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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
Q

complications of CKD

A
  • CVD from hypertension, vascular calcification, hyperlipidaemia
  • renal bone disease = mix of hyper-parathyroid bone disease, osteomalatia and osteoporosis
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26
Q

what is haemodialysis

A
  • blood passed over a semi-permeable membrane against the flow of dialysis fluid
  • hydrostatic gradient
  • AV fistula
  • 3+ times per week
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27
Q

what is peritoneal dialysis

A
  • uses the peritoneum as a semi-permeable membrane
  • catheter into peritoneal cavity and fluid infused (with osmotic agents)
  • drainage
  • at home
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28
Q

what is hemofiltration

A
  • water cleared by positive pressure

- low haemodynamic stability so only used in critical care when BP too low for HD

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29
Q

what is glomerulonephritis

A

-inflammation and damage to the glomeruli which allows protein +/- blood into the urine

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30
Q

what is the condition that causes glomerulonephritis that doesn’t lead to kidney failure

A
  • minimal change disease
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31
Q

pathology of glomerulonephritis

A
  • 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
Q

what are the different types of GN and how do they cause damage to the glomerulus

A
  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
Q

what does GN cause

A
  • haematuria and proteinuria
  • damage to glomerulus restricts blood flow; leading to compensatory hypertension
  • loss of filtration capacity leads to AKI
34
Q

clinical manifestations of GN

A
  • asymptomatic urine abnormalities (haem/proteinuria)
  • acute nephritis syndrome
  • nephrotic syndrome
  • CKD
35
Q

investigations for GN

A
  • 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
Q

what is acute nephritic syndrome

A
  • 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
Q

what is the most common primary cause of acute nephritic syndrome

A
  • IgA nephropathy
38
Q

what are the symptoms of acute nephritic syndrome

A
  • haematuria
  • proteinuria
  • hypertension
  • oedema
  • low vol of urine <300ml/day
39
Q

what is IgA nephropathy

A
  • immune complex GN related to glomerular deposition of immune complexes containing IgA
40
Q

causes of IgA nephropathy

A
  • 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
Q

what are the pathological features of IgA nephropathy

A
  • IgA causes glomerular changes from mild mesangial hypercellularity only to glomerular hypercellularity.
  • crescents seen in most severe cases
42
Q

presentation of IgA nephropathy

A
  • asymptomatic non-visible haematuria
  • episodic haematuria
  • hypertension
43
Q

investigations/ diagnosis of IgA nephropathy

A
  • renal biopsy = IgA deposition in mesangium
44
Q

treatment of IgA nephropathy

A
  • ACE inhibitors to reduce BP and protein in urine
45
Q

what is nephrotic syndrome

A
  • proteinuria due to podocyte pathology = leakage from basement membrane
46
Q

what is the triad of signs for nephrotic syndrome

A
  • 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
Q

causes of nephrotic syndrome

A
  • primary renal disease = minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN
  • secondary causes = DM, lupus nephritis, myeloma, amyloid, pre-eclampsia
48
Q

pathophysiology of nephrotic syndrome

A

podocyte damage leads to proteinuria

49
Q

what makes up the kidneys filtration barrier

A

podocytes, GBM, endothelial cells

50
Q

presentation of nephrotic syndrome

A
  • generalised pitting oedema to ankles, genital and abdominal wall (rapid and severe)
  • hypoalbuminemia
  • frothy urine
  • systemic symptoms
51
Q

differential diagnoses for nephrotic syndrome

A
  • congestive heart failure (oedema and raised jugular venous pressure)
  • cirrhosis (oedema and hypoalbuminenia)
52
Q

investigations for nephrotic syndrome

A
  • renal biopsy (find cause)
  • urine dipstick (high protein)
  • serum albumin low
53
Q

management of nephrotic syndrome

A
  • reduce oedema (fluid and salt restriction, diuretics with loop diuretics)
  • treat cause
  • ACEi/ARB reduce proteinuria
54
Q

what are the complications of nephrotic syndrome

A
  • thromboembolism
  • infection
  • hyperlipidaemia
55
Q

what is the pathology of minimal change disease

A
  • nephrotic syndrome
  • loss of podocyte foot processes, vacuolation, appearance of microvilli in glomerulus
  • proteinuria
  • doesn’t progress to renal failure
56
Q

investigations/diagnosis of MCD

A
  • biopsy= electron microscope shows abnormal podocytes
57
Q

what is the natural history of MCD

A

relapsing- remitting course

58
Q

treatment of MCD

A
  • supportive care
  • prednisolone (steroid)
  • 2nd line = cyclophosphamide or cyclosporine (immunosuppressants)
59
Q

what is focal segmental glomerulosclerosis (FSGS)

A
  • nephrotic syndrome
  • primary (genetic mutations)
  • secondary (HIV/ reflux nephropathy)
60
Q

investigations for FSGS

A
  • specific segments of certain glomeruli develop sclerosed lesions
  • Ab tests all negative
61
Q

treatment for FSGS

A
  • salt and water restriction and diuretics
  • antihypertensives
  • statins (for hyperlipidaemia)
  • transplant
62
Q

what is membranous glomerulonephritis

A
  • nephrotic syndrome
  • slowly progressive
  • usually idiopathic but can be from Hep B/ malaria/ penicillamine/SLE
63
Q

pathology of membranous glomerulonephritis

A
  • immune complex deposition results in complement activation against GBM proteins
64
Q

investigations for membranous glomerulonephritis

A
  • microscopic analysis = thickened GBM

- immunofluorescence = diffuse uptake of IgG

65
Q

treatment of membranous glomerulonephritis

A
  • steroids (prednisolone)
66
Q

what is the prognosis for membranous glomerulonephritis

A

1/3 have chronic membranous glomerulonephritis
1/3 go into remission
1/3 progress to end-stage renal failure

67
Q

what is polycystic kidney disease

A
  • inherited disorder

- clusters of cysts develop primarily within kidneys = enlarge and lose function over time

68
Q

adult (dominant) polycystic kidney disease

A
  • 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
Q

extra-renal manifestations of PKD

A
  • liver cysts

- berry aneurysms

70
Q

presentation of PKD

A

symptomatic due to size/haemorrhage

  • loin pain
  • visible haematuria
  • cyst infection
  • renal calculi
  • hypertension
  • progressive renal failure
71
Q

investigations for PKD

A
  • US
  • genetic testing
  • CT for renal colic
72
Q

treatment for PKD

A
  • 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
Q

infantile (recessive) PKD

A
  • 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
Q

treatment for infantile PKD

A
  • continuous renal replacement therapy
75
Q

what is renal colic

A
  • a type of pain when urinary stones block part of your urinary tract
  • upper urinary tract obstruction
76
Q

what are the symptoms of renal colic pain

A
  • 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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