Renal Flashcards

1
Q

What is acute kidney injury?

A

A significant deterioration in renal function

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2
Q

What causes AKI?

A

Pre-renal: hypoperfusion (severe drop in BP) - ischaemia, sepsis, drugs, cardiogenic shock
Renal: intrinsic renal disease - glomerulonephritis, infection, drugs
Post-renal: obstruction to urine flow - benign prostatic hyperplasia

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3
Q

How does AKI present?

A

Oliguria, pulmonary oedema, fatigue, shortness of breath

Hyperkalaemia - medical emergency

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4
Q

How is AKI diagnosed?

A

Blood: elevated serum urea an creatinine (>50%)
Decrease in urine output
Imaging

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5
Q

How is AKI managed?

A

Hypovolaemia - give crystalloid for volume replacement
Hypervoleaemia - fluid restriction and diuretics
Treat sepsis, stop NSAIDs, ACEi
Consider gastroprotection (H2 antagonist and PPI)

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6
Q

What is chronic kidney disease?

A

Irreversible loss of nephrons

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7
Q

What classifies CKD?

A

GFR <15 is kidney failure

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8
Q

What are some abnormalities of kidney function/structure?

A

Decreased glomerular filtration rate (GFR)
Increased albuminuria
Urinary sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders

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9
Q

What are some causes of CKD?

A

Acute renal failure, hypertension, diabetes, kidney disease e.g. PKD

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10
Q

Describe the pathology of CKD

A

Injury may primarily affect glomeruli or vessels but eventually it leads to reduction in nephron mass with reduction in renal function.
The reduction in nephron mass then causes haemodynamic stress in remaining nephrons, leading to further nephron loss.

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11
Q

How does CKD present?

A

Early disease is asymptomatic
Loss of appetite, fatigue, bone pain
End-stage renal failure - fluid overload and metabolic derangement (vomiting and diarrhoea)

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12
Q

How is CKD diagnosed?

A

Bloods - glucose, increased PTH, low calcium
Urine dipstick - albumin:creatinine ratio
Imaging - US for size and to exclude obstruction

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13
Q

How is CKD renal disease progression slowed?

A

Target to lower blood pressure, offer treatment with renin-angiotensin system antagonist (ACEi)

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14
Q

How are renal complications of CKD managed?

A

Anaemia: treat underlying cause
Acidosis: consider sodium bicarbonate supplements
Oedema: restrict fluid and sodium intake
CKD bone mineral disorders: give vitamin D supplements

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15
Q

What are the 2 biggest complications of CKD?

A

CVD due to hypertension, vascular calcification and hyperlipidaemia - patients more likely to die of CVD than need RRT
Renal bone disease (hyper-parathyroid bone disease, osteomalacia and osteoporosis)

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16
Q

What is renal replacement therapy?

A

Haemodialysis, peritoneal dialysis, haemofiltration

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17
Q

What symptoms of renal failure indicate the need for long-term dialysis?

A

Inability to control volume status or blood pressure
Acid-base or electrolyte abnormalities
Cognitive impairment

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18
Q

What is haemodialysis?

A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction.
Access if via an AV fistula
3+ times a week

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19
Q

What is peritoneal dialysis?

A

Uses the peritoneum as a semi-permeable membrane. Catheter is inserted into the peritoneal cavity and fluid infused. Solutes diffuse slowly across.
Continuous process with intermittent drainage and refilling at home

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20
Q

What is haemofiltration?

A

Water cleared by positive pressure, dragging solutes into the waste by convention. The ultra filtrate is replaced with an appropriate volume of clean fluid

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21
Q

What are the complications of RRT?

A

CVD: increased BP, calcium/phosphate disregulation

Renal bone disease, infection

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22
Q

What immunosuppression is provided at the time of a kidney transplant?

A

Monoclonal antibodies e.g. daclizumab

23
Q

What is polycystic kidney disease?

A

An inherited disorder in which clusters of cysts develop primarily within your kidneys, causing your kidneys to enlarge and lose function over time

24
Q

What causes polycystic kidney disease?

A

Inherited mutation in PKD1 gene. Defects in the function of the PKD1 protein lead to cystic change in renal tubules and loss of normal renal tissue

25
How does polycystic kidney disease present?
Hypertension, flank pain, haematuria, renal calculi
26
How is polycystic kidney disease diagnosed?
USS, genetic testing, CT for renal colic as cysts obscure view on ultrasound
27
How is polycystic kidney disease managed?
Water intake 3-4L/day suppresses cyst growth, treat high BP (ACEi), severe pain - cyst decompression
28
What is renal colic?
A type of pain you get when urinary stones block part of your urinary tract
29
What are the features of renal colic?
Rapid onset - woken from sleep Pain from upper UT obstruction from loin to groin Associated with nausea and vomiting Often cannot lie still - patient writhing in pain from excruciating ureteric spasms
30
What is glomerulonephritis?
Inflammation and damage to the glomeruli that allows protein +/- blood to leak out into the urine
31
What are the features of glomerular disease?
``` Caused by pathology in the glomerulus Present with proteinuria, haematuria Diagnosed on a renal biopsy Cause CKD Can progress to kidney failure ```
32
How does glomerulonephritis present?
Acute nephritis syndrome, nephrotic syndrome, chronic kidney disease
33
How is glomerulonephritis diagnosed?
Renal biopsy is required for diagnosis
34
What is IgA nephropathy?
Immune complex GN related to glomerular deposition of immune complexes containing IgA Causes acute nephritis syndrome
35
What causes IgA nephropathy?
Primary - abnormal mucosal immune system | Secondary - IgA deposited in glomeruli, associated with liver/ bowel disease
36
How does IgA nephropathy present?
Asymptomatic non-visible haematuria, episodic visible haematuria, high BP
37
How is IgA nephropathy diagnosed?
Renal biopsy - IgA deposition in mesangium
38
How is IgA nephropathy treated?
ACE inhibitors - reduce BP and protein in the urine
39
What is nephrotic syndrome?
Proteinuria due to podocyte pathology
40
What is the classic triad of nephrotic syndrome?
Proteinuria >3.5g/24 hours Hypoalbuminemia Oedema
41
What causes nephrotic syndrome?
Primary renal disease e.g. membranous nephropathy, or secondary causes e.g. DM, lipid nephritis
42
How does nephrotic syndrome present?
Oedema of ankles, genital, abdominal wall | Hypoalbuminaemia, frothy urine, systemic symptoms
43
How is nephrotic syndrome diagnosed?
Establish cause via renal biopsy, urine dipstick shows high protein, serum albumin is low
44
How is nephrotic syndrome managed?
Reduce oedema - fluid and salt restriction, loop diuretics Reduce proteinuria - ACEi / ARB Treat underlying cause and complications
45
What are the features of minimal change disease?
Loss of podocyte foot processes, vacuolation and appearance of microvilli in the glomerulus Does not progress to renal failure
46
How is minimal change disease diagnosed and managed?
Electron microscopy shows abnormal podocytes (biopsy) | Steroids (prednisolone), second line is cyclophosphamide
47
What is acute nephritic syndrome?
Loss of blood in the urine due to damage of the glomeruli in the kidney
48
What is nephritic syndrome characterised by?
Haematuria, proteinuria, hypertension and oedema. | Low volume of urine
49
What are the features of focal segmental glomerulosclerosis?
Nephrotic syndrome. Primary (genetic) or secondary (HIV) | Diagnosis: Ab tests all -ve. Glomeruli develop sclerosed lesions.
50
How is focal segmental glomerulosclerosis managed?
Salt restriction and diuretics to reduce oedema Antihypertensives Statins - treat hyperlipidaemia Transplant
51
What are the features of Membranous glomerulonephritis?
Nephrotic syndrome. Slowly progressive. Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins.
52
How is Membranous glomerulonephritis diagnosed?
Microscopic analysis shows thickened glomerular basement membrane Immunofluorescence shows diffuse uptake of IgG
53
How is membranous glomerulonephritis managed?
Steroids if disease progresses