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medicine specialities > Renal > Flashcards

Renal Flashcards

1
Q

what are the nice criteria for AKI?

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours

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2
Q

what are the risk factors for AKI?

A
  • CKD
  • HF
  • DM
  • Liver disease
  • > 65
  • cognitive impairment
  • nephrotoxic meds - NSAID, ACEi
  • contrast during CT scans
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3
Q

what are the causes of renal impairment?

A
  • pre renal
  • renal
  • post renal
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4
Q

what are the pre renal causes of AKI?

A

inadequate blood supply to kidneys -
dehydration
hypotension
HF

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5
Q

what are the renal causes of AKI?

A

reduced filtration of blood -
ATN
interstitial nephritis
glomerulonephritis

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6
Q

what are the post renal causes of AKI?

A

obstruction of outflow of urine…backpressure and reduced kidney function -
kidney stones
masses in abdomen and pelvis
ureter or urethral strictures
BPH or prostate cancer

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7
Q

how do we investigate AKI?

A

urinalysis:
bloods, protein - acute nephritis/infection
leucocytes, nitrites - infection
glcuose - diabetes

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8
Q

how is post renal aki diagnosed?

A

USS of KUB - obstruction

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9
Q

how is AKI managed?

A
  • fluid resus - pre renal
  • stop nephrotoxic drugs - renal
  • relieve obstruction, ie catheter - post renal
    if severe - renal specialist +/- dialysis
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10
Q

what are the complications of AKI?

A

Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis

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11
Q

define CKD

A

chronic reduction in kidney function

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12
Q

what are the causes of CKD?

A
  • DM
  • HTN
  • age
  • glomerulonephritis
  • PCKD
  • medications - NSAIDS, PPI, lithium
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13
Q

what are the risk fx for CKD?

A

Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys

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14
Q

what are the signs and sx of CKD?

A

Pruritus (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

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15
Q

which investigations are required for CKD?

A

UandE’s - eGFR , two tests 3 months apart to diagnose CKD
urine albumin:creatinine ratio - >3mg/mmol
urine dipstick - 1+ blood (malignancy)
renal USS

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16
Q

what are the stages of CKD?

A

G score - eGFR
G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)
A score - albumin:creatinine ratio
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol

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17
Q

what stage does a patient need to HAVE CKD?

A

not have if A1 + G1 or G2
require either eGFR<60 or proteinuria

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18
Q

what are the complications of CKD?

A

Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems

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19
Q

what are the guidlines for referring to a specialist with CKD?

A

eGFR < 30
ACR ≥ 70 mg/mmol
Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
Uncontrolled hypertension despite ≥ 4 antihypertensives

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20
Q

how is CKD managed?

A

Slowing the progression of the disease-
Optimise diabetic control
Optimise hypertensive control
Treat glomerulonephritis

Reducing the risk of complications-
Exercise, stop smoking
Special dietary advice about phosphate, sodium, potassium and water intake
Offer atorvastatin 20mg for primary prevention of cardiovascular disease

Treating complications-
Oral sodium bicarbonate to treat metabolic acidosis
Iron supplementation and erythropoietin to treat anaemia
Vitamin D to treat renal bone disease
Dialysis in end stage renal failure
Renal transplant in end stage renal failure

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21
Q

what is the first line drug in treating HTN for CKD?

A

ACEi
offered to all -
Diabetes plus ACR > 3mg/mmol
Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol

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22
Q

what is the target for blood pressure in pts with HTN?

A

<140/90 or <130/80 if ACR >70

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23
Q

what is a complication shared by treatment and as a consequence of CKD?

A

hyperkalamia from CKD and ACEi

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24
Q

why is anaemia is caused by CKD and how can it be treated?

A

damage kidney cells can not produce EPO - reduced production of RBC’s
treated with exogenous EPO and IV/oral iron (blood transfusions should be limited as they sensitise the immmune system so transplated organs more likely to be rejected)

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25
Q

what are the features of renal bone disease and how dot they appear on x ray of the spine?

A

osteomalacia - softening of bone - less white in centre
osteoporosis - brittle bones
osteosclerosis - denser white at booth ends
…‘rugger jersey’ spine - stripes

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26
Q

why does CKD cause mineral bone disease?

A

reduced phosphate excretion
low active vit D as kidney usually metabolises to active form
active vit D is required for calcium absorption from intestines and kidneys and regulates bone turnover
due to reduced serum calcium and high serum phosphate - secondary hyperparathyroidism - this increases osteoclast activity leading to absoption of calcium from bone
Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.
Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.

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27
Q

how is mineral bone disease managed?

A
  • active forms of vit D - calcitriol
  • low phosphate diet
  • bisphosphonates to treat osteoporosis
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28
Q

acute tubular necrosis

A

urine is very pale even if dehydrated

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29
Q

acei

A

decreases tubular pressure as decreases BP, so less protein in urine but lower eGFR….helps CKD long term but also potentiates it

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30
Q

what is the biggest consequence of dialysis?

A

cardiovascular event

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31
Q

when is dialysis considered?

A

end stage renal failure
any acute indications which continue long term

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32
Q

what are the indications for acute dialysis?

A

A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness

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33
Q

what are the three main options for dialysis when required long term?

A

continous ambulatory peritoneal dialysis
automated peritoneal dialysis
haemodialysis

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34
Q

how does peritoneal dialysis work?

A

uses peritoneal membrane as filtration membrane and a dextrose solution is added to the peritoneal cavity. Ultrafiltration occurs from the blood across the membrane and into the solution…the solution is then replaced - so waste products that have been filtered are taken away
- tenckhoff catheter - plastic tube used to insert solution into peritoneal cavity
if continious - eg: 2L changed 4 times a day
or automated - overnight, replaces fluid overnight

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35
Q

what are the complications of peritoneal dialysis?

A
  • bacterial peritonitis - due to glucose solution
  • peritoneal sclerosis - thickening and scarring of membrane
  • ultrafiltration failure - absorbs the dextrose in the filtration solution so gradient less
  • weight gain - absorb carbs from dextrose
  • psychosocial
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36
Q

what is a typical regime for haemodialysis?

A

4 hours 3 days a week

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37
Q

what are the access options for haemodialysis?

A

tunnelled cuffed catheter (right side below clavicle) - tube into subclavian or jugular vein with a tip that sits in SVA or RA
two lumens - one where blood exits and one where enters
ring called dacron cuff that surrounds catheter - promotes healing and adhesion of tissue to cuff so catheter is more permanent and provided barrier to infection…infection and bloods clots are main complications
AV fistula - artificial connection between artery to a vein, bypasses capillary system and allows blood to flow under high pressure.you create the fistula during surgery and requires 4 weeks-months without use,permanent large easy access blood vessels with high flow - radio cephalic, brachio-cephakic, brachio-basilic

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38
Q

how do you examine an AV fistula?

A

Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
Stereotypical “machinery murmur” on auscultation

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39
Q

what are the complications of AV fistula?

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure

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40
Q

define STEAL syndrome

A

inadequate blood supply to limb distal to AV fistula, the blood is diverted away from where it is supposed to supply and flows to venous system causing distal ischaemia

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41
Q

define high output heart failure

A

where AV fistula blood is flowing v quickly from arterial to venou system through fistula…rapid return of blood to heart..increasing pre load in heart causing hypertrophy and HF

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42
Q

never….from a fistula

A

NEVER TAKE BLOOD

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43
Q

what is the examination of the renal system?

A
  • tunnel cuffed catheter scar - right side, below clavicle
  • hockey stick scar on abdomen - renal transplant
  • peritoneal dialysis scars
  • fistula on arms
  • palpable implanted kidney in RIF or LIF
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44
Q

how are donors matched for kidney transplants?

A

based on HLA type A, B, C on chromosome 6…do not have to match and would be immunocompromised to desensitise them to donor HLA if a living donor

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45
Q

how does a kidney transplant work?

A
  • patient’s kidneys left
  • donor’s kidney blood vessels are anastomosed with patient’s pelvic vessels…external iliac
  • donor’s ureter is anastomosed with patient’s bladder
    -donor kidney in anterior of abdomen, palpated in ILIAC area
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46
Q

which drugs are used to immunosuppress the patient?

A

Tacrolimus - IL 2 inhibition
Mycophenolate mofetil
Prednisolone - not for a long term

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47
Q

what are the complications of a renal transplant?

A

Transplant rejection (hyperacute, acute and chronic)
Transplant failure
Electrolyte imbalances

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48
Q

what are the complications relating to immunosuppressants?

A

Ischaemic heart disease
Type 2 diabetes (steroids)
Infections are more likely and more severe
Unusual infections can occur (PCP, CMV, PJP and TB)
Non-Hodgkin lymphoma
Skin cancer (particularly squamous cell carcinoma)

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49
Q

what are the criteria for nephritic syndrome?

A

Haematuria- microscopic (not visible) or macroscopic (visible).
Oliguria - reduced urine
Proteinuria - there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention

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50
Q

what is the criteria for nephrotic syndrome?

A

Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia

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51
Q

define glomerulonephritis

A

conditions that cause inflammation of or around the glomerulus and nephron

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52
Q

define interstitial nephritis

A

inflammation of the space between cells and tubules (the interstitium) within the kidney:
acute interstitial nephritis and chronic tubulointerstitial nephritis.

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53
Q

define glomerulosclerosis

A

scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses
- can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.

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54
Q

what are the specific types of glomerulonephritis?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
Mesangiocapillary glomerulonephritis
Rapidly progressive glomerulonephritis
Goodpasture Syndrome

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55
Q

how are most types of glomerulonephritis treated?

A

Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)

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56
Q

how might nephrotic syndrome look on examination?

A

oedema
frothy urine from proteinuria

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57
Q

what does nephrotic syndrome predipose a patient to?

A

thrombosis, hypertension and high cholesterol.

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58
Q

what is the most common cause of nephrotic syndrome in children?

A

minimal change disease
- treated with steroids

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59
Q

what is the most common cause of nephrotic syndrome in adults?

A

focal segmented glomerulosclerosis

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60
Q

what is the aetiology of primary glomerulonephritis?

A

IgA nephropathy (berger’s disease)
- 20’s
- IgA deposits and mesangial proliferation

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61
Q

what is the aetiology of membranous glomerulonephritis?

A

Most common type of glomerulonephritis
bimodal peak in age in the 20s and 60s
“IgG and complement deposits on the basement membrane”
usually idiopathic
Can be secondary to malignancy, rheumatoid disorders and drugs (e.g. NSAIDS)

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62
Q

define post strep glomerulonephritis

A

<30
1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
They develop a nephritic syndrome
There is usually a full recovery

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63
Q

what is goodpasture’s syndrome and how might a patient present?

A

antibodies attack glomerulus and pulmonary basement membranes….glomerulonephritis and pulmonary haemorrhage
- AKI + haemopytsis

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64
Q

what is a differential for goodpasture’s syndrome?

A

granulomatosis with polyangiitis (AKA Wegener’s granulomatosis)
type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA). Patients with Wegener’s granulomatosis may also have a wheeze, sinusitis and a saddle-shaped nose.

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65
Q

histology shows cresenteric glomerulonephritis, what is the diagnosis?

A

rapidly progressive glomerulonephritis
- very acutely unwell
- often secondary to goodpastures

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66
Q

what is the most common cause of CKD in Uk?

A

diabetic nephropathy- chronic high levels of glucose passing through glomerulus causes glomerulosclerosis

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67
Q

how should patients with diabetes be managed with regards to kidney damage?

A

regular screening for diabetic neuropathy - albumin:creatinine ratio and UE

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68
Q

how is diabetic nepropathy managed?

A

glucose levels and blood pressure

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69
Q

what is acute interstitial nephritis caused by?

A

hypersensitivity reaction to drugs (nsaids, abx) or infection

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70
Q

how can patients with acute interstitial nephritis present?

A

AKI
hypertension
rash
fever
eosinophilia

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71
Q

how is acute interstitial nephritis managed?

A

treat underlying cause
steroids

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72
Q

how does chronic tubointerstital nephritis present?

A

CKD

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73
Q

what are the causes of chronic tubointerstitial nephritis?

A

autoimmune, infectious, iatrogenic and granulomatous disease…treat underlting cause + steroids

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74
Q

what is the most common cause of AKI?

A

ATN

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75
Q

define ATN

A

damage and death (necrosis) of the epithelial cells of the renal tubules

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76
Q

is ATN reversible?

A

epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover

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77
Q

what are the causes of ATN?

A

hypoperfusion - Shock, Sepsis, Dehydration
direct damage - Radiology contrast dye, Gentamycin, NSAIDs
…managed the same as AKI

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78
Q

what is found on urinalysis of ATN?

A

muddy brown casts on histology

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79
Q

what is the aetiology of renal tubular acidosis?

A

metabolic acidosis due to pathology in the tubules of the kidney. The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH

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80
Q

what is type 1 renal tubular acidosis caused by?

A

pathology in DCT…so unable to excrete H ions
Genetic -both autosomal dominant and recessive forms.
Systemic lupus erythematosus
Sjogren’s syndrome
Primary biliary cirrhosis
Hyperthyroidism
Sickle cell anaemia
Marfan’s syndrome

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81
Q

how does type 1 renal tubular acidosis present?

A

Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)

82
Q

what are the biochemical results of type 1 renal tubular acidosis?

A

hypokalaemia
metabolic acidosis
urinary pH of 6

83
Q

how is type 1 renal tubular acidosis treated?

A

bicarbonate

84
Q

what is the cause of type 2 renal tubular acidosis?

A

PCT - can not reabsorb HCO3- from urine into blood so excess in urine
usually caused by falconi’s syndrome

85
Q

what are the biochemical results of type 2…acidosis?

A

Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)
…also treated with HCO3-

86
Q

what is type 3 renal..acidosis?

A

combination of type 1 and type 2 with pathology in the proximal and distal tubule. This is rare and unlikely to appear in your exams or clinical practice.

87
Q

what is type 4 renal tubular acidosis caused by?

A

reduced aldosterone - due to adrenal insuffiency, ACEi and sprinolactone or lupus, DM, HIV

88
Q

what is the biochemical results of type 4…acidosis?

A

Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH

89
Q

how is type 4 renal tubular acidosis treated?

A

fludrocortisone
sodium bicarbonate and tx of hyperkalaemia

90
Q

define haemolytic uraemic syndrome

A

thrombosis in small blood vessels throughout the body - usually triggered by shiga toxin

91
Q

what is the triad of haemolytic uraemic syndrome?

A

Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)

92
Q

where is shiga toxin produced from?

A

e.coli 0157
shigella
- use of abx and anti motility meds such as loperamide increases risk

93
Q

how does a pt with e.coli present in contrast to later when they develop HUS?

A

gastroenteritis - bloody diarrhoea
then 5 days later -
Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability (anaemia)
Confusion (uraemia)
Hypertension (renal failure)
Bruising (low platelets)

94
Q

how is HUS managed?

A

medical emergency -
Antihypertensives
Blood transfusions
Dialysis

95
Q

define rhabdomyolysis

A

skeletal muscle breaks down and releases breakdown products into the blood..myocytes undergo apoptosis
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine kinase

96
Q

what are the consequences of the breakdown products of rhabdomyolysis being released?

A

potassium - hyperkalaemia - cardiac arrhythmias
myoglobin - toxic to kidney - AKI

97
Q

what are the causes of rhabdomylosis?

A

Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)
Crush injuries
Seizures

98
Q

what are the signs and sx of rhabdomyolsis?

A

Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine

99
Q

which investigations are used for rhabdo?

A

CK - very elevated - typically to thousands until 12 hours then remains elevated for 1-3 days and then starts reducing
urine dipstick - myglobin causes blood to be positive
UE - AKI and hyperkalaemia
ECG - hyperkalaemia

100
Q

how is rhabdomyolysis managed?

A

IV fluids
IV sodium bicarb to make urine more alkaline reducing toxicity of myoglobin on kidneys
IV mannitol - increase GFR and reduce oedema
treat complications - hyperkalaemia

101
Q

what are the causes of hyperkalaemia?

A

Acute kidney injury
Chronic kidney disease
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
Medications - Aldosterone antagonists (spironolactone and eplerenone)
ACE inhibitors
Angiotensin II receptor blockers
NSAIDs
Potassium supplements

102
Q

what may result in a falsely elevated potassium?

A

haemolysis

103
Q

what are the ECG changes of hyperkalaemia?

A

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

104
Q

when is hyperkalaemia concerning?

A

Patients with a potassium ≤ 6 mmol/L with otherwise stable renal function don’t need urgent treatment and may just require a change in diet and medications (i.e. stopping their spironolactone or ACE inhibitor).

Patients with a potassium ≥ 6 mmol/L and ECG changes need urgent treatment.

Patients with a potassium ≥ 6.5 mmol/L regardless of the ECG need urgent treatment.

105
Q

how is hyperkalaemia managed?

A

insulin and dextrose infusion and IV calcium gluconate
other options-
nebulised salbutamol
IV fluids
oral calcium resonium
sodium bicarb
dialysis

106
Q

define polycystic kidney disease

A

genetic
multiple fluid filled cysts
may also develop hepatic cysts and cerebral aneurysms

107
Q

how is polycystic kidney disease found on examination?

A

palpable enlarged kidneys

108
Q

what is the genetic inheritance of polycystic kidney disease?

A

auto dom or auto rec

109
Q

what are the auto dom associated genes?

A

PKD-1: chromosome 16 (85% of cases)
PKD-2: chromosome 4 (15% of cases)

110
Q

what are the extra renal manifestations of aut dom polycystic kidney disease?

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation

111
Q

what are the complications of polycystic kidney disease auto dom?

A

Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria can occur with cyst rupture
Renal stones
End-stage renal failure

112
Q

which gene is associated with polycystic kidney disease aut rec?

A

gene on chromosome 6

113
Q

how does aut rec polycystic kidney disease often present?

A

in pregnancy with oligohydramnios as the fetus does not produce enough urine…causing resp failure after birth due to underdevelopment of lungs
- underdeveloped ear cartilage, low set ears and a flat nasal bridge. They usually have end-stage renal failure

114
Q

how is polycystic kidney disease managed?

A

Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease

115
Q

how are the complications of PCKD managed?

A

Antihypertensives for hypertension.
Analgesia for renal colic related to stones or cysts.
Antibiotics for infection. Drainage of infected cysts may be required.
Dialysis for end-stage renal failure.
Renal transplant for end-stage renal failure.

116
Q

how else can PCKD be managed?

A

Genetic counselling
Avoid contact sports due to the risk of cyst rupture
Avoid anti-inflammatory medications and anticoagulants
Regular ultrasound to monitor the cysts
Regular bloods to monitor renal function
Regular blood pressure to monitor for hypertension
MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history

117
Q

which fluids should be used in AKI (majority)?

A

high risk of hyperkalaemia - so not Hartmann’s as has K, use NaCl instead

118
Q

define cirrhotic AKI

A

cirrhosis causes portal hypertension resultingin splanchnic arterial vasodilation, reducing arterial blood volume causing AKI and encephalopathy

119
Q

how must mycophenolate moeftil be given

A

come off if acutely unwell and double prednisolone

120
Q

why might a patient have hypercalcaemia?

A

immobilisation
mineral bone disease from CKD

121
Q

how often is haemodialysis performed

A

3 times a week for 4 hours

122
Q

in what forms can haemodialysis access be given?

A

central line or AV fistula or graft

123
Q

how is PD different?

A

at home
risk of peritonitis
given through catheter

124
Q

When is alfacalcidol used?

A

Suppresses PTH, lowering serum calcium so not activating osteoclast activity…used in osteoporosis and vit d deficiency

125
Q

What is a proteus infection?

A

Usually UTI causing pyelonephritis
In young boys, elderly and structural abnormalities

126
Q

Which hypertension must be removed in fluid overload?

A

Amlodipine - blocks calcium ion channels resulting in vasodilation and fluid exudate

127
Q

What is used if a dialysis catheter is occluded?

A

Urokinase infusion

128
Q

What can cyclosporin not be used with?

A

Anti fungals- fluconazole

129
Q

What electrolyte abnormalities are common in CKD?

A

Hyperkalaemia - kidneys excrete potassium, met acidosis,
Dysnatriaemia - depending of fluid overload or depleted

130
Q

What is important ro measure in every patient on a renal ward?

A

JVP!
From sterna angle - straight line up..should be less than 3cm
Otherwise +1, +2, +3 - fluid overload

131
Q

Classification of CKD - severity heat map

A

See

132
Q

In what circumstances is ACR very important?

A

Diabetes

133
Q

What is the prognosis of ESRD?

A

Majority of CKD 1-3 do not progress ro ESRF
Risk of CV death is higher than risk of progression

134
Q

What are the complications of CKD and how are they treated?

A

Sodium retention - sodium restriction
Volume overload - diuretics, fluid restriction
Hyperkalaemia - dietary restrictions, avoid NSAIDS
Metabolic acidosis - sodium bicarbonate
High phosphate - phosphate binders
Low serum calcium -pans calcitriol - calcimimetrics
Anaemia - EPO, iron

135
Q

Why should you avoid blood transfusions in CKD?

A

Iron overload
Exposure of HLA antigens

136
Q

what are the sx of uraemia?

A

N+V
anorexia
weight loss
fatigue
pericarditis
sei\ures

137
Q

what is a type of living donation?

A

paired and pooled living kidney donation

138
Q

what are the contraindications of kidney transplant?

A

cardiac/resp
cancer
chronic infection - hep B, C
life expectancy < 5 yrs

139
Q

what are the early and late complications of kindey transplant?

A

early - bleeding, thrombosis, infection, ureteric, lymphocele
rejection
renal artery stensois
late - rejection, lympho-prolierative disorder (EBV), CMV disease, BK nephropathy, PCP, hypertension, DM
LATER - chronic antibody mediated rejection, recurrent UTI, CV disease, swuamous cell carcinoma

140
Q

what is the optimal way to transplant?

A

pre emptive, liver donor

141
Q

What are the causes of metabolic acidosis which have a normal anion gap?

A

Hyperchoraemia
Renal tubular acidosis
Addison’s
Diarrhoea

142
Q

What are the causes of metabolic acidosis which have a raised anion gap?

A

DKA, salicylate overdose, lactic acidosis, methanol poisoning

143
Q

What are the biochemical results of renal tubular acidosis?

A

Hyperchloraemia
Low bicarbonate

144
Q

What is associated with ADPKD?

A

Berry aneurysm (sudden onset headache…can lead to subarachnoid haemorrhage)
Cysts I’m kidney, liver, ovaries and spleen

145
Q

Over how many hours is an AKI defined?

A

<0.5 mL/kg/hr over 6 hrs

146
Q

Define amyloidosis, how it presents?

A

50-65 yr olds
Presents as breathlessness and weakness
Loss of renal function and Proteinuria
Hepatosplenomegaly

147
Q

How should a patients with a raised ACR (>3mg/mmol) and DM be managed?

A

Commence acei

148
Q

How does nephrotic syndrome predispose a patient to VTE?

A

Loss of antithrombin 111

149
Q

What is the indication for haemodialysis in a patient with AKI?

A

If they have pulmonary oedema

150
Q

What are some side effects of EPO?

A

Bone aches
Flu like sx
Skin rash

151
Q

How is ATN diagnosed?

A

Nephrotoxic causes
Urine osmolality <350 mOsm/kg
High sodium

152
Q

What is a cause of cranial diabetes insipidus?

A

Sx of CDI - high serum osmolality, low urine osmolality , retuns to normal with desmopressin
Urinary sx
Hereditary haemochromatosis -lethargy and arthralgia…causing CDI

153
Q

How does acute graft failure present and when does it occur?

A

Usually asx h(different from ATN of graft)
Pyuria
Proteinuria
Rising creatinine
6 months post transplant

154
Q

What can cause deranged liver function tests?

A

TPN

155
Q

When should patients with CKD be started on ACEi?

A

ACR >30mg/mmol

156
Q

What drug has shown to reduce the rate of CKD progression in ADPKD?

A

Tolvaptan - vasopressin receptor 2 antagonist

157
Q

What is the first indicator of diabetic nephropathy?

A

Microalbuminuria

158
Q

What drug is used to treat hyperphosphataemia in CKD with mineral bone disease?

A

Sevelamer

159
Q

How can acute interstitial nephritis present?

A

Allergic type - raised WCC, IgE and eosinophils
Impaired renal function

160
Q

What can be used ro differentiate ATN from AIN causing AKI?

A

Urine dip -
If protein - not pre or post renal
If no nitrites - no infection
AIN has high white cell count in urine wheras ATN doesn’t

161
Q

How can diabetic neuropathy be distinguished from other causes of CKD?

A

Large/normal sized on USS
Most patients with CKD have bilateral small kidneys

162
Q

What does a raises serum urea:creatinine ratio indicate?

A

Pre renal cause

163
Q

What drug can cause rhabdomyolysis?

A

Statin

164
Q

What drug must be stopped in AKI?

A

ARB - valsartan

165
Q

What is the most likely causative organism of peritonitis secondary to peritoneal dialysis?

A

Staph epidermidis

166
Q

How can renal artery stenosis be differentiated from other causes of refractory hypertension?

A

High renin

167
Q

What is the treatment of a hyper acute transplant rejection?

A

Remove immediately

168
Q

Define henoch-schonlein purpura

A

IgA autoimmune mediated Vasculitis
Abdo pain
Arthritis
Haematuria
Pupuric rash over buttocks amd extensor surfaces

169
Q

How does ATN present?

A

Poor response to fluids

170
Q

what are the causes of hyponatraemia?

A

diuretics
PPI
anti-epileptics
malignancy
head trauma
…..

                              Hypovolaemia   Euvolaemia	             Hypervolaemia Urine [Na+] <20mmol	Vomiting or Diarrhoea      Acute fluid overload	Congestive Cardiac Failure or Liver Cirrhosis* Urine [Na+] >20mmol	Diuretics	SIADH	Acute Tubular Necrosis
171
Q

how do you investiagte hyponatraemia?

A

the first step when investigating hyponatraemia should be to measure serum osmolality, to see whether it is hypo-osmotic, iso-osmotic or hyper-osmotic. However, in clinical practice, most cases* of hyponatraemia encountered will be hypo-osmotic hyponatraemia, whereby there is either sodium depletion or water excess (or both

172
Q

how do you manage hyponatraemia?

A

careful fluid balance. Start close fluid monitoring, catheterising if necessary; this is particularly important during the intraoperative and post-operative period.

Intravenous fluids (such as 0.9% sodium chloride) are generally advised over enteral hydration for the hyponatraemic patient, as they will provide a greater control to the serum electrolyte levels. Monitor renal function and electrolyte levels regularly, as potential derangement may occur during any fluid redistribution during your management.

If the cause is unknown or evidence of prolonged and marked hyponatraemia, urine osmolality and sodium concentration should be measured to inform additional diagnosis.

173
Q

what are the sx of hyponatraemia?

A

mostly asx
malaise, headache, and confusion, before progressing to reduced consciousness and seizures

174
Q

HLA antigens renal transplant

A

When HLA matches for a renal transplant the most important HLA antigen is DR, followed by B and then A. Other antigens to consider include C, DP, and DQ but these are not the most important. Although donors who are closely genetically related to the patient have an increased likelihood of being an organ donor match, it may be the case that they are still not a close enough match to donate.

175
Q

what is the most common causative organism of peritoneal dialysis related peritonitis?

A

Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis - staph epidermiditis

176
Q

what drugs must be stopped in AKI?

A

Diuretics
Aminoglycosides and ACE inhibitors
Metformin
NSAIDs.

177
Q

which nephropathy is most likely to be associated with malignancy?

A

membranous nephropathy

178
Q

tolvaptan

A

Tolvaptan has been shown to reduce the rate of CKD progression in ADPKD (and is approved by NICE)

179
Q

HIV infection is a cause of …

A

HIV infection is a cause of focal segmental glomerulosclerosis

180
Q

acute interstitial nephritis

A

Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function

181
Q

iga nephropathy investigations

A

his would show diffuse mesangial IgA deposition and is required to make a definitive diagnosis of IgA nephropathy. This is the most common primary glomerulonephritis in high-income countries. Approximately half of all patients with IgA nephropathy will present with recurrent episodes of frank haematuria following respiratory or gastrointestinal infections, usually occurring 1-2 days after the onset of infection.

182
Q

haemolytic uraemic syndrome

A

Normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS

183
Q

ADPKD triad

A

Renal impairment, flank masses, hypertension → ?ADPKD

184
Q

renal USS

A

An ultrasound is required in the investigation of all patients presenting with an AKI of unknown aetiology

185
Q

rapidly progressive glomerulosclerosis CAUSES

A

Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis

186
Q

low vitamin D ckd

A

Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys

187
Q

primary v secondary hyperaldosteronism

A

Primary and secondary aldosteronism can be differentiated by looking at the renin levels. If renin is high then a secondary cause is more likely, i.e renal artery stenosis.

188
Q

HUS

A

Haemolytic uraemic syndrome - classically caused by E coli 0157:H7

189
Q

screening of AKPD

A

LIVER USS

190
Q

glomerulonephritis what is it

A

Glomerulonephritis can present with any of the following:

Isolated haematuria or proteinuria
Nephrotic syndrome
Nephritic syndrome
Acute renal failure
Chronic renal failure

191
Q

causes of normal anion gap in metabolic acidosis

A

Causes of a normal anion gap metabolic acidosis are ABCD:
Addison’s
Bicarb loss
Chloride
Drugs

192
Q

causes of normal anion gap in metabolic acidosis

A

Causes of a normal anion gap metabolic acidosis are ABCD:
Addison’s
Bicarb loss - diarrrhoea
Chloride
Drugs

193
Q

dehydration

A

presenting with confusion, which is an unspecific symptom in elderly patients, especially with dementia, and anuria. The blood tests show that the patient has high sodium and urea. The urine test shows normal osmolarity with sodium inferior to 20 mmol/L. This is a hallmark in the diagnosis of prerenal uraemia. One of the most common causes of prerenal uraemia, especially in elderly patients is dehydration.

194
Q

if peritonitis from PD

A

staph epidermdiits

195
Q

minimal change disease fx

A

Her normotension and preceding history of viral illness are also typical features of MCD. 80% of cases will be steroid responsive.

196
Q

diabetic patient with > ACR

A

All diabetic patients with a urinary ACR of 3 mg/mmol or more should be started on an ACE inhibitor or angiotensin-II receptor antagonist

197
Q

alports v goodpastures

A

Alport’s patient with a failing renal transplant. This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.

198
Q

high urine osmolality and low urine sodium

A

pre renal AKI

199
Q

acute interstitial nephritis

A

Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function

200
Q

aki

A

results in hyperkalaemia

medicine specialities (11 decks)

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