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4TH YEAR - CSIM2 > Renal > Flashcards

Renal Flashcards

1
Q

What are the functions of the kidneys?

A

Endocrine release - epo, renin, prostaglandins
Removal of waste products - urea, drugs
Metabolism - proteins, vit D
Fluid regulation

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2
Q

What are the 3U’s that must always be remembered in investigation for renal disease?

A

U&E, urinalysis, USS

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3
Q

How is proteinuria measured?

A

Albumin:creatinine ratio (<2.5 men, <3.5 women)
24 hr collection albumin

If they have proteinuria do culture of urine

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4
Q

What is the main cause of haematuria? What are some other causes?

A
  1. Glomerular disease (>1g)
  2. Transient causes - orthostatic, exercise, fever (<1g)
  3. Tubulointerstitial disease (<1g)
  4. Upper/lower UTI (<1g)
  5. Diabetes (30-300mg)
  6. Minimal change disease (30-300mg)
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5
Q

In terms of proteinuria, what are the indications for biopsy?

A

Persisent (>3g) or alongside haematuria

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6
Q

How much blood is usually lost in the urine?

A

<1uL/day

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7
Q

What is the main cause of proteinuria? What are some other causes?

A
  1. Glomerular disease (IgA nephropathy, thin basement membrane disease)
  2. Transient causes (UTI, exercise, menstruation)
  3. Neoplasia (painless, bladder/renal)
  4. Drugs
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8
Q

Which drugs may cause haematuria?

A

Cephalosporins
Ciprofloxacin
Furosemide
NSAIDS

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9
Q

What is the 2WW criteria for haematuria?

A

Visible >45 yers
Non-visible >60yrs

Do renal USS and cystography

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10
Q

What are the normal values for glucose in the urine?

A

0-0.8mmol/L

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11
Q

What causes glycosuria?

A

DM
Pregnancy
Sepsis
Renal tubular damage

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12
Q

What causes nitrites/leucocytes in the urine?

A

UTI, high protein meal

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13
Q

What causes ketones in the urine?

A

Starvation, ketoacidosis

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14
Q

What does urine microscopy look for? What do they show?

A

CASTS
white cell casts - UTI, acute interstitial nephritis
red cell casts - glomerular bleeding, vasculitis, nephritis
epithelial casts - acute tubular necrosis

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15
Q

What factors influence creatinine levels?

A

Muscle mass
Muscle catabolism
Liver function

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16
Q

What causes high creatinine levels?

A
  • Kidney dysfunction
  • Hypertension
  • Drugs (statins)
  • Rhabdomyolysis
  • Large muscle mass
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17
Q

What are the problems associated with measuring creatinine levels?

A
  • Muscle mass
  • Log relationship to GFR ( as GFR decreases lots, creatinine only increases a little)
  • Tubular and gut secretion
  • Variability of assay
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18
Q

How is eGFR calculated?

A

Takes into account creatinine, age, gender and ethnicity

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19
Q

What is the definition of AKI?

A

A rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine and leading to a failure to maintain fluid, electrolyte and acid-base homeostasis

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20
Q

How is AKI diagnosed?

A
  • Rise in creatinine >26umol/L in 48hours
  • Rise in creatinine >1.5 x the baseline
  • Urine output <0.5ml/kg/h for 6 consecutive hours

1st line investigations - U&Es and creatinine

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21
Q

What are the symptoms of AKI?

A

Urinary - dysuria, oliguria, anuria, haematuria,
Systemic - fever, vomiting, myalgia, diarrhoea
Kidney dysfunction - oedema, bruising

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22
Q

What are the risk factors for AKI?

A
  • Age>75
  • CKD
  • Cardiac failure
  • Sepsis/infection
  • PVD
  • Chronic liver disease
  • Diabetes
  • Drugs
  • Poor fluid intake
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23
Q

Which investigations results would raise your index of suspicion for AKI secondary to CKD?

A
  • Small kidneys
  • Anaemia
  • Low calcium
  • High phosphate
  • Previous bloods
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24
Q

What investigations should be done in AKI?

A

BEDSIDE - urinalysis, BP, ECG

BLOODS - FBC, U&E, CRP, LFTs, bone profile, CK, clotting, ESR, cultures, immunoglobulins, complement, autoantibodies

IMAGING - renal USS, CXR

SPECIAL - kidney biopsy

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25
Q

What are the indications for kidney biopsy for AKI?

A

Intrinsic cause other than ATN is suspected, such as glomerulonephritis

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26
Q

How can you tell it is a pre-renal cause of AKI?

A

Restoration of blood flow will resolve the problem with no cell injury

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27
Q

What are some pre-renal causes of AKI?

A

Volume depletion - GI bleed, diarrhoea, vomiting, burns

Low CO - tamponade, massive PE, MI

Distributive - sepsis, anaphylaxis, hepatorenal, pancreatitis

Drugs - NSAIDS, contrast, antihypertensives

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28
Q

How do NSAIDs cause kidney injury?

A

Vasoconstriction of the afferent arteriole (supplying the kidney) and therefore decreased GFR

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29
Q

How do antihypertensives cause kidney injury?

A

Cause vasodilation of efferent arteriole, causing a decrease in filtration pressure, causing decreased GFR

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30
Q

What are some renal causes of AKI?

A
  1. Tubulointerstitial disease - ATN, cast obstruction, acute allergic interstitial nephritis (no haematuria/proteinuria)
  2. Glomerular disease - glomerulonephritis (haematuria, proteinuria)
  3. Microvascular - HUS, MAHA, vasculitis, microemboli
  4. Infection
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31
Q

What is the main cause of renal AKI?

A

Acute tubular necrosis - this is when ischaemia to tubular cells or exposure to a toxin causes cell death.

Patients will be oliguric first as a compensatory mechanism, but then become polyuric, as the tubules grow back.

Recovery may take weeks

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32
Q

What causes ATN?

A

Ischaemia - can progress from pre-renal AKI involving hypo perfusion

Toxins - aminoglycosides, cisplastin, contrast

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33
Q

What kind of casts can obstruct the tubules causing renal AKI?

A

Paraprotein - myeloma
Myoglobin - rhabdomyolysis
Urate - tumour lysis syndrome
Crystals - drugs, alcohol

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34
Q

What is acute interstitial nephritis?

A

Abnormal inflammatory response, often accompanied by a fever, painful joints and a rash - can cause renal AKI.

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35
Q

How is acute interstitial nephritis diagnosed?

A

White cell casts, eosinophils

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36
Q

How is acute tubular necrosis diagnosed?

A

Epithelial casts

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37
Q

What causes allergic acute interstitial nephritis?

A

NSAIDS, pencilllins, PPIs

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38
Q

What can cause glomerulonephritis?

A

Immune, drugs, infection

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39
Q

What can cause microvascular damage in intrinsic AKI?

A
  • Haemolytic uraemia syndrome - post-viral
  • MAHA - anaemia, shistocytes
  • Vasculitis - ANCA
  • Microemboli of cholesterol post angiography, causing distal necrosis
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40
Q

What are the post-renal causes of AKI?

A

Luminal - stones, clots
Mural - malignancy, BPH, strictures, fibrosis
Extrinsic compression - malignancy, retroperitoneal fibrosis
Retention - UTI, constipation

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41
Q

How is AKI managed?

A
  1. IV fluids - give boluses then assess
  2. Stop nephrotoxic drugs
  3. Monitor (fluid status, U&E)
  4. Treat sepsis
  5. Give inotropes if low BP
  6. Treat cause
  7. Manage complications
  8. Dialysis
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42
Q

Which nephrotoxic drugs need to be stopped in AKI?

A

NSAIDS, antihypertensives, gentamicin, metformin, morphine

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43
Q

How do you treat a pre-renal cause of AKI?

A

IV fluids, abx, inotropes

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44
Q

How do you treat an intrinsic cause of AKI?

A

Refer to nephrology

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45
Q

How do you treat a post-renal cause of AKI?

A

DO USS, catheterize, CTKUB, relieve obstruction

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46
Q

What complications might arise secondary to AKI, and how can they be managed?

A

Hyperkalaemia - IV calcium gluconate, salbutamol, dextrose and insulin, sodium bicarb, fluids

Pulmonary oedema secondary to fluid retention - MONA

Uraemia - dialysis

Metabolic acidosis - sodium bicarb, dialysis

NB any of these complications could be an indication for dialysis

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47
Q

What is the pathophysiology of glomerulonephritis, and how does this lead to AKI?

A
  1. Damage to the glomerulus restricts blood flow, leading to compensatory rise in BP
  2. Damage to the filtration mechanisms from rise in BP, allows protein and blood to enter the urine
  3. Loss of usual filtration capacity, leading to AKI
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48
Q

How do patients with glomerulonephritis present?

A
  • Hypertension
  • Proteinuira/haematuria
  • AKI or other renal impairment
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49
Q

What is a nephritic picture?

A
  • Inflammatory
  • Blood + protein on urine
  • Very high BP and low eGFR
  • Implies immune pathology
  • Rarely pain
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50
Q

What are the primary cause of nephritis?

A
  • IgA nephropathy

- Mesangiocapillary glomerulonephritis

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51
Q

What are the secondary causes of nephritis?

A
  • Goodpastures syndrome
  • SLE
  • Vasculitis
  • Post-strep infection
  • HSP
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52
Q

What is a nephrotic picture?

A
  • Disturbance of permeability barrier
  • Triad of proteinuria, hypo albumin and oedema
  • Protein ++++ on urine
  • Rarely pain
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53
Q

What are the primary causes of nephrotic syndrome?

A
  • Minimal change disease
  • Focal and segmental glomerulosclerosis
  • Membranous
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54
Q

What are the secondary causes of nephrotic syndrome?

A
  • Diabetes
  • SLE
  • Amyloidosis
  • HepB/C
  • Drugs
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55
Q

Describe the normal structure of the glomerular filtration barrier

A

3 layers of filtration, all negatively charged to repel plasma proteins:

  1. Fenestrated capillary endothelium, made from podocalyxin (50-100nm holes)
  2. Thick basement membrane, made from heparan sulphate proteoglycans
  3. Filtration slits in between the interdigitating processes of the podocytes (4-14nm)

These ensure that large molecules are not filtered out

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56
Q

What is the pathophysiology of IgA nephropathy, and how is it diagnosed??

A

At times of infection, IgA deposits in the kidney and attacks the glomeruli.

Diagnosis

  • Increased IgA and C3 on immunofluorescnece
  • Mesangial proliferation on renal biopsy
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57
Q

What are the clinical features of IgA nephropathy?

A

Typically young patient with episodic macroscopic haematuria and rapid recover, at times of illness

58
Q

How is IgA nephropathy managed?

A

Good BP control with ACEis

Immunosuppression

59
Q

What is the pathophysiology of HSP and how is it diagnosed?

A

Small vessel vasculitis due to deposition of IgA complexes, post infection (type of IgA nephropathy)

Diagnosis

  • Usually clinical
  • Increased IgA and C3 on IF
60
Q

What are the clinical features of HSP?

A

Post-viral, abdo pain, purpuric rash on extensor surfaces and buttocks, polyarthritis

61
Q

How is HSP managed?

A

Usually self-limiting

62
Q

What is the pathophysiology of SLE and how is it diagnosed?

A

Autoantibodies cause tissue damage via immune complex formation and complement activation

Diagnosis

  • Anti-dsDNA, ANA, anti-Sm antibodies
  • Low C3/4 on IF
  • Presence of cellular casts on microscopy
63
Q

What are the clinical features of SLE?

A

Varied - malar rash, photosensitivity, alopecia, oral ulcers, malaise, arthritis, raynauds, nephritis, relapsing/remitting course etc

64
Q

How is SLE managed?

A
  • Steroids
  • Immunosuppresion
  • Dialysis/transplant
65
Q

What is the pathophysiology of Anti-GBM disease (good pastures) and how is it diagnosed?

A

Type II hypersensitivity reaction in which IgG is formed against against type IV collagen, found in the BM of the kidneys and the lungs

Diagnosis

  • Anti-GBM antibodies
  • Kidney biopsy - shows crescents (this is more of a prognostic investigation)
  • Also do CXR to look for lung involvement
66
Q

What are the clinical features of Anti-GBM disease?

A

AKI, haematuria and lung haemorrhage

67
Q

How is Anti-GBM disease managed?

A
  • Immunosuppresion
  • Steroids
  • Plasmaphoresis to remove antibodies
68
Q

What are crescents?

A

They are a marker of severity of renal damage, representing infiltration of the Bowmans space with cells and inflammatory mediators

They indicate rapidly progressive nephritis

69
Q

Which small vessel vasculitis can cause glomerulonephritis? How are they diagnosed?

A
  • Wegeners (granulomatous polyangitis ) - cANCA, RP3
  • Microscopic polyangitis - pANCA, MPO
  • Eosinophilic polyangitis (Churg Strauss) - pANCA, MPO
70
Q

Which small vessel vasculitis is associated with:

a) ENT/URTI problems
b) rapidly deteriorating kidney function
c) asthma

A

a) Wegeners (granulomatous)
b) Microscopic
c) Eosinophilic (churg strauss)

71
Q

What is the pathophysiology of post-strep glomerulonephritis and how is it diagnosed?

A

Generally self-limiting immune complex deposition in the kidney 1-4 weeks after a pharyngeal infection (typically with strep pyogenes)

Diagnosis
- Antistreptolysin O antibodies

72
Q

What are the clinical features of post-strep glomerulonephritis?

A

Slight fever, nausea, smoky-brown urine

73
Q

What is the diagnostic criteria for nephrotic syndrome?

A
  1. Proteinuria (>3.5g/24h or ACR>250)
  2. Hypoalbuminuria (<25)
  3. Oedema

You also often get severe hyperlipidemia (TC>10mmol/L) due to overproduction of the liver to compensate for low protein

74
Q

What are the signs and symptoms of nephrotic syndrome?

A

Severe oedema
Frothy urine
Wight gain

75
Q

What is the pathology of minimal change disease and how is it diagnosed?

A

T cells release a cytokine that injures the processes of podocytes

Diagnosis
- Nothing seen at microscopy (‘minimal change’) so need to do electron microscopy which would show foot effacement

76
Q

What are the causes of minimal change disease?

A

Idiopathic, drug associated, lymphoma

77
Q

What is the pathology of membranous nephropathy and how is it diagnosed?

A

Immune deposition and spike formation due to autoantibodies against epithelial cell receptor PHOSPHOLIPASE A2

Diagnosis

  • Diffusely thick GBM without hyper proliferation of cells
  • IgG and C3 increased on IF
78
Q

What is the pathology of membranous nephropathy and how is it diagnosed?

A

Immune deposition and spike formation due to autoantibodies against epithelial cell receptor PHOSPHOLIPASE A2

Diagnosis

  • Diffusely thick GBM without hyper proliferation of cells
  • IgG and C3 increased on IF
79
Q

What is the pathology of FSGS and how is it diagnosed?

A

Sclerosis of certain areas of the glomerulus

Diagnosis

  • Increase in hyalin, collagen and fat cells on biopsy (segmental pattern)
  • IgM, C3 increased in certain areas
80
Q

What are the causes of FSGS?

A

Idiopathic, malignancy, obesity, HIV (poor prognosis), alport syndrome, heroine use

81
Q

What are the complications of nephrotic syndrome?

A
  • Increased susceptibility to infection
  • Thromboembolsim due to increased production of clotting factors
  • Hyperlipidemia

NB - renal function may be normal in bloods

82
Q

How is nephrotic syndrome managed?

A

1st line - Reduce oedema - diuretics

  1. Reduce proteinuria - ACEi/ARB
  2. Reduce complication risk - anticoagulants, statins
  3. Treat cause - immunosuppression, steroids

Dont recommend bed rest as patients are already in a hyperthrombotic state

83
Q

What is the main cause of CKD? What else causes it?

A
  1. Diabetes
  2. Hypertension
  3. Glomerular disease
  4. Other - urinary obstruction, inherited disease
84
Q

How does diabetes cause CKD?

A
  • Mesangial expansion due to hyperglycaemia
  • GBM thickening
  • Sclerosis due to intraglomerular hypertension
85
Q

How does hypertension cause CKD? (and vice versa)

A

Thick vessels encroach on the lumen, leading to decreased renal perfusion. This has numerous effects:

  • activates the RAAS system which further increases BP
  • decreases GFR causing sodium retention, which increases BP

ie. it is a cycle!!

86
Q

What is the pathophysiology of CKD?

A
  • Various causes lead to expansion, proliferation and eventual fibrosis and scarring of nephrons
  • This causes irreversible loss of nephrons
  • Remaining nephrons have to work harder to maintain renal function
  • This leads to up regulation of the RAAS and further damange and fibrosis
  • The end result is widespread GLOMERULOSCLEROSIS and TUBULOINTERSTITIAL FIBROSIS
87
Q

What are the symptoms of CKD?

A

Often asymptomatic

May present stage 4/5 with weight loss, oedema, SOB, fatigue, itch, neuropathy, pallor, uraemia etc

88
Q

What investigations should be done if you suspect CKD?

A

FIRST CHECK PREVIOUS KIDNEY RESULTS - NEED TO COMPARE

  1. Bedside - urinalysis (ACR, mc&s)
  2. Bloods - FBC, glucose, U&E, ESR, calcium (low), phosphate (high) , PTH (high)
  3. Imaging - USS (<9cm kidneys), APKD, MRangiogram
  4. Special - histology
89
Q

What are the indications for kidney biopsy?

A

Unclear cause and normal sized kidneys on USS

90
Q

How is kidney disease staged?

A 
According to GFR
1  >90
2  >60
3a  >45
3b  >30
4  >15
5 - 0-15

Stage 4/5 - refer to nephrologist

91
Q

How can you stop progression of CKD?

A
  1. Treat underlying cause
  2. BP control
  3. ACEis for proteinuria
  4. Glycaemic control
  5. Low salt diet
  6. Lifestyle
  7. Reduce CVS risk (aspirin, statins)
92
Q

What BP should you aim for in CKD?

A

<140/90 (or<130/80 if ACR>30mg/mol)

Higher ACR indicates worse disease

93
Q

What are the symptoms of uraemia and how can it be treated?

A

Fatigue, appetite loss, itch, nausea (non-specific)

Treat with dialysis

94
Q

What are the symptoms of oedema and how can it be treated?

A

Breathlessness, hypertension

Treat with diuretics, ACEis/ARBs

95
Q

What are the symptoms of hyperkalemia and how can it be treated?

A

Arrhythmia, sudden death

Treat with IV calcium gluconate, salbutamol, dextrose and insulin, sodium bicarbonate and fluids

96
Q

What are the symptoms of acidaemia and how can it be treated?

A

Fatigue

Treat with sodium bicarbonate, dialysis

97
Q

What are the symptoms of hyperphosphataemia and how can it be treated?

A

Itch, bone disease

Treat with phosphate binders, diet restriction (no milk, dairy, eggs) and vit D analogues

98
Q

What are the symptoms of anaemia and how can it be treated?

A

Fatigue, pallor etc (this is due to decreased epo production)

Treat with epo replacement and iron

99
Q

What are the symptoms of hyperparathyroidism and how can it be treated?

A

Osteoporosis, bone disease

Treat with hydroxylated vit D (can’t be normal form as kidney can’t metabolise it)

100
Q

What is the biggest cause of mortality in CKD?

A

Cardiovascular complications

101
Q

What are the indications for dialysis?

A 
Chronic - GFR<10ml/min 
ACUTE - AEIOU
Acidosis
Electrolyte imbalance
Intoxicants 
Overload/oedema
Uraemic symptoms
102
Q

What are the symptoms of uraemia?

A

Fatigue, pericarditis, bleeding, nausea and vomiting

103
Q

How does dialysis work?

A

Filters out toxin urea and electrolytes by maintaining a diffusion gradient, allowing solutes to diffuse across a semi-permeable membrane.

Essentially acts as an artificial glomerular basement membrane??

104
Q

How does haemodialysis work?

A

Blood is circulated outside the body - 4 hours, 3 times a week

Risk of infection at entry site

105
Q

How do you access circulation in haemodialysis?

A

Artifical AV fistula (permanent)

Central venous catheter (temp)

106
Q

How does peritoneal dialysis work?

A

Uses the peritoneum as a semi-permeable membrane - continuous or overnight

Risk of peritonitis

107
Q

How do you access circulation in peritoneal dialysis?

A

Use a Tenckhoff catheter

108
Q

What is the gold standard treatment for kidney failure and why?

A

Kidney transplant - improves survival, corrects metabolic acidosis and is cost-effective

109
Q

What are the requirements for transplant?

A

Patient must be fit (no chronic infection, malignancy, CVS disease)

110
Q

What is the diagnostic criteria of haemolytic uraemic syndrome?

A

Triad of:

  • Haemolytic anaemia
  • AKI
  • Thrombocytopenia
111
Q

What are the features of HUS?

A
  • Commonly affects children (most common cause of AKI in kids)
  • Usually preceded by E.coli infection (diarrhoea)
  • Thrombotic microangiopathy (thrombosis in small vessels)
112
Q

What is the definition for UTI?

A

> 10^5 organisms per mL of fresh MSU

113
Q

What are the symptoms of UTI?

A

Lower - dysuria, lower back pain, frequency

Upper - fever, rigors, vomiting, loin pain

114
Q

What is lower and upper UTI?

A

Lower - cystitis urethritis, prostatitis

Upper - pyelonephritis

115
Q

What is the difference between a complicated and uncomplicated UTI?

A

Complicated - abnormal renal tract, virulent organism, pregnant, obstruction, abnormal function

Uncomplicated - normal renal tract

116
Q

How is UTI diagnosed?

A

Leucocytes and nitrites on urine dip

117
Q

What organisms most commonly cause UTI?

A

E.coli

Proteus mirabilis

118
Q

What are the RF for UTI?

A
  • Sex
  • Pregnancy
  • Catheter
  • Condom use
  • Menopause
  • Kidney stones
119
Q

How is UTI treated?

A

Uncomplicated - 3 days trimethoprim/nitrofurantoin

Complicated - 7 day course

Only treat if symptomatic!!

120
Q

How is UTI treated in pregnancy?

A

1st trim - can’t give trimethoprim
3rd trim - can’t give nitrofurantoin

Amoxicillin fine always, always treat, even if asymptomatic

121
Q

How is UTI treated in men?

A

Quinolone, will need imaging as it could indicate structural problem

122
Q

How is UTI treated in pregnancy?

A

1st trim - can’t give trimethoprim
3rd trim - can’t give nitrofurantoin

Cephalexin/amoxicillin fine always (although growing resistance to amoxicillin)
Always treat, even if asymptomatic

123
Q

What would haematuria from bladder pathology be like?

A

Through voiding

124
Q

What would haematuria from prostate pathology be like?

A

End of voiding

125
Q

What would haematuria from urethral pathology be like?

A

Beginning of voiding

126
Q

Which investigation is best for detecting kidney stones?

127
Q

What investigations is best for detecting renal artery stenosis?

128
Q

What are some signs of diabetic nephropathy?

A

Normocytic anaemia
Proteinuria
High ESR

129
Q

What is the classic presentation of bladder cancer?

A

Painless, gross haematuria throughout voiding

130
Q

What is the classic presentation of renal cell carcinoma?

A

Triad of:

  • Haematuria
  • Flank pain
  • Abdo/flank mass

Non specific symptoms

131
Q

What is the best
a)initial
b)diagnostic
investigation for PCKD?

A

a) Abdo USS

b) MRI??

132
Q

What is Alport syndrome?

A

A genetic defect in synthesis of type IV collagen causing:

  • hereditary nephritis
  • sensorineural deafness
  • ocular abnormalities - ‘retinal fleeks’ and cataracts
133
Q

What is the best investigation for renal artery stenosis?

A

Renal arteriography - can show the exact location of the occlusion
Uses radiological dyes which are then detected using xray

134
Q

What is a common complication of bladder cancer?

A

Bilateral hydronephrosis - due to obstruction to urine-outflow, creating a back pressure upon the kidneys

135
Q

What is the best way to monitor renal function following a diagnosis of diabetes?

A

Microalbuminuria

136
Q

What is the best management for minimal change disease?

A

Steroids eg. oral prednisolone

137
Q

What are the characteristic biopsy changes in diabetic nephropathy?

A

Kimmel-Stiel nodules

138
Q

What HbA1c should you aim for in CKD?

139
Q

What are the 2 most useful tests for looking for the cause of AKI?

A

Urinalysis

Urine microscopy

140
Q

Positive MBO?

A

Microscopic polyangitis

COCAINE

141
Q

In CKD how should you measure iron stores?

A

Transferrin

142
Q

How should you usually measure iron stores?

4TH YEAR - CSIM2 (20 decks)

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