12.4 - Urological & Renal Disorders Flashcards

1
Q

What are the main normal functions of the kidney?

A
  1. filtration - removal of waste substance, keeping the essential substances within the blood e.g. blood cells, large proteins including albumin
  2. control salt and water balance
  3. control of acid/base balance
  4. hormones e.g. erythropoietin production - essential for Hb synthesis
  5. vitamin D - 1-alpha-hydroxylation of vitamin D
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2
Q

What happens when each of the normal functions of the kidneys go wrong?

A
  1. filtration failure - unwell with accumulation of waste substance, haematuria and proteinuria, low serum protein including albumin in blood
  2. hypertension, water retention (sometimes dehydration because unable to make concentrated urine)
  3. metabolic acidosis
  4. anaemia (reduced EPO)
  5. vitamin D deficiency and secondary hyperparathyroidism
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3
Q

What inflammatory diseases are there?

A
  • infection including cystitis
  • non-infective causes can be:
  1. metabolic, including diabetic nephropathy
  2. immunological - nephritic syndrome, nephrotic syndrome
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4
Q

What obstructive diseases are there?

A
  • stones
  • benign prostatic hypertrophy
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5
Q

What neoplastic diseases are there?

A

Kidney, bladder, prostatic, testicular cancer

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6
Q

What developmental/genetic diseases are there?

A
  • polycystic kidneys
  • horseshoe kidney (due to incorrect embryological development)
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7
Q

What are the possible locations for an infection of the urological system?

A
  • bladder - cystitis
  • kidney - pyelonephritis
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8
Q

What are the potential pathogen types causing infection of the urological system?

A
  • bacteria - most common
  • virus and fungal in immunocompromised patients
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9
Q

How do we make a diagnosis for a urinary tract infection (UTI)?

A
  • history
  • physical examination
  • urine dipstick
  • urine microscopy, culture and sensitivity
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10
Q

What do we look out for in a physical exam for a UTI?

A
  • temperature - e.g. 38oC
  • blood pressure - e.g. 105/70 mmHg
  • pulse - e.g. 80/min (normal)
  • abdomen - soft, slightly tender over suprapubic area and left loin
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11
Q

What investigations do we do for a UTI?

A
  • urine dipstick - e.g. 2+ leukocytes, + nitrite, trace of blood
  • urine microscopy, culture and sensitivity
  • (blood tests e.g. renal profile: electrolyte, urea and creatinine)
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12
Q

What is the treatment and overall clinical management for UTI?

A
  • antibiotics - choice depends on severity of illness, common bacteria in local area, modified when sensitivity from urine culture is available
  • some patients may be very ill + treated as inpatient
  • pain control
  • supportive e.g. hydration through IV fluid replacement
  • imaging/differential diagnosis important too
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13
Q

How can the immune system damage the kidney?

A
  • antibodies
  • inflammatory cells (neutrophils, monocytes/macrophages, T cells)
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14
Q

What is glomerulonephritis?

A
  • inflammation of the microscopic filtering units of the kidney
  • wide variety which presents as:
  • nephritic syndrome
  • proteinuria
  • nephrotic syndrome
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15
Q

What are the patterns of organ involvement for immunological causes of inflammation?

A
  • kidney only
  • kidney and lung
  • multiple organs/tissues involved
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16
Q

What is the diagnostic approach?

A
  • history and physical examination
  • urine test
  • blood test - including immunology tests
  • imaging - start with ultrasound
  • kidney biopsy
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17
Q

How does nephritic syndrome present?

A
  • haematuria
  • variable amount of proteinuria
  • may have hypertension, reduced urine output, increased urea and creatinine
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18
Q

How is nephritic/nephrotic syndrome diagnosed?

A
  • history
  • physical examination
  • urine dipstick
  • urine microscopy
  • urine protein : creatinine ratio
  • blood tests - kidney function, immunology test
  • kidney biopsy
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19
Q

What do we look out for in a physical exam for nephritic syndrome?

A
  • temperature - normal
  • inflamed tonsil
  • blood pressure - 140/100 (high)
  • pulse - normal around 70/min
  • chest: normal
  • abdomen: normal
  • ankle: no peripheral oedema
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20
Q

What investigations do we do for nephritic syndrome?

A
  • urine dipstick - 3+ blood, 2+ protein
  • blood tests - raised serum urea and creatinine concentration, reduced eGFR, no autoantibodies
  • urine - raised urine protein : creatinine ratio
  • kidney biopsy - IgA nephropathy
21
Q

What is IgA nephropathy (nephritic syndrome)?

A
  • most common primary glomerulonephritis worldwide - high prevalence in Far East
  • deposition of IgA antibody in kidney (detected by immunohistochemistry)
  • inflammation and scarring
  • about 30% progress to kidney failure
22
Q

What is the supportive treatment for IgA nephropathy (nephritic syndrome)?

A
  • treat hypertension and reduce proteinuria
  • first line treatment - angiotensin receptor inhibitor (ARB e.g. irbesartan) or angiotensin converting enzyme inhibitor (ACEI e.g. ramipril)
23
Q

What is the immunotherapy like for IgA nephropathy (nephritic syndrome)?

A
  • renal replacement therapy - when reaching late stage kidney disease:
  • kidney transplantation
  • dialysis
24
Q

Give an example of an organ specific (kidney and lung) immunological condition?

A
  • anti-glomerular basement membrane (GBM) antibody mediated - Goodpasture’s disease
  • shared common antigen between lung and kidney - alpha3chain of type IV collagen
25
Q

What are systemic inflammatory conditions?

A
  • systemic lupus erythematosus (SLE) - autoantibodies: antinuclear factor, anti-dsDNA
  • vasculitis - antineutrophil cytoplasm antibody (ANCA)
26
Q

What is the pathogenesis of diabetic nephropathy?

A
  • inflammation and fibrosis
  • most common cause of chronic kidney disease and kidney failure in Western world
  • damaged glomerulus of nephron - glomerular damage compromises the filtration function
  • reduced kidney functionality - could cause tiredness (loss of detoxifying kidney function + reduced EPO = anaemia), swollen ankles (water retention in periphery due to loss of proteins and reduced kidney function)
27
Q

What are the risk factors for diabetic nephropathy?

A
  • hypertension
  • poor diabetic control
  • smoking
28
Q

What are the clinical features of diabetic nephropathy?

A
  • microalbuminuria (increased albumin in urine)
  • proteinuria
  • association with other complications of diabetes mellitus - diabetic retinopathy, diabetic neuropathy
29
Q

What does diabetic nephropathy do to the glomerulus?

A
  • thickens glomerular basement membrane
  • deposits ECM in glomerulus
30
Q

What are the treatments and clinical management for diabetic nephropathy?

A
  • optimised diabetic control
  • optimised treatment of hypertension
  • reduce proteinuria using ARB / ACEI
  • stop smoking
  • new treatments - SGLT2 inhibitor
  • transplantation (including combined pancreas and kidney transplantation)
  • dialysis
31
Q

How does nephrotic syndrome present?

A
  • peripheral oedema
  • severe proteinuria
  • low serum albumin
  • variable amount of microscopic haematuria
  • associated with hyperlipidaemia
32
Q

What do we look out for in a physical exam for nephrotic syndrome?

A
  • preorbital oedema
  • temperature normal
  • blood pressure around 110/70
  • ankle - pitting oedema
33
Q

What investigations do we do for nephrotic syndrome?

A
  • urine dipstick - no blood, 4+ protein
  • blood tests - normal serum urea and creatinine concentration, normal eGFR, very low serum albumin concentration (11g/L), no autoantibodies
  • very high urine protein : creatinine ratio 1000mg/mmol
  • kidney biopsy - minimal change glomerulopathy
34
Q

What are the causes for nephrotic syndrome?

A
  • minimal change glomerulopathy
  • membranous nephropathy
  • focal segmental glomerulosclerosis
  • lupus nephritis
  • others
35
Q

What are the key features of minimal change glomerulopathy (nephrotic syndrome)?

A
  • most common in children, also affect other age groups
  • normal light microscopy
  • electron microscopy - podocyte effacement - abnormal flattened appearance
  • complication - high risk of thrombosis
36
Q

What are the treatments for nephrotic syndrome?

A
  • immunotherapy - corticosteroid, cyclophosphamide, recent development: tacrolimus, antibody therapy targeting B cell pathway
  • diuretics - to reduce peripheral oedema
  • prevention of thrombosis - anticoagulation - nephrotic patients more likely to get DVT
37
Q

What are the possible locations for stones? (Obstructive conditions)

A
  • kidney
  • ureter
  • bladder
38
Q

How are stones clinically presented?

A
  • pain (abdomen, back-loin)
  • blood in urine
  • associated with urine infection
  • about 90% of kidney stones are radio-opaque, so are visible under X-ray
39
Q

What imaging tests can be used to detect stones in the urinary tract?

A
  • X-ray - quick, easy, readily available in hospitals - but patient exposed to radiation
  • ultrasound - can detect dilation of urinary system due to obstruction which can be useful in spotting loss of function
  • CT scan - highly sensitive in detecting small stones but involves radiation exposure
40
Q

What are the possible causes for stone formation?

A
  • prostate enlargement - can obstruct urine excretion, causing stones to form in bladder from minerals in urine
  • any nervous system disease damaging the bladder nerves - causes partial urine excretion, causing stones to form in bladder e.g. motor neurone disease
  • gout - increased blood uric acid levels –> increased risk of kidney stone development
  • hydration - being dehydrated concentrates the urine, increasing chances of stones
  • diet - diet rich in sodium/animal protein/poor in calcium can lead to stone formation as it can cause an increase in calcium, uric acid and oxalate levels (different stone types) respectively in urine
41
Q

What is the supportive treatment for stones?

A
  • pain control
  • hydration
42
Q

What does specific treatment for stones depend on?

A
  • size and location of stones
  • availability of local expertise
  • fitness of patient for general anaesthetics
43
Q

What are three specific treatments for stones?

A
  • shockwave lithotripsy - high energy ultrasound waves to break up large kidney stones into smaller ones
  • ureteroscopy - through urethra, bladder and ureter
  • percutaneous nephrolithotomy - small percutaneous incision, insertion of nephroscope, stone is removed (may need to be broken into smaller pieces)
44
Q

What are the different types of polycystic kidneys? (Developmental/genetic condition)

A
  • neonatal - autosomal recessive
  • adult onset - autosomal dominant
  • some patients without any family history
45
Q

What are the consequences of polycystic kidneys?

A
  • loss of kidney function
  • pain
  • bleeding into the renal cysts
  • infection of renal cysts
  • asymptomatic in some patients
46
Q

What are the treatment options for polycystic kidney disease?

A
  • new medication - Tolvaptan (vasopressin receptor 2 antagonist) to slow down cyst formation
  • treat hypertension, infection
  • pain control
  • renal replacement therapy (transplantation, dialysis)
47
Q

How may we know if the patient has horseshoe kidney? (Developmental/genetic condition)?

A

Imaging of abdomen/pelvis

48
Q

What are the consequences of horseshoe kidney?

A

Increased risk of:

  • obstruction
  • stone
  • infection