convoluted tubule

80
Q

describe vasopressin analogues

A

o Desmopressin
o Treats patients with high urinary flow – diabetes insipidus

Affects collecting duct

81
Q

describe vasopressin inhibitors

A

o In the case of over production of vasopressin, SIADH
o Demeclocycline
o Tolvaptan

Affects collecting duct

82
Q

what are epoietins

A

o Epoetin beta
o Darbopoietin

Replacement product for erythropoietin

83
Q

describe vitamin D analogues

A

o Alfacalcidol
o Calcitriol

replacement for vit D

84
Q

what is sodium bicarbonate for?

A

acidosis

85
Q

what drugs cause dehydration

A

• Diuretics
o Loop diuretics
o Thiazide diuretics

•	Drug-induced diarrhoea
o	Laxatives
o	Proton pump inhibitors
o	Antibiotics
o	Many others (digoxin, colchicine)

• Drug induced vomiting
o Chemotherapy
o Many others

86
Q

what drugs alter renal perfusion

A

• Drugs that supress the renin-angiotensin system
o ACE inhibitors
o Angiotensin receptor antagonists
o Adverse effects are particularly likely if renal function is already threatened by hypovolaemia, hypotension or renal artery stenosis

• NSAIDs
o Reduce cortical blood flow and glomerular perfusion by blocking production of vasodilating prostaglandins by cyclooxygenase

87
Q

what drugs are toxic

A 
•	Acute tubular necrosis
o	Aminoglycosides (e.g gentamicin)
o	Amphotericin B 
o	Calcineurin inhibitors (e.g. ciclosporin)
o	Chemotherapy (e.g. cisplatin)
o	Acyclovir
o	Poisons (e.g. ethylene glycol)
o	Radiocontrast agents

• Acute interstitial nephritis
o 2/3 drug induced
o Antibiotics (e.g. cephalosporins, sulphonamides)
o NSAIDs (e.g. ibuprofen, diclofenac)
o Proton pump inhibitors (e.g. omeprazole)

• Other drugs and poisons affecting tubular function
o Lithium compete with other cations in cells – polyuria
o Heavy metals - excessive losses of glucose, amino acids, phosphate and small proteins

88
Q

how do you calculate renal clearance

A

Clearance = conc. urine x (urine output/conc. plasma)

89
Q

how do you calculate GFR

A

GFR = curine x UO/cplasma units mL/min

The substance must:
• Not alter GFR
• Be freely filtered by the glomerulus
• Not be reabsorbed/ actively secreted by nephron
• Not be metabolized/ produced by the kidney

90
Q

what are methods for calculating GFR

A

• A substance completely lost in urine

o Exogenous substances

 Inulin (fructose polymer)
• Continuous IV infusion combined with timed urine collections
• Not generally used outside of research

 radioisotope tracers
• 51Cr-EDTA or 125I-iothalamate
• Single injection, followed by serial blood tests
• Again rarely used outside of research

 Iohexol
• Non-radioactive contrast agent
• Single injection, followed by serial blood tests
• Sometimes used in paediatrics

o Endogenous substances

 Creatinine
• Small molecule
• Produced at a relatively constant rate (muscle metabolism)
• Some active tubular secretion
• Long-established role in GFR measurement

	Cystatin C
•	Small protein, inhibitor of proteinases
•	Produced by all nucleated cells
•	So significant tubular secretion
•	10-20x more expensive to measure
•	Relatively new method of measuring GFR
91
Q

describe creatinine measurement

A
  • 24 hour urine collection
  • Plasma creatinine measurement
  • Inconvenient for patient
  • Inaccurate - may not be complete, may be mistimed
  • Imprecise – involves combination of imprecision from 4 variables

At very low GFR – renal failure
• Less creatinine filtered
• Amount of creatinine secreted becomes proportionally larger

Measuring plasma creatinine alone
• Reciprocal relationship with GFR
• But large inter-individual differences – e.g. muscle mass
• Plasma creatinine of 80 umol/L in young muscly man would correspond with a fairly high 130ml/min GFR but in a thin elderly woman it would be a GFR of 40ml/min

92
Q

what equations are there to calculate GFR which attempt to overcome the problems associated with it

A

Cockcroft-gault equation
• eGFR = (140-age) x (weight)/(Cr * x) x-man = 0.81 x-woman = 0.85

another eGFR equation (MDRD) derived from a large study with patients with renal disease
equation is only applicable to those with low GFR due to this and those with a score of more than 60 are said to have a GFR of >60ml/min
takes into account age, sex and ethnicity (although this is rarely recorded)

EPI equation comes from a study which included higher GFRs so allows results to be recorded up to 90ml/min/1.73m2
Not yet widely adopted in UK

These equations lose applicability in these patients:
•	children, pregnancy, very elderly
•	muscle mass extremes
•	rapidly changing renal function
•	very low GFR
93
Q

what does CKD diagnosis require

A

CDK diagnosed based on eGFR and urinary albumin to creatinine ratio
Usually requires GFR <60 ml/min but can involve less than that if
• persistent proteinuria/ microalbuminuria
• haematuria
• renal anatomical/genetic abnormality

94
Q

describe AKI

A

• abrupt loss of renal function
• commonly characterised by acute oliguria and increases in plasma urea and creatinine
• often accompanied by a loss of water regulation, electrolyte and acid/base balance
• eGFR is not accurate for rapidly changing renal function
• e-alerts use lab-computer based algorithm to determine creatinine baseline and then calculate magnitude of creatinine rise
o this warning + clinical context = recommended response

95
Q

what can significant damage to tubules do

A

impair urine acidification
However overt rise in urine pH is relatively rare
• Renal Tubular Acidosis (RTA) type I can lead to pHurine >5.5
• Distal tubular cells unable to secrete H+ (abnormally permeable to H+)
• Many possible causes: autoimmune, paraproteinaemia, nephrocalcinosis etc

96
Q

how can you work out if an electrolyte imbalance is renal in origin?

A

Renal causes may be identified/excluded by investigation of plasma & urine
Example: Hypokalaemia, K+ <3.5mmol/L
If the urine concentration of K is also low it usually excludes renal cause

Often a simple “spot” urine does not suffice… … as urine conc varies considerably throughout day
Two ways to get round this:
1) 24-hour urine collection
2) Measure creatinine (or osmolality) to correct for variability in urine conc. e.g. fractional excretion of phosphate (FEP)

97
Q

describe fluid balance and sodium

A

Fluid balance & sodium
Plasma sodium – more an indicator of fluid balance, rather than total body sodium
e.g. hypernatraemia tends to reflect water deficit, rather than sodium overload
Urine sodium can be used to determine if tubular function appropriate
Example: plasma Na+ 120 mmol/L (ref range: 135 – 145), SBP 90 mmHg i.e. low

Urine Na+ <30 mmol/L  tubules appropriately re-absorbing Na (and water) e.g. pre- renal failure caused by hypotension

Urine Na+ >30 mmol/L  inappropriate loss tubular dysfunction / damage / inadequate aldosterone action e.g. pre-renal failure caused by hypotension e.g. intrinsic /established renal failure caused by untreated pre-renal failure

98
Q

how does urine and plasma osmolarity differ in conditions

A

o Chronic renal failure Osmurine ≅ Osmplasma
 end-stage: oliguric

o Acute tubular necrosis Osmurine ≅ Osmplasma
 e.g. following pre-renal failure
 initially oliguric, “recovery phase” often polyuric

o Diabetes mellitus Osmurine ≅ or > Osmplasma
 “osmotic diuresis”, polyuria, high glucose overwhelms urine conc ability

o Diabetes insipidus Osmurine < Osmplasma
 polyuria, dilute urine

99
Q

how do you diagnose diabetes insipidus

A

water deprivation test
• Involves with-holding fluids over several hours
• Potentially dangerous, must be monitored very closely (true DI  hypernatraemia)
• DI involves failure of action of vasopressin (or ADH)
• May be cranial (hypothalamic/pituitary pathology), nephrogenic (tubular problem)
• Normal response: plasma osmolality static, urine osmolality rises i.e. kidney conc urine
• DI: plasma osmolality will rise… urine remains dilute
• Cranial DI should be responsive to DDAVP (synthetic vasopressin)

100
Q

describe dipstick urinalysis

A 
•	Rapid, simple, convenient, cheap 
•	Number of tests varies by manufacturer 
•	Readout: coloured strip, or printed report 
•	Tests may include: 
o	 Glucose (diabetes?) 
o	Ketones (ketoacidosis?) 
o	 Protein (albumin) – not as sensitive as lab measurement 
o	 Blood (detects Hb: calculi, bladder ca., glomerulonephritis) 
o	Leukocytes (UTI) 
o	 Nitrites (produced by nitrate-reducing UTI bacteria) 
o	Bilirubin (jaundice) 
o	 Urobilinogen (absent in cholestaGc jaundice) 
o	pH, specific gravity (related to osmolality) etc.
101
Q

describe proteinuria

A

• Physiological vs. pathophysiological urine protein levels
o Glomeruli prevent passage of most large plasma proteins
o Tubules actively re-absorb/catabolise low MW proteins

• However renal pathology may lead to:
o Increased glomerular permeability – increasing urinary albumin, detectable levels of large MW proteins not normally found in urine
o Decreased tubular protein reabsorption – increased conc. of low MW proteins

• Proteinuria may be detected via
o dipstick testing (not as sensitive as lab urine testing)
o lab-based albumin / protein measurement, sometimes 24 hr collection but usually a spot urine using creatinine to adjust for urinary conc:
 protein : creatinine ratio (PCR)
 Albumin : creatinine ratio (ACR) – used to classify CKD

• Microalbuminuria
o Refers to abnormal level of albumin, usually too low for detection by urine dipstick
o ACR > 3.5 mg/mmol in men, >2.5 mg/mmol in women
o Important for prevention of significant diabetic nephropathy
o Can occur transiently e.g. post-trauma, surgery, pyrexia, vigorous physical exercise!

Year 2 - Semester 2 (8 decks)

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