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3rd Year Medicine UoM > Nephrology > Flashcards

Nephrology Flashcards

1
Q

how is the anion gap calculated?

A

(Sodium and potassium - positive cations) - (chlorine and bicarbonate - negative anions)

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2
Q

what is the anion gap?

A

the blood serum should have a neutral charge. the number of cations (positive) should equal the number of anions (negative). the reason we have an anion gap is because we don’t calculate all the anions present in the blood stream. we only look at chlorine and bicarbonate.

there are other anions e.g. sulphate, phosphate and organic acids. when there is a big anion gap - these anions are making up a bigger proportion of the anion molecules e.g. raised lactic acid (lactate anion)

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3
Q

how does lactic acidosis widen the anion gap?

A

lactic acid dissociates to form a lactate anion and hydrogen ion. the hydrogen is buffered by the bicarbonate, lowering its numbers.
less bicarbonate and more lactate anions leads to a bigger anion gap

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4
Q

what are causes for a raised anion gap?

A

lactic acid
ketoacids
urate - renal failure
acid poisoning - methanol (formic acid) and salicylate

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5
Q

what happens in a normal anion gap acidosis?

A

the bicarbonate falls and kidney compensates for the decrease in anions by increasing the production of chlorine anions.
therefore, can also be known as a hyperchloraemic acidosis

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6
Q

what are causes of normal anion metabolic acidosis?

A

loss of bicarbonate in the GI tract = e.g. diarrhoea
renal tubular acidosis (RTA) e.g. decreased bicarb re-absorption in DCT
addissons disease

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7
Q

what causes metabolic alkalosis?

A

caused by a loss of hydrogen ions or gain of bicarb
mainly due to problems in the kidneys or GI tract
- diuretics
- vomiting/aspiration
- cushings syndrome
- primary hyperaldosteronism
- hypokalaemia

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8
Q

what is diabetes insipidus?

A

characterised by raised plasma osmolarity and low urinary osmolarity
due to a deficiency of ADH (cranial DI) or decreased sensitivity to ADH (nephrogenic DI)

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9
Q

what are causes of cranial DI?

A

idiopathic
head injury
pituitary surgery
craniopharyngomas

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10
Q

what are causes of nephrogenic DI?

A

genetic - mutations affection vasopressin receptor / aquaporin channel
electrolytes- hypercalcaemia, hypokalaemia
tubulo-interstital disease (pyelonephritis, sickle-cell, obstruction)

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11
Q

what are features of diabetes insipidus?

A

polyurea
polydipsia
high plasma osmolarity
low urine osmolarity (<700 )

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12
Q

what is rhabdomyolosis?

A

break down of muscle fibres and the release of their content into the blood stream - can cause serious complications such as renal failure
due to direct or indirect muscle injury

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13
Q

what is myoglobinuria?

A

the presence of myoglobin in the urine

usually associated with rhabdomyolosis or muscle destruction

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14
Q

what can cause renal tubular apoptosis?

A

aminoglycosides and radio contrast medium

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15
Q

what can cause renal tubular necrosis? ATN

A

myoglobinuria and haemolysis

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16
Q

how is an AKI defined?

A

an AKI is a syndrome of reduced renal function, measured by creatinine or urine output. There are a number of different aetiologies
clinically defined as:

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17
Q

how is AKi clinically defined?

A

1) creatinine rise >26 in 48 hours
2) Creatinine rise in adults by 50% + in 7 days
3) eGFR fall in children by 25% + in 7 days
3) urine output < 0.5ml/kg/h for >6 consecutive hours

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18
Q

what are the clinical parameters for the severity staging of AKIs?

A

Stage 1 = Creatining rise 1.5x baseline or Urine output <0.5 for > 6 hours
Stage 2 = Creatinine rise 2-2.9 x baseline or Urine output <0.5 for >12 hours
Stage 3 = creatinine rise >3 x baseline or urine output <0.3 for >24 hours

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19
Q

how are causes for AKI classified?

A

Pre-renal 85%
Renal 10%
Post renal 5%

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20
Q

what are pre-renal causes for an AKI?

A

anything causing decreased renal perfusion

  • sepsis, shock
  • haemorrhage, burns, pancreatitis, D and V
  • cardiogenic shock, severe HF, MI (decreased cardiac output)
  • drugs - vasodilation
  • hypotension
  • ACE-I, ARBs, hepatorenal syndrome, NSAIDs ( renal vasoconstriction)
  • dehydration
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21
Q

what are renal causes for AKI?

A

anything damaging the actual kidney
glomerular = glomerularnephritis, acute tubular necrosis
interstitial = drug reaction, infection, infiltration
vessels = vasculitis, DIC (disseminated intravascular coagulation), TTP (Thrombotic thrombocytopenic purpura), HUS (haemolytic ureamic syndrome)

drugs - NSAIDs, ARBs, ACEi, gentamycin, radio contrast,
rhabdomyelosis

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22
Q

what are post-renal causes of AKI?

A

anything obstructing the output

  • within renal tract: stone, renal tract malignancy, clot, stricture
  • extrinsic pressure: retroperitoneal fibrosis, pelvic malignancy, prostatic hypertrophy
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23
Q

what are the most common causes of AKI?

A
  1. sepsis
  2. major surgery
  3. cardiogenic shock
  4. other hypovolaemias
  5. drugs
  6. hepatorenal syndrome
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24
Q

how does a patient with an AKI present?

A

dizzy, nausea, vomiting, fluid overload (orthopnea, pulmonary oedema etc), hypotension, tachycardia,

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25
Q

how is an AKI managed?

A

need to treat underlying cause
almost all AKI patients will need to have the following addressed: (regardless of aetiology): fluid balance (overload or dehydration), acidosis and hyperkalaemia.

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26
Q

how is fluid resuscitation in hypovolaemic AKI patients carried out?

A

500mL crystalloid bolus given over 15 mins and then reassessed. continue giving boluses of 250-500mL and then reassessing. stop when euvolaemic
if 2L given and no change - seek advice

Buffered solutions e.g. Hartmanns/ Ringers contain Potassium - be cautious if patient hyperkalaemic
non-buffered solutions e.g. 0.9% saline = contains chlorine. be wary of hyperchloraemic acidosis
Blood components should be used in haemorrhage (colloid)

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27
Q

how is fluid overload managed in AKI patients?

A
  • oxygen if patient has pulmonary oedema
  • fluid restriction
  • venous vasodilator e.g. diamorphine (with antiemetic)
  • diuretics can be used in symptomatic overload. not useful if the cause is oliguria

a patient with persistent fluid overload and oliguria/anuria needs urgent referral to critical care

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28
Q

what are causes of fluid overload?

A

sepsis - increased capillary permeability
aggressive fluid resuscitation
oliguria
Heart failure

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29
Q

how is hyperkalaemia treated in AKI?

A

1) calcium gluconate/calcium chloride (calcium chloride best given via central line) - stabilises heart cell membrane potentials
2) IV insulin - encourages cell take up of K+
3) salbutamol (nebuliser) - also shifts K+ into cells, at high doses

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30
Q

when is renal replacement therapy indicated?

A
  • persistent fluid overload despite medication
  • persistent hyperkalaemia
  • severe/prolonged acidosis
  • uraemic symptoms e.g. encephalopathy, pericarditis
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31
Q

what does the SALFORD pneumonic for AKI checklist stand for?

A 
Sepsis?
ACEi/ARBs/NSAIDs? - suspend!
Labs - repeat creatinine levels 
Fluid resuscitation 
Obstruction - US for non- resolving AKI 
Renal replacement therapy? 
Dip the urine
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32
Q

how does the RAAS counteract hypovolaemia?

A

it attempts to increase circulating volume by
1) increasing reabsorption of Sodium and water
2) causing vasoconstriction of efferent arteriols to maintain GFR
(ACEi, ARBs and NSAIDs prevent this protective mechanism)

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33
Q

what is Acute Tubular Necrosis?

A

a condition involving the death of tubular epithelial cells that make up the renal tubules.
ATN presents with AKI and is one of the most common causes of AKI

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34
Q

what are common causes of ATN?

A

sepsis and nephrotoxic drugs

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35
Q

what are the 3 phases of ATN?

A

1) oligoruic phase
- patient produces <500ml urine /day
- at risk of fluid overload and electrolyte imbalance
- creatinine levels shoot up
2) maintenance phase
- creatinine levels stabilise/ rise slowly
- normal urine quantities produced
- fluid and electrolyte balance maintained
3) polyuric recovery phase
- large amounts off dilute urine produced
- patients can become hypovolaemic and unwell, hypokalaemic (electrolyte loss)
- DCT and collecting ducts recover last so water not reabsorbed by aquaporins
- creatinine levels drop

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36
Q

what is sepsis?

A

overwhelming and damaging systemic inflammatory response to infection.
can cause organ dysfunction
recognised by worsening vital signs

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37
Q

what is the pathophysiology of sepsis?

A

pathogen gains access to patient - risk increased with surgery, foreign bodies e.g. catheter and poor immunity
widespread inflammation leads to the systemic release of inflammatory molecules. NO causes vasodilation, other molecules activate endothelins - causing increase capillary permeability. fluid leaks out into tissue - causing oedema and hypovolaemia.
increased coagulapathy causes formation of microthrombi
the above compounds organ hypo-perfusion and dysfunction.
lactic acidosis and multi organ failure results

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38
Q

what are the SIRS criteria for sepsis?

A 
need 2 or more of the below criteria 
tachycardia >90bpm
RR> 22
acutely altered mental state
temp >38.3 or <36 
leukocytosis or leukopenia 
hyperglycaemia >7.7
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39
Q

what is the SOFA score for sepsis?

A 
Sequential Organ Failure Assessment 
if a patient with infection scores 2 or  more, suspect sepsis 
Resp; PaO2
liver: bilirubin 
Coagulation: platelets
renal; urine output 
CV; catecholamine doses
CNS; GCS score
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40
Q

what is the risk stratification approach to sepsis and how are moderate and high risk patients classified?

A

identifying infective patients who are high risk for sepsis
looking at
1) history
2) respiratory, >20 in moderate, >25 in severe
3) blood pressure, high in moderate, low in severe
4) circulation and hydration - raised HR, prolonged anuria
5) skin - cyansis, non-blanching skin rash

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41
Q

what investigations should be performed in suspected sepsis?

A 
examination and culture of potential sites of infection 
blood culture 
FBC, LFTs, U and E, renal profile 
ABGs - hypoxia and Lactate?
coagulation screening 
CRP, procalcitonin - raised in inflammation/sepsis 
glucose 
ECGs, CXR, CT - source of infection?
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42
Q

what is the sepsis six?

A 
must be completed within the first hour 
mnemonic  -O2 FLUID
1. Oxygen therapy - high flow
2. Fluid challenge - bolus
3. Lactate levels checked 
4. Urine output - hourly measurement 
5. Infection, blood culture 
6. Drugs - ASAP antibiotics - broad spec at max dose
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43
Q

what electrolyte imbalance can omeprazole and furosemide cause?

A

hyponatraemia

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44
Q

what is chronic kidney disease?

A

impaired renal function or structure for >3 months with implication for health
or markers of kidney damage and GFR <60 (on 2 separate occasions) for over 3 months

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45
Q

what are the 5 stages of CKD?

A

1) >90
2) 60-89
3a) 45-59
3b) 30-44
4) 15-29
5) <15

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46
Q

at what GFR do symptoms of renal failure become apparent?

A

usually <30 GFR

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47
Q

what are causes of CKD?

A

1) hypertension and diabetes are responsible for majority of cases
2) glomerulonephritis - mainly IgA nephropathy
3) renovascular disease
5) pyelonephritis / reflux nephropathy
others = following AKI, ATN, adult polycystic kidney disease, interstitial nephritis, obstructive uropathy, lupus

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48
Q

what are symptoms of CKD??

A

often vague - requiring lab evidence
begins with fatigue, nausea, possible oedema

then as renal function worsens = uraemic symptoms such as pruritis, bone pains, restless legs, vomiting, fatigue, weakness, yellowish tinge to skin

signs of fluid overload
signs of hyperkalaemia - seizures, encephalopathy, coma, arrhythmias

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49
Q

what investigations should be performed in suspected CKD?

A
  • Renal profile; GFR and creatinine levels
  • Urine dipstick and analysis - haematuria, proteinuria, Pyuria?
  • renal ultrasound
  • diabetes revision/screen - glucose levels etc
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50
Q

how is proteinuria defined?

A

ACR - albumin: Creatinine ratio > 30 mg/mmol
Albumin >200mg/L
PCR: urine protein: creatinine ration > 45mg /mmol
ACR is more conclusive than PCR

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51
Q

how is STAGE 1-4 CKD treated?

A
  • aim to slow down renal damage and prevent RRT

1) ACEi or ARBs = decreases the pressure in the kidneys (ramipiril or losarton)
2) Statins
3) additional hyptertensive medication - beta blockers, thiazide diuretics
2nd line = non -dilhydropyridine CCB e.g. diltiazam or verpamil

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52
Q

how is STAGE 5 CKD treated?

A

1st line = dialysis

2nd line = kidney transplant

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53
Q

what is the pathophysiological mechanisms behind diabetic nephropathy?

A

1) Raised glomerular pressure - due to HTN and RAAS activation by hyperglycaemia
2) barotrauma of mesangial cells
3) nephron ischaemia (microvascular damage, efferent arteriole vasoconstriction)

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54
Q

what are side effects of ACEi/ ARBs?

A 
dry cough 
hyperkalaemia
hypotension 
angio oedema 
AKIs - must be stopped in this case ( they prevent body's protective mechanism against pre-renal AKI)
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55
Q

how do ACEi and ARBs work in CKD?

A

they prevent salt retention and vasoconstriction
this reduced bllood volume and pressure in the kidneys
relaxes the efferent arteriole
- prevents the viscous cycle HTN causing hypoperfusion of kidney, which then activates the RAAS, raising BP

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56
Q

can you take ACEi/ARBs in pregnancy?

A

NO

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57
Q

what are the metabolic complications of CKD?

A

1) anaemia - decreased erythropoietin produced
2) Acidosis - failure to excrete various anions
3) CKD mineral bone disease - bone pain and muscle cramps

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58
Q

how is metabolic acidosis treated in CKD?

A

oral sodium bicarbonate

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59
Q

How is anaemia treated in CKD?

A

EPO stimulating agents e.g.
epoetin-alfa
darbepoetin-alfa

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60
Q

how does CKD lead to mineral bone disease?

A

hypocalcaemia is caused by kidneys inability to activate Vit D, and inability to excrete adequate phosphate.
Hypocalcaemia leads to secondary hyperparathyroidism - excess PTH causes excess phosphate

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61
Q

how is mineral bone disease in CKD treated?

A

alfacalcidol - vitamin D supplement / calcitriol

phosphate binding medication

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62
Q

when should a CKD patient be referred to a renal specialist?

A

Stage 5 - immediate referral
Stage 4 - urgent referral, or routine if stable
Stage 3 - routine referral if any of the following: uncontrolled BP, PCR>45, GFR fall by 15% after ACEi, unexplained anaemia, abnormal K, Ca, Phosphate, microscopic haematuria, systemic illness e.g. SLE
Stage 1 and 2 - referral not required

proteinuria w/ oedema and decreased serum albumin (nephrotic syndrome)
hyperkalaemia
malignant hypertension

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63
Q

which diabetic medication is contraindicated if eGFR < 30 ?

A

metformin

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64
Q

what is the target BP in all stages of CKD?

A

130/80

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65
Q

what are the features of hemodialysis?

A
  • AV fistula created (better flow, less complications for needle insertion)
  • dialysis carried out 3 times a week for 4 hours
  • diet and fluid is restricted
  • difficult to go abroad, unless dialysis clinics arranged
  • lots of time travelling to/from hospital, spent in hospital
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66
Q

what are features of peritoneal dialysis ?

A
  • tenckhoff catheter is fitted
  • usual requirement = 4-6 exchanges per day with 4-6 hours of dwell time per exchange
  • absolute CIs : IBD, ischaemic bowel, abdo abscess, pregnancy 3rd trimester, diverticulitis
  • carried out at home, less bulky, portable equipment
  • there are 2 forms: CAPD (continuous ambulatory PD) or APD (assisted PD).
  • CAPD doesn’t require a machine - the patient fills the stomach with dialysate, leaving it to dwell whilst carrying out normal daily activities and then drains it with gravity
  • APD uses a machine that automatically does exchanges whilst you sleep. the dwells are shorter. in the morning you fill with dialysate and leave it to dwell all day.
  • risk of peritonitis, malnutrition
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67
Q

what is the average waiting time for a kidney transplant in manchester?

A

3 years

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68
Q

what is the annual cost of dialysis per patient?

A

£30800

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69
Q

how is the new kidney plumbed into the patient?

A

the renal artery is anatomised onto the iliac artery
the renal vein onto the iliac vein
and the ureter onto the bladder
the old kidney is left where it was

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70
Q

what immunosuppressant drugs can be used for kidney transplant patients?

A

calcineurin inhibitors: cyclosporine or tacrolimus
antiproliferative agents: mycophenolate mofitil, mycophenolate sodium or azathioprine
prednisolone
mTOR inhibitor: sirolimus

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71
Q

what are the complications of a kidney transplant?

A

1) Rejection
2) Infection- most commonly UTI then Chest. Diverticulitis = ~100% mortality in transplant patients
3) Malignancy
4) CV disease
5) Immunosuppressant drug interacts.
6)

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72
Q

how is transplant rejection diagnosed?

A

via US guided transplant biopsy
biopsy shows lymphocyte infiltration of tubularinterstitium and tubules.
Can be treated with steroids
if lymphocytes have infiltrated vasculature - under endothelium - this is very serious.

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73
Q

risk of which malignancy is increased most in transplant patients?

A

squamous cell carcinoma of the skin

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74
Q

which immunosuppressant drug has numerous interactions?

A

tacrolimus

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75
Q

give examples of phosphate binders used in CKD?

A

lanthanum, sevelamer, calcium carbonate/acetate

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76
Q

what is tertiary hyperparathyroidism?

A

after a long period of secondary hyperparathyroidism, the regulation of PTH hormone can become autonomous and dysregulated.
excessive PTH can be secreted leading to hypercalcaemia
treated with cinacalcet

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77
Q

what are side effects of erythropoietin treatment?

A

accelerated hypertension (leading to encephalopathy or seizures)
increased risk of thrombosis (b/c increased PCV)
iron deficiency
bone aches
flu-like symptoms
skin rashes
red cell aplasia (due to autoimmune antibodies)

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78
Q

how much protein and albumin is excreted daily in the urine?

A

<150 mg protein
<30 mg albumin
30-300 mg albumin = moderately increased albuminurea

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79
Q

what is glomerulonephritis?

A
  • A group of diseases which cause injury to the glomeruli
  • present with proteinuria and/or haematuria
  • covering a spectrum from nephrotic syndrome to nephritis
  • can cause CKD
  • diagnosed on biopsy
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80
Q

what is nephrotic syndrome? (triad)

A

1) Proteinuria (hyperalbuminuria) >3.5g/24hr, PCR>300, ACR>250
2) Hypoalbuminaemia
3) Oedema
ALSO
hyperlipidaemia (serum proteins suppress lipid production usually)
lipiduria

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81
Q

what is the pathophysiology of Nephrotic syndrome?

A

damage to the filtration barrier of the glomeruli leads to proteins entering the urine. (>3.5g/24hr)
decreased protein in the serum leads to decreased oncotic and osmotic pressures. Fluid leaves the blood causing Oedema.
(?)lack of proteins/albumin in blood causes a rise in lipids. this results in hyperlipidaemia and lipiduria

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82
Q

which diseases fall under the umbrella of nephrotic glomerulonephritis?

A

Minimal Change disease
Focal Segmental Glomerulosclerosis
Membranous nephropathy
mebranoproliferative GN

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83
Q

which diseases fall under the umbrella of nephritic GN?

A

IgA nephropathy
Post-streptococcal GN
Anti GBM disease (Good Pastures)

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84
Q

What causes Minimal change disease?

A 
most cases are idiopathic 
10-20% have cause 
- drugs: NSAIDs, rifampicin 
- Hodgkin's lymphoma, thymoma 
- infectious mononucleosis
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85
Q

what are features of minimal change disease?

A
  • nephrotic syndrome
  • normotensive
  • highly selective proteinuria (only intermediate sized proteins leek through)
  • change only visible on electron microscopy - shows effacement of podocytes.
  • responsible for 75% cases of GN in children
  • and 25% cases in adults
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86
Q

what is the pathophysiology of minimal change disease?

A

t cell and cytokine mediated damage of the glomerular basement membrane leads to polyanion loss and podocyte foot damage

the loss of the electrostatic charge barrier leads to increased permeability of the glomerular filter and thus passage of albumin into the urine

87
Q

how is minimal change disease treated?

A

steroids
this works in 90% cases
cyclophosphamide is second line

88
Q

what is Focal Segmental Glomerulosclerosis?

A

scarring of segments in glomeruli. not all glomeruli are affected - only a small section.
characterised by sclerosis and hyalonosis
- where scarring occurs, the filtration barrier is damaged and proteins escape into the urine
- most common GN in adults
- can cause chronic renal failure

89
Q

what are causes of FSGS?

A

in primary FSGS - idopathic
in secondary FSGS - clear underlying cause.
secondary is associated with Sickle cell, HIV, heroin abuse, lithium, kidney hyperpurfusion, raised pressure in glomeruli

90
Q

how is FSGS treated?

A

steroids
ACEi/ARBS and BP control
2nd line = calcinuerin inhibitors e.g. tacrolimus , cyclosporine

91
Q

what is membranous nephropathy?

A
  • the glomerular basement membrane becomes inflammed.
    this leads to increased permeability and proteins escaping into the urine.
    nephrotic syndrome
92
Q

what is the pathophysiology of membranous nephropathy ?

A

inflammation of the basement membrane leads to nephrotic syndrome
the damage is caused by immune complexes. these immune complexes are either
1) auto-antibodies which target the GBM. these include M type phospholiase A2 antibodies and neutral endopeptidase
or
2) complexes which are formed outside of the kidney and then carried to the GBM. these include complexes with the antigen: cationic bovine serum albumin, from beef and cows milk.
these immune complexes are known as subepithelial deposits - sandwiched between the GBM and podocytes.
they activate the complement system - leading to damage of podocytes and mesangial cells and recruits further inflammatory mediators which cause damage to the GBM.
in response to the subepithelial deposits, GBM matrix is laid down - creating a spiky thickened GBM

93
Q

which antibodies are found in membranous nephropathy?

A

M type phospholipase A2 antibody
Neutral endopeptidase
complexes with cationic bovine serum albumin

94
Q

what are the causes for membranous nephropathy?

A 
primary = idiopathic 
secondary = autoantibodies are generated in response to malignancy, infections (Hep c,b, strep, malaria), autoimmune conditions (lupus, arthritis), and drugs (gold, penincilinamine)
95
Q

how is membranous nephropathy treated?

A 
secondary = treat underlying cause 
primary = steroids, BP control and ACEi/ARBs
96
Q

what is the pathophysiology of membranoproliferative GN (MPGN)??

A

a mixture of:
(1) immune complex deposition in btwn the endothelial layer and basement membrane. (subendothelial deposits)
(2) inappropriate complement activation - (perhaps by IgG binding C3 activase which stabilises it and causes it to continually activate C3 - this antibody is known as nephritic Factor (C3NeF))
The inflammation leads to mesangial cell proliferation and growth into the BM
Type 1 MPGN = mixture of (1) and (2)
Type 2 MPGN = only complement deposits - no immune complexes. this is also known as Dense Deposit Disease
Type 3 MPGN = mixture of (1) and (2). deposits are also found in subepithelial space as well as subendothelial space

97
Q

how does MPGN present?

A
  • present as nephrotic and maybe nephritic syndrome
98
Q

what are characteristics of nephritic syndrome?

A

INFLAMMATION
haematuria
oliguria
azotemia (nitrogen containing compounds in urine)

99
Q

how is MPGN treated?

A

steroids

ACE/ARB/BP control

100
Q

what is IgA nephropathy?

A

abnormal, galactose deficient IgA antibodies are not recognised by the body. they accumulate in high numbers. IgG anti-glycan antibodies are formed against them and complexes are formed which are then carried to the kidney.
immune complexes are deposited in the mesangium

101
Q

what is the most common cause of renal AKI?

A

Acute tubular necrosis

102
Q

how do you differentiate between pre-renal AKI and ATN (renal AKI)?

A

in prerenal AKI, the kidneys hold onto sodium to preserve volume.
In ATN: raised sodium in the urine, wont respond to fluid challenge

103
Q

what fluid challenge should be given to a patient without known HF?

A

500mls 0.9% saline

104
Q

what fluid challenge should be given to a patient with known HF?

A

250mls 0.9% saline

105
Q

what are the requirements for maintenance fluids?

A

25-30 ml/kg/24hours saline
1mmol/kg/day sodium, potassium and chloride
50-100g glucose/day

106
Q

what are the complications of nephrotic syndrome??

A

1) hypocalcaemia (vit d not activated)
2) infection - immunoglobulin lost in urine
3) coagulopathy - antithrombin 3 and plasminogen lost in urine (can cause renal vein thrombosis)
4) acute renal failure
5) hyperlipidaemia

107
Q

how is lupus nephritis picked up?

A

regular urine testing of all lupus patients, even if asymptomatic
proteinuria will be present

108
Q

what is the commonest cause of GN worldwide?

A

IgA nephropathy

109
Q

what is the histology of IgA nephropathy?

A

mesangial hypercellularity and positive immunofluoresence for IgA and C3

110
Q

how does IgA nephropathy typically present?

A

young male
recurrent episodes of macroscopic haematuria
associated with infection, usually URTI
renal failure

111
Q

how do you differentiate between IgA Nephropathy and Post-strep GN?

A 
POST STREP: 
- GN is seen 1-2 weeks after URTI 
- proteinuria also seen 
- 
IGA NEPH
- seen 1-2 days after URTI 
- macroscopic haematuria 
proteinuria very rarely seen
112
Q

what is Henoch Schonlein purpura ??

A

small vessel vasculitis and system variant of IgA nephropathy
IgA complexes are deposited in joints/skin/gut/kidney

113
Q

how does henoch schonlein purpura present?

A

purpuric rash on extensor surfaces
polyarthritis
abdo pain
GI bleeding
renal biopsy identical to IgA nephropathy
IgA nephropathy - renal failure, haematuria

114
Q

How is IgA nephropathy treated?

A

steroids

115
Q

What are features of post-strep GN?

A
  • occurs ~2 weeks after an infection

- strep antigen deposits in the glomerulus leading to immune complex formation and inflammation

116
Q

how is maintenance fluid prescribed for children?

A

100ml/kg for the first 10 kg
50ml/kg for the next 10kg
and 20ml/kg for the remainder of the kgs

117
Q

how does post-strep GN present?

A

haematuria
oedema
raised BP
oliguria

118
Q

how is post-strep GN treated?

A

supportive antibiotcis

119
Q

what are the features of Anti - GBM disease (Good Pastures)?

A
  • autoimmune antibodies against type 4 collagen - found in glomerular and alveolar BM
  • diagnosed by presence of Anti-GBM antibodies in circulation/kidney
120
Q

how does Good-Pastures disease present?

A

renal disease (oliguria, haematuria, AKI, RF) and lung disease (pulmonary haemorrhage, SOB, haemoptysis)

121
Q

what is rapidly progressive GN (Crescentric GN) ?

A

a type of nephritic syndrome
inflammation in the glomerulus leads to proliferation of cells producing a crescent like shape in the bowmans space. this change leads to renal failure in weeks to months

122
Q

what causes rapidly progressing GN?

A

idiopathic

1) type 1 - Anti-GBM antibodies (Goodpastures)
2) Type 2 - immune complex mediated e.g. Post-strep GN, lupus, IgA nephropathy and henoch schonlein
3) type 3 - Pauci- immune (no immune complexes/abs in kidney) - ANCA in blood (Anti Neutrophil Cytoplasmic Antibodies)

123
Q

what are the autosomal dominant cystic kidney diseases?

A

1) AD polycystic kidney disease
2) Von Hippel Landau
3) tuburous sclerosis
4) medularry cystic disease

124
Q

what are the features of AD PKD?

A
  • commonst genetic renal disease
  • make up 10% of the end stage renal failure ppln
  • 50% reach ESKF by 60s
  • 1 in 800 births
  • patient also presents with extra renal cysts e.g. hepatic cysts (most common), berry aneurysm, pancreas, spleen and mitral valve prolapse)
125
Q

how does a patient with ADPKD present?

A 
flank/abdo pain 
renal colic 
gross haematuria 
renal stones 
cystitis
headaches 
recurrent UTIs 
history of dysuria, suprapubic pain and urgency 
HTN 
often Hernias
chronic kidney disease
early satiety = kidneys occupy large amount of space in abdo
126
Q

what imaging should be performed if ADPKD is suspected?

A

1) ultrasonography

2) contrast enhanced CT or MRI

127
Q

what are the US diagnostic criteria for ADPKD?

A

for patients with 50% risk:

  • < 30 yrs = 2 cysts unilaterally or bilaterally
  • 30-60 yrs = 2 cysts in each kidney
  • > 60 yrs = 4 cysts in each kidney
128
Q

what is a common finding in ADPKD patients?

A

renal stones are found in 20% cases

low urine citrate and pH predisposes to this

129
Q

how is ADPKD treated?

A

1) treat HTN -lifestyle mods and medication
2) UTIs - antibiotics
3) infected renal cyst = antibiotics, drainage and 2nd line = nephrectomy
4) analgesia for renal pain
5) nephrolithiasis (renal stones) =potassium citrate
6) symptomaic polycysts - drainage, resection and then nephroctomy

130
Q

what antibiotic do we use in renal cyst infection?

A

ciprofloxacin

131
Q

which new medication may slow cyst progression in PKD?

A

Tolvaptan (Jinarc) - a vasopressin receptor 2 antagonist

  • patient needs regular blood tests to monitor liver and kidney
  • and annual imaging of kidney
132
Q

what are examples of large vessel vasculitis?

A 
Giant Cell (elderly, headaches, raised ESR)
Takayasu arteritis (pulseless disease, aorta and main branches)
133
Q

what are examples of medium vessel vasculitis??

A

kawasaki disease

polyarterius nodosum - assoc. with Hep C and B

134
Q

what are examples of small vessel vasculitis?

A

ANCA associated

others… SLE

135
Q

what does ANCA stand for?

A

Anti Neutrophil Cytoplasmic Antibodies

136
Q

what are the 3 clinical entities of ANCA assoc. vasculitis?

A

1) microscopic polyangitis
2) granulomatosis polyangitis
3) eosinophilic granulomatosis polyangitis

137
Q

what are the 2 types of ANCA?

A

pANCA = perinuclear staining. specific for myeloperioxidase staining. seen mostly in Pauci immune GN

cANCA = diffuse cytoplasmic staining. specific for proteinase 3 enzmye

both enzymes are present in neutrophil granules

138
Q

what is the pathogenesis of ANCA assoc. vasculitis??

A

1) neutrophil is primed - expression of auto antibodies
2) binding of ANCA and activation of neutrophil
3) tissue damage

139
Q

how does ANCA assoc. vasculitis present?

A

renal - Pauci immune GN / RPGN

lungs - haemoptysis, granuloma/alveolar haemorrhage, cough, dyspnoea

140
Q

how is ANCA + vasculitis treated?

A

1) induction of remission = steroids and cyclophosphamide

2) maintenance of remission = azathioprine and steroids

141
Q

what are features of von hippel landau disease?

A
  • a mutation in the tumour suppressor gene (VHL protein)
  • autosomal dominant
  • 1 in 36000
  • presents in 20’s-30’s with an array of benign tumours and cysts in the CNS, abdomen, pancreas, retina
142
Q

what are the kidney mainfestations of VHL syndrome?

A
  • cortical renal cysts (70%)
  • renal cell carcinoma (20-40%)
  • renal cell adenoma, renal haemaginoma
143
Q

how is VHL syndrome monitored?

A

annual US

3 yearly CT scan

144
Q

what are causes of transient non-visible haematuria?

A

sexual intercourse
vigorous exercise
UTI
menstruation

145
Q

what are causes of persistent non-visible haematuria?

A 
cancer (bladder, prostate, renal)
stones 
BPH
Renal causes (GN nephritis, IgA nephropathy,)
prostasis 
urethritis (chlamydia)
146
Q

when do you make an urgent referal for haematuria?

A

> 45 years with haematuria without UTI or after successful treatment of UTI
65 years with haematuria without UTI AND dysuria or raised WBC

147
Q

when do you make a non-urgent referral for haematuria?

A

unexplained persistent/recurrent UTIs in > 60 YO

148
Q

which GN presents with nephrotic syndrome?

A

minimal change GN
FSGN
membranous GN

149
Q

which GN presents with nephritic syndrome?

A

IgA nephropathy

Rapidly progressing GN

150
Q

which GN present with mixed nephritic/nephrotic picture?

A

Post - strep GN

membranoproliferative GN

151
Q

what are extra-renal features of ADPKD?

A

hepatic cysts - manifest as hepatomegaly
ovarian cysts
intracranial aneurysms
diverticulosis

152
Q

what is the prognosis of Henoch schonlein purpura?

A

usually excellent, self-limiting disease

1/3 will relapse

153
Q

how may contrast media nephrotoxicity defined?

A

25% rise in creatinine within 3 days of IV contrast media administration

154
Q

how is the risk of contrast media administration reduced in CKD patients?

A

administration of 0.9% saline solution at a rate of 1mL/kg/h for 12 hours pre-and post-procedure
N acetyl cysteine (oral) has been shown to help but poor evidence base

155
Q

what are risk factors for contrast media nephrotoxicity?

A 
known renal impairment 
dehydration 
cardiac failure
>70 YO
nephrotoxic drugs
156
Q

how would a patient with a ruptured berry aneurysm present?

A

subarachnoid haemorrhage
-sudden severe headache
-meningitic features= neck stiffness and vomiting
CT findings = hyper attentuation around circle of willis

157
Q

what is the characteristic triad of haemolytic uraemic syndrome?

A

1) haemolytic anaemia
2) thrombocytopenia - low platelet count
3) acute kidney failure (Uraemia)

158
Q

what are causes of haemolytic uraemic syndrome?

A 
post dysentry e.g. E Coli 
tumours
pregnancy
cyclosporin, the pill 
HIV 
SLE
159
Q

how does minimal change disease present?

A

young child
periorbital swelling
frothy urine

160
Q

what is the prognosis of minimal change disease?

A

1/3 have 1 episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

161
Q

what is the first step after receiving a patients blood results which show hyperkalaemia?

A

urgent ECG

if ECG changes consistent with hyperkalaemia are seen - stabilise myocardium with calcium gluconate infusion

162
Q

how is severity of hyperkalaemia classified??

A

mild 5.5-5.9
moderate 6 - 6.4
severe >6.5mmol/l

163
Q

what are features of rhabdomyolosis?

A
  • renal failure with disproportionately raised creatinine
  • CK rise
  • myoglobinuria
  • hypocalcaemia (myoglobin binds calcium)
  • elevated phosphate - released from myocytes
164
Q

eosinophilic casts are found on microscopic inspection of urine. what is this a sign of?

A

acute interstitial nephritis

usually caused by a drug reaction e.g. penicillin

165
Q

which bacteria is associated with post-strep GN?

A

streptococcus pyogenes

166
Q

what are the different causes of anaemia in CKD?

A

reduced erythropoietin
reduced erythropoiesis in bone marrow due to toxic ureamic affect
reduced iron absorption
nausea and vomiting due to uraemia
reduced red cell survival (especially in haemodialysis)

167
Q

what are signs/symptoms of anaemia?

A

pallor
tachycardia
fatigue
aortic flow murmur

168
Q

what are acceptable changes in CK and GFR after starting on an ACEi in patients with CKD?

A

a rise in creatinine of 30%

and fall in GFR of 25%

169
Q

what antihypertensive medication should be used if GFR falls below 45 (or 30)?

A

furosemide

170
Q

what is the most commonly used formula for calculating eGFR?

A

MDRD

modification of diet in renal disease

171
Q

what variables does the MDRD formula take into account?

A 
CAGE
creatinine 
age
gender
ethnicity
172
Q

which factors may affect the eGFR?

A

pregnancy
muscle mass
eating red meat 12 hours prior to tests

173
Q

what are causes for diffuse proliferative GN?

A

post-strep

SLE

174
Q

why are diuretics nephrotoxic?

A

they prevent water being reabsorbed into the capillaries. this means the capillaries have a lower volume as they move to the end of the nephrons. this can cause hypoxia and then acute tubular necrosis

175
Q

muddy brown casts found in urine microscopy are suggestive of?

A

acute tubular necrosis

176
Q

what is an example regime for immunosuppression following a transplant?

A

initial: ciclosporin/tacrolimus with monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus
add steroids after 1 rejection episode

177
Q

what is Alports syndrome?

A

a rare X linked dominant genetic disease

caused by a mutation in gene coding for collagen 4 resulting in abnormal glomerular basement membrane

178
Q

what are features of Alports syndrome?

A
  • presents in childhood
  • progressive renal failure
  • microscopic haematuria
  • bilateral sensorineural loss
  • retinitis pigmentosa
  • lenticonus - protrusion of the lens into the anterior chamber
179
Q

what is seen on electron microscopy of a renal biopsy from a patient wit Alport syndrome?

A

splitting of the lamina densa

180
Q

what is gold standard for bladder cancer diagnosis?

A

cystoscopy

181
Q

what are complications of peritonal dialysis ?

A

peritonitis

sclerosing peritonitis

182
Q

which bacteria is most commonly responsible for peritonitis in peritoneal dialysis?

A

staphylococcus epidermidis

staph aureus is another common one

183
Q

how is diabetes insipidus treated?

A

cranial DI = treated with vasopressin analogue e.g. desmopressin
nephrogenic DI = treated with thiazide diuretic. prevents the plasma serum osmolarity for getting too high e..g chlorothiazide

184
Q

what changes predispose to thrombosis in CKD?

A

loss of antithrombin 3, proteins C and S

and subsequent raise in fibrinogen

185
Q

what are potential complications of an arteriovenous fistula?

A

infection
thrombosis
stenosis
steal syndrome

186
Q

when should calcium glucanate be administered for hyperkalaemia?

A

if potassium >6.5 or ECG changes

187
Q

what are symptoms of hypokalaemia?

A

weakness, leg cramps, ascending paralysis, arrhythmias causing palpitations

188
Q

what are ECG changes seen in hypokalaemia?

A

u waves
absent/flat T waves
prolonged PR interval
ST depression

189
Q

how is hypokalaemia treated?

A

depends on severity
mild to moderate: 2.5 - 3.4 treated with oral potassium
severe < 2.5 : cardiac monitoring and saline with potassium infusion. not exceeding 20mml/hr

190
Q

what are the 2 types of ADPKD?

A

type 1 - 85% cases. mutation in polycistin 1 on chromosome 16
type 2 - 15% cases, mutation in polycistin 2 on chromosome 4

191
Q

what is Wilm’s nephroblastoma?

A

one of the most common childhood malignancy

typically presents in under 5s (mean age 3)

192
Q

what are features of Wilm’s nephroblastoma?

A 
abdominal mass
painless haematuria 
flank pain 
other = fever, anorexia 
unilateral in 95% cases
20% metastasised
193
Q

how does acute graft rejection present?

A

<6 months post transplant

signs and symptoms of infection

194
Q

what is the most common viral infection in organ transplant recipients?

A

cytomegalovirus

treated with ganciclovir

195
Q

what are causes for hypokalaemia associated with hypertension?

A

cushings syndrome
conns syndrome (primary hyperaldosteronism)
liddle’s syndrome

196
Q

what are causes of hypokalaemia without HTN?

A

GI loss
diureti
renal tubular acidosis

197
Q

can a CKD diagnosis be made on eGFR alone?

A

no, need supporting evidence from urinalysis or renal ultrasound

198
Q

how does a urine dip differentiate between causes of AKI?

A
  • presences of proteins basically rules out any pre or post renal causes
  • absence of nitrates rules out infection
  • high white blood count will point towards an inflammatory process
199
Q

what is the most likely cause of death for CKD patient on haemodialysis?

A

ischaemic heart disease

CV events acount for over 50% of mortality

200
Q

what can spironolcatone be switched for?

A

eplerenone (another aldosterone antagonist)

201
Q

what are features of renal cell carcinoma?

A

-classic triad = loin pain, abdo mass, haematuria
-pyrexia
- left varicocele (due to occlusion of left testicular vein)
-endocrine effects -may secrete erythropoietin, PTH, renin, ACTH
-

202
Q

what are the investigations for goodpastures?

A

renal biopsy - linear IgG deposits along linear BM

increased transfer factor b/c of haemorrhage

203
Q

how is pyelonephritis treated?

A

24-48 hours of IV gentamicine or temocillin

204
Q

what abnormalities may predispose a patient to UTIs?

A

urinary tract tumours
urinary stones
incomplete bladder emptying
vesicoureteral reflux

205
Q

what is defined as recurrent UTIs?

A

> 3 episodes /year

206
Q

how do urological stones present?

A 
pain 
haematuria 
infection 
3rd-5th decade of life 
male > female
207
Q

what are causes of urological stones?

A

metabolic (50%) - renal tubular acidosis, hyperparathyroidism, crohns disease, cystinuria, sarcoidosis

  • infection
  • immobilisation
  • urological
208
Q

what are urological stones composed of?

A

75% calcium oxalate
10% struvate
10% urate

209
Q

how are urological stones managed?

A

increase fluid intake
treat infection
surgery for large stones >8mm

210
Q

what is the most common kidney malignancy?

A

renal cell carcinoma (80%)

next is TCC

211
Q

what are benign renal tumours?

A

angiomyolipomas

oncocytoma

212
Q

what is papillary necrosis?

A

necrosis and shedding of medullary papillae

the papillae may cause obstruction and pyonephrosis

213
Q

what are RFs for papillary necrosis?

A

analgesia, sickle cell, infection, DM

214
Q

how is papillary necrosis treated?

A

emergency drainage

and antibiotics

3rd Year Medicine UoM (9 decks)

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