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2MBChB Renal > Kidney Disease > Flashcards

Kidney Disease Flashcards

1
Q

What is chronic kidney disease (CKD)?

A

Abnormal kidney function and/or structure.

  • Often co-exists with other conditions e.g. CVD and diabetes.*
  • Requires at least 2 samples (abnormal U&Es [eGFR/creatinine]) at least 90 days apart.*
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2
Q

What is moderate to severe CKD associated with?

A

Increased risk of CVD, acute kidney injury, falls, frailty and mortality.

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3
Q

What are markers of GFR?

A

Creatinine - on its own not very useful.

eGFR - based upon serum creatinine level, age, sex and race.

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4
Q

What is eGFR based upon?

A

Serum creatinine level.

Age.

Sex.

Race.

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5
Q

How if eGFR creatinine estimated?

A

Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI).

Reported as either eGFR >60, or if below 60 then a numerical value is given.

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6
Q

What are the stages of CKD?

A
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7
Q

What test investigates proteinuria?

A

Albumin/creatinine ratio (ACR).

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8
Q

What are the categories of ACR?

A

A1 is barely any albumin detectable.

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9
Q

Why is the albumin to creatinine ratio in urine calculated rather than the level of albumin in urine on its own?

A

Albumin presence on its own can just be an indication of concentrated urine, dehydration, post-exercise muscle breakdown.

Whereas, by calculating the ratio of albumin to creatinine means you can determine if there is more albumin than there should be in the urine or not.

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10
Q

What are the guidelines for management of anyone with acute kidney injury (AKI)?

A

They need to be monitored for at least 2-3 years after acute kidney injury even if serum creatinine has returned to baseline.

This is because people who have had AKI puts them at increased risk of CKD developing or progressing.

In severe cases of AKI, the patient may have an annual review lifelong.

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11
Q

What is an eGFRcystatinC?

A

A more accurate measure of eGFR using cystatinC rather than creatinine to confirm or rule out CKD in people with an eGFRcreatinine of 45-59ml/min/1.73m2 or no proteinuria or other marker of CKD.

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12
Q

Who is ACR and eGFRcreatinine testing offered to?

A

Diabetes.

Hypertension.

Acute kidney injury.

CVD.

Structural renal disease.

Multisystem diseases with potential kidney involvement, recurrent renal calculi or prostatic hypertrophy.

Family history of end-stage kidney disease or hereditary kidney disease.

Opportunistic detection of haematuria.

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13
Q

How is accelerated progression of CKD defined?

A

A sustained decrease in GFR of 25% or more and a change in GFR category within 12 months.

OR

A sustained decrease in GFR of 15ml/min/1.73m2 per year.

This is normally plotted on a graph in the patient’s notes.

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14
Q

What risk factors are associated with CKD progression?

A

CVD.

Proteinuria.

AKI.

Hypertension.

Diabetes.

Smoking.

African, African-Caribbean or Asian family origin.

Chronic used of NSAIDs.

Untreated urinary outflow tract obstruction.

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15
Q

What is the target range for BP in people with CKD without proteinuria?

A

<140/90mmHg.

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16
Q

What is the target range for BP in people with CKD with proteinuria (ACR >70mg/mmol) and/or diabetes?

A

<130/80mmHg.

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17
Q

What medications for prevention of associated risks should CKD patients be on?

A

Atorvastatin 20mg for primary/secondary prevention of CVD.

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18
Q

What are the causes of CKD?

A

Diabetes.

Hypertension.

Glomerular nephritides (primary/secondary).

Macro- and microvascular causes (renal artery stenosis; small vessel vasculitidis).

Tubulointerstitial.

Post-renal (obstruction: calculi, prostatic, bladder, urethral structure).

Main causes are in bold.

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19
Q

What are the clinical signs of CKD?

A

Anaemia - conjunctival and palmar pallor.

Weight loss.

Advanced uraemia:

  • Lemon yellow.
  • Uraemic frost (sweating out uraemic toxins visible on skin that smells of urea).
  • Twitching.
  • Encephalopathic flap.
  • Confusion.
  • Pericardial rub or effusion.
  • Kussmaul breathing (respiratory compensation of metabolic acidosis).
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20
Q

What are the symptoms of uraemia in CKD?

A

Nausea & vomiting.

Anorexia.

Weight loss.

Fatigue.

Itch.

Altered taste.

Restless legs.

Muscle twitching.

Difficulties concentrating.

Confusion.

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21
Q

What are the symptoms of anaemia in CKD?

A

Fatigue.

Muscle weakness.

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22
Q

What are the symptoms of pain in CKD?

A

Bony.

Neuropathic.

Ischaemia.

Visceral.

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23
Q

What are the renal consequences of CKD?

A

Local pain/haemorrhage/infection.

Urinary haematuria/proteinuria (frothy urine).

Impaired salt and water handling.

Hypertension.

Electrolyte abnormalities.

Acid-base disturbance.

All leads to end-stage renal dysfunction.

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24
Q

What are the extra-renal consequences of CKD?

A

CVD.

Mineral and bone disease (CKD-MBD).

Anaemia.

Nutrition.

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25
Q

What are the treatments for end-stage renal disease?

A

Renal replacement therapies (haemodialysis, peritoneal dialysis, transplantation).

Conservative management.

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26
Q

At what eGFR does increased risk of CVD start?

A

eGFR <50mls/min.

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27
Q

When should you not use the CVD calculators to calculate risk of CVD?

A

In patients with renal disease, you should not use cardiovascular risk calculators because they significantly underestimate the risk.

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28
Q

How do you modify CV risk in people with CKD?

A

Smoking cessation.

Weight loss.

Aerobic exercise.

Limiting salt intake.

Control of hypertension.

Lipid-lowering therapy.

Consider aspirin for secondary prevention but there is a significantly increased risk of bleeding complications for patients on multiple anti-thrombotic agents.

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29
Q

What are the consequences of CKD mineral and bone disease?

A

Secondary/tertiary hyperparathyroidism.

Vascular calcification.

Bone pain.

Fractures.

CV events.

Lower life quality.

High morbidity and mortality.

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30
Q

What dietary advice is given to patients with CKD and mineral and bone disease?

A

Phosphate restriction (if high).

Consider:

  • Salt reduction.
  • Potassium restrictions (if persistently elevated).
  • Fluid resuscitation to 1-1.5L/day if volume overload.
  • Consider other dietary restrictions also (e.g. DM/coeliac/etc.).
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31
Q

What is renal anaemia?

A

Anaemia in CKD with an eGFR of <45 (less common with eGFRs >45; CKD 3a and above).

Diabetics are more at risk.

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32
Q

What is the target haemoglobin range in renal anaemia?

A

100-120g/L.

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33
Q

How can kidney disease present?

A

Asymptomatic.

Loin pain/urinary symptoms.

Haematuria:

  • Microscopic.
  • Painless macroscopic haematuria.

Proteinuria.

Hypertension:

  • Asymptomatic.
  • Accelerated.

Acute kidney injury.

Chronic kidney disease.

Nephrotic syndrome.

Nephritic syndrome.

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34
Q

What are the functions of the kidney?

A

Excretion of nitrogenous waste (urea).

Fluid balance.

Electrolyte balance.

Acid-base balance.

Vitamin D metabolism/ phosphate excretion.

Production of erythropoietin.

Drug excretion.

Barrier to loss of proteins.

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35
Q

Where does the problem lie if a patient presents with uraemia (pericarditis/encephalopathy/neuropathy/asterixis/gastritis)?

A

In excretion of nitrogenous waste (urea).

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36
Q

Where does the problem lie if a patient presents with fluid retention and oedema?

A

Fluid balance.

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37
Q

Where does the problem lie if a patient presents with hyperkalaemia and arrhythmia?

A

Electrolyte balance.

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38
Q

Where does the problem lie if a patient presents with metabolic acidosis and Kussmaul’s respiration?

A

Acid-base balance.

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39
Q

Where does the problem lie if a patient presents with renal bone disease and vascular calcification?

A

Vitamin D metabolism/phosphate excretion.

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40
Q

Where does the problem lie if a patient presents with anaemia?

A

Production of erythropoietin.

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41
Q

Where does the problem lie if a patient presents with drug toxicity e.g. digoxin, gabapentin?

A

Drug excretion.

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42
Q

Where does the problem lie if a patient presents with proteinuria and nephrotic syndrome?

A

Problem with the barrier to loss of proteins.

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43
Q

Which renal function may or may not be impaired in association with significant loss of renal function?

A

Barrier to loss of proteins.

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44
Q

What is the presentation of accelerated hypertension?

A

Diastolic BP >120mmHg.

Papilloedema.

End-organ decompensation (encephalopathy, fits, cardiac failure, acute renal failure).

This is a medical emergency.

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45
Q

What is a urinary cast?

A

Formed by precipitation of Tamm-Horsfall mucoprotein which is secreted by renal tubule cells.

It is seen more in environments favouring protein denaturation and precipitation (low urine flow, low pH).

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46
Q

What is seen on an ECG suggestive of hyperkalaemia?

A

Peak T-waves.

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47
Q

What is acute kidney injury?

A

Decline in GFR over hours/days/weeks with or without oliguria (<400ml urine output/day).

Can occur in a patient with normal or impaired baseline renal function.

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48
Q

What are the symptoms of nephrotic syndrome?

A

Triad of symptoms and signs fur to glomerular disease:

  • Proteinuria >3g/day (mostly albumin, also globulins).
  • Hypoalbuminaemia.
  • Oedema (hypercholesterolaemia).

Often normal renal function.

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49
Q

What is nephritic syndrome?

A

Signs and symptoms of glomerulonephritis:

  • Acute kidney injury.
  • Oliguria.
  • Oedema/fluid retention.
  • Hypertension.
  • Active urinary sediment (RBC’s, RBC and granular casts, proteinuria).
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50
Q

What is acute kidney injury (AKI)?

A

An abrupt (<48hrs) reduction in kidney function defined as:

  • An absolute increase in serum creatinine by >26.4micromol/L.
  • OR increase in creatinine by >50%.
  • OR a reduction in urine output.
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51
Q

How is acute kidney injury categorised?

A

KDIGO staging classification 1-3.

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52
Q

What are the risk factors for acute kidney injury?

A

Older age.

CKD.

Diabetes.

Cardiac failure.

Liver failure.

Peripheral vascular disease.

Previous AKI.

Hypotension.

Hypovolaemia - blood loss.

Sepsis.

Deteriorating NEWS.

Recent contrast.

Exposure to certain medications.

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53
Q

What are the causes of acute kidney injury?

A

Pre-renal (functional).

Renal (structural).

Post-renal (obstruction).

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54
Q

What are the pre-renal causes of acute kidney injury?

A

Hypovolaemia (haemorrhage, volume depletion e.g. D&V, burns).

Hypotension (cardiogenic shock, distributive shock e.g. sepsis, anaphylaxis).

Renal hypoperfusion (NSAIDs, COX-2, ACEI, ARBs, hepatorenal syndrome).

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55
Q

What is pre-renal AKI?

A

Reversible volume depletion leading to oliguria and an increase in creatinine.

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56
Q

What is the volume of normal urine output?

A

0.5ml/kg/hour.

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57
Q

What is the volume of oliguria?

A

<0.5ml/kg/hour.

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58
Q

What is the effect of ACEI on GFR?

A

ACE inhibitors reduce Angiotensin II.

Angiotensin II mediates arteriolar vasoconstriction, therefore, increasing GFR.

ACEI, therefore, can cause a fall in GFR by causing efferent arteriolar vasodilation.

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59
Q

What is acute tubular necrosis?

A

Death of tubular epithelial cells that form the renal tubules of the kidneys.

Due to a combination of factors leading to decreased renal perfusion.

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60
Q

What are the causes of acute tubular necrosis?

A

Sepsis.

Severe dehydration.

Rhabdomyolysis.

Drug toxicity.

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61
Q

What is the treatment of pre-renal AKI?

A

Assess for hydration.

  • Clinical observations (BP, HR, UO).
  • JVP, capillary refill time, oedema.
  • Pulmonary oedema.

Fluid challenge for hypovolaemia.

  • Crystalloid (0.9% NaCl) or colloid (Gelofusin).
  • Do NOT use 5% dextrose as the dextrose goes into the extravascular space so has no effect in increasing BP.
  • Give bolus of fluid then reassess and repeat as necessary.
  • If >1000mls in and no improvement, seek help.
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62
Q

What are the renal causes of AKI?

A

Diseases causing inflammation or damage to the cells causing AKI.

Vascular:

  • Vasculitis, renovascular disease.

Glomerular:

  • Glomerulonephritis.

Interstitial Nephritis:

  • Drugs (e.g. penicillin, NSAIDS, PPIs).
  • Infection (e.g. TB).
  • Systemic (e.g. sarcoid).

Tubular injury:

  • Ischaemia — prolonged renal hypoperfusion.
  • Drugs (e.g. gentamicin).
  • Contrast.
  • Rhabdomyolysis.
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63
Q

What are the signs and symptoms of AKI?

A

Non-specific symptoms:

  • Constitutional symptoms (anorexia, weight loss, fatigue, lethargy).
  • Nausea & vomiting.
  • Itch.
  • Fluid overload.
  • Oedema, SOB.

Signs:

  • Fluid overload incl hypertension, oedema, pulmonary oedema, effusions (pleural & pulmonary).
  • Uraemia incl itch, pericarditis.
  • Oliguria.
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64
Q

What drugs are important when taking a drug history in someone with an AKI?

A

NSAIDs.

PPIs.

ACEI.

ARB.

Gentamicin.

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65
Q

What initial investigations would you do for someone with AKI?

A

U&Es

  • Marker of renal function (Na, K, Ur, Cr).
  • Look at the potassium, is it high?.

FBC & Coagulation Screen

  • Abnormal clotting.
  • Anaemia.

Urinalysis

  • Haematoproteinuria.

USS

  • ?Obstruction.
  • ?Size (1 big kidney and 1 small kidney means potential renal artery stenosis).

Immunology

  • ANA, ANCA, GBM (myeloma - will also have high calcium and anaemia in this case).

Protein electrophoresis & BJP.

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66
Q

What are the life-threatening complications of AKI?

A

Hyperkalaemia.

FLuid overload (pulmonary oedema).

Severe acidosis (pH <7.15).

Uraemic pericardial effusion.

Severe uraemia (>40).

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67
Q

What are the post-renal causes of AKI?

A

Stones.

Cancers.

Strictures.

Extrinsic pressure.

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68
Q

What is post-renal AKI?

A

Due to obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability.

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69
Q

What is the treatment of post-renal AKI?

A

Relieve obstruction (catheter, nephrostomy).

Refer to urology if ureteric stenting required.

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70
Q

What is hyperkalaemia associated with?

A

Cardiac Arrhythmias.

  • Normal K = 3.5-5.0.*
  • Hyperkalaemia = >5.5.*
  • Life-threatening hyperkalaemia = >6.5.*
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71
Q

How do you assess hyperkalaemia?

A

ECG.

Muscle weakness.

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72
Q

What is the medical treatment for hyperkalaemia?

A

Cardiac Monitor & IV access.

Protect myocardium:

  • 10mls 10% calcium gluconate (2-3mins) - life-saving as prevents cardiac arrest.

Move K+ back into the cells:

  • Insulin (actrapid 10units) with 50mls 50% dextrose (30 mins).
  • Salbutamol Nebs (90 mins).

Prevent absorption from GI tract:

  • Calcium resonium (NOT in the acute setting).
73
Q

What would you give someone with severe hyperkalaemia who is away to arrest?

A

Calcium gluconate 10mls 10%.

Insulin (actrapid 10 units) with 50mls 50% dextrose.

Sodium bicarbonate to treat acidosis which exacerbates hyperkalaemia.

74
Q

What are the urgent indications for haemodialysis?

A

Hyperkalaemia (>7 or >6.5 unresponsive to medical therapy).

Severe Acidosis (pH < 7.15).

Fluid overload.

Urea >40, pericardial rub/effusion.

75
Q

What is the cause of this patient’s AKI?

40-year-old male presenting with general malaise & haemoptysis (urea 28, creatinine 600, elevated ant-glomerular membrane disease [GBM]).

A

Goodpasture’s syndrome.

76
Q

What is the cause of this patient’s AKI?

25-year-old IVDA found collapsed at home.

A

Rhabdomyolysis.

77
Q

What is the cause of this patient’s AKI?

82-year-old man admitted with BP 70 30, T 39, pulse 140bpm, K+ 7.0, urea 48, Cr 789, CRP 250, CXR left basal consolidation.

A

Acute tubular necrosis from sepsis.

78
Q

What is the cause of this patient’s AKI?

72-year-old man presenting with difficulty passing urine and reduced urine output.

A

Obstructive uropathy.

79
Q

Which of the following drugs do not cause hyperkalaemia?

  1. Spironolactone.
  2. Ramipril.
  3. Amiloride.
  4. Furosemide.
  5. Atenolol.
A

4 - furosemide.

80
Q

80-year-old male admitted with 4-5 day history of diarrhoea. On admission BP 80 40, pulse 30bpm. Bloods phone back: Na 135, K+ 8.0, Urea 50, Cr 1000, Bicarb 9.

Which drugs would you administer first?

A

Calcium gluconate.

81
Q

Which of the following is not an indication for emergency dialysis?

  1. Pulmonary oedema (in context of AKI).
  2. Life-threatening hyperkalaemia.
  3. Uraemic pericarditis.
  4. Elevated creatinine > 500.
  5. Severe acidosis.
A

4 - elevated creatinine >500.

82
Q

Which drugs would you avoid in patients with AKI?

A

NSAIDs.

ACE/ARB.

Diuretics.

Gentamicin.

Contrast.

Trimethoprim and co-trimoxazole as they work by causing hyperkalaemia which puts creatinine up.

Potassium-sparing diuretics.

83
Q

What are the glomerular diseases?

A

Diabetic nephropathy.

Glomerulonephritis.

Amloid/light chain nephropathy.

Transplant glomerulopathy.

84
Q

What is glomerulonephritis?

A

Immune-mediated disease of the kidneys affecting the glomeruli with secondary tubulointerstitial damage.

85
Q

What is the pathogenesis of glomerulonephritis?

A

Antibody-mediated.

Causing a cell-mediated (T cell) response.

Inflammatory cells, mediators and complements.

86
Q

What type of barrier is the glomerular capillary wall?

A

Size and charge-selective barrier.

87
Q

In glomerulonephritis, what happens to the glomerular capillary wall?

A

Disruption of the barrier which leads to haematuria and/or proteinuria.

88
Q

In glomerulonephritis, what happens if the damage is to the endothelial or mesangial cells?

A

Leads to a proliferative lesion and red cells (blood) in the urine (haematuria).

Nephritic type picture.

89
Q

In glomerulonephritis, what happens if the damage is to the podocytes?

A

Non-proliferative lesion and protein in the urine (proteinuria).

Nephrotic type picture.

90
Q

24-year-old man incidentally found to have ++ blood and + protein on dip, BP 148/92.

Protein quantified at 0.7g/day. Creat 72.

What glomerular cells are most likely to be injured?

A

Mesangial cell.

91
Q

What urine microscopy features are suggestive fo glomerular disease?

A

RBCs are squished (dysmorphic) as they’ve been pushed through the tubules.

Red cell casts (suggestive of endothelial injury e.g. vasculitis.

92
Q

What is nephritic syndrome?

A

Acute renal failure (rapidly declining renal function).

Oliguria.

Oedema/fluid retention (from not peeing much).

Hypertension.

Active urinary sediment (RBCs, RBC and granular casts).

93
Q

What is a nephritic syndrome indicative of?

A

Proliferative process affecting endothelial cells.

94
Q

What is nephrotic syndrome?

A

Proteinuria >3g/day (mostly albumin but also globulins).

Hypoalbuminaemia (<30).

Oedema.

Hypercholesterolaemia.

Usually normal renal function.

95
Q

What is a nephrotic syndrome indicative of?

A

A non-proliferative process affecting podocytes.

96
Q

What are the complications of nephrotic syndrome?

A

Infections due to loss of opsonising antibodies.

Renal vein thrombosis (due to blood being thicker because of lack of protein in the blood).

Pulmonary emboli.

Volume depletion (overaggressive use of diuretics) - may lead to acute renal failure (pre-renal).

  • Vitamin D deficiency.*
  • Subclinical hypothyroidism.*
97
Q

How does the presentation of glomerulonephritis differ from a non-glomerular disease like Interstitial Nephritis?

A

Protein will be seen in the urine of glomerulonephritis.

98
Q

What are the secondary causes of glomerulonephritis?

A

Infections.

Drugs.

Malignancies.

Part of systemic disease (e.g. ANCA-associated systemic vasculitis, lupus, Goodpasture’s, HSP).

99
Q

How can glomerulonephritis bee classified histologically?

A

Proliferative or non-proliferative.

Focal or diffuse.

Global or segmental.

Cresentic (presence of crescents - extracapillary proliferation).

100
Q

What are the aims of treatment in glomerulonephritis?

A

Reduce the degree of proteinuria.

Induce remission of nephrotic syndrome.

Preserve long-term renal function.

101
Q

What are the 2 main types of treatment in glomerulonephritis?

A

Immunosuppressive.

Non-immunosuppressive.

102
Q

What are the risks of immunosuppressing a patient who is nephrotic?

A

Patients are already at high risk of infection due to leaking protein so if you then immunosuppress them, they are even more at risk of septic infections.

103
Q

74-year-old woman.

Hypoxic.

Haemoptysis.

Creatine 430.

Blood and protein on dip.

Red cell casts on microscopy.

Purpuric rash.

What cells are affected?

A

Endothelial cells.

104
Q

74-year-old woman.

Hypoxic.

Haemoptysis.

Creatine 430.

Blood and protein on dip.

Red cell casts on microscopy.

Purpuric rash.

What’s the diagnosis?

A

ANCA-positive vasculitis.

105
Q

74-year-old woman.

Hypoxic.

Haemoptysis.

Creatine 430.

Blood and protein on dip.

Red cell casts on microscopy.

Purpuric rash.

What investigation would you do?

A

Blood test for ANCA.

106
Q

Describe the ECG changes caused by hyperkalaemia?

A
107
Q

What is the medical treatment for hyperkalaemia?

A

Cardiac monitor and IV access.

10mls 10% calcium gluconate (over 2-3mins) - protects myocardium.

Insulin (actrapid 10 units) with 50mls 50% dextrose (over 30mins) - moves K back into the cells.

Salbutamol nebulised (over 90 mins) - moves K back into the cells.

Calcium resonium (NOT given in the acute setting) - prevents absorption from the GI tract.

108
Q

What is the non-immunosuppressive treatment for glomerulonephritis?

A

Anti-hypertensives (ACEI/ARBs; target BP <130/80 or <12/75 if proteinuria).

Diuretics.

Statins.

? anticoagulants/aspirin/antiplatelets.

? omega 3 fatty acids/fish.

109
Q

What are the immunosuppressive treatments for glomerulonephritis?

A

Corticosteroids.

Azathioprine.

Alkylating agents.

Calcineurin inhibitors.

Mycophenolate mofetil.

Plasmapheresis.

IV immunoglobulin or MAB.

110
Q

What is the general treatment for nephrotic patients?

A

Fluid restriction.

Salt restriction.

Diuretics.

ACE inhibitors/ARBs.

? anticoagulation.

IV albumin (only if volume is depleted).

Immunosuppression.

Aim is to induce sustained remission: complete remission (proteinuria <300mg/day) or partial remission (proteinuria <3g/day).

111
Q

What are the main types of primary (idiopathic) glomerulonephritis?

A

Minimal change.

Focal segmental glomerulosclerosis.

Membranous.

Membranoproliferative.

IgA nephropathy.

112
Q

What is minimal change disease?

A

Commonest type of glomerulonephritis in children.

Normal renal biopsy on light and immunofluorescent microscopy with foot process fusion of the podocyte on electron microscopy.

Does not cause progressive renal failure.

Thought to be caused by IL-13

113
Q

What is focal segmental glomerulosclerosis?

A

Commonest cause of nephrotic syndrome in adults.

Causes are primary or secondary HIV, heroin use, obesity, reflux nephropathy.

Renal biopsy shows minimal immunoglobulin under light microscopy and complement deposition under immunofluorescence.

50% progress to end-stage renal failure after 10 years.

Remission with prolonged steroids in 60%.

114
Q

What is membranous nephropathy?

A

Second commonest cause of nephrotic syndrome in adults.

Renal biopsy shows subepithelial immune complex deposition in the basement membrane.

Steroids/alkylating agents/B cell monoclonal antibodies.

30% progress to end-stage renal failure in 10 years.

115
Q

What are the important secondary causes of membranous nephropathy?

A

Infections (hepatitis B/parasites).

Connective tissue diseases (lupus).

Malignancies (carcinomas/lymphoma).

Drugs (gold/penicillamine).

116
Q

What antibody presents in >70% of patients with primary membranous nephropathy?

A

Anti-PLA2r antibody.

117
Q

What is IgA nephropathy?

A

Commonest glomerulonephritis in the world.

Asymptomatic microhaematuria +/- non-nephrotic range proteinuria.

Macroscopic haematuria after resp/GI infection.

Associated with Henoch-Schonlein Purpura (HSP; arthritis/colitis/purpuric skin rash).

Renal biopsy shows mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on immunofluorescence.

25% progress to end-stage renal failure in 10-30 years.

BP control/ACEI and ARBs/fish oil.

118
Q

What is rapidly progressive glomerulonephritis?

A

A treatable cause of acute renal failure.

Rapid deterioration in renal function over days/weeks.

Active urinary sediment (RBCs, RBC and granular casts).

May be part of systemic disease (ANCA positive or negative).

Associated with glomerular crescents on biopsy.

119
Q

Which ANCA positive conditions are associated with rapidly progressive glomerulonephritis?

A

Systemic vasculitis.

Granulomatosis with polyangiitis.

Microscopic polyangiitis.

120
Q

Which ANCA negative conditions are associated with rapidly progressive glomerulonephritis?

A

Goodpasture’s disease - anti-GBM.

Henoch-Schonlein purpura - HSP/IgA.

Systemic lupus erythematosus (SLE).

121
Q

What is the treatment for rapidly progressive glomerulonephritis?

A

Should be prompt and consist of strong immunosuppression (IV steroids, cytotoxics) with supportive care including dialysis if needed.

Plasmapheresis.

122
Q

What are the physical effects of chronic kidney disease?

A

Thirst -> dehydration.

Loss of interest in food -> nausea, depression.

Vitamin/mineral imbalances -> osteopaenia.

Malnutrition.

Anaemia -> fatigue, tiredness.

123
Q

What are the dietary restrictions for people on dialysis?

A

Low K (excess affects heart, hypertension and neurological system).

Low PO4 (excess affects bones).

Low salt (excess affects hypertension and neurological system).

124
Q

What does renal replacement therapy do, in general?

A

Restores electrolyte balance.

Removes urea/creatinine etc. from the blood.

Restores fluid balance.

Maintains erythropoietin production, etc.

125
Q

What are the forms of polycystic kidney disease?

A

Autosomal recessive.

Autosomal dominant (common).

126
Q

What genes are involved in autosomal dominant polycystic kidney disease (ADPKD)?

A

PKD gene 1 (chromosome 16).

PKD2 (chromosome 4).

127
Q

What is the pathology of autosomal dominant polycystic kidney disease (ADPKD)?

A

Massive cyst enlargement -> large kidneys.

Epithelial lined cysts arise from a small population of renal tubules.

Benign adenomas (in 25% of kidneys).

128
Q

What are the renal clinical features of autosomal dominant polycystic kidney disease (ADPKD)?

A

Reduced urine concentration ability.

Chronic pain.

Hypertension (common early sign of the disease).

Haematuria (due to cyst rupture, cystitis, stones).

Cyst infection.

Renal failure.

129
Q

What are the extra-renal clinical features of autosomal dominant polycystic kidney disease (ADPKD)?

A

Hepatic cysts (present 10yrs after renal cysts; function generally preserved but can result in SOB, pain, ankle swelling).

Intra-cranial aneurysms (4-8% patients, mainly in the anterior circulation territory).

Cardiac disease (mitral/aortic valve prolapse, valvular disease).

Diverticular disease.

Hernias.

130
Q

How is autosomal dominant polycystic kidney disease (ADPKD) diagnosed?

A

USS - presence of bilateral cysts.

Renal enlargement.

CT/MRI - when unclear on USS.

Genetic testing - linkage and/or mutation analysis.

131
Q

What is the management of autosomal dominant polycystic kidney disease (ADPKD)?

A

Rigorous control of hypertension.

Hydration.

Proteinuria reduction.

Cyst haemorrhage and cyst infection prevention.

Tolvaptan - new treatment to reduce cyst volume and progression.

For those in renal failure: dialysis, transplantation.

132
Q

What is autosomal recessive polycystic kidney disease (ARPKD)?

A

Rare genetic mutation in the PKDH1 gene on chromosome 6.

Bilateral and symmetrical renal involvement.

Urinary tract is generally normal.

133
Q

Where are cysts found in autosomal recessive polycystic kidney disease (ARPKD)?

A

The collecting duct system.

134
Q

Where are cysts found in autosomal dominant polycystic kidney disease (ADPKD)?

A

Cysts form in the renal tubules of the nephrons.

135
Q

What is the clinical presentation of autosomal recessive polycystic kidney disease (ARPKD)?

A

Varies and depends on renal/liver lesions.

Kidneys are always palpable.

Hypertension.

Recurrent UTIs.

Slow decline in GFR (less <1/3 reach dialysis).

136
Q

What is acquired cystic kidney disease?

A

Over time, cysts develop in the kidneys.

Occurs in people with CKD or end-stage renal disease.

This is different from PKD.

137
Q

What is Alport syndrome (hereditary nephritis)?

A

Disorder of the Type IV collagen matrix causing loss of kidney function (haematuria and later on proteinuria), sensorineural deafness, ocular defects (anterior lenticonus) and leiomyomatosis of the oesophagus/genitalia (rare).

138
Q

What is the genetic cause of Alport syndrome (hereditary nephritis)?

A

X-linked inheritance (85%) of a mutation in the COL4A5 gene.

139
Q

What constitutes a diagnosis of Alport syndrome (hereditary nephritis)?

A

Haematuria +/- hearing loss.

Renal biopsy -> variable thickness of the glomerular basement membrane with splitting of the lamina densa.

140
Q

What is the treatment of Alport syndrome (hereditary nephritis)?

A

No specific treatment.

Treatment is aggressive treatment of BP and proteinuria.

Dialysis/transplantation.

141
Q

What is Anderson-Fabry disease?

A

X-linked lysosomal storage disease that affects the kidneys, liver, lungs and erythrocytes.

Inborn error of glycosphingolipid metabolism (deficiency of a-galactosidase A).

Uncommon.

142
Q

What are the clinical features of Anderson-Fabry disease?

A

Renal failure.

Cutaneous angiokeratomas.

Cardiomyopathy.

Cardiac valvular disease.

Stroke.

Acroparaesthesia.

Psychiatric illness.

143
Q

How is Anderson-Fabry disease diagnosed?

A

Plasma/leukocyte a-GAL activity.

Renal biopsy.

Skin biopsy.

144
Q

What is the treatment for Anderson-Fabry disease?

A

Enzyme replacement (Fabryzyme).

Management of the complications.

145
Q

What is medullary cystic kidney disease?

A

A rare inherited cystic disease (autosomal dominant inheritance) which involves abnormal renal tubules leading to fibrosis.

Cysts are in the corticomedullary junction or medulla.

146
Q

How is medullary cystic kidney disease diagnosed?

A

CT scan and family history.

147
Q

What is the best treatment for medullary cystic kidney disease?

A

Renal transplant.

148
Q

What is medullary sponge kidney?

A

Uncommon, sporadic inheritance that causes dilatation of the collecting ducts due to cysts forming in the tubules or collecting ducts.

Calculi form in the cysts.

Renal failure is unusual.

149
Q

How is medullary sponge kidney diagnosed?

A

Excretion urography (to demarcate the calculi).

150
Q

What are the causes of CKD?

A
151
Q

What is dysproteinaemia?

A

Overproduction of immunoglobulin by clonal expansion of cells from B-cell lineage.

152
Q

What is myeloma?

A

Cancer of the plasma cells (a type of WBC normally responsible for producing antibodies).

  • Collections of abnormal plasma cells accumulate in the bone marrow.*
  • Impairment of production of normal blood cells.*
  • Monoclonal production of a paraprotein (abnormal antibody).*
  • Potentially cause renal dysfunction.*
  • ​*
153
Q

What are the symptoms of myeloma?

A

Bone pain.

Weakness.

Fatigue.

Weight loss.

Recurrent infections.

Classic presentation is back pain and renal failure.

154
Q

What are the signs of myeloma?

A

Anaemia.

Hypercalcaemia.

Renal failure.

Lytic bone lesions.

Classic presentation is back pain and renal failure.

155
Q

What are the renal manifestations of myeloma?

A

Glomerular (AL amyloidosis, monoclonal Ig deposition [light/heavy chains]).

Tubular (light chain cast nephropathy).

Dehydration, hypercalcemia, contrast, bisphosphonates, NSAIDs affecting renal failure.

156
Q

What investigations are done to diagnose myeloma?

A

Bloods: serum protein electrophoresis, serum free light chains.

Urine: Bence Jones protein (abnormal protein filtered through the collecting system; small proteins).

Bone marrow biopsy.

Skeletal survey.

Renal biopsy.

157
Q

What is the management of myeloma?

A

Stop nephrotoxic medication.

Manage hypercalcaemia (saline +/- bisphosphonates).

Chemotherapy.

Stem cell transplant.

Plasma exchange (to remove light chains).

Supportive: dialysis.

158
Q

What is the classic presentation of myeloma?

A

Back pain and acute kidney injury.

159
Q

What is the baseline investigation for diagnosing myeloma?

A

Protein electrophoresis (from bloods) and Bence Jones protein (from urine).

160
Q

What is amyloidosis?

A

Deposition of extracellular amyloid (insoluble protein fibrils) in tissues or organs.

Occurs due to abnormal folding of proteins which then aggregate and become insoluble.

Breakdown of usual degradation pathways for abnormally folded proteins.

Inherited and acquired problems.

161
Q

What are the most common types of amyloidosis?

A

Primary/light chain amyloidosis (AL).

Secondary/systemic/inflammatory amyloidosis (AA).

Dialysis amyloidosis (due to the accumulation of ABeta2 microglobulin not being filtered by dialysis from the kidney).

Hereditary and old age amyloidosis (ATTR).

162
Q

What is AL (immunoglobulin light chain) amyloidosis?

A

Production of abnormal Ig light chains from plasma cells.

Light chains enter the bloodstream and cause amyloid deposits.

Commonly affects the heart, bowel, skin, nerves, kidneys.

  • Age at diagnosis 55-60 years.*
  • Life expectancy 6 months – 4 years (untreated).*
163
Q

What is AA (amyloid-associated) amyloidosis?

A

Associated with systemic inflammation.

Production of acute phase proteins (serum amyloid protein [SAA]).

Commonly affects the liver, spleen, kidneys and adrenal glands.

Develops in approx. 5% of patients with chronic inflammatory conditions or chronic infections: RA, inflammatory bowel disease, psoriasis, TB, osteomyelitis, bronchiectasis.

164
Q

What is the pathogenesis of amyloidosis?

A
165
Q

How does amyloidosis present?

A

Depends on the organs or tissues involved.

Renal: nephrotic range proteinuria +/- impaired renal function.

Cardiac - cardiomyopathy.

Nerves - peripheral or autonomic neuropathy.

Hepatomegaly/splenomegaly.

GI - malabsorption.

166
Q

What are the renal investigations for diagnosing amyloidosis?

A

Urinalysis & uPCR.

Blood tests (renal function, inflammatory markers, protein electrophoresis, SFLC).

Renal biopsy (is a must for amyloidosis) - Congo red staining (apple green birefringence under polarised light).

  • [**Other biopsy* - abdominal fat pad or rectal biopsy].
  • SAP scan – Scintigraphy with radiolabelled serum amyloid – shows the extent of disease.*
167
Q

What is the management for amyloidosis?

A

Aim is to reduce further deposition and preserve organ function (no cure).

AA - treat underlying condition causing the amyloidosis.

AL - immunosuppression (steroids, chemotherapy, stem cell transplant).

168
Q

What are small vessel (ANCA associated) vasculitides?

A

Necrotising polyangiitis that affects capillaries, venules and arterioles.

  • Usually presents in 5th, 6th and 7th decade.*
  • Patients present with constitutional symptoms e.g. fever, migratory arthralgia, weight loss, anorexia and malaise.*
  • Vasculitis is a systemic disease.*
  • Pro-dromal symptoms may last for weeks to months before specific organ involvement.*
169
Q

What are the investigations done to diagnose ANCA associated vasculitis?

A

Urinalysis showing blood ++ and protein ++.

Bloods with raised inflammatory markers, AKI and anaemia.

Immunology: anti-ANCA positive (anti-MPO [pANCA] and anti-PR3 [cANCA]).

Renal biopsy.

170
Q

What is granulomatosis with polyangiitis?

A

Predominantly anti-PR3 antibodies.

Necrotising granulomatous inflammation.

Lung involvement (pulmonary/renal syndrome).

171
Q

What is microscopic polyangiitis?

A

Predominantly anti-MPO antibodies.

Small vessel vasculitis with no granulomas.

Systemic features/renal/lung/skin/GI/nerves.

172
Q

What is eosinophilic GPA?

A

GPA associated with asthma and eosinophilia.

2/3 have skin involvement.

173
Q

What is the management of small vessel ANCA associated vasculitides?

A

Immunosuppression (steroids, cyclophosphamide/rituximab).

Plasma exchange.

Supportive: dialysis, ventilation.

174
Q

What is systemic lupus erythematosus?

A

Chronic auto-immune inflammatory disease of unknown origin.

Affecting skin, joints, kidneys, lungs, nervous system, serous membranes.

  • Women in their 20s-30s more commonly affected (10:1).*
  • African Americans and Hispanics.*
175
Q

How can SLE be diagnosed?

A

High index of suspicion in a young lady with non-specific symptoms.

Blood tests: raised inflammatory marks; immunology (ANA positive, anti-dsDNA positive); low levels of complement.

Urinalysis (to check renal function).

176
Q

When considering SLE, what are the differential diagnoses?

A

Sjogren’s syndrome.

Fibromyalgia.

Primary antiphospholipid syndrome.

Thrombotic micro-angiopathies.

SLE can be on the differential diagnosis list of virtually any presentation.

177
Q

What is lupus nephritis?

A

Up to 50% of lupus patients will have renal involvement at presentation and up to 60% during the course of their disease.

The most frequently observed abnormality is proteinuria.

A number of types of renal disease can occur and are differentiated by renal biopsy.

178
Q

How is lupus nephritis classified?

A

ISN classification.

Class I: minimal mesangial.

Class II: mesangial proliferative.

Class III: focal proliferative.

Class IV: diffuse proliferative.

Class V: membranous.

Class VI: advanced sclerosing.

179
Q

What is the management for SLE?

A

Hydroxychloroquine - all patients.

As the renal function worsens then immunosuppression needs to be commenced and stepped up as required.

2MBChB Renal (20 decks)

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