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Y3 med old > RENAL MEDICINE > Flashcards

RENAL MEDICINE Flashcards

1
Q

What blood tests may you order to investigate a patient’s renal function? (For each you can think of, state what you might be looking for. )

A

FBC - signs of anaemia, infection
Haematinics - iron, folate, b12 deficiency
U&E - Potassium, urea, creatine, bicarbonate
Bone profile - Calcium, phosphate, PTH, Alkaline Phosphatase, Albumin
CRP - Infection, Inflammation
HbA1c - diabetic control

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2
Q

What urinary tests may you order to investigate a patient’s renal function? (For each you can think of, state what you might be looking for. )

A

Urine dipstick - infection (leukocytes, nitrites), any pathology of glomerulus (blood, protein)
Urine protein:creatinine ratio - quantifies amount of protein in urine
Urine albumin:creatinine ratio - quantifies amount of albumin
Urine microscopy, culture and sensitivity (MC&S)

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3
Q

What imaging may you order to investigate a patient’s renal function?

A

US KUB - good for peri-nephric (i.e. around the kidney) collections, size of the kidneys, corticomedullary differentiation, hydronephrosis

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4
Q

What would VBG show for metabolic acidosis?

A

pH would be low
Bicarb would be low
pCO2 would be normal (maybe low if compensation)

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5
Q

What would VBG show for metabolic alkalosis?

A

pH would be high
Bicarb would be high
pCO2 would be normal

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6
Q

What causes metabolic alkalosis?

A

GI losses - vomiting.
Renal losses - primary hyperaldosteronism, tubular transporter defects, diuretics
Intracellular shifts - Hypokalaemia

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7
Q

What is a normal anion gap range?

A

8-12

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8
Q

What are specific causes of metabolic acidosis? (Split into causes of lactic acidosis, ketoacidosis, GI losses, renal losses and toxins)

A

Lactic acidosis - due to sepsis, anaerobic exercise, organ ischaemia
Ketoacidosis - diabetic, starvation, alcohol abuse
GI losses of bicarb - diarrhoea
Renal losses of bicarb - renal tubular acidosis, Addison’s
Toxins - Aspirin, Isoniazid (used in TB), see others on pg5 of booklet

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9
Q

Why may a patient have a metabolic acidosis? (HINT: 2 main overarching reasons)

A

Due to having increased acid OR acidosis due to reduced alkali

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10
Q

What are RF for AKI?

A

DM
CKD
IHD, CCF (congestive heart/cardiac failure),CVD
Liver disease
Elderly 75+ (Z2F says 65+)
Sepsis
Cognitive impairment
Nephrotoxic Meds - ACEi, ARBs, NSAIDs, Abx
Use of contrast medium e.g. during CT scans

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11
Q

How many stages of AKI are there?

A

3

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12
Q

How can causes of AKI be grouped?

A

Pre renal
Intrinsic
Postrenal

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13
Q

Name pre renal causes of AKI

A

Z2F: Dehydration, Hypotension(shock), HF

Renal Booklet: Hypovolameia
Decreased cardiac output
Decreased effective circulating volume - in CCF, Liver failure
Impaired renal autoregulation - due to NSAIDs, ACEi, ARBs, Cyclosporine

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14
Q

Name intrinsic/renal causes of AKI

A

Z2F: Glomerulonephritis, Interstitial nephritis, Acute Tubular necrosis

Renal booklet: Acute glomerulonephritis
Ischamia
Sepsis / infection
Vasculitis
Malignant HTN
Nephrotoxins - e.g contrast, haemolysis, cisplatin, aminoglycosides e.g. gentamicin

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15
Q

Name post renal causes of AKI

A

Z2F: kidney stones, masses, ureter or urethral strictures, BPH, prostate cancer

Renal booklet: Bladder outlet obstruction e.g. renal calculi, BPH
Pelvoureteral obstruction

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16
Q

What is the most important investigation in suspected AKI?

A

URINE DIP - look for abnormal proteins and blood
(This is according to renal booklet)

Z2F: Urinalysis - protein and blood (for acute nephritis), leucocytes and nitrites (for infection), glucose (for diabetes)

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17
Q

What investigations would you want to do in patient with suspected AKI?

A

Urine dip
FBC, U&E, LFTs, bone profile, CRP
Urine PCR, Urine MC&S,
USS KUB - look for obstruction

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18
Q

Potential presenting complaint in AKI

A

Symptoms: Nausea, vomiting, diarrhoea, tiredness/fatigue, changes to urine colour

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19
Q

How is AKI managed?

A

Treat underlying cause (prerenal, itrinsic, post renal). Send off investigations
Stop any nephrotoxic agents
Dehydrated? IV fluids
Overloaded? Diuretics
Monitor urine output (catheterise if needed) and daily bloods
Avoid hyperglycaemia

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20
Q

What are indications for renal replacement therapy?

A

Hyperkalaemia even after medical therapy
Metabolic acidosis even after medical therapy
Fluid overload which is not helped by diuretics
Uraemic pericarditis
Uraemic encephalopathy
Intoxications

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21
Q

What is uraemia?

A

High urea.

Waste products that should be removed via urination accumulate in the blood. This is due to reduced kidney function

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22
Q

What are signs of uraemic encephalopathy?

A

Vomiting, confusion, drowsiness, reduced consciousness

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23
Q

What triad of signs are characteristic of nephrotic syndrome?

A

Oedema
Albumin <30
Unine PCR (protien:creatinine ratio) >350 aka more than 3.5g/24hrs

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24
Q

What are the complications of nephrotic syndrome?

A

Higher risk of infection
VTE
Progression to CKD
Hypertension
Hyperlipidaemia

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25
Q

What can cause nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis
Amyloidosis, Myeloma, DM

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26
Q

Who does minimal change disease affect?

A

Children under 6yrs.

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27
Q

Describe the pathophysiology of membranous glomerulonephritis

(AR of Urinary module)

A

Subepithelial deposition of immune complexes - i.e. these deposit between the basement membrane and podocytes.

This causes thickening of the BM

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28
Q

What conditions can predispose to secondary focal segmental glomerulosclerosis?

A

Sickle cell disease
HIV
Heroin abuse
Kidney hyper perfusion

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29
Q

Define AKI

A

An acute drop in kidney function

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30
Q

How is AKI diagnosed?

A

By measuring the serum creatinine

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31
Q

What are NICE criteria for AKI?

A

Rise in creatinine of 25< micromol/L in 48hrs
Rise in creatinine of 50%< in 7 days
Urine output of <0.5ml/kg/hr for more than 6 hours

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32
Q

What are complications of AKI?

A

Hyperkalaemia
Fluid overload, HF, pulm oedema
Metabolic acidosis
Ureaemia

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33
Q

What are features of nephritic syndrome?

A

Haematuria
Oliguria
Proteinuria <3.5g/24hr
Fluid retention
Its may also have hypertension

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34
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy aka Berger’s disease

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35
Q

What is the most common cause of nephrotic syndrome in:

a) children?
b) adults?

A

a) Minimal change disease
b) Focal segmental glomerulosclerosis or in older people = diabetes

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36
Q

A patient with post-streptococcal glomerulonephritis may have ____what?____ in their recent PMH?

Hint: there are 2.

A

1-2 weeks after tonsillitis/pharyngitis
3-4 weeks after impetigo/cellulitis

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37
Q

What are main treatments for most types of glomerulonephritis?

A

Immunosupression using steroids
Blood pressure control - ACEi/ARBs

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38
Q

A patient has IgA nephropathy. What may be present in their PMH?

A

URTI: 1-2 days ago
GI infection
Strenuous exercise

Associated with: alcoholic cirrhosis

coeliac disease/dermatitis herpetiformis

Henoch-Schonlein purpura

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39
Q

In what age groups do Goodpastures syndrome incidence peak?

A

30s - usually male
60+ - usually female

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40
Q

What is the pathophyisology of Goodpastures Syndrome?

A

Antibodies against type 4 collagen (in glomerular basement membrane) develop .

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41
Q

What are complications of Goodpastures?

A

Pulmonary haemorrhage
Rapidly progressive glomerulonephritis

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42
Q

Define CKD

A

Chronic kidney damage which is permanent and progressive.
Have:
- abnormal albumin excretion / decreased kidney function
- present for more than 3 months

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43
Q

What can cause CKD?

A

DM, HTN, age (decline as age +), glomerulonephritis, polycystic kidney disease, medications - NSAIDs, PPIs, lithium. Obstructive nephropathy. Recurrent pyelonephritis

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44
Q

What are RF for CKD?

A

Older age, HTN, DM, smoking, medications which affect kidney

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45
Q

How does CKD present?

A

Asymptomatic
Pruritis (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN

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46
Q

What investigations would you do for suspected CKD?

A

1) U&Es - to check eGFR. Need to be 2 tests 3 months apart to confirm ddx of CKD
2) Urinanalysis - urine albumin:creatinine ratio. >3mg/mmol is significant
3) Urine dipstick - haematuria
4) Renal USS

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47
Q

A patient has haematuria. What are your differentials?

A

Bladder cancer, prostate cancer, CKD, kidney stones, UTI, pylenonephritis, period, acute protastitis, BPH, trauma (depends on context of hx)

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48
Q

Write out/speak aloud stages of CKD (the G score):
G1 = eGFR ?
G2 = eGFR ?
G3a = eGFR ?
G3b = eGFR ?
G4 = eGFR ?
G5 = eGFR ?

A

G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15

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49
Q

In CKD, what is the A score based on?

A

The ALBUMIN: creatinine ratio

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50
Q

What are the stages involved in the A score in proteinuria?
A1 = ?
A2 = ?
A3 = ?

A

A1 = <3mg/mmol so normal to mildly increased
A2 = 3-30mg/mmol so moderately increased
A3 = 30+ mg/mmol so severely increased

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51
Q

What eGFR is needed for a diagnosis of CKD?

A

less than 60

OR proteinuria has to be present

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52
Q

What are complications of CKD?

A

Anaemia of chronic disease
Renal bone disease
CVD = number 1 cause of mortality!!!
Hyperparathyroidism (secondary or tertiary)
HTN
Malnutrition
Dialysis related problems

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53
Q

Who is needed in MDT meeting to manage patients with CKD?

A

Renal physicians
GPs
Renal specialist nurses/home care teams
Dieticians
Pharmacists
Vascular/Transplant surgeons

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54
Q

What are main aims of management in CKD?

A

Slow progression of disease
Reduce CVD risk
Reduce risk of complications
Treat complications

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55
Q

What can be implemented to slow down progression of CKD?

A

Optimising diabetic control
Optimising HTN control
Treat infections promptly
Immunosuppression for GN

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56
Q

How to reduce the risks of CKD complications?

A

Main complication is CVD, so advice on this is appropriate:

  • Exercise, weight loss/maintain healthy weight,
  • Stop smoking
  • control BP - so dietary advice regarding sodium and water intake (+potassium and phosphate)
    -Advise on starting statin
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57
Q

What dose of atorvastatin is offered for primary prevention of CVD?

A

20mg

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58
Q

Why do potassium levels need to be monitored in patient with CKD?

A

CKD can cause hyperkalaemia
ACEi used to treat HTN in CKD also cause hyperkalaemia

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59
Q

Describe how CKD causes anaemia

(the main reasoning taught in Urinary module)

A

Kidney cells produce erythropoietin (EPO)
EPO is a hormone that stimulates production of RBC

In CKD, kidney cells are damaged = can not produce as much EPO = can not produce as many RBC = anaemia

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60
Q

How can anaemia in CKD be managed?

A

Measure haematincis - Vit B12, folate, ferritin, iron, transferrin saturation, reticulocyte Hb. If deficient in any of these, replace these first.

  • Note: IV iron may be better tolerated than PO

If this does not treat anaemia, discuss with renal team to offer EPO stimulating agents - e.g. exogenous EPO

Aim for Hb of 100-120

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61
Q

What features may be present in CKD MBD (mineral bone disease)?

A

Osteomalacia
Osteoporosis
Osteosclerosis `

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62
Q

CKD MBD is a complication of CKD. How would you manage this?

A

Vit D

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63
Q

ESRD is a complication of CKD. How would you manage this?

A

Dialysis
Renal transplant

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64
Q

What is the most important antigen to match in renal transplant?

A

HLA-DR

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65
Q

How does Anti-glomerular basement membrane disease (Goodpastures) present?

A

Typically with haemoptysis + AKI/proteinuria/haematuria

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66
Q

How does an acute graft rejection present?

A

Presents like infection: fever, rigors Usually picked up by rising creatinine, pyuria and proteinuria

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67
Q

What part of the kidney does Nephrotic syndrome affect?

A

Glomerulus or Bowman’s capsule

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68
Q

What does proteinuria and/or haematuria indicate?

A

Damage to the glomerulus

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69
Q

A patient is losing > to 3g in 24hrs of protein in their urine. what conditions could it be?

A

Diseases that cause Nephrotic syndrome:
Diabetes
Minimal changes disease
Membranous
Focal segmental glomerular sclerosis
Amyloid

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70
Q

What is nephrotic syndrome symptoms?

A

Oedema- often periorbital swelling
Proteinaemia (> 3g in 24hrs)
Hypoalbuminaemia

Hyperlipidaemia
Hypercoagulable state

71
Q

What is nephrotic syndrome proteinuria range?

A

> 3g in 24hrs

72
Q

What are nephritic syndrome symptoms?

A

Haematuria
Proteinuria (less than 3g over 24hrs)
Hypertension

73
Q

What diseases present with nephritic syndrome?

A

IgA nephropathy
Lupus
Mesangial proliferative glomerulonephritis
Vasculitis

74
Q

What is the difference between nephrotic and nephritic syndrome?

A

Both manifestations of glomerulonephritis, different diseases present as either one but they are both due to damage to the glomerulus/bowmans capsule

75
Q

How is kidney function affected by glomerulonephritis?

A

V often kidney function is not affected, the damage is to the glomerulus

76
Q

What investigations would you do for a patient with suspected glomerulonephritis?

A

Urine dip- protein:creatinine, 24 hr- nephrotic syndrome: diagnostic criteria is 300. If less than this may be nephritic syndrome
Bloods- U&Es, FBC,Bone, serum glucose
Imaging

77
Q

What is the pathophysiology of minimal change syndrome?

A

Podocytes become flattened- lose ability to control amount of protein that goes into the urine

78
Q

After diabetes and hypertension, what is the most common glomerulonephritis?

A

IgA nephropathy

79
Q

What type of kidney injury can vasculitis cause?

A

Acute

80
Q

How may vasculitis present?

A

Non-blanching rash
Knee/ankle pain
Inflammation of blood vessels in ENT
Neuro conditions

Pt with vague symptoms, haematuria and presence of ANCA

81
Q

What type of kidney injury does glomerulonephritis cause?

A

Mostly chronic, however some may cause acute e.g. vasculitis

82
Q

How is vasculitis treated?

A

Plasma exchange- take blood from pt and pass through filter which removes the antibodies driving the condition

Cyclosporin
Tacrolimus
Mycophenate motefil
Cylcophosphamide

83
Q

What antibody is implicated in vasculitis?

A

p-ANCA- anti-neurophil anti-cytoplasmic antibodies, they target neutrophil nucleus

c-ANCA- attaches to cytoplasm of nucleus

84
Q

Name three investigations you would do for suspected glomerulonephritis

A

Urine dip - protein creatinine ratio
Bloods - U&Es, FBC, Bone, Serum glucose
Imaging - USS of renal system

85
Q

What is common clinical presentation of minimal change disease in children/young adults?

A

Swelling - facial - peri-orbital swelling

86
Q

What are ddx for swelling/odema in pt with pmh of proteinuria and angina?

A

Nephrotic syndrome, HF, Liver disease

87
Q

What do patients with nephrotic syndrome need to help find cause?

A

Renal biopsy

88
Q

A lady attends a&e with DVT and oedema. What renal condition must you rule out?

A

Nephrotic syndrome - dvt can be first sign; pts with nephrotic syndrome are at risk of dvt and stroke

89
Q

How can you check pt with MCD is responding to steroids given?

A

Look at serum albumin - should be increasing if steroids are working.

90
Q

What are risks of steriods?

A

Risk of osteoporosis
Risk of DM
Weight gain
Skin thinning
Risk of infection

91
Q

What risk is associated to kidney biopsy?

A

Heamatoma - biopsy can damage kidney and pt presents with heamaturia

92
Q

What antibodies can cause vasculitis?

A

P-ANCA
C-ANCA

93
Q

What extra renal complications are related to AKPD?

A

Liver cysts
Berry aneurysms - check FHx of sudden death

94
Q

What are complications of AKPD?

A

Renal failure
Hypertension
Infection
Pain

95
Q

Why isn’t it useful doing genetic testing for AKPD?

A

High number of mutations - i.e. can not just test for ne mutation, have to test for 100s.

96
Q

What is inheritance pattern of AKPD?

A

Autosomal dominant

97
Q

Where is the mutation in Adult Polycystic Disease?

A

Polycystine gene, on chromosome 16 and chromosome 4

98
Q

How is Adult polycystic disease inherited?

A

Autosomal dominant

99
Q

How do you diagnose adult polycystic ovary syndrome?

A

Family history
Ultrasound- done over the age of 16 as cysts too small to be seen before then

100
Q

What are the features of adult polycystic kidney disease?

A

Bilateral cysts on the kidneys
HTN
Risk of berry aneurysms

101
Q

What are the complications of adult polycystic kidney disease?

A

Pain
Discomfort
Haematuria
Kidney failure

102
Q

What are the extra renal involvements of adult polycystic kidney disease?

A

Liver- doesn’t affect function too much, but pts may feel bloated and uncomfortable
Berry aneurysms

103
Q

What major complications result in patients needing dialysis?

A

Hyperkalaemia- give calcium gluconate and dextrose
Pulmonary oedema

104
Q

What are the aims of renal replacement therapy?

A

Remove toxic metabolites
Normalise electrolyte disturbances
Correct volume deficit

105
Q

What is Renal Replacement Therapy?

A

Dialysis- Peritoneal or Haemodialysis
Renal transplant

106
Q

How does haemodialysis work?

A

Movement of solute across semi-permeable membrane- molecules that shouldn’t be there ie. ‘dirty’ molecules move across into water, thus cleaning blood Driven by osmotic pressure
3x weekly 4 hr treatment

107
Q

Why do you need a AvF in haemodialysis?

A

To get blood out of the patient, most veins will collapse so need to arterialise the vein

108
Q

What are the types of AvF

A

Radial artery joined to cephalic vein
Brachial artery joined to cephalic vein

109
Q

How do you know if the AvF is working?

A

You can feel a thrill or hear a bruit

110
Q

When do you use a central line in dialysis?

A

When you can’t get a AvF

111
Q

Where does the end of the central line sit?

A

Superior vena cava

112
Q

What is the risks with central line for dialysis?

A

Endocarditis
SVC obstruction

113
Q

How often do you need to do PD?

peritoneal dialysis

A

4 x a day, every day, as less efficient

114
Q

What is the biggest complication of PD

A

Peritonitis due to infection

115
Q

What is encapsulating sclerosing peritonitis?

A

In PD- Peritoneal membrane becomes thickened due to constant exposure due to sugar water, becomes a fibrosis capsule so bowel cannot move- sx of small bowel obstruction

116
Q

What is renal bone disease?

A

Renal failure- cannot hydroxylate Vit d–> means they cannot reabsorb calcium from gut–> serum calcium falls–> parathyroid hormone activated–>uses osteoclastic activity to increase serum calcium

Parathyroid goes out of control–> tertiary hyperparathryoidism–>Parathyroid increases calcium even when it doesn’t need to–> hypercalcaemia

117
Q

How do you try to avoid hyperparathryoidism?

A

vit D

Or parathyroidectomy–> give calcium in the long time

118
Q

What is renal anaemia?

A

Reduction in EPO
Normocytic anaemia

119
Q

How do you treat renal anaemia?

A

Oral iron tablets, if that doesn’t work give
Give EPO injection
IV Iron

120
Q

What is the complication to giving EPO?

A

May increase BP
Too much Hb can lead to viscous blood leading to hypercoaguable state

121
Q

Why are pts on dialysis at risk of not surviving transplantation?

A

Due to cardio complications- pts likely to have diabetes or HTN which leads to increase CVS risk

122
Q

What do you need to suppress during transplantation?

A

CD4 + T helper cell–> can’t produce NKC or B cells

123
Q

What are the complications of immunosuppression for kidney transplant?

A

Opportunistic infection e.g. miliary TB
Cancer: melanoma, lymphoma
Karposi sarcoma

124
Q

What drugs do you give to immunosuppress a patient prior to transplant?

A

Mycophenolate
Azathioprine
Calcineurin inhibitors- tacrolimus and cyclosporin
Steroids

125
Q

What are some long term side effects of ciclosporin?

A

Nephrotoxicity- tubular atrophy and fibrosis
Gum hypertrophy
Hypertension
Atherosclerosis

126
Q

What is the rule of thirds in membranous glomerulonephritis?

A

1/3 get better
1/3 have a relaxing and remitting condition
1/3 progress to ESRD

127
Q

What metabolic abnormality does alcohol poisoning cause?

A

Raised anion gap metabolic acidosis

128
Q

What metabolic abnormality Renal tubular acidosis cause?

A

Normal anion gap metabolic acidosis

129
Q

What metabolic abnormality does renal failure cause?

A

Raised anion gap metabolic acidosis

130
Q

Potential clinical findings in pt with AKI?

A

Signs: Reduced urine output (oliguria), dehydrated (NO moist mucous membranes, reduced skin turgor, sunken eyes). Confusion, drowsiness,

Who: over 65, RF present (see BS on this), Hx off AKI.

131
Q

Differentials of AKI?

A

CKD (i.e. a progression of CKD staging/acute on chronic kidney disease)

BMJ also states 1) increased muscle mass which shows elevated Cr. 2) Drug side effect leading to elevated creatinine (trimethoprim).

132
Q

Important differentials of CKD?

A

Diabetic kidney disease
Glomerulonephritis
Obstructive uropathy

133
Q

Indication for dialysis in CKD patient?

A

CKD stage 5 - end stage renal disease

134
Q

Which protein is lost in nephrotic syndrome?

A

Antithrombin III

135
Q

Features of osteomalacia?

A

bone pain, proximal myopathy, and waddling gait

136
Q

Link between CKD and osteomalacia?

A

phosphate is renally excreted, if there is impaired renal function - phosphate will build up, ‘dragging’ the calcium out of the bones resulting in osteomalacia

137
Q

First line management of CKD induced osteomalacia?

A

Limit dietary phosphate

138
Q

Aside from diet, how else can you manage CKD induced osteomalacia?

A

phosphate binder e.g Sevelamer- non-calcium-based phosphate binder, it binds to dietary phosphate and prevents its absorption.

139
Q

Why would a patient with Nephrotic syndrome develop a DVT /PE ?

A

Nephrotic syndrome is associated with a hypercoagulable state due to loss of antithrombin III and plasminogen via the kidneys

Antithrombin III inhibits coagulation by inhibiting the action of thrombin while plasminogen is involved in fibrinolysis.

140
Q

Which is higher in nephrotic syndrome LDL or HDL?

A

LDL

141
Q

What is Dialysis disequilibrium syndrome?

A

Rare
Usually caused by cerebral oedema- treat by reducing ICP
Neurological symptoms due to rapid removal of urea
Headache, nausea, vomiting, disturbed consciousness, convulsions, coma

142
Q

Who is at risk of diabetic nephropathy?

A

T1 DM or long duration of T2 DM patients

143
Q

A patient has diabetic nephropathy. What 2 additional microvascular complications may be present?

A

Retinopathy
Peripheral neuropathy

144
Q

What is glomerulosclerosis?

A

In Diabetic nephropathy - chronic high levels of glucose pass through glomerulus and cause scarring = glomerulosclerosis

145
Q

What is key feature of diabetic nephropathy?

A

Proteinuria

146
Q

Why do we get proteinuria in diabetic nephropathy?

A

Glomerulus is damaged - so allows protein to be filtered from the blood into the urine.

147
Q

What is involved in screening for diabetic nephropathy ?

A

Urine Albumin:creatinine ratio
U&Es

148
Q

What does albumin:creatinine ration show for patient with diabetic nephropathy?

A

Raised urine albumin:creatinine ratio

149
Q

How is diabetic nephropathy managed?

A

Key: want to optimise blood sugar levels and blood pressure.

ACEi/ARB - reduces proteinuria and controls blood pressure
CVS risk modification (may involve lifestyle changes)
Continue screening for microvascular complication of diabetes e.g. retinal screening, foot checks.

150
Q

What should always be started in patients with diabetic nephropathy, regardless of their BP reading?

A

ACEi (even if BP is normal)

151
Q

Signs present in patient with diabetic nephropathy?

A

Presence of RF: Hyperglycaemia, HTN, FHx of DM, obesity, smoker

Retinopathy, odema, foot ulcers.

152
Q

Drugs that cause acute interstitial nephritis?

A

Penicillin
Rifampicin
NSAIDS
Allopurinol
furosemide

153
Q

Most common complication of haemo-dialysis?

A

Diaslysis induced hypotension

154
Q

What are principals of management in AKI?

A

Find and treat causes (e.g. sepsis, drugs, obstruction):

Bloods/Blood Cultures, urine dip, bladder scan, ultrasound renal tract, ECG

Stop renotoxic drugs

Give IV fluid

Treat complications

Consider dialysis if indicated

155
Q

What is alport syndrome?

A

X-linked (usually affects males) Mutation in gene coding for Type V collagen
Associated with hearing loss and abnormalities of the eyes
Often leads to ESRF

156
Q

Presentation of alport syndrome?

A

Persistent microscopic haematuria with intermittent visible haematura Sensorineural hearing loss Biopsy: splitting of GBM and alternating thickening & thinning of GBM
Genetic studies – family history

157
Q

Clinical features of pyelonephritis?

A

Fever, rigors
Loin pain
Vomiting
White cell casts in urine

158
Q

Hb target for CKD patients being treated for anaemia?

A

Hb 100-120

159
Q

What factors contribute to anaemia in CKD?

A

Decreased production of EPO from kidney
Absolute iron deficiency - poor absorption/malnutrition
Functional iron deficiency - inflammation/infection
Blood loss
Shortened RBC survival
Bone marrow suppression from uraemia
Medication induced anaemia
Deficiency of B12 or folate

160
Q

What needs to be present for CKD-MBD to be diagnosed in a pt with CKD?

A

Evidence of one or more of:
- Abnormal metabolism of vitamin D or levels of PTH, calcium, phosphate, alkaline phosphatase
- Vascular and/or soft tissue calcification
- Abnormal bone turnover, metabolism, volume, linear growth or strength

161
Q

A pt with CKD has a low bone turnover. What could this mean they have?

A

Adynamic bone disease
Osteomalacia

162
Q

What is Osteitis Fibrosa?
1. give the features
2. Give symptoms

A

Features:
* loss of bone mass
* weakening of bones and calcified structures - this is replaced with fibrous tissue (peritrabecular fibrosis)
* formation of small cyst-like brown tumours

Symptoms:
* Bone pain
* tenderness
* fractures
* skeletal deformities

163
Q

What causes Osteotits fibrosa cystica?

A

Cause: Unchecked hyperparathyroidism
* overproduction of PTH
* PTH causes Ca release from bones - blood - reabsorption of calcium in kidney
* this results in hypercalcaemia

164
Q

What conditions might lead a pt to develop hyperparathyroidism and therefore develop a complication such as Osteitis fibrosa cystica ?

A
  • Parathyroid adenoma (majority)
  • Genetics -( i.e. familiar hyperarathyroidsim, MEN type 1)
  • Parathyroid carcinoma
  • Renal - End stage renal disease
165
Q

Why does End stage renal disease lead to hyperparathyroidism?

A
  • In ESRD the kidneys fail to produce calcitriol (a form of vitamin D)
  • Vit D facilitates the absorption of calcium into bones.
  • When calcitriol levels decrease, parathyroid hormone levels increase
  • This causes calcium to be removed from the bones and released into the blood
166
Q

A patient has CKD which has progressed. Describe the levels of the following as either increased or decreased:
1. Fibroblast growth factor-23
2. ALP
3. Phosphate
4. PTH
5. Serum calcium
6. Vit D

A
  1. Fibroblast growth factor-23 = Increased
  2. ALP = Increased
  3. Phosphate = Increased
  4. PTH = Increased
  5. Serum calcium = Decreased
  6. Vit D = Decreased
167
Q

Define tertiary hyperparathyroidism

A

Occurs when PTH release continues despite raised serum Calcium levels

168
Q

What is Secondary hyperparathyroidism?

A
  • elevation of parathyroid hormone (PTH) secondary to hypocalcaemia.
169
Q

What causes secondary hyperparathyroidism ?

A
  • Any disorder that results in hypocalcaemia will elevate parathyroid hormone.
  • CKD - MOST COMMON
  • malabsorption syndromes
  • chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium.
170
Q

Secondary hyperparathyroidism (SHPT) is a complication of CKD. This is important in the pathogenesis of CKD-mineral bone disorder (MBD).

Define CKD-MBD

A
  • a systemic disorder of mineral and bone metabolism due to CKD.

This is due to either one or a combination of the following:
* abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism
* abnormalities in bone turnover, mineralisation, volume, linear growth, or strength
* vascular or other soft tissue calcification

171
Q

How is CKD-MBD managed?

A

Reduce the severity/occurrence of renal bone disease
Reduce CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload.

AIM: control serum phosphate, calcium and vit D levels.
* Dietary phosphate reduction
* Phosphate binder
* Vit D supplemenation (if low) / vit D analaogue
* Ca - treat if hypo/hyper (can be either) either by supplementing or binder
* Persistently elevated PTH - parathyroidectomy or calcimimetic therapy is indicated.

172
Q

When do you use Ramipril in kidney disease?

A

In patients with proteinuria, an ACE inhibitor such as ramipril is used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol.

They are also used regardless of a patient’s blood pressure if the ACR is > 70 mg/mmol.

173
Q
A

Y3 med old (8 decks)

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