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2A revision > Renal > Flashcards

Renal Flashcards

1
Q

what is acute kidney injury

A
  • a significant deterioration in renal function
  • over hours or days
  • 3 stages of severity
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2
Q

what are the three types of causes for AKI

A
  • pre-renal (decreased perfusion to kidney)
  • renal (intrinsic renal disease)
  • post-renal (obstruction to urine flow)
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3
Q

give 3 pre-renal causes of AKI

A
  • renal artery stenosis
  • heart failure
  • haemorrhage
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4
Q

give 4 renal causes of AKI

A
  • acute tubular injury
  • glomerulonephritis
  • acute interstitial nephritis
  • renal vasculitis
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5
Q

give 3 post-renal causes of AKI

A
  • benign prostatic hyperplasia
  • kidney stones
  • tumour
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6
Q

what is the pathology of pre-renal AKI

A
  • low vascular volume
  • decreased cardiac output
  • systemic vasodilation
  • renal vasoconstriction
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7
Q

what is the pathology of renal AKI

A
  • glomerular
  • interstitial
  • vessels
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8
Q

what is the pathology of post-renal AKI

A

extrinsic compression

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9
Q

clinical manifestations of AKI

A
  • oliguria (passing small volume of urine)
  • severe = pulmonary oedema, encephalopathy, pericarditis
  • fatigue
  • SOB
  • can cause HYPERKALAEMIA = medical emergency
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10
Q

differential diagnoses of AKI

A
  • CKD
  • hyperkalaemia/hypernatremia
  • acute tubular necrosis
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11
Q

investigations for AKI

A
  • bloods = elevated serum urea and creatinine

- imaging

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12
Q

diagnostic markers for AKI

A
  • rise in creatinine>26umol/L in 48h
  • rise in creatinine >50%
  • urine output <0.5ml/kg for >6 consecutive hours
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13
Q

management of AKI

A
  • dialysis may be needed while renal function improves
  • manage complications (hyperkalaemia, pulmonary oedema, uraemia, acidaemia)
  • IV fluid for hypovolaemia (crystalloid to increase intra-vascular volume)
  • oxygen, fluid restriction +/- diuretics for hypervolemia
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14
Q

what is chronic renal failure (chronic kidney disease)

A
  • abnormalities of the kidney structure or function with implications for health
  • present for >3months
  • irreversible loss of nephrons
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15
Q

how is CKD classifies

A
  • based on the cause, GFR category and presence of albuminuria
  • GFR<15 is kidney disease
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16
Q

abnormalities of kidney functions/structure

A
  • decreases GFR
  • increased albuminuria
  • urinary sediment
  • electrolyte and other abnormalities
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17
Q

causes of CKD

A
  • acute renal failure
  • hypertension
  • diabetes
  • kidney disease (polycystic kidney disease, dysplastic kidneys, reflux or obstructive nephropathy)
  • infections
  • drugs
  • systemic disease
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18
Q

pathology of CKD

A
  • primary injury to glomeruli, vessels or the tubulo-interstitium
  • leads to reduction in nephron mass
  • haemodynamic stress on remaining nephrons causes further loss.
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19
Q

clinical manifestations of CKD

A
  • early can be asymptomatic
  • tired
  • bony pain (decalcification due to metabolic acidosis)
  • loss of appetite
  • end-stage = fluid overload and metabolic derangement
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20
Q

differential diagnoses for CKD

A
  • AKI
  • diabetic nephropathy
  • chronic glomerulonephritis
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21
Q

investigations for CKD

A
  • bloods = U&E, Hb, glucose, low calcium, high phosphate, increased PTH
  • urine dipstick = albumin:creatinine ratio, protein:creatinine ratio
  • US
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22
Q

management of CKD to slow disease progression

A
  • lower BP

- ACE inhibitor

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23
Q

treatment of complications of CKD

A
  • treat anaemia
  • sodium bicarbonate supplements if acidosis
  • restrict fluid and Na for oedema
  • vit D for bone mineral density
  • atorvastatin and antiplatelets to prevent CVD and atherosclerosis
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24
Q

renal replacement therapy

A
  • dialysis
  • transplant
  • preparation should begin when risk of renal failure is 10-20% in a year
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25
complications of CKD
- CVD from hypertension, vascular calcification, hyperlipidaemia - renal bone disease = mix of hyper-parathyroid bone disease, osteomalatia and osteoporosis
26
what is haemodialysis
- blood passed over a semi-permeable membrane against the flow of dialysis fluid - hydrostatic gradient - AV fistula - 3+ times per week
27
what is peritoneal dialysis
- uses the peritoneum as a semi-permeable membrane - catheter into peritoneal cavity and fluid infused (with osmotic agents) - drainage - at home
28
what is hemofiltration
- water cleared by positive pressure | - low haemodynamic stability so only used in critical care when BP too low for HD
29
what is glomerulonephritis
-inflammation and damage to the glomeruli which allows protein +/- blood into the urine
30
what is the condition that causes glomerulonephritis that doesn't lead to kidney failure
- minimal change disease
31
pathology of glomerulonephritis
- damage to glomerulus with leakage of proteins and blood | - may be rupture of glomerular basement membrane and a cellular reaction in the Bowman's space
32
what are the different types of GN and how do they cause damage to the glomerulus
1. immune complex GN and monoclonal immunoglobulin GN = deposition of immune complexes causes local cellular proliferation and inflammation. 2. pauci-immune GN = glomerular necrosis. 3. anti-GBM GN = Abs against the GBM 4. C3 glomerulopathy = abnormalities in the regulation of alternative complement activation with deposition of C3 in the glomerulus
33
what does GN cause
- haematuria and proteinuria - damage to glomerulus restricts blood flow; leading to compensatory hypertension - loss of filtration capacity leads to AKI
34
clinical manifestations of GN
- asymptomatic urine abnormalities (haem/proteinuria) - acute nephritis syndrome - nephrotic syndrome - CKD
35
investigations for GN
- assess cause and damage - bloods: FBC, U&E, LFT, CRP, ANCA, culture, hapatitis serology - urine: MC&S, bence jones protein, RBC casts - imaging: CXR (pulmonary haemorrhage), renal US - renal biopsy required for diagnosis.
36
what is acute nephritic syndrome
- GN - immune response triggered by an infection or other disease - podocytes develop large pores allowing blood and protein into urine. - red cell casts = distinguishing feature = formed in nephrons and indicate glomerular damage
37
what is the most common primary cause of acute nephritic syndrome
- IgA nephropathy
38
what are the symptoms of acute nephritic syndrome
- haematuria - proteinuria - hypertension - oedema - low vol of urine <300ml/day
39
what is IgA nephropathy
- immune complex GN related to glomerular deposition of immune complexes containing IgA
40
causes of IgA nephropathy
- primary = abnormal mucosal immune system produces abnormally glycosylated IgA - secondary = associated with liver disease, bowel disease and dermatitis herpetiformis. - systemic form with small-vessel vasculitis
41
what are the pathological features of IgA nephropathy
- IgA causes glomerular changes from mild mesangial hypercellularity only to glomerular hypercellularity. - crescents seen in most severe cases
42
presentation of IgA nephropathy
- asymptomatic non-visible haematuria - episodic haematuria - hypertension
43
investigations/ diagnosis of IgA nephropathy
- renal biopsy = IgA deposition in mesangium
44
treatment of IgA nephropathy
- ACE inhibitors to reduce BP and protein in urine
45
what is nephrotic syndrome
- proteinuria due to podocyte pathology = leakage from basement membrane
46
what is the triad of signs for nephrotic syndrome
- proteinuria >3.5g/24hours - hypoalbuminemia - oedema due to oncotic pressure decrease from hypoalbuminemia - severe hyperlipidaemia (liver goes into overdrive from albumin loss which increases risk of blood clots and raises cholesterol)
47
causes of nephrotic syndrome
- primary renal disease = minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN - secondary causes = DM, lupus nephritis, myeloma, amyloid, pre-eclampsia
48
pathophysiology of nephrotic syndrome
podocyte damage leads to proteinuria
49
what makes up the kidneys filtration barrier
podocytes, GBM, endothelial cells
50
presentation of nephrotic syndrome
- generalised pitting oedema to ankles, genital and abdominal wall (rapid and severe) - hypoalbuminemia - frothy urine - systemic symptoms
51
differential diagnoses for nephrotic syndrome
- congestive heart failure (oedema and raised jugular venous pressure) - cirrhosis (oedema and hypoalbuminenia)
52
investigations for nephrotic syndrome
- renal biopsy (find cause) - urine dipstick (high protein) - serum albumin low
53
management of nephrotic syndrome
- reduce oedema (fluid and salt restriction, diuretics with loop diuretics) - treat cause - ACEi/ARB reduce proteinuria
54
what are the complications of nephrotic syndrome
- thromboembolism - infection - hyperlipidaemia
55
what is the pathology of minimal change disease
- nephrotic syndrome - loss of podocyte foot processes, vacuolation, appearance of microvilli in glomerulus - proteinuria - doesn't progress to renal failure
56
investigations/diagnosis of MCD
- biopsy= electron microscope shows abnormal podocytes
57
what is the natural history of MCD
relapsing- remitting course
58
treatment of MCD
- supportive care - prednisolone (steroid) - 2nd line = cyclophosphamide or cyclosporine (immunosuppressants)
59
what is focal segmental glomerulosclerosis (FSGS)
- nephrotic syndrome - primary (genetic mutations) - secondary (HIV/ reflux nephropathy)
60
investigations for FSGS
- specific segments of certain glomeruli develop sclerosed lesions - Ab tests all negative
61
treatment for FSGS
- salt and water restriction and diuretics - antihypertensives - statins (for hyperlipidaemia) - transplant
62
what is membranous glomerulonephritis
- nephrotic syndrome - slowly progressive - usually idiopathic but can be from Hep B/ malaria/ penicillamine/SLE
63
pathology of membranous glomerulonephritis
- immune complex deposition results in complement activation against GBM proteins
64
investigations for membranous glomerulonephritis
- microscopic analysis = thickened GBM | - immunofluorescence = diffuse uptake of IgG
65
treatment of membranous glomerulonephritis
- steroids (prednisolone)
66
what is the prognosis for membranous glomerulonephritis
1/3 have chronic membranous glomerulonephritis 1/3 go into remission 1/3 progress to end-stage renal failure
67
what is polycystic kidney disease
- inherited disorder | - clusters of cysts develop primarily within kidneys = enlarge and lose function over time
68
adult (dominant) polycystic kidney disease
- mutation in PKD1 gene on chromosome 16 - defects in function of PKD1 protein leads to cystic change in renal tubules and loss of normal renal tissue. - kidneys massively enlarged and completely replaced with cysts
69
extra-renal manifestations of PKD
- liver cysts | - berry aneurysms
70
presentation of PKD
symptomatic due to size/haemorrhage - loin pain - visible haematuria - cyst infection - renal calculi - hypertension - progressive renal failure
71
investigations for PKD
- US - genetic testing - CT for renal colic
72
treatment for PKD
- 3-4 L/day water may supress growth - high BP treated to target <130/80mmHg (ACEi/ ARB first line) - treat infections - cyst decompression for severe/ persistent pain
73
infantile (recessive) PKD
- rare - causes bilateral polycystic kidneys with congenital hepatic fibrosis - mutations in the PKHD1 on chromosome 6p which encodes a component of the cilia on collecting duct epithelial cells - kidneys enlarged and numerous cysts - severe cases cause neonatal death from pulmonary hypoplasia - less severe cause congenital hepatic fibrosis and portal hypertension - poor prognosis if respiratory distress
74
treatment for infantile PKD
- continuous renal replacement therapy
75
what is renal colic
- a type of pain when urinary stones block part of your urinary tract - upper urinary tract obstruction
76
what are the symptoms of renal colic pain
- rapid onset - excruciating ureteric spasms - pain is from loin to groin - nausea and vomiting - worse with fluid loading - radiates to ipsilateral testis/labia - can't lie still

2A revision (10 decks)

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