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Nephrology Flashcards

1
Q

List 3 functions of the kidney?

A

Primary role: maintain fluid and electrolyte homeostasis in response to blood pressure and hormones

  • Metabolic waste excretion
  • Endocrine functions
  • Drug metabolism/excretion
  • Control of solutes and fluid status
  • BP control
  • Acid/Base
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2
Q

How do you measure kidney function?

A

Measure what is going out in urine or what’s left in the blood

  • Metabolic waste excretion: urea, creatinine
  • Endocrine fxn: Vit D, EPO, PTH
  • Control of solutes and fluid status: sodium, potassium, fluid
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3
Q

What is the role of the glomerulus?

A
  • To filter blood
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4
Q

What is the glomerular filtration barrier (GFB)?

A
  • Semi-permeable membrane preventing the passage of a majority of proteins in urine
  • Controls the glomerular filtration rate
  • Glomerular basement membrane and podocytes make up the GFB
  • Blood cells and large molecules (albumin, immunoglobulins) are not filtered due to size and charge barrier
  • Electrolytes, amino acids and small molecules pass through Bowman’s space
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5
Q

What controls blood flow through the glomerulus?

ie. describe what happens when a low blood volume is recognised

A

Reduced blood vol / low BP

  • Baroreceptos stimulated causing juxtaglomerular cells to release renin causing angiotensin II production
  • Angiotensin II: efferent arteriole vasoconstriction, inc. Na and water reabsorption and systemic vasoconstriction
  • Sympathetic NS: systemic vasoconstriction
  • Osmoreceptors of the hypothalamus cause ADH (from ant/ pituitary) to increase water retention and insert aquaporin channels in collecting duct
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6
Q

What is the pathway for filtration/reabsorption etc at the nephron?

A
  • Blood is filtered at the glomerulus which goes to tubules
  • 99% is reabsorbed
  • Small amount is secreted into the tubules
  • What’s left in tubules exits via urine
  • Tubules adjust filtrate content, with collecting ductules absorbing water
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7
Q

In context of kidney function, which aspects of a dipstick are important?

A
  • Presence of blood and protein
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8
Q

How do you measure urinary protein excretion?

A
  • 24hr urine collection: not routine as not standardised between patients
  • Protein:Creatinine Ratio (PCR) on a morning spot sample (mg/mmol). Urine PCR (uPCR) of 100 is equivalent to 1g/day of protein in urine
  • Albumin:Creatinine ratio (mg/mmol), measuring just albumin rather than all the protein in the urine
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9
Q

What is proteinuria and what’s the pathology?

A
  • Normal: less than 150mg/day (15% albumin, rest is other proteins)
  • Protein: abnormal quantities of protein in urine, suggestive of kidney damage
  • Damage to GFB: lose albumin into the urine
  • When protein in the urine is pathological and due to glomerular dysfunction: 70% protein is albumin
  • Urinalysis detects albumin
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10
Q

What is haematuria and how is it caused?

A

Haematuria: presence of blood in the urine

  • Non-visible haematuria: can be detected on dipstick and is caused by disruption of the GFB
  • Visible haematuria: can come from anywhere in the urinary tract. More likely to come from kidney stones/malignancy/UTI rather than the glomerulus
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11
Q

What makes a substance ideal to measure in urine?

What is the best substance to measure kidney function?

A
  • Freely filtered at the glomerulus
  • Not reabsorbed
  • Not secreted
  • Creatinine isn’t this straightforward but is the best marker
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12
Q

What are the 3 most important measurements for determining kidney function?

A
  • Urea
  • Creatinine
  • eGFR
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13
Q

how is creatinine released into the blood and what affects it?

A
  • From muscle breakdown
  • Concentration affected by plasma volume
  • Affected slightly by diet (high protein diet) or muscle building supplements
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14
Q

When is urea released into the blood and how are levels affected?

What is the pathway in the nephron?

A
  • Tissue breakdown product
  • Diet: high protein or GI bleed
  • Dehydration causes more passive reabsorption at proximal tubule, so urea is usually higher
  • In liver failure, breakdown products aren’t processed as well so urea is lower
  • Freely filtered at glomerulus but 40% is reabsorbed so less reliable in indicating kidney function
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15
Q

Define renal clearance

A

Renal clearance = volume of plasma which would be cleared of the substance per unit time

  • Expressed as ml/min
  • Usually described as the glomerular filtration rate
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16
Q

What information is needed to measure eGFR?

What units is it expressed in?

In what situation can it not be used?

What else needs taken into account?

A

MDRD*4 formula:

  • Plasma creatinine concentration
  • Age (need to be >16)
  • Gender
  • Race
  • Units: ml/min/1.73m2

Not suitable in AKI (ie. not valid when kidney function is changing rapidly)

  • eGFR assumes stable renal function
  • Creatinine levels are related to muscle mass, so what’s normal for one patient may not be normal for another
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17
Q

What are the stagings for chronic kidney disease with eGFR?

A

Stage 1: eGFR >90 with another abnormality*

Stage 2: eGFR 60-89 with another abnormality*

*patients with eGFR >60 should be regarded as normal unless other evidence of kidney disease eg. persistant haematuria or proteinuria

Only considered to have CKD if eGFR <60

Stage 3: eGFR 30-59 is CDK with moderate impairment

Stage 4: 15-29 is CDK with severe impairment

Stage 5: <15 is CKD with advanced impairment. Any patient on dialysis is considered stage 5.

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18
Q

Define glomerulonephritis

What is a complication of glomerulonephritis?

A

Inflammatory disease involving the glomerulus and disruption of the glomerular filtration barrier

  • It can develop into end-stage renal failure (ESRF)
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19
Q

What cells are present in the glomerulus?

What are their roles?

What would damage of these cells lead to?

A

Parietal epithelial cell: lines Bowman’s capsule

  • Damage is called a crescent lesion

Podocyte: sits on the outside of the glomerular membrane

  • Has zipper-like foot processes
  • Controls the charge and filtration barrier
  • Damage: lose zipper effect and filtration barrier. Lots of protein will be present in urine

Mesangial cell: controls the matrix between the capillaries and produces mesangial matrix

  • keeps the filter (GBM) free from debris

Endothelial cell: affected more often in systemic disease

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20
Q

What are the targets for injury in glomerulonephritis?

What are the pathological mechanisms involved in glomerulonephritis

A

Targets: cells

  • Parietal epithelial cells, podocytes, mesangial cells, endothelial cells

Pathological mechanisms

  • Pre-formed antibodies that travel to the glomerulus and cause damage ie. form immune complexes or activate complement
  • Cell-mediated mechanisms (cells infiltrate the kidney) eg. cytokines
  • Metabolic e.g. diabetes, genetic, vascular disease (HTN)
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21
Q

Many conditions are associated with glomerulonephritis. Give 3 examples

A

CV: SBE (subacute bacterial endocarditis)

Resp: lung cancer, TB

Infectious Disease: Hepatitis, HIV, chronic infection, Abx

Rheum: RA, lupud, amyloid, CT disease

Drugs: NSAIDs, bisphosphonates

Gastro: ALD, IBD, coeliac disease

Diabetes

Haem: myeloma, CLL, polycythaemia rubra vera (PRV)

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22
Q

Label the diagram

A
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23
Q

When do symptoms appear with kidney damage?

A
  • When eGFR falls below 50%
  • Creatinine only begins to rise when eGFR falls below 50%
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24
Q

How do you approach a patient with suspected glomerulonephritis?

A
  1. Detailed medical and drug history (if symptoms, how long have they been present?)
  2. Basics: U&Es, dipstick for blood and to quantify proteinuria, check albumin, USS (1/2 kidneys)
  3. Glomerulonephritis screen: ANCA, ANA/dsDNA, RF, anti-GBM, immunoglobulins, virology (Hep B, C, HIV)
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25
Q

What is required for a clinical diagnosis of glomerulonephritis?

A
  • Kidney biopsy of the cortex (where the glomeruli are found)
  • Bleeding risk so avoid is possible
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26
Q

What is the spectrum of presentation for glomerulonephritidies?

A
  • Incidental finding with urinary abnormalities +/- impaired kidney function
  • Visible haematuria (usually lower urinary tract problem but could be glomerulus)
  • Synpharyngitic: sore throat and coke-looking urine. This is classic of IgA nephropathy
  • Nephritic syndrome (pt. often ends up in hospital): high BP, declining kidney function and blood and protein in urine
  • Nephrotic syndrome (odematous patient): unwell with rapidly progressing GN
  • Acutely unwell with rapidly progressive glomerulonephritis
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27
Q

How do you diagnose nephrotic syndrome?

What is the risk of nephrotic syndrome?

A

Triad:

  • Massive proteinuria: 3.5g proteinuria per 24hr (ie. urine PCR >300)
  • Hypoalbuminaemia: Low serum albumin <30 liver tries to accomodate loss of albumin but usually unable to keep up
  • Oedema: ankles, puffy face, around the eyes. Due to salt and water retention and low serum albumin
  • Usually see hyperlipidaemia

RIsk: loss of anticoagulants therefore risk of venous thromboembolism and inc. risk of infection

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28
Q

What are the classic causes of nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephritis
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29
Q

How do you diagnose nephritic syndrome?

A
  • Hypertension
  • Blood in urine (coke-coloured urine), sometimes protein
  • Oliguria: production of abnormally small amounts of urine
  • Usually caused by inflammation often involving the endothelium
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30
Q

Compare and contrast the mechanisms of nephritic and nephrotic syndrome

A

Nephrotic: oedema and injury to podocytes

Nephritic: inflammation

Nephrotic: altered architecture with scarring and matrix deposition

Nephritic: reactive cell proliferation, breaks in the GBM and Crescent formation

Nephrotic: always protein, sometimes blood

Nephritic: always blood, sometimes protein

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31
Q

What are the classic causes of nephritic syndrome?

A
  • Crescentic GN
  • Vasculitis
  • Post-infectious
  • IgA (usually presents with nephritis but can present as nephrotic)
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32
Q

What is IgA nephropathy?

What is the aetiology?

A
  • IgA deposition in the mesangial cells
  • The most common GN type in adults

Aetiology

  • Secondary to infection: synpharyngitic IgA nephropathy until proven otherwise (sore throat and coke-coloured urine)
  • Secondary to coeliac disease, cirrhosis, HSP (IgA vasculitis)
  • IgA vasculitis: purpuric spots on extensor surfaces and protein in urine

-

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33
Q

What is the pathophysiology of IgA nephropathy?

What is the clinical presentation?

What is the treatment?

A
  • Abnormal/Over-production of IgA immune complexes that deposit in the mesangium
  • Mesangium responds bu proliferating, disrupting the GFB

Presentation

  • Haematuria, usually HTN, proteinuria
  • 1/3 progress to ESRF

Treatment

  • Antihypertensive therapy ie. BP control (ideally <125/75)
  • ACEi (Ramipril) or ARB
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34
Q

What is membranous glomerulonephritis?

What are the causes?

A
  • Damage to podocytes and glomerular basement membrane due to deposits

Causes

  • Idiopathic
  • 10% due to underlying disease
  • 70% have an antibody (anti-phospholipase A2 receptor antibody Anti-PLA2R) that binds to receptors on podocytes and causes dysfunction ie. immune complexes found in basement membrane
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35
Q

How does membranous glomerularnephritis present?

What is the natural history?

A

Presentation: nephrotic syndrome

  • Oedema, inc. risk of infection and clots
  • Fatigue

Natural history

  • 1/3 spontaneous remission
  • 1/3 progress to ENRF over 1-2yrs
  • 1/3 persistent to proteinuria, maintain GFR
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36
Q

How is membranous glomerulonephritis treated?

A
  • If secondary: treat underlying disease e.g. stop NSAIDs

ACEi/ARB, statin, diuretics

  • BP control is essential, to <125/75
  • Anything blocking RAAS will affect both BP and GMB to reduce proteinuria

Specific immunotherapy (if still deteriorating)

  • Steroids along with alkylating agents for 6 months
  • Rituximab
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37
Q

What age bracket is minimal change disease most common?

What is it’s pathogenesis?

What’s seen with a microscope?

A
  • Commonest form of GN seen in children
  • 90% of GN <10yrs is Minimal Change Disease I therefore don’t need to biopsy

Pathogenesis: disorder of the T cell that targets podocytes

  • Damage to the GFB

Light microscope: normal glomerulus, no sign of inflammation or proliferation

Electron microscope: podocytes fused together and lose of finger-like processes (characteristic of MCD I)

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38
Q

What causes MCD and how does it present?

A

Cause: idiopathic

  • Can be seen 2o to malignancy

Presentation: nephrotic syndrome

  • MCD I: rapid presentation
  • MCD II: acute presentation (overnight), 50% will relapse
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39
Q

How is minimal change disease treated?

A

Children: prednisolone (high dose corticosteroid) for 8 weeks

Adult: ACEi/ARB or diuretics

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40
Q

What is the mainstay for treatment of glomerulonephritis?

A

ACEi (ramipril)/ARB or statin or diuretics

  • Ie. BP control <125.75mmHg
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41
Q

What primary causes of nephrotic syndrome are prevalent in different age categories?

A

Children: Minimal Change Disease (MCD)

  • <45: Minimal change

45-65: Focal Segmental Glomerular Sclerosis (FSGS)

>65: Membranous GN

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42
Q

What is the pathology of Focal Segmental Glomerular Sclerosis (FSGS)?

What is the aetiology?

How does it present?

A

Pathology:

  • Focal: only some glomeruli are affected

Segmental: only part of each glomerulus

Aetiology:

  • Idiopathic or systemic disease

Presentation:

  • Nephrotic syndrome
  • 50% progress to ESRF
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43
Q

What are cresentic/rapidly progressing glomerulonephritidies?

What is the pathology?

How does the disease progress?

A
  • A group a conditions demonstrating glomerular crescents on kidney biopsy
  • Glomerular crescents = defined as 2+ layers of proliferating cells in Bowman’s space
  • Presence of active proliferative disease
  • Inside the glomerulus looks normal but the Bowman’s capsule has expanded out due to inflammatory cells, necrosis and ECM

Aggressive disease therefore will progress to ESRF

  • Needs urgent treatment
  • When crescents heal, the whole glomerulus scleroses and dies
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44
Q

Describe some common causes of Crescentic GN

A

ANCA Vasculitis

  • Systemic disease, patient usually has other symptoms e.g. rash, joint paint, deaf, neuropathy
  • ANCA positive

Goodpasture’s syndrome

  • Autoimmune condition with anti-GBM antibodies
  • Glomerulus and lungs are affected
  • Symptoms: haematuria and haemoptysis
  • Treatment: steroids

Lupus Nephritis

  • ANA +ve, anti-dsDNA +ve, anti-histone +ve

HSP Nephritis

  • ANA positive
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45
Q

What are the embryological stages of the kidney?

When is urine produced?

How much kidney function is developed by the 3rd trimester?

A

Pronephros: appears in the 4th week of development and regresses by end of week 4

Mesonephros: regresses by end of 2nd month

Metanephros: appears in week 5 and becomes functional around the 12th week. This is the definitive kidney

Urine production starts at week 10

Only 60% of kidney function (ie. 60% of glomeruli) by 3rd trimester

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46
Q

What is the most common cause of ESRF in children?

A

Congenital anomalies

  • 50% of congenital problems lead to CKD needing renal replacement therapy (RRT)
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47
Q

Define renal agenesis

What stage of embryogenesis does this occur?

What is the prognosis?

A
  • Congenital absence of renal parenchymal tissue, with less glomerli
  • Occurs in the metanephric stage

Prognosis

  • Bilateral: not compatible with life
  • Unilateral: good prognosis
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48
Q

What is the most common congenital abnormality that progresses to ESRF?

A
  • Renal hypodysplasia
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49
Q

What is renal hypodysplasia?

A

Renal hypodysplasia: congenitally small kidneys with dysplastic features

  • Can be accompanied by a cystic component
  • Renal hypoplasia: reduction in the number of nephrons but normal architecture
  • Renal dysplasia: malformed renal tissue
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50
Q

How would a patient with renal hypodysplasia present?

How is renal hypodysplasia managed?

A

Presentation:

  • Antenatal US: reduced kidney growth, reduction in amniotic fluid
  • Neonate: lung issues (need ventilated), intrauterine growth restrictions, acidosis, raised creatinine

Children: failure to thrive (FTT), anorexia, vomiting, proteinuria

Management: supportive

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51
Q

What is MCDK?

How would multi-cystic dysplastic kidney (MCDK) present?

What are the risks of MCDK?

A
  • Large low-functioning kidney with multiple fluid-filled cysts, which may get smaller over time causing the kidney to shrink
  • 50% involute (shrink): monitoring is required

Presentation

  • Mainly antenatal detection on US
  • Neonate: abdominal mass
  • Usually unilateral (unaffected kidney does all the work), rarely bilateral (incompatible with life)

Risks

  • Non-functioning kidney
  • Malignancy
  • HTN
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52
Q

What is the main risk factor for renal disease in infancy?

A
  • Male
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53
Q

Define hydronephrosis

What is hydronephrosis associated with?

What modality is it usually discovered on?

A

Definition: distension of the kidney with urine, caused by obstruction to urinary outflow

  • Associated with renal injury and impairment
  • Usually unilateral (60-80%)
  • Commonly seen on ultrasound (enlarged renal pelvis w/ diameter >10mm)
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54
Q

What are the causes of hydronephrosis?

A
  • Vesico-ureteric reflux
  • Obstruction in urinary tract
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55
Q

Define obstruction (in relation to hydronephrosis)

What are the levels of obstruction in the urinary tract?

A

Def: impedence to urinary flow which causes progressive damage

Levels of obstruction:

  • Pelvic-Ureteric Junction (PUJ)
  • Ureter
  • Vesico-ureteric junction (VUJ)
  • Bladder
  • Urethra
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56
Q

How is PUJ obstruction diagnosed?

What is the effect of PUJ obstruction?

A

Effect: partial or total urine blockage at ureter junction

  • usually unilateral

Diagnosis:

  • Antenatal diagnosis (US)
  • Neonate: abdominal mass (enlarged renal pelvis), UTI, FTT
  • Children: abdominal/flank pain
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57
Q

What is vesico-ureteric junction obstruction?

What causes it?

What are the effects?

A
  • Functional/Anatomical abnormality at vesico-ureteric junction, causing obstruction of urinary flow

Causes:

  • Primary: reflex or obstruciton
  • Secondary: bladder issues

Effect: develop a megaureter

  • Ureteric dilatation >7mm (>1cm is significant)
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58
Q

What are posterior urethral valves?

How would they present?

What is the diagnosis, management and outcome?

A
  • They are obstructive membranes that develop in the urethra, close to the bladder
  • Only seen in boys

Presentation: UTI (bilateral hydronephrosis)

Diagnosis: US

Management: cystoscopy

Outcomes: 1/3 normal renal function, 1/3 with bladder problems and incontinence, 1/3 with ESRF

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59
Q

Define vesico-ureteric reflux

What are the consequences?

How is it diagnosed?

How is it graded?

A

Def: retrograde passage of urine from the bladder into the upper urinary tract

Consequences: can lead to scarring, HTN, ESRF

Diagnosis: MCUG (Micturating Cystourethrogram)

Graded I-V

  • Grade I&II: reflux into ureters
  • Grade I-III: usually resolve spontaneously
  • Grade IV&V: need intervention
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60
Q

Define pyelonephritis

A

Bacterial infection of the kidneys causing inflammation

  • Aka UTI (urinary tract infection)
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61
Q

How does pyelonephritis present?

A
  • More common in girls (unless <3 months)

Upper tract pyelonephritis:

  • Pyrexia, vomiting, systemic upset, abdominal pain
  • More likely to cause kidney damage

Lower tract pyelonephritis:

  • Dysuria, frequency, haematuria, wetting
  • Similar to adult clinical presentation
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62
Q

What is the commonest caustive organism of pyelonephritis?

A

E. Coli

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63
Q

How do you diagnose pyelonephritis?

What are the complications of pyelonephritis?

A

Urine sample

  • Need proper urine collection
  • Significant bacteriuria: >105 colony forming units (CFU)/ml

Investigations

  • US, MCUG (<1yr), nuclear medicine (if questioning obstruction)

Complications

  • Scarring, HTN, ESRF
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64
Q

What is the epidemiology of diabetic nephropathy

A

30-40% diabetes develop kidney problems (usually T2DM)

  • 26% of people starting RRT (ie. dialysis or transplant) are diabetic
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65
Q

Describe the pathophysiology of diabetic nephropathy

A

Structural changes of the glomerulus:

  • inc. number of mesangial cells
  • thickening of the glomerular basement membrane
  • mesangial matrix expansion
  • fusion of foot processes

Progression:

hyperglycaemia → volume expansion → intra-glomerular hypertension → hyperfiltration → proteinuria → hypertension and renal failure

  • Often takes 5-10 years for microalbuminuria to occur
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66
Q

What is the clinical presentation for diabetic nephropathy

A

Early on: may be asymptomatic

Later:

  • worsening BP control
  • proteinuria
  • peripheral oedema (ankles, feet, hands)
  • inc. frequency
  • confusion / difficulty concentrating
  • SOB, nausea, loss of appetite, persistent itch, fatigue
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67
Q

Describe the histology of diabetic nephropathy

A

Pathognominic hyaline material containing nodules (excess mesangial matrix) in glomerular capillary loops

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68
Q

What are 3 complications of diabetic nephropathy

A

anaemia

bone and mineral metabolism

retinopathy

neuropathy

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69
Q

What is the management for reducing diabetic nephropathy and it’s progression to needing dialysis

A
  • tight glycaemic control
  • BP control
  • SGLT-2 inhibitors
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70
Q

What is the pathophysiology of renovascular disease?

A
  • progressive narrowing of the renal arteries with atheroma (degradation of the walls due to fatty deposits)
  • perfusion through kidney falls by 20%: GFR falls but tissue oxygenation of cortex and medulla are maintained
  • a hypoxic medulla can be compensated for
  • RA stenosis progresses to 70%: if it becomes so hypoxic, the compensation is overwhelmed and the medulla becomes ischaemic and dysfunction develops
  • cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways
  • Parenchymal inflammation and fibrosis progress and become irreversible. Restoration of blood flow provides no benefit
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71
Q

At what stage do symptoms develop with renal artery stenosis and list 3

A

Symptoms usually develop after advanced stage

  • hypertension with sudden onset or worsens without explanation
  • hypertension that begins <30yrs or >50yrs

As RA stenosis develops..

  • HTN that’s difficult to maintain
  • Bruit over the kidneys
  • Proteinuria
  • worsening kidney function with HTN treatment
  • fluid overload and oedema
  • treatment resistant HF
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72
Q

What is the aim of treatment for RA stenosis

Give 2 medical and lifestyle and one surgical management option(s) for renal artery stenosis

  • when would the surgical option be considered?
A

Aim: Treat underlying systemic disease and always control BP as it will always affect kidney function

Medical:

  • BP control (not ACEi/ARB, think verapamil or amlodipine or bisoprolol)
  • Statin: lower cholesterol
  • If diabetic, tight glycaemic control
  • Stop ACEi, and avoid it and ARBs in future

Lifestyle

  • smoking cessation, exercise, low Na diet

Surgical: angioplasty

  • rapidly deteriorating renal failure
  • uncontrolled inc. BP on multiple agents
  • flash pulmonary oedema
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73
Q

A 42yr old male attends medical receiving unit

PC: leg swelling

HPC: normal ECG, albumin low, BP 105/65mmHg

Urinalysis: uPCR 742

PMH: 20yr hostory of ulcerative colitis

Comment on any significant results

What are the differentials and what investigations are needed to confirm/exclude these differentials

A

Low albumin

  • either losing albumin in urine or failure to make albumin (liver disease - no evidence in this case)

uPCR 742 = excreting about 7.5g/day ie. proteinuria - nephrotic syndrome

Nephrotic syndrome on background of colitis

Differentials: diabetic nephropathy, lupus nephritis, virual infections (HBV, HCV, HIV), amyloidosis, myeloma

Investiagtions:

  • Bloods: glucose (diabetes), ANA (lupus nephritis), viral infection screen, protein electrophroesis (myeloma - looking for light chains), kidney biopsy (amyloidosis)
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74
Q

Define amyloidosis

What are the primary organs that are affected?

A

A group of diseases that result from the abnormal deposition of a highly stable insoluble proteineous material, amyloid, in the extracellular space

  • Amyloid is made of beta-pleated sheets
  • mainly found in the kidneys, heart, liver, gut
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75
Q

How is amyloidosis diagnosed?

A

For the kidney: biopsy

  • Light microscope with Congo red stain: apple green birefringence
  • Electron microscope: Amyloid fibrils causing mesangial expansion
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76
Q

What are the two classes of amyloidosis and what conditions are they associated with

A

AA: systemic amyloidosis

  • inflammation/infection
  • more widely seen in TB and IBD

AL: immunoglobulin fragments

  • haematological conditions eg. myeloma
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77
Q

How are the two classes of amyloidosis treated?

A

AA amyloid: treat underlying cause of infection or inflammation

AL amyloid: treat the underlying haematological condition

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78
Q

What is protein in the urine associated with

A

GLOMERULI disease

  • if no protein: damage to another part of the kidney other than the glomerulus
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79
Q

36yr old attends the rheumatology ward

Investigations: SCrumol/l 200 (70 in Jan)

  • Urinalysis P4+ and B3+, uPCR 400 and albumin 29
  • Presents with butterfly rash, hair loss, Ryanoids’, some arthritis associated

Comment on noteworthy values

What are the differentials and what investigations are needed to confirm/exclude these differentials

A

SCr elevated: kidney dysfunction and rapidly progressing

Urinalysis: haematuria and proteinuria

Nephritic syndrome: rapidly progressing, haematuria and proteinuria

Differentials:

  • Crescentric nephritis: ANCA vasculitis, Goodpasture’s, HSP nephritis, Lupus nephritis
  • IgA nephropathy

Investigations: antibodies: ANCA (ANCA vasculitis), anti-GBM (Goodpasture’s), ANA (HSP/lupus), anti-dsDNA and anti-histone (lupus nephritis)

  • check C4 (low in SLE)
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80
Q

Define systemic lupus erythematous

What is the pathology of this ocndition?

A

A chronic inflammatory condition caused by an autoimmune disease

  • It’s a immune complex mediated glomerular disease

Pathology:

  • multiple autoantibodies directed against DNA (anti-dsDNA), histones (anti-histone), snRNPs, translational machinery, nucleus (ANA)
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81
Q

Describe the pathophysiology of systemic lupus erythematous (SLE)

A
  • auto-antibodies produced against dsDNA or nucleosomes (anti-histone)
  • form intravascular immune complexes or attach to GBM
  • activate complement, resulting in a low C4
  • renal damage
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82
Q

How is systemic lupus erythematous diagnosed and treated?

A

Diagnosis: kidney iopsy

Treatment: immunosuppression ie. steroids

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83
Q

What genes are involved in the development of adult polycystic kidney disease?

A

PKD 1 gene mutation (chromosome 16) - 85%

  • Typical rapid progression with ESRD <50yrs

PKD 2 gene mutation (chromosome 4) - 15%

  • Slower progression, may never reach ESRD
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84
Q

Define autosomal dominant polycystic kidney disease (ADPKD)

A
  • the most common form of polycystic kidney disease characterised by the progressive development of innumerable kidney cysts, causing HTN, renal pain and renal insufficiency
  • usually mutations of PKD 1 gene on chromosome 16, less often PKD 2 gene on chromosome 4
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85
Q

Define autosomal recessive polycystic kidney disease (ADPKD)

A
  • early onset disorder characterised by the presence of innumerable kidney cysts and enlarged kidneys that can usually be detected via ultrasound before birth or in the neonatal period
  • mutated gene found on chromosome 6
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86
Q

What are the roles of the PKD 1 and 2 genes?

A

They code for polycystin 1 and 2

  • membranr proteins found all over (kidneys, brain, bone, heart)
  • located in the renal tubular epithelial
  • involved in intracellular calcium regulation

Overexpressed in cyst cells

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87
Q

Describe the progression of ADPKD

A

Cysts gradually enlarge causing pressure, and the normal kidney tissue starts getting replaced

  • Kidney volume increased and eGFR falls
  • cyst infection, rupture, haematuria and pain
  • extra-renal manifestations explained as polycystin proteins are found systemically

Hepatic cysts: originate from bile ducts, so can enlarge and cause enlargement of the liver but will not cause liver failure

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88
Q

Describe the presentation of ADPKD at different ages

A

Antenatal: antenatal US

Childhood: haematuria, flank pain, HTN, UTIs, renal US findings

Adult (usual presentation):

  • HTN, impaired renal function, loin pain, haematuria, UTIs, renal US findings

Family associated

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89
Q

Describe the presentation of ARPKD at different ages

A

Antenatal: US or oligohydramnios (deficiency of amniotic fluid)

Infancy:

  • large palpable renal mass, resp. distress, renal failure, HTN, hyponatraemia

Childhood:

  • Renal failure, HTN
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90
Q

Describe the histpathology and associated anomalies of ARPKD

A

Histopathology:

  • Cystic dilatations of collecting tubules with flattening of the epithelium that runs perpendicular to the renal capsule

Associated anomalies:

  • congenital hepatic fibrosis → portal HTN → ascending cholangitis
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91
Q

Compare the prognosis of ADPKD and ARPKD

A

ADPKD:

  • progression of ESRF in adulthood, 50% by 60yrs

ARPKD:

  • 20-30% mortality in neonate period
  • 5yr survival: 70-88%
  • Progression to ESRF >50% (often >15yrs)
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92
Q

List 3 extra-renal manifestations associated with polycystic kidney disease (PKD)

A

Heart: mitral valve prolapse, AV malformation

Brain: cerebral aneurysm

GI: hepatic/pancreatic cysts, colonic diverticula, colonic hernia

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93
Q

How is polycystic kidney disease managed?

A
  • Supportive
  • Early detection and BP management
  • Treat complications
  • Manage extra-renal associations
  • Prepare for renal replacement therapy (RRT): dialysis or kidney transplant

For ADPKD: Tolvaptan (only in CKD that’s stage II/II at start of treatment and evidence of rapidly progressing kidney disease)

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94
Q

Define acute kidney injury

A

A sudden decline in renal function over hours or days, recognised by the rise in serum urea and creatinine

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95
Q

What are the diagnostic classifications of AKI and list three causes of each

A

Pre-renal failure: Due to circulatory failure ie. shock

  • occurs secondary to renal hypoperfusion
    1. hypovolaemia and hypotension eg. diarrhoea, dehydration, haemorrhage, burns
    2. Reduced effective circulatory volume eg. septic shock, cardiac failure, cirrhosis
    3. drugs eg. NSAIDs and ACEi together
    4. renal artery stenosis

Renal failure: due to an injury/failure of the cells of the kidney

  1. glomerular: glomerulonephritis and other glomerular pathology
  2. Tubulointersitial: ischaemic and nephrotoxic acute tubular necrosis (ATN) caused by pre-renal failure, drugs, myeloma, sarcoid
  3. Vascular: renal artery stenosis causing structural abnormalities

post-renal failure: due to obstruction

  • renal papillary necrosis, kidney stones
  • retroperitoneal fibrosis
  • carcinoma of the cervix, prostatic hypertrophy/maligancy
  • urethral strictures
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96
Q

How does septic shock affect the kidneys?

A

Causes systemic vasodilation which reduces renal perfusion pressure and leads to hypoperfusion

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97
Q

How does the combination of NSAIDs and ACEi induce vascular changes that could lead to renal failure?

A

NSAIDs: vasoconstrict the afferent glomerular arteriole

ACEi: vasodilate the efferent glomerular arteriole

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98
Q

How does hypoperfusion of the kidneys lead to renal failure?

A

hypoperfusion results in ischaemia of the renal parenchyma

  • if this lasts, intrinsic damage may occur and acute tubular necrosis will develop
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99
Q

Explain the development of intrinsic renal failure

A

3 categories: glomerular, tubulointerstitial and vascular

Pre-renal failure can cause intrinsic renal failure due to lack of blood supply to the kidney parenchyma

Tubulointerstitial causes:

  • due to damage of the parenchyma which leads to scarring and fibrosis
  • most common is acute tubular necrosis (ATN)
  • always occurs due to prolonged renal hypoperfusion (pre-renal) and / or direct toxicity
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100
Q

List 3 symptoms of acute kidney injury

A

Non-specific

  • nausea or vomiting
  • diarrhoea
  • dehydration
  • oligouria
  • confusion, drowsiness
  • irregular heart beat (due to hyperkalaemia)
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101
Q

What can acute kidney injury result in?

A

Decline in renal function can result in dysregulation of

  • fluid balance
  • acid-base homeostasis
  • electrolytes
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102
Q

List the classification systems used for AKI and their stages

What measurements are used for their classification

A

RIFLE: Risk, Injury, Failure, Loss, ESRD

  • sCr / GFR and urine output

AKIN: Stages 1-3

  • sCr and urine output

KDIGO: Stages 1-3

  • sCr and urine output
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103
Q

What are the stages involved in the RIFLE classification of AKI

A

Risk:

  • inc. sCr x1.5 or GFR dec. by >25%
  • UO <0.5ml/kg/hr for 6hrs

Injury:

  • inc. sCr x2.0 or GFR dec. by >50%
  • UO <0.5ml/kg/hr for 12hrs

Failure:

  • inc. sCr x3.0 or GFR dec. by >75% or Cr >4mg/dl with acute rise >0.5mg/dl
  • UO <0.3ml/kg/hr for 24hrs or anuria for 12hours

Loss:

  • persistant acute renal failure = complete loss of renal function for >4 weeks

ESRD: End stage renal disease

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104
Q

What are the stages involved in AKIN?

A

Stage 1:

  • sCr inc. x1.5 or >0.3mg/dl
  • UO <0.5mg/kg/hr x6hrs

Stage 2:

  • sCr inc. x2.0
  • UO <0.5mg/kg/hr x12hrs

Stage 3:

  • sCr inc. x3.0 or >4mg/dl with acute rise of >0.5mg/dl
  • UO <0.3ml/kg/hr x24hrs or anuria x12hrs
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105
Q

Where are patients on renal replacement therapy placed on the AKIN classification?

106
Q

What are the criteria to warrent an AKI e-alert?

What are AKI e-alerts used for?

A

Used in hospitals to highlight when creatinine has changed to indicate underlying AKI

Criteria:

Serum creatinine 1.5x higher than median of all creatinine values of 8-365 days ago

Serum creatinine 1.5x higher than the lowest creatinine within the last 7 days

Serum creatinine >26 umol/l than the lowest creatinine within 48hrs

107
Q

What is the KDIGO classification based on and what’s involved in each stage

A

Based on:

  • absolute sCr rise in 38hrs
  • sCr inc. 1.5x baseline in last 7 days
  • UO <0.5ml/kg/hr for 6hours

Stage 1:

  • sCr >26umol/l (48hours) or >1.5-1.9x inc. in 7 days
  • UO <0.5ml/kg/hr for 6 hours

Stage 2:

  • sCr >2.0-2.9x inc. in 7 days
  • UO <0.5ml/kg/hr for 12 hours

Stage 3:

  • sCr >354 umol/l or 3x reference or if on RRT
  • UO <0.3ml/kg/hr for 24hrs or anuria for 12hrs
108
Q

Define oliguria

A

urine output <1ml/kg/h in infants and <0m5ml/kg/h in children and <400ml-500ml/24h in adults

109
Q

Describe the pathophysiology of acute kidney injury

A
  • largely dependent on cause
  • common link: reduction in GFR
  • as the pressure within the afferent arteriole falls and approaches 80mmHg, prostglandins dilate the arteriole to inc. flow through the vessel
  • NSAIDs prevent this from occuring
  • ACEi dilate the efferent arteriole thus decreasing glomerular pressure
110
Q

How is acute kidney injury diagnosed?

A

Need for urgent action > making final diagnosis

Determination of acute or chronic kidney injury dependent on timeline

Bloods: raised urea and creatinine

Potassium: severe hyperkalaemia (K >6.5mmol/l) is a common complication of AKI

Urine output: <400ml/day (oliguria in adults)

Fluid assessment:

  • raised JVP and oedema: fluid overload
  • BP and heart sounds

Consider sepsis and medications (ie. underlying causes)

Perform urinalysis (protein/blood) and renal USS

GN screening for glomerulonephritis cause: bloods (ANA, anti-GBM, ANA, Ig, complement)

Renal USS to exclude obstruction

  • Loss of cortico-medullar differentiation suggests CKD as well as smaller kidneys
111
Q

How is acute kidney injury treated?

A

ABCDE protocol

May need emergency correction of:

  • Circulatory shock: hypovolaemia, hypotension, shock and hyperkalaemia. Restore renal perfusion
  • Remove causes and correct them quickly: eg. drugs or sepsis
  • Exlude obstruction and consider renal causes
112
Q

What is the main complication of AKI

A

Hyperkalaemia = serum potassium >5.5mmol/l

Mild: 5.5-5.9mmol.l

Moderate: 6-6.4mmol/l - risk of arrythmias and should be treated

Severe: >6.5mmol/l - medical emergency

113
Q

How is hyperkalaemia treated?

A
  1. Reduce absorption from the gut
    - calcium resonium
  2. Drive K back into cells
    - insulin and dextrose
  3. Portect heart by stabilising cardiac membrane
    - calcium gluconate
114
Q

What are the absolute indications for needing dialysis

In which scenarios would dialysis be adviced but not necessary

A

Absolutely:

  1. Refractory severe hyperkalaemia (>6.5mmol/l)
  2. Refractory pulmonary oedema
    refractory: uncontrolled/resistant

Beneficial:

  1. acidosis ie. pH <7.1
  2. Uraemia esp. if urea >40 or pericarditis
115
Q

Define chronic kidney disease

A

The presence of kidney damage or reduced kidney function for 3 or more months, suggested by a reduction to a GFR <60ml/min/1.73m2

116
Q

What pathological markers can be used to characterise CKD?

A
  • albuminuria
  • radiological abnormalities (polycystic kidneys)
  • evidence of kidney pathology
117
Q

What problems arise as kidney function begins to fall in CKD

A

Dysregulation of

  • fluid balance
  • acid/base homeostasis
  • electrolyte balance
  • calcium/phosphate handling (secondary hyperparathyroidism)
118
Q

What is the relationship between serum creatinine and the glomerular filtration rate

What is the main association with creatinine and why

A
  • sCr is inversely proportionate to GFR
  • creatinine is strongly dependent on muscle mass as it is a product of muscle metabolism (breakdown)
119
Q

What are the two downfalls for using serum creatinine as a marker for kidney function?

A

An exponential relationship exists leading to inaccuracies:

  • loss of the first 70% of renal function is not recognised quickly enough (lag time)
  • late renal referral - may encounter sudden, sharp rise in creatinine

Due to the effects of muscle mass:

  • renal function tends to be over-estimated in women, elderly and amputees who all have a lower muscle mass
120
Q

What is the formula to calculate eGFR and what’s involved?

A

MDRD 4 formula

  • age, gender, race, serum creatinine
121
Q

List 3 situations where eGFR cannot be used and one other downfall

A
  • Not validated in the elderly
  • Not useful in AKI
  • Not useful for pregnancy
  • Only validated for white and African-American populations

Downfall: not distinguishable above 60ml/min/1.73m2

122
Q

What markers are involved in the classification of CKD?

A

eGFR: stages 1-5

ACR (albumin creatinine ratio)

these are used in combination to work out a provisional prognosis for a patient

A1: normal (male <2.5; female <3.5)

A2: microalbuminura (male 2.2-25; female 3.5-35)

A3: macroalbuminuria (male >25; female >35)

123
Q

What is a normal amount of protein excretion per day in urine

A

<150mg per day

124
Q

What protein is measured on a dipstick for proteinuria?

125
Q

How is proteinuria quantified?

A

Concentration of urine changes based on hydration status, therefore need to test urine conc. against something that’s excreted independently of urine conc. - urine creatinine concentration

ie. uPCR: urine protein creatinine ratio

126
Q

What are the normal ACR and PCR values?

How can ACR be converted into PCR?

A

Albumin:Creatinine Ratio (ACR) - normal ACR <2.5

Protein:creatinine ratio (PCR) - normal PCR <20

Conversion: ACR = 2/3 of PCR

ie. ACR 70 = PCR 100 = 1g protein excreted /24hrs

127
Q

Define proteinuria

A

The presence of excess levels of protein in the urine

PCR >300 ie. 3g protein excreted / day

128
Q

Describe the pathophysiology of CKD

A

As we age, there is a progressive loss in renal mass and structural changes occur resulting in a decline in renal function

  • Irrespective of cause, CKD leads to progressive loss of nephrons and a subseuqent reduction in GFR
129
Q

List 3 causes of Chronic Kidney Disease (CDK)

A

Majority are secondary to diabetes, HTN and glomerulopathies

  • Diabetic nephropathy
  • Renovascular disease/Ischaemic nephropathy eg. artery occlusion, venous thrombosis
  • Chronic glomerulonephritis: membranous or IgA nephropathy
  • Reflux nephropathy or chronic pyelonephritis
  • Adult polycystic kidney disease
  • obstructive uropathy: hydronephrosis
130
Q

How can diabetic nephropathy cause CKD?

A
  • glycosuria damages the glomerular filtration barrier
  • small vessel damage in the glomerulus
  • develop nodular lesions
131
Q

How can renovascular disease cause CKD?

A
  • Naorriwng or blockage of renal vasculature usually stemming from artery occulsion, venour thrombosis or renal atheroembolism
  • Glomerulus gets eroded and you get local sclerosis of the vessels
132
Q

How can reflux nephropathy lead to CKD

A
  • urinary reflux from the bladder causes scarring of the renal tissue
  • bladder contracts and urine goes back up ureters
  • if consistant efflux of urine, it will present with an inflammatory response
  • this can happen over time and scar the tissues
133
Q

Which part of the kidney is damaged in APKD

A

The parenchyma

134
Q

List 3 symptoms and 3 signs of CDK

A

Early stage CKD: usually asymptomatic

Advanced CKD: non-specific features ie. when eGFR falls beow 45ml/min

Symptoms of advanced CKD:

  • pruritus/itch
  • nausea, anorexia, weight-loss, fatigue
  • SOB/breathlessness
  • leg swelling, bone/joint pain
  • nocturia (impaired ability to concentrate urine)
  • confusion

Signs of advanced stage CKD

  • peripheral and pulmonary oedema
  • pericardial rub
  • rash, pallor and/or yellow tinge
  • HTN, tachypnoea
  • cachexia (muscle weakness/wasting)
135
Q

Describe the management for CKD

A

3-fold: renal protection; complications; RRT

  • there are interventions to slow progression of CKD and may reduce cardiovascular risk
  • dialysis shown to slow progression of CKD and drop in eGFR

Renoprotection

  • Agressive BP control (ACEi/ARB)
  • Diabetic control, improve diet, stok smoking
  • Improve lipid profile, treat acidosis

RRT: 4 domains

  1. Transplant
  2. Home haemodialysis
  3. Hospital based therapies (haemodialysis or self-care unit)
  4. Conservative care
136
Q

List and explain the development of two complications of CKD

A

Anaemia

  • normocytic-normochromic anaemia
  • occurs when eGFR falls below 30
  • due to reduction of EPO production (stimulates BM to produce more RBCs)
  • can also occur due to suboptimal iron absorption and utilisation

Mineral Bone Disorders

  • Reduction of Vitamin D
  • Vit. D needed for cellular Ca uptake, and with CKD there’s reduced Vit D production
  • So intracellular Ca falls leading to stimulationg of parathyroid gland to inc. PTH production
  • Inc. PTH production inc. bone turnover leading to metabolic deposition of calcium in other body parts, mostly blood vessels
  • Secondary hyperparathyroidism may occur due to abnormal handling of calcium and phosphate
  • once eGFR <30: hypocalaemia, hyperphosphatemia and hyperparathyroidism occur leading to bone pathology
137
Q

What is the treatment for bone mineral disorders due to CKD

A

manage the underlying conditions:

Hypocalcaemia: supplement with calcitriol

Hyperphosphataemia: restrict diet and give phosphate binders

  • Calcium based treatments: calcium carbonate/acetate

Hyperparathyroidism: calcimimetics or surgery

138
Q

List 4 functions of the kidney

A

Water and waste

  • Regulates total body water
  • waste excretion eg. urea and creatinine
  • regulate electrolyte balance
  • regulate acid-base

Hormonal

  • mineral metabolism
  • renin production
  • EPO production
  • glucose metabolism
139
Q

List the indications for starting renal replacement therapy

A
  • Medically resistant severe hyperkalaemia (>6.5)
  • Medically resistant pulmonary oedema
  • Medically resistant acidosis
  • Urinemic pericarditis
  • Uraemic encephalopathy

Some drugs are only cleared by dialysis and therefore dialysus is used alongside normal kidney function in acute reatment of certain drug overdoses

140
Q

Define uraemia

A

Raised levels of urea and nitrogenous waste products in serum

  • Uraemia manifests as uraemic syndrome (renal failure) and can affect several body systems
141
Q

List 3 symptoms of uraemia

A
  • itch
  • vomiting
  • anorexia, weight-loss
  • restless leg
  • metallic taste
142
Q

What is the importance of GFR when deciding on RRT?

What is the timing of RRT based on?

A

There is no absolute rule nor absolute threshold with regards to a GFR at which it is appropriate/adviced to initiate GFR

  • RRT should be considered on a patient-by-patient basis
  • Generally start RRT when GFR falls to 5-10ml/min/1.73m2
  • Most start with RRT at a GFR of 7-8ml/min

Timing is symptom based with no absolute threshold

143
Q

What are the three main options for a patient requiring RRT?

A
  • Haemodialysis
  • Peritoneal dialysis
  • Renal transplant
144
Q

In what setting would haemodialysis be done and how long does it take?

A

Setting: either home or hospital (more common)

  • can e either daily or nocturnal

Timing: usually a 4-hour procedure 3x week

  • Can be 6hrs 3x a week, short daily or daily overnight
145
Q

What are the aims of haemodialysis

A

Aims:

  1. Removal of solutes eg. urea, potassium, creatinine via diffusion
  2. Removal of fluid via ultrafiltration - hydrostatic pressure filtration
146
Q

Describe the process of haemodialysis

A
  • Blood removed from body and pumped through the dialysis machine in one direction
  • dialysis fluid (purified water with added ions - dialysate) is pumped through in the opposite direction (counter-current flow)
  • Blood and dialysis fluid are separated by a semi-permeable membrane
  • Diffusion: Urea, creatinine and waste products diffuse down conc. gradient
  • Hydrostatic pressure Filtration: drives fluid and solute through the membrane from blood into dialysate

NB heparin is needed in the machine to prevent blood clotting

  • An air detected and bubble trap are placed on the line taking blood back to the blood to prevent air-emboli
147
Q

Where are the access points on the body for haemdialysis?

A

AVF (Arteriovenous Fistula)

  • Gold standard
  • the connection between artery and vein
  • increases blood flow through the vein leading to inc. venous diameter and becomes stronger
  • the vein can now withstand repeated needle insertions and provides good flow without collapsing
  • rate of infection and thromboembolic event is low

TCVC (tunelled central venous catheter)

  • required central line access
  • doesn’t last as long as AVF but more prone to complications and infections
  • lines are wide bore and have red and blue cap for the venous and arterial vessels

AV graft

  • if veins aren’t good enough to form a fistula, and a tube is attached to the artery
148
Q

List 3 complications of haemodialysis

A
  • May go into shock due to acute hypotension
  • May be problems with vascular access eg. infection, thromboembolic events, fatigue, blood loss
  • Cramps
  • Hypokalaemia (over dialysed)
  • Air embolism
  • Blood loss
  • Dialysis disequilibrium: rapid shift in urea leads to rapid shift in cerebral water flow and can cause cerebral oedema
149
Q

List three advantages and three disadvantages of using haemodialysis

A

Pros:

  • can be used even when no kidney function left
  • replaces many functions of the normal kidney
  • quicker than peritoneal dialysis

Cons:

  • massive impact on QoL and not definitive
  • Expensive
  • Preferable to be hospital-based
150
Q

In what setting would peritoneal dialysis be used?

What are the procedures used for peritoneal dialysis?

A

Setting: allows for home-based therapy

Procedures:

  • can be daily or nocturnal
  • continuous ambulatory peritoneal dialysis
  • automated peritoneal dialysis: machine will filter blood as they sleep and don’t need to carry it around during the day
151
Q

Describe the process of peritoneal dialysis

A

The exchange occurs between the peritoneal capillary blood and dialysis fluid (dialysate) which is put into the peritoneal cavity

  • 2l of glucose rich (K depleted) dialysate is used
  • blood should be high in K and low in glucose
  • gradual in nature therefore not appropriate for AKI
  • glucose conc. can be changed to alter rate of ultrafiltration
  • need some residual renal function (not good options if no/minimal kidney function)

Two mechanisms:

  1. Osmotic fitration (ultrafiltration): movement of water and small solutes due to presence of glucose in dialysate inc. osmolarity
  2. Diffusion down the conc. gradient: urea, creatinine and electrolytes cross into the fluid from blood down the conc. gradient
    - the longer the dialysate remains within the peritoneal cavity, the smaller the gradient becomes and the lower the rate of diffusion
152
Q

List 3 complications of peritoneal dialysis

A
  • infection of peritoneum may occur (peritonitis)
  • glucose load may impact existing or lead to development of diabetes
  • can inc. risk of hernias, diaphragmatic leaks or other mechanical issues
  • hyperalbuminaemia
153
Q

List 3 advantages and 3 disadvantages of peritoneal dialysis

A

Pros:

  • Maintains independence and less impact on QoL
  • Needs to be taight
  • Can be altered/controlled to a degree

Cons:

  • Requires some residual kidney function
  • Infection risk
  • Not suitable for obese or frail patients or those with intra-abdominal adhesions
154
Q

List 3 practicalities of peritoneal dialysis

A
  • home-based therapy
  • better with some residual kidney function
  • gradual treatment: no good for AKI
  • different glucose concs. of dialysate to provide more or less ultrafiltration
  • maintain independence
  • simple procedure once taught
155
Q

What patients wouldn’t be suitable for peritoneal dialysis?

A
  • Grossly obese
  • Frail
  • Intra-abdominal adhesions
156
Q

In what situation in conservative care used in RRT?

A
  • Symptom based management
  • With an increasingly frail and elderly population, the survival on RRT may only be marginally greater but with a much reduced quality of life
  • reserved for the older population
157
Q

List 3 factors taken into consideration to decide the type of RRT that should be used for a patient

A
  • frailty
  • ability to gain vascular access
  • time constraints (time to travel to/from hospital)
  • physical - concurrent medical problems eg. severe dementia, psychiatric disease, disseminated malignancy
  • patient lifestyle and wishes ie. patient choice
  • need someone living with patient at home for home-based therapies
158
Q

How much GFR can dialysis provide?

A

only around 10ml/min GFR, nowhere near as good as a transplant

159
Q

Explain how kidney transplants can be acquired

A

Cadaveric transplant

  • there’s a waiting list for patients who can receive a kidney from a registered donor following brainstem death or cardiac death
  • average wait: 3 years

Live donor kidneys

  • best success
  • altruistic donor - an individual who donates one of their kidneys

NB not all patients are suitable for a transplant as surgery is demanding and requires immunosuppressant lifelong to prevent organ rejection

160
Q

What immunosuppression can be offered after a kidney transplant?

A

Immunosuppression is given following the procedure lifelong

  • Tacrolimus: inhibits IL-2 thus effectively blocking proliferation of T-cells
  • Mycophenolate: blocks nucleosynthesis of B and T cells
  • Methotrexate: inhibits DNA production

Given to prevent organ rejection

161
Q

List 3 advantages and 3 disadvantages of a renal transplant

A

Pros:

  • no need for dialysis
  • better renal fucntion
  • longer independent living
  • increased life expentancy
  • improved fertility

Cons:

  • lifelong immunosuppression
  • inc. CVS risk
  • increased infection risk
  • post-transplant diabetes may occur
  • skin malignancy associations
162
Q

What is the class, indication and action of methotrexate

A

Class: immunosuppressant

Indication

  • Post-transplantation immunosuppression
  • Inflammatory bowel disease
  • Renal vasculitis
  • Paediatric leukaemia

Action:

  • disrupts DNA synthesis
  • blocks the action of the enzyme dihydrofolate needed for DNA production
163
Q

Define bacteruria

A

The presence of bacteria in the urine in the absence of symptoms

164
Q

List 3 groups in which bacteruria is common

A
  • girls > boys
  • pre-school age
  • adult males
  • non-pregnant females
165
Q

List 3 high-risk groups of bacteruiria

A
  • hospitalised patients
  • catheterised patients
  • diabetics
  • patients with structural abnormalities
  • immunocompromised patients
  • pregnant patients
166
Q

How is bacteruria managed?

A

Asymptomatic bacteriuria should only be treated in the following:

  • pre-school children
  • pregnant women (can escalate to pyelonephritis)
  • those who have undergone a renal transplant
  • immunocompromised

Treatment in other asymptomatic patients is not indicated

167
Q

Outline the classification of urinary tract infections

A

Ascending:

  • urethral colonisation
  • more common in females
  • bacteria multiply in the bladder and ureters are involved

Descending:

  • aka ‘haematogenous’
  • often blood-borne infections (blood filters through the kidney)
  • usually an abnormal causative organism
  • involed renal parenchyma
168
Q

List a gram negative and 3 gram positive organisms that commonly cause urinary tract infections (UTIs)

A

Gram -ve Bacilli

  • E. Coli

Gram +ve

  • Streptococcus sp.
  • Enterococcus sp.
  • Staphylococcus sp. (S. aureus, s. saprophyticus)
    • S. saureus found more often in UTIs of catheterised patients*
169
Q

Outline the clinical features seen with a UTI

Outline the additional features seen in neonates, children and the elderly with a UTI

A
  • suprapubic discomfort
  • dysuria
  • urinary frequency
  • cloudly, blood stained, smelly urine
  • low grade fever (potentially complicated)
  • features of SIRS or sepsis (complicated)

Neonates: failure to thrive and jaundice

Children: abdominal pain and vomiting

Elderly: nocturia, incontinence, confusion

170
Q

In what situations would the following most likely occur:

Multiple-organism infections

Multi-drug resistant organisms

A

Multi-organism infections:

  • long-term catheterisation
  • long term infection
  • structural and neurological abnormalities

Multi-drug resistant organisms:

  • abnormalities
  • frequent infections
  • courses of prophylactic antibiotics
171
Q

Outline the investigations and treatment for a uncomplicated suspected UTI in non-pregnant women

A

1st presentation: culture not mandatory

  • Dipstick (high false positive rate)
  • check previous culture results (multi-resistant organism will change treated)
  • trimethoprim for 3-7 days
  • hydrate, rest, paracetamol (analgesics)

No response to treatment:

  • urine culture and change abx
172
Q

Outline the investigations and treatment needed for a suspected uncomplicated UTI in children and men

A
  • send urine samples for culture with each presentation and treat accordingly
173
Q

Outline the investigations and treatment for a suspected UTI in pregnant women

A

Send urine culture with each presentation

Treat with abx for 7-10 days

  • amoxicillin and cefalexin are fairly safe

Avoid:

  • Trimethoprim in 1st trimester (teratogenic)
  • Nitrofuratonin near term

Hospital admission may be neccessary for IV abx if infection is severe: progression pyelonephritis occurs in around 30% cases

174
Q

Define a recurrent UTI

Who are mostly affected and why?

A

occurance of more than two episodes in 6 months or more than 3 episodes in a year

  • mostly affects women due to shorter urethra
175
Q

Outline the management for recurrent UTIs

A
  • abx may be given as a short-course therapy or single doses given as a post-coital dose
  • abx prophylaxis is given when simple measures fail and usually involve trimethoprim and nitrofuratoin ideally for 6 months
  • NB risk of antibiotic resistance
176
Q

What is a complicated UTI?

A

Upper UTIs which are associated with systemic signs and symptoms and/or catheter associated infection (CAUTI)

177
Q

How can catheter-associated UTIs develop and what are the likely causative organisms?

A

Development due to the disturbance of:

  • the flushing-system
  • colonisation of urinary catheters
  • production of biofilm by the bacteria

Likely causative organisms:

  • patient’s flora
  • healthcare environment
178
Q

Outline three complications of catheter use

A
  • catheter associated UTI (CAUTI)
  • obstruction leading to hydronephrosis than can progress into (chronic) renal inflammation
  • urinary tract stones
  • long-term risk of bladder cancer
179
Q

Outline the prevention strategies for catheter associated UTIs

A
  • only catheterise when necessary (do not catheterise if urine can be produced and measured without catheter)
  • promptly remove catheters when no longer needed
  • continually assess the need for a catheter
  • signs of infection, remove catheter immediately
  • catheter bundle care
180
Q

Outline the management for cstheter associated UTIs

A

empirical antiboitics

  • check previous microbiology results
  • remove catheter if needed
  • replace catheter: ensure catheters are changed under abx cover (gentamicin or ciprofloxacin)
  • broad spec abx
181
Q

Differentiate upper and lower urinary tract infections

A

upper UTI: ureters and kidney

lower UTI: involves bladder and urethra

182
Q

Define acute pyelonephritis

A

moderate to severe upper UTI which is ascending and involves the renal pelvis

  • acute inflammation of the kidney
183
Q

Outline the clincal and morphological features of acute pyelonephritis

A

Clinical: UTI symptoms

Morphologically:

  • kidney enlargement with possible abscess formation on the surface
  • US changes
  • hydronephrosis can contribute
184
Q

How is acute pyelonephritis diagnosed and managed

A

Diagnosis:

  • check previous microbiology
  • request urine samples +/- blood culture +/- imaging (US)

Management:

community prescription of co-amoxiclav / ciprofloxacillin / trimethoprim

hospital prescription: usually broad spec abx

  • uncomplicated pyelonephritis: 7-14 days
  • complicated pyelonephritis: >14 days
185
Q

Outline the main complication of acute pyelonephritis

What are the outcomes of this complication?

A

Renal abscess

  • clinical features similar to acute pyelonephritis
  • positive urine and blood cultures
  • usually due to Gram -ve bacilli

Outcome:

  • life-threatening with a poor response to antibiotics
186
Q

Outline the investigations that are needed for patients with suspected complicated UTIs

A

Bloods:

  • FBC, U&Es, CRP
  • Blooc cultures who are pyrexial or hypothermic

Urine sample (microscopy and culture)

Imaging:

  • renal ultrasound
  • CT kidneys, ureters, bladder
187
Q

How are the following results with urine microscopy interpreted?

Epithelial cells

Bacteria with no WBCs

Bacteria with WBCs but no catheter

bacteria with WBCs with catheter

A

epithelial cells: contamination

bacteria with no WBCs: contamination

bacteria with WBCs but no catheter: infection

bacteria with WBCs with catheter: assess clinically

188
Q

If a urine sample is continually negative in a patient but presenting with UTI complaint, what diagnoses would need investigated?

A

Gonorrhoea and chlamydia

189
Q

List 3 causes of pyruia with no bacteria

A

Pyruia = pus in the urine

  • recent/recent abx
  • tumour
  • calculi
  • urethritis (check for chlamydia)
  • TB
190
Q

Outline the antibiotic options for uncomplicated UTIs

A

prescription of oral:

  • trimethoprim
  • amoxicillin
  • nitrofuratoin
  • co-amoxiclav, ciprofloxacin, cefalexin
191
Q

Outline the antibiotic options for a complicated UTI

A

treated with IV therapy

  • amoxicillin or vancomycin
  • Gentamicin (require monitoring)
192
Q

What are the recommendations for the following antibiotics in a UTI:

Amoxicillin

Co-amoxiclav

Ciprofloxacin

Trimethoprim

Nitrofuratoin

Gentamicin

Vancomycin

A

Amoxicillin: some gram -ves and strep

Co-amoxiclav: inc. gram -ve cover, some anaerobes and strep

Ciprofloxacin: gram negatives

Trimethoprim and Nitrofuratoin: both gram +ves and -ves

  • used in uncomplicated UTIs

Gentamicin: Gram -ves and most staph

Vancomycin: Gram +ves only, includes MRSA

193
Q

What antibiotics would be recommended for the following

Strep

Staph

Gram -ves

Gram +ves

uncomplicated UTIs

MRSA

A

Strep: amoxicillin, co-amoxiclav

Staph: Gentamicin, Vancomycin

Gram -ves: Ciprofloxacin, Gentamicin, trimethoprim, nitrofuratoin

Gram +ves: amoxicillin, vancomycin, trimethoprim, nitrofuratoin

uncomplicated UTIs: trimethoprim, nitrofuratoin

MRSA: vancomycin

194
Q

Define acute bacterial prostatitis

List 3 aetiologies

A

Define: often spontaneous, localised infection and inflammation of the prostate gland, which may be secondary to urethral instrumentation

Aetiology:

  • gram -ve bacilli eg. E. coli
  • S. aureus (MRSA, MSSA)
  • N. gonorrhoea
195
Q

Outline the clinical presentation of acute bacterial prostatitis

A
  • Fever
  • Perineal and back pain
  • UTIs, urinary retention
  • Diffuse oedema
  • Micro-abscesses
196
Q

Outline the diagnosis and management for acute bacterial prostatitis

A

Diagnosis:

  • urine cultures usually +ve
  • blood cultures
  • trans-rectal US: prostatic enlargement
  • DT/MRI: prostatic enlargement

Management:

  • Check previous microbiology results
  • Abx: ciprofloxacin
197
Q

List 3 complications with acute bacterial prostatitis

A
  • Prostatic abscesses
  • Spontaneous rupture of urethra/rectum
  • Epididymitis
  • Pyelonephritis
  • Sepsis
198
Q

List 3 aetiologies of chronic prostatitis

Outline the clinical presentation

A
  • often secondary to chlamydia urethritis
  • Gram -ve bacilli (E. coli)
  • Enterococci
  • S. aureus (MSSA, MRSA)

Presentation:

  • asymptomatic, perineal discomfort or back pain with low-grade fever
199
Q

List 3 risk factors for prostate cancer

A

age (>65yrs)

genetics: Hereditary Prostate Cancer 1 gene (HPC1) or BRCA2
familial: 2x risk if 1st degree relative diagnosed <60yrs
environment: UV light

sexual activity from a young age

hormones: the normal function of the prostate gland is regulated by testosterone and DHT. Higher incidence of PC associated with elevated 5-alpha reductase (converts testosterone to DHT)

200
Q

Outline the pathology of prostate cancers

A

Majority of malignant cancers of the prostate are primary adenocarcinomas which usually arise in the peripheral zone of the gland

201
Q

Outline the local and metastatic clinical presentations of prostate cancer

A

Local:

  • asymptomatic
  • painful or slow miturition, urinary retention, UTI
  • haematuria
  • lymphadenopathy

Metastatic:

  • Bone pain
  • Renal failure (ureteric obstruction)
  • Fatigue, weight loss etc.
202
Q

Outline the investigations to diagnose prostate cancer

A

PSA (Prostate Specific Antigen)

  • not very specific (also elevated with an enlarged prostate (occurs with age), prostatitis, UTI)
  • PSA is a serine protease secreted into seminal fluid and causes the release of sperm

DRE (Digital Rectal Examination)

  • Palpation of the prostate: should have a smooth surface with two, equal and palpable hemispheres

MRI

True Biopsy

  • biopsy taken trans-rectally under US guidance
203
Q

Outline how prostate cancers are graded and stages

A

Grading: Gleason Score

  • sum of two prominent Gleason Grades seen histologically within a sample
  • <4: histologically characteristics are well differentiated, unlikely to progress locally
  • 5-7: moderately differentiated, 50% likelihood of local progression
  • >7: poorly differentiated with 75% likelihood of local progression

Staging: TNM (Tumour-Nodes-Metastases)

204
Q

Outline the management for early/localised prostate cancer

A

Watchful waiting

Active surveillance: regular DRE, PSA, MRI and biopsy

Radiotherapy:

  • external beam radiotherapy
  • brachytherapy: radioactive seeds put inside the prostate
  • Radiotherapy usually alongside hormone therapy: LHRH therapy (causes initial testosterone surge but anti-androgens given to stop this)

Radial prostatectomy:

  • removal of all or part of the prostate
  • can be done robotically
205
Q

OUtline the management for advanced prostate cancer

A

Androgen ablation

Medical castration (orchiectomy): removal of the testes

Hormone therapy (LHRH / GnRH agonists)

Chemotherapy

TURP (transurethral resection of the prostate) for symptomatic relief

Radiotherapy

206
Q

Outline two complications of metastatic prostatic cancer and the clinical presentation they would elicit

A

Spinal cord compression

  • severe pain, retention and constipation
  • urgent MRI and intervention
  • radiotherapy and/or spinal decompression surgery

Ureteric Obstruction

  • Anorexia, weight loss, raised creatinine
207
Q

Outline the epidemiology of bladder cancer

A

More common in males

Incidence increases with age

208
Q

Identify 3 risk factors of bladder cancer

A
  • Age (increased age)
  • Causacian
  • Environmental carcinogens
  • Chronic inflammation (causes: renal stones, infection, long-term catheterisation)
  • pelvic radiotherapy
  • smoking
209
Q

What cancer types are most commonly seen in the bladder?

A
  • transitional cell carcinoma (90%)
  • squamous carcinoma
  • adenocarcinoma
210
Q

Outline the clinical presentation of cancer of the bladder

A

painless frank haematuria

  • some may present with microscopic haematuria
211
Q

Outline the investigations for a case of suspected bladder cancer

A

Diagnosis: need flexible cystoscopy (can visualise inside of the bladder with a camera)

  • Also can do renal ultrasound
212
Q

Outline the staging and grading for bladder cancer

A

Staging

  • NMIBC: non-muscle invasive bladder cancer
  • MIBC: muscle invasive bladder cancer

Grading

  • dependent on the grade of inflammation
  • Grade 1: well differentiated
  • Grade 2: moderately differentiated
  • Grade 3: poorly differentiated
213
Q

How is bladder carcinoma in-situ staged?

A

Based on degree of invasion through the bladder wall

T1: confined by lamina propria

T4a: through bladder wall and invading prostate

214
Q

Outline the management for bladder cancer following flexible cystoscopy

A

Surgical:

  • trans-urethral resection of bladder tumour (TURBT)

Medical:

  • Mitomycin C: chemotherapy, targets DNA synthesis
  • Immunotherapy: induction and maintenance
  • radial cystectomy: removal of the bladder +/- prostate/uterus, with urine being directed into an ileal conduit or neobladder
215
Q

What is the main cancer type seen in renal cancer?

A

renal cell carcinoma

  • conventional or clear cell tumour
216
Q

Identify 3 risk factors for renal cell carcinoma

A
  • smoking
  • obesity
  • HTN
  • acquired renal cystic disease
  • genetics
  • haemodialysis
217
Q

Outline the clinical features seen with renal carcinoma

A

80% - incidental finding (asymptomatic)

Non-specific features:

  • weight loss, night sweats, fever, fatigue

Classic Kidney Cancer triad:

- mass, pain, haematuria

Small maj can present with:

  • oedema of the left leg
  • paraneoplastic syndrome
  • varicocele (more common of the left due to the angle at which the left testicular vein enters the left renal vein)
218
Q

Define paraneoplastic syndromes

Outline it’s common presentation

A

Def: set of signs or symptoms in the body caused by underlying cancer but not due to local presence of cancer cells

Common presentation:

  • HTN: due to renin secretion
  • Hypercalcaemia: due to PTH secretion or osteolytic hypercalaemia
  • Polycythaemia: inc. EPO production

Abnormal LFTs

Rarer:

  • CTH (Cushing’s syndrome), prolactin (galactorrhoea), insulin (hypoglycaemia)
219
Q

how is renal carcinoma diagnosed?

A

initial diagnosis: US

bloods:

  • fbc, U&E, lft, crp, ldh

CT of Kidneys and MRI

220
Q

Outline how renal carcinomas are staged

A
  • staging based on the size of tumour and extent of invasion

T1a: <4cm

T1b: 4-7cm

T2: >7cm

T3a: extends to renal vein

T3b: extends into IVC below diaphragm

T4: extends to IVC above diaphragm

T4: extends beyond adrenal gland

221
Q

Outline the management for renal carcinoma

A

Dependent on tumour stage and patient preference

Radical Nephrectomy

  • removal of kidney + gerota’s fascia (encapsulates kidneys and adrenal glands)
  • indication: large renal mass

Nephron Sparing Surgery

  • resection-type surgery in which only part of the kidney is removed

Tyrosine Kinase Inhibitors

  • metastatic disease treatment
  • inhibits angiogenesis
  • indications: small renal mass, single kidney, patient has CKD, CV risk factors, stage is only T1

-

222
Q

Identify 3 risk factors for testicular cancer

A
  • age: 20-40yrs
  • cryptorchidism
  • HIV infection
  • Caucasian
223
Q

Outline the cell types commonly seen in testicular cancers

A

Germ cell tumours

  • Teratomas, seminomas

Stromal tumours

  • Leydig cell tumours, Sertoli cell tumours

Others:

  • lymphoma, metastases
224
Q

Outline the clinical presentation and investigations for testicular cancer

A

Presentation: painless lump

Diagnosis:

  • Scrotal US
  • tumour markers: AFP (alpha fetoprotein), beta-HCG, LDH
  • CT staging
225
Q

Outline the management for testicular cancer

A

Radical orchidectomy

Chemotherapy

it’s important to check lymph nodes and if necessary:

  • para-aortic nodal radiotherapy
  • retroperitoneal lymph node dissection
226
Q

What are the treatment options for a patient with kidney failure (eGFR 7-10ml)

A
  • renal dialysis: haemodialysis peritoneal dialysis
  • renal transplant
  • conservative care
227
Q

Identify three disadvantages of renal dialysis

A
  • always exhausted
  • fluid restriction
  • diet restriction (K and phosphate restrictions)
  • women are infertile
228
Q

Identify three indications for renal transplant

A
  • increased life expectancy
  • improved quality of life
  • less time in hospital
  • Cost saving
229
Q

identify 3 contra-indications for a renal transplant

A

reduced life expectancy:

  • older age
  • co-morbidities
  • unlikely to survive 5 years post-transplant

surgical contra-indications:

  • calcified blood vessels
  • bladder removed

medical contraindications

  • hypertension / hypotension
  • disease that will recur in the transplanted kidney
230
Q

What is the challenge of a renal transplant?

What treatment is given to avoid this?

A

The immune system recognises foreign cells and proteins

  • it responds to destroy foreign tissue through complex amplification pathways
  • evolved to deal with infection and malignancy

Therefore, the immun system will attack the new kidney which could lead to organ rejection

  • Therefore immunosuppression is needed to prevent rejection
231
Q

What causes rejection of an organ in organ transplant?

A
  • Recognising cell proteins as non-self
  • Blood group incompatibility
  • HLA compatibility
  • T cell mediated and antibody mediated rejection
232
Q

What immunosuppression treatment is given following a renal transplant and outline what each drug does?

A
  • Basiliximab: monoclonal antibody directed against IL-2 receptor
  • Tacrolimus: calcineurin inhibitor
  • Mycophenolate mofetil: depletes guanosine nucleotides in T and B lymphocytes and inhibits proliferation

+/- steroids

233
Q

Outline the 3 major complications of organ transplantation

A

Rejection

  • cell mediated rejection: interstitial inflammation and tubulitis. Often easily treated with steroids if caught early
  • antibody-mediated rejection: endothelial swelling, glomerulitis and peritubular capillaries. Difficult to treat, usually inc. immunosuppression

Infection

  • Chest infection, skin wound infection, UTI

Malignancy

  • melanoma, non-Hodgkin’s lymphoma, Hodgkin’s lymphoma
  • treatment: reduce immunosuppression +/- rituximab or chemotherapy
234
Q

identify 3 diseases that would indicate need for renal dialysis over transplant

A
  • renovascular disease
  • T2 diabetic nephropathy
  • vasculitis
  • obstructive uropathy
235
Q

Identify 3 conditions that would indicate need for renal transplant rather than dialysis

A
  • adult polycystic kidney disease
  • glomerulonephritis
  • reflux nephropathy
  • T1 diabetic nephropathy
236
Q

What two sources are there for renal transplants?

A

Deceased donors

  • Following brainstem death
  • Need good kidney function
  • Average wait time: 2-3 years

Living donors:

  • friend, family altruistic donor
237
Q

Identify three advantages of getting a renal transplant from a living donor rather than a deceased donor

To be a living donor, what matches must be made with the patient?

A
  • pre-emptive transplantation
  • better kidneys
  • better outcomes and longer kidney survival

Donor:

  • must be fit and healthy
  • have excellent kidney function
  • blood and HLA compatible
238
Q

List the segments of the ureters at which renal stones are most likely to get trapped

A

Narrowed segments of ureter:

  • Proximal: pelviureteric junction
  • Mid: pelvic brim (segment over the sacral bone)
  • Distal: uretero-vesical junction
239
Q

List the layers of the ureter wall

A
  • Urothelial mucosa
  • Lamina propria
  • Muscular layer
  • Adventitial layer
240
Q

Identify 3 intrinsic and 3 extrinsic risk factors for developing kidney stones

A

Intrinsic:

  • Age: 20-50yrs
  • Gender: men (males have a higher oxalate production and females have higher urinary citrate (stops stone formation)
  • Caucasians
  • Familial renal tubular acidosis
  • Cystinuria
  • Co-morbidity

Extrinsic:

  • Low fluid intake
  • Diet and lifestyle
  • More likely in summer (higher urinary concentrations, lower pH, sunlight and Vit D - inc. calcium with inc. Vit D levels)
  • Hot climates
  • Sedentary (occupation, exercise etc.)
241
Q

What is the clinical importance of the content of kidney stones?

A
  • If patients are presenting as an emergency, it doesn’t matter what type of stone it is, immediately want to treat the patient eg. sepsis, AKI, pain
  • Content of stone is useful as it influences management
    eg. urate stones can be managed with medication, ESWL is unlikely to be successful for calcium oxalate dihydrate which are much harder stones
242
Q

Identify the main renal stone morphologies

A

Calcium Stones (80%):

  • Calcium oxalate monohydrate
  • Calcium oxalate dihydrate

Infection stones:

  • Struvite (Mg-ammonium-phosphate)

Uric acid stones

Cystine (genetic)

Xanthine stones

243
Q

Outline the mechanism for development of calcium-oxalate monohydrate and dihydrate renal stones

A

Ca-oxalate stones are the most common renal stones

Calcium-Oxalate Monohydrate:

  • Due to excess of oxalate
  • Oxalate commonly found in fruit, vegetables, nuts and chocolate

Calcium-Oxalate Dihydrate:

  • Calcium driven
244
Q

Outline the mechanism for development of Struvite stones

A

aka. magnesium-ammonium-phosphate stones
- infection driven
- staghorn calculi that grow quickly and become quite large
- Staghorn calculi: branched stones that fill part or all of the renal pelvis and branch into several or all calyces

245
Q

Outline the mechanism for development of uric acid stones

A
  • metabolic syndromes
  • these form due to chronic dehydration
  • the risk of development increases in those with gout, a genetic tendency or a high protein diet
246
Q

Outline the mechanism of development of cystine stones

A

genetic - runs in families

  • inherited disorders that cause the kidneys to excrete certain types of amino acids
247
Q

Outline the mechanism of development of xanthine renal stones

A
  • enzyme deficiency that causes build-up of xanthine deposits
248
Q

Identify the three accepted mechanisms that lead to formation of renal stones

A
  1. Abnormal urine
  2. Urinary obstruction
  3. Urinary infection
249
Q

Identify the causes of abnormal urine can lead to the formation of renal stones

A

Normal urine is understanderated, but if the composition of urine changes making it abnormal, stone formation becomes more likely

Too much salt

Abnormalities of blood

  • Elevated calcium eg. underlying hyperparathyroidism
  • Metabolic syndrome causing elevated uric acid levels

Abnormal urine

  • Hypercalciruia, Hyperoxaluria

Dehydration (insufficient intake or excess output)

250
Q

Identify levels of factors and inhibitors that affect stone formation

A

Low levels can predispose to stone formation

  • low urine volume
  • pH, citrate, magnesium
  • Lack of inhibitors: citric acid, magnesium, pyrophosphate, glycoproteins

Inc. in certain substances promote stone formation

  • high uric acid, calcium, oxalate
251
Q

Identify the causes of urinary obstruction that can lead to formation of renal stones

A

Congenital

  • abnormalities preventing normal outflow of urine through the ureters into the bladder
  • medullary sponge kidney
  • uretourocele
  • pelvico-urinary junction obstruction

Acquired

  • ureteric strictures
  • anastomotic strictures
252
Q

Outline the causes of urinary infection that can lead to formation of renal stones

A

Organisms that produce urease are linked to urinary stone formation

Proteus mirabilis

  • Gram -ve, anaerobic rod
  • forms characteristic bullseye patterns
  • splits urea into ammonium and raises the pH of urine

Struvite

  • magnesium ammonium phosphate precipitates in alkaline urine to form stones which means infection with proteus can potentiate the formation of stones
253
Q

Outline the clinical presentation of kidney stones

A
  • can be asymptomatic and found incidentally on imaging

Typical presentation:

  • colicky pain which radiates from loin to groin without settling
  • the patient may be unable to sit still, constantly moving
  • Haematuria (frank or microscopic)
  • UTI or sepsis with no known cause (confirmed with imaging)
254
Q

What initial investigations are needed for a patient with suspected kidney stones

A

History and Examination

Bloods: U&Es, CRP, FBC

Urine: urinalysis (blood and infection) and cultures

Biochemistry:

  • First stone: U&Es, Ca, urate, stone analysis
  • Recurrent stone: U&E, Ca, urate, venous bicard, two sets of 24hr urine analysis

Imaging:

  • CT KUB (CT of kidneys, ureters and bladder): gold standard
  • US
  • X-Ray KUB: cannot detect uric acid stones
255
Q

What are the advantages of CT KUB scan for a renal stone?

A
  • suggests the fluoroscopic appearance of a stone, which determines whether it can be targeted with extra-corporeal shock wave lithrotripsy (ESWL)
  • stone diameter
  • skin to stone distance: if >10cm, can consider EWSL
  • lower radiation dose
256
Q

Identidy the management options for kidney stones and what affects management

A
  • Observation: small and asymptomatic stones
  • Medical therapy: involves dissolution therapy
  • Non-invasive
  • Invasive

Affecting management plan: size of stones

  • <4mm: 75% chance of passing passively
  • <7cm: 25% chance of passing if proximal, 35% chance if mid, 64% chance if distal
257
Q

Describe the medical treatment used for kidney stones

A

For acute pain: NSAIDs or opiates

  • NSAIDs: reduce pain as they reduce GFR, reduce renal pressure and ureteric peristalsis
  • Medical Expulsive Therapy: alpha-blocker, only used for large, distal stones
258
Q

Identify the surgical options for renal stones

A

Dependent on size and location

Ureteroscopy

  • ureteric or renal stones <2cm
  • Ureteroscopy and basket
  • Ureteroscopy and fragmentation
  • FURS: flexible ureteroscopy

ESWL: extracorporeal shockwave lithrotripsy

  • proximal ureteric stones of <10mm or <20mm renal stones (location dependent)

PCNL: percutaneous stent or nephrostomy

  • Stones >2cm that are within the kidney
  • Used for staghorn calculi

Nephrostomy

  • laparoscopic or open surgery
  • suitable for huge stones in non-functioning kidneys
  • required reconstruction afterwards
259
Q

Identify three situations in which admission to hospital with renal stones would be required

A
  • Uncontrollable pain
  • Fever or signs of sepsis
  • Solitary kidney with a ureteric stone
  • Bilateral ureteric stones
  • Renal failure caused by an obstructing stone
260
Q

Outline the emergency presentation of kidney stones

A

Pain

  • worst pain ever (worse than labour)
  • typical loin pain which radiates to the groin

*Watch for AAA - similar presentation

261
Q

What are the differentials for the clinical presentation of pain (‘worst pain ever’), typically in the loin that radiates to the groin

A
  • Kidney stone
  • Appendicitis
  • Ovarian cysts / gynaecological pathology

Phase 3 (12 decks)

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