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taz- year 3 med > renal > Flashcards

renal Flashcards

1
Q

what are the common renal presenting complaints

A 
Dyspnoea 
Leg swelling 
Nausea &/or Vomiting
Upper Airway Symptoms
Constitutional Symptoms
Lower Urinary Tract Symptoms
Flank pain
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2
Q

what features of the history of presenting complaint would you ask about for theses symptoms in a renal patient

Dyspnoea 
Leg swelling 
Nausea &/or Vomiting
Upper Airway Symptoms
Constitutional Symptoms
Lower Urinary Tract Symptoms
Flank pain
A
  • Dyspnoea – Exercise tolerance, triggers, relieving
    factors, diurnal variation, orthopnoea, PND, associated symptoms
  • Leg swelling – site, severity, time of onset,
    amount of fluid intake
  • Nausea/Vomiting – triggers, relieving factors, able to keep down food, frequency, associatedsymptoms, bowel frequency
  • ENT symptoms – nasal secretions, sinusitis, epistaxis, haemoptysis, sore throat, visual
    disturbances, hearing loss
  • Constitutional Symptoms – fever, joint pains, muscle aches, weight changes, lethargy, night
    sweats, pruritus
  • Lower Urinary Tract Symptoms – dysuria,
    frequency, quantity of urine, colour of urine, frothiness, haematuria
  • Flank pain – duration, radiation, associated
    symptoms, intensity, aggravating/relieving factors
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3
Q

what OTC medicine is important to ask about in renal patients

A

NSAIDs

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4
Q

what are the stages of the WHO performance status

A

0 Normal - Fully active without restriction

1 Restricted in physically strenuous activity but ambulatory and able to carry out light work e.g., light house work, office work

2 Ambulatory and capable of all self-care but unable to carry out any work activities. Up and about more than 50% of waking hours

3 Capable of only limited self-care, confined to bed or chair more than 50% of waking hours

4 Completely disabled. Cannot self-care. Totally confined to bed or chair

5 Dead

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5
Q

what are the 7 functions of the kidney

use the pneumonic A WET BED

A

Acid/base balance

water balance regulation
erythropoesis
toxin removal

blood pressure regulation
electrolyte balance
vit D activation

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6
Q

what are some common renal function tests

A

Bloods

  • FBC – Anaemia, infection, allergic reactions,
  • Haematinics – Iron/Folate/B12 deficiency
  • U&Es – Potassium, Urea, Creatinine, Bicarbonate
  • Bone profile – Calcium, Phosphate, PTH, Alkaline Phosphatase
  • CRP – Infection/Inflammation
  • HbA1c – Diabetic control

Urine

  • Urine Dipstick – Infection (leukocytes, nitrites); Glomerular pathology (blood, protein)
  • Urine Protein:Creatinine Ratio – Quantifies the amount of all protein in the urine
  • Urine Albumin:Creatinine Ratio – Quantifies just albumin (good for monitoring diabetic nephropathy)
  • Urine microscopy, culture and sensitivity

Imaging
- US KUB – look for peri-nephric collection, size of kidneys, corticomedullary differentiation, hydronephrosis.

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7
Q

what are the acid base disturbances in metabolic acidosis

A

pH low
bicarbonate LOW
pCO2 normal/low

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8
Q

what are the acid base disturbances in metabolic alkalosis

A

pH high
bicarbonate HIGH
pCO2 normal

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9
Q

what are some causes of metabolic alkalosis

A

GI

  • diarrhoea
  • vomiting

renal losses

  • primary hyperaldosteronism
  • tubular transport defects
  • diuretics

intracellular shift
- hypokalaemia

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10
Q

what is the anion gap used for

A

Can be useful to work out what could be causing the acidosis

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11
Q

how do you calculate anion gap

A

Anion Gap = Sodium - (Chloride + Bicarbonate)

[Na+] – ([Cl-]+[HCO3-])

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12
Q

what is the normal anion gap

A

8-12mmol/l

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13
Q

what are some causes of a high anion gap

A

Acidosis due to increased acid

  • lactic acidosis- Anaerobic exercise; Sepsis; Organ ischaemia
  • ketoacidosis- Diabetic; alcohol abuse; Starvation
  • toxins- Ethylene Glycol; Methanol; Isoniazid; Aspirin; Salicylate
  • renal failure
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14
Q

what are some causes of a normal anion gap

A

Acidosis due to reduced alkali

  • GI losses of HCO3- Vomiting; diarrhoea
  • Renal losses of HCOs- Renal tubular acidosis; mineralocorticoid deficiency (Addison’s)
  • Toxins- Ammonium Chloride; Acetazolamide
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15
Q

what is the most common cause of Hypernatraemia

what are the symptoms

how do you treat

A

Usually due to water deficit.

Symptoms of thirst, apathy, irritability, weakness,
confusion, reduced consciousness, seizures, hyperreflexia, spasticity & coma.

Generally – free water

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16
Q

what are some Hypovolaemic, Euvolaemic, Hypervolaemic causes of Hypernatraemia

A

Hypovolaemic High Na

  • Renal free water losses (Osmotic diuresis [NG feed etc], loop diuretics, intrinsic renal disease)
  • Non-Renal free water losses (Excess sweating, Burns, Diarrhoea, Fistulas)

Euvolaemic High Na

  • Renal Losses (Diabetes Insipidus, Hypodipsia)
  • Extra-Renal Losses (Insensible, Respiratory losses)

Hypervolaemic High Na (Sodium Gains)

  • Primary hyperaldosteronism
  • Cushing’s Syndrome
  • Hypertonic dialysis
  • Hypertonic Sodium Bicarbonate
  • Sodium Chloride tablets
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17
Q

how does Hyponatraemia

present

A

Low Na causes decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy,
confusion, seizures, coma.

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18
Q

how do you investigateHyponatraemia

A
  • plasma osmolality (if normal or raised then pseudohyponatraemia),
  • hypokalaemia of hypomagnesaemia potentiates ADH release
  • Urine sodium (if <20 then non-renal salt losses, if >40 then SIADH) (diuretics may confound)
  • TSH and 9am cortisol, Calcium, albumin, glucose, LFT
  • CT head or chest if
    suspect SIADH.
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19
Q

what are some renal and non renal causes of Hypovolaemic Hyponatraemia and how do you treat

A

Renal loss [Urine Na+ >20mmol/L]
- Diuretics (thiazides), Osmotic diuresis (glucose, urea in
recovering ATN), Addison’s disease (mineralocorticoid
deficiency)

Non-renal loss [Urine Na+ <20mmol/L]
- Diarrhoea, Vomiting, Sweating, Third space losses
(burns, bowel obstruction, pancreatitis)

Treatment – give IV fluids (0.9% NaCl at 1-3ml/kg/hour) Give K if necessary

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20
Q

what are some causes of Euvolaemic Hyponatraemia

A

Hypothyroidism, Primary polydipsia – (if urine
osmolality <100)
Glucocorticoid deficiency – adrenal insufficiency, SIADH

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21
Q

when should you suspect SIADH and how would you manage it

A
  • Low serum osmolality
  • Inappropriately concentrated urine – Urine osmolality >100
  • Urine Na >20
  • Clinical euvolaemia
  • Not on diuretics
  • Diagnosis of elimination – normal renal, thyroid, adrenal function

Management of SIADH – Fluid restrict <800ml/day. PO sodium chloride, may give furosemide, Demeclocycline induces diabetes insipidus (reversing ADH effect), alternatively Tolvaptan

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22
Q

what are some causes of Hypervolaemia Hyponatraemia

how do you treat

A

CCF, Nephrotic syndrome, Liver cirrhosis

Treatment – fluid restrict and consider furosemide

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23
Q

what is the Risk of correcting hyponatraemia quickly

how much should you aim to decrease it by a day

A

Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis. Aim to correct <12 mmol/L/day

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24
Q

how would you manage acute vs chronic Hyponatraemia

A

Acute (tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy)
- If acute hyponatraemia (within 48 hours) and symptomatic
– Give 3% hypertonic saline IV boluses +/- Furosemide

Chronic If chronic (>48 hours) and symptomatic – hypertonic saline boluses if having seizures.

Otherwise isotonic saline and furosemide – aim to correct 8mmol/L in 24 hours

If chronic and asymptomatic – water restriction, stop offending drug, if dehydrated – restore volume, if overloaded – Na and water restriction and diuretics

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25
Q

what are some causes of Hyperkalaemia

A
  • CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)
  • Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/
    Heparin/ LMWH/Cyclosporin or calcineurin
    inhibitors/High dose Trimethoprim/ Digoxin toxicity/B-blockers)
  • Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use
  • Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome
  • Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis
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26
Q

what are the egg changes for Hyperkalaemia

A
  • Tented T waves
  • Prolonged QRS
  • Slurring of ST segment
  • Loss of P waves
  • Asystole
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27
Q

how would you treat Hyperkalaemia

A
  1. Stabilizing the myocardium to prevent arrhythmias
    - 10mls of 10% Calcium Gluconate over 5-10
    minutes
  2. Shifting potassium back into the intracellular space
    - IV fast acting insulin (actrapid)- 10 units and IV glucose/dextrose 50% 50mls
    - Sodium Bicarbonate- 500mls of 1.4% Sodium Bicarbonate. Only effective at driving Potassium intracellullarly if the patient is acidotic
    - Salbutamol- 5-10mg via nebulizer
  3. Eliminating Potassium From the Body:
    - Calcium Resonium- 15-45g orally or rectally, mixed with sorbitol or lactulose
    - Frusemide- 20-80mg depending on hydration status
    - Dialysis- If resistant to medical treatment
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28
Q

what are the symptoms of Hypokalaemia

A

Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension

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29
Q

what are the causes of Hypokalaemia

A
  • Pseudohypokalaemia – acute leukaemia
  • Extra-renal losses - Inadequate PO intake, Gut losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)
  • Redistribution – Delirium tremens, beta agonists,
    insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)
  • Refeeding syndrome, alkalosis, vigorous exercise,
    glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)
  • Primary hyperaldosteronism (conn’s syndrome)
    Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),
  • Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.
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30
Q

what are the egg changes for Hypokalaemia

A
  • Small T waves
  • U wave (after T)
  • Increased PR interval
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31
Q

what is the treatment of Hypokalaemia

A
  • Replace magnesium
  • Oral K replacement
  • IV K replacement (Usually in 0.9% NaCl - avoid in dextrose as induces further hypokalaemia)
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32
Q

what are some examples, main indications, MOA and common side effects of loop diuretics

A

eg Furosemide, Bumetanide, Torsemide

main indication Fluid Overload

MOA- Inhibits Na+K+Cl- transporter in Loop of Henle

common side effects- Hyponatraemia, hypokalaemia, diuresis, dehydration, alkalosis

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33
Q

what are some examples, main indications, MOA and common side effects of Thiazide/Thiazide-like Diuretics

which drug should you take caution prescribing it with

A

eg Bendroflumethiazide, Indapamide

main indications- Hypertension, Fluid Overload

MOA- Inhibits NaCl channel in distal convoluted tubule

common side effects- Hyponatraemia, Hypokalaemia, Dehydration, Hypercalcaemia, Hyperuricaemia, Hypomagnesaemia, Alkalosis

Use with caution in combination with loop diuretics.

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34
Q

what are some examples, main indications, MOA and common side effects of K sparing Diuretics

which drug should you take caution prescribing it with

A

eg Aldosterone antagnosists - Spironolactone
Epithelial Na channel blockers - Amiloride

main indication- K-losing tubulopathies, Hypertension, Heart failure

MOA- Block epithelial Na channel. Antagonises the action of aldosterone at mineralocorticoid receptors

side effects - Hyperkalaemia Gynaecomastia

Caution when combined with ACEi/ARB for increased risk of hyperkalaemia

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35
Q

what are some examples, main indications, MOA and common side effects of Carbonic Anhydrase Inhibitors

A

eg Acetazolamide, Brinzolamide

main indications- Benign Intracranial hypertension, Glaucoma

MOA- Inhibits carbonic anhydrase

side effects- Flushing, metabolic acidosis, agranulocytosis, liver failure

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36
Q

what are some examples, main indications, MOA and common side effects of CORTICOSTERIODS (GLUCOCORTICOID)

A

eg Prednisolone (PO), Hydrocortisone (IV/IM), Dexamethasone (PO/IV), Triamcinolone (IM)

main indication- Supress inflammation, allergy & immune responses

MOA- Alters gene transcription

side effects- Adrenal suppression (especially courses > 3 weeks), hyperglycaemia, psychosis, insomnia, indigestion, mood swings

important info- May need PPI (reduce GORD), Bisphosphonates (bone protection) and steroid card. Used both in short- term and long-term. Long-term steroid courses should NOT be withdrawn abruptly.

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37
Q

What is the triad of Diabetes Insipidus?

A

Polydipsia, Polyuria, Dilute Urine

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38
Q

Give two causes of Central DI

A

TB

Sarcoidosis

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39
Q

Give two causes of Nephrogenic DI

A

Congenital

Drugs (Lithium, Amphoterecin, Demeclocycline)

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40
Q

What three investigation results would prove DI

A

Serum Osmolality>295
Urine Osmolality<300
Water Deprivation test causes weight loss

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41
Q

Using the mnemonic THANKS CYCLE, what drugs contribute to HYPERkalaemia?

A 
Trimethoprim
Heparin 
ACEI 
NSAIDs 
K+ Sparing DIuretics 
Succinyl Choline 
Cyclosporine
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42
Q

Define AKI

A

Reduced renal function occurring over hours to days

A rise in creatinine more than 50% in the last 7 days

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43
Q

Give two broad causes of PRE RENAL AKI

A

Reduced cardiac output

Reduced circulating volume

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44
Q

Give a tubular, glomerular and vascular cause of INTRARENAL AKI

A

Glomerular - Acute Glomerulonephritis
Tubular - Toxins (endo - myoglobin, exo - aminoglycosides)
Vascular - Vasculitis

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45
Q

Give two causes of POSTRENAL AKI

A

BPH

Bladder Outflow Obstruction

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46
Q

If you thought the AKI might be due to Post Streptococcal Glomerulonephritis, what investigation would you do?

A

Anti Streptolysins Titre

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47
Q

Name would you investigate a suspected AKI

A

Urinalysis: dipstick for blood, nitrates, leukocytes, glucose, osmolality
Bloods: FBC, Blood film, U&Es, coag studies (DIC), CK, myoglobinurea (?rhabdomyalysis), autoantibody screen virology
USS when ?obstruction
CXR- pulmonary odema, AXR- renal calculi
Doppler USS to look for stenosis or renal arteries and veins

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48
Q

How do you calculate IV flow rate?

A

IV Flow Rate = (drop factor * vol)/time

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49
Q

What Nephrotoxic agents should you discontinue in an AKI?

A 
Aminoglycosides
Vancomycin 
Acyclovir 
NSAIDs
Cisplatin
Lithium
ACE-I (if RAS)
Cyclosporin
Radiocontrast
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50
Q

what are some indications for Renal Replacement Therapy in an AKI

A
  • Hyperkalaemia (>6.5) refractory to medical management
  • pulmonary odema/ fluid overload refractory to medical management
  • metabolic acidosis refractory to medical therapy
  • uraemia complications (pericarditis or uraemic encephalopathy)
  • CKD stage 4/5
  • dialysable nephrotoxin
  • intrinsic renal disease (vasculitis, GN, SLE) suspected
51
Q

what are the diagnostic criteria of AKI

A

one of

  • Rise in serum creatinine of > 26 umol/L over 48hrs
  • 50% or greater increase in creatinine within 7 days
  • fall in urine output to less than 0.5 ml/kg/hr for more than 6 hrs
52
Q

how would you manage AKI

A
  • monitor fluid and electrolyte balance closely
  • treat cause
  • pre renal aki: fluid replacment
  • withdraw nephrotoxic drugs
  • identify and treat complications (hyperalaemia, acidosis, pulmonary odema, bleeding)
  • restrict oral K+ and monitor carefully
53
Q

what is the commonest cause of AKI in children

A

Hemolytic uremic syndrome (HUS)

54
Q

What are the four characteristics of Nephrotic Syndrome?

A

Oedema
Proteinuria (>3.5g in 24 hours)
Hypoalbuminaemia (<30)
hyperlipidaemia

55
Q

How does nephrotic syndrome usually present?

A
  • pitting odema in legs
  • odema in face worse in morning
  • any age
  • infections
  • predisposing factor eg diabetes, fhx
  • frothy urine
  • incidental finding of gross protein urea
56
Q

Give 3 secondary causes of nephrotic syndrome?

A
  • diabetes
  • lupus nephritis
  • myeloma
  • amyloid
  • pre- eclampsia
57
Q

give 3 primary causes of nephrotic syndrome

A
  • FSGS
  • minimal change
  • membranous nephropathy
58
Q

What are the classical findings of nephritic syndrome?

A
  • blood and small amounts of protein in urine
  • no swelling
  • vague symptoms
59
Q

Give primary and secondary causes of nephritic syndrome

A

primary

  • IgA Nephropathy
  • Mesangiocapillary GN

secondary

  • Post-streptococcal
  • Vasculitis
  • SLE (other classes)
  • Anti-GBM diseases
60
Q

Describe the pathophysiology of Post Streptococcal GN

A
  • Occurs weeks after Group A/B Strep Infection
  • 1-2 weeks post tonsillitis
  • 3-4 weeks post impetigo/cellulitis
  • Normally affects children aged 3-12
61
Q

What would a serum sample of Post Streptococcal GN show?

A

Low C3

Anti Strep Antibodies

62
Q

How would you manage Post Streptococcal GN?

A

Self Limiting

ACEI/ARB for proteinuria

63
Q

Describe the pathophysiology of IgA Nephropathy

A

Haematuria after an URTI, GI Infection
↑IgA in response to URTI
This IgA is abnormally glycosylated
o → resistant to degradation o → antigenic ∴ incites auto-antibodies against it (anti-glycan IgG)
• Immune complex deposition in mesangium • Complement pathway activation • Proinflammatory cytokine release + macrophage infiltration • Glomerular injury → Nephritic Syndrome

Peak incidence in 20-30 y/o

64
Q

Describe the findings in a serum/urine/biopsy of IgA Nephropathy

A

Serum - High IgA, Normal C3/C4
Urine - Asymptomatic microhaematuria with intermittent visible
Biopsy - mesangial proliferation + IgA + C3

65
Q

State the three different types of ANCA/Small Vessel Vasculitis

A

Granulomatosis with Polyangitis
Microscopic Polangitis
Churg Strauss

66
Q

Describe the features of Granulomatosis with Polyangitis

A
  • C-ANCA

- Pulmonary and Nasopharyngeal involvement (haemoptysis and nasal polyps)

67
Q

Describe the features of Microscopic Polyangitis

A

P-ANCA

Mild Respiratory Symptoms

68
Q

Describe the features of Churg Strauss

A

P-ANCA

Asthma, Allergic Rhinitis, Peripheral Neuropathy

69
Q

Describe the pathophysiology of Anti GBM disease/ Goodpasture’s Syndrome

A

Antibodies against type 4 collagen

Type 4 collagen also lies in Respiratory System therefore haemoptysis

70
Q

What would serum sample/CXR/biopsy of Anti GBM show

A

Serum - Anti GBM Antibodies
CXR - Pulmonary Infiltrates
Biopsy - Deposition of IgG along basement membrane

71
Q

How would you treat Anti GBM disease?

A

Plasma Exchange and Immunosupression

72
Q

Describe the pathophysiology of Thin Basement Membrane Disease

A

Hereditary Abnormalities of Type 4 collagen cauisng microscopic haematuria
Biopsy shows diffuse thinning of GBM

73
Q

What is Alport Syndrome?

A

X linked abnormalities in Type 4 collagen, also causing hearing loss and eye abnormalities

74
Q

How does the biopsy of Alport and Thin Basement Membrane disease differ

A

Thin Basement Membrane - Diffuse thinning

Alport - Alternate thinning and thickening

75
Q

Why should you give LMWH prophylactically in Nephrotic Syndrome?

A

Low albumin increases VTE risk

It is an acute phase reactant normally with anticoag properties

76
Q

define Glomerulonephritis

A

A group of disorders resulting from glomerular damage.
They are a common cause of ESRF in adults.
Broadly, they can be divided in terms of their presentation (nephritic vs. nephrotic).
These are then further subdivided based on their histological appearances.

77
Q

what is the pathophysiology of Nephrotic syndrome

A

Podocyte damage → loss of:

  • Albumin → oedema
  • IgG/Complement → infection
  • AT3, PC, PS → DVT/PE
78
Q

how would you investigate nephrotic syndrome

A
  • Dipstick: protein ++++
  • Blood: ↓Albumin, ↑lipids, coagulation tests
  • Biopsy: will reveal cause
79
Q

how would you manage nephrotic syndrome

A

Children → straight into empirical steroids (as 90% = minimal change; no point in biopsy)
Adults → Full examination + biopsy

Medical
• Main Rx → ACE-i/ARB
• Hyperlipidaemia → Statins
• Oedema → Furosemide + fluid restriction
• Infection/Sepsis → Abx
• DVT/PE → Anticogulation
80
Q

what is nephritic syndrome due to and how does it present

A

Nephritic Syndrome is due to endothelium damage and mesangium

acute inflammation of the glomerulus. This is manifested as:

  1. Haematuria
  2. Oliguria + Hypertension
  3. Uraemia
81
Q

what is the general treatment of nephritic syndrome

A

Salt restriction, fluid restriction, loop diuretics, vasodilators

82
Q

what is minimal change nephrotic disease, how does it present and how do you treat

A

A nephrotic syndrome of microscopic damage to podocytes visible only by electron microscopy

Features

  • Highly-Selective proteinuria (albumin & transferrin only)
  • Facial/peri-orbital swelling and frothy urine

Management
• Steroids: 90% of children and 70% of adults undergo remission
• If recurrence → Cyclophosphamide or CNIs (ciclosporin/tacrolimus

83
Q

what is an example of mixed Nephrotic/Nephritic Syndrome

A

Membranoproliferative GN (Mesangiocapillary GN)- A mixed nephrotic-nephritic syndrome characterised by both mesangial and endocapillary proliferation

84
Q

how do you manage Membranoproliferative GN

A
  • ACE-i/ARB; Steroids ± Cyclophosphamide if ↓renal function

- Anti-Complement eculizumab may be trialled

85
Q

how would you manage IgA Nephropathy (Berger’s Disease)

A

ACE-i/ARB for all patients

Steroids ± Cyclophosphamide

86
Q

what is Henoch-Schönlein Purpura (IgA Vasculitis): how does it present and how do you treat

A

Definition: a systemic variant of IgA nephropathy, causing IgA small vessel vasculitis; it is the most common systemic vasculitis of children. Type III hypersensitivity → immune complex deposition in small vessels → local damage to blood vessels → purpura (NO thrombocytopenia)

Features
• Nephritis + 
• Purpuric extensor rash (typically legs) 
• Flitting polyarthritis 
• Abdominal pain (GI bleeding)

Diagnosis: IgA + C3 in skin/renal biopsy (identical to IgA nephropathy)

Treatment: as IgA nephropathy but steroids/Immunosupression don’t help

87
Q

how would Anti-GBM Disease (Goodpasture’s Syndrome) present and how would you investigate

A

presents

  • haemoptysis
  • haematuria/nephritic syndrome

investigations
Renal Biopsy: linear IgG deposits along GBM = pathognomonic

88
Q

what is Lupus Nephritis and how does it present

A

Definition: SLE is a systemic auto-immune condition targeting nuclear blebs. Lupus nephritis is a severe manifestation of systemic lupus erythematosus (SLE) that can result in end-stage renal disease. SLE patients should be monitored by performing urinalysis at regular check-up appointments to rule out proteinuria.

Presentation
• Malar rash, discoid rash, photosensitivity, arthralgia, etc.
• 1/3 patients will have evidence of renal disease; renal involvement is variable:
o vascular, glomerular, tubulointerstitial damage
• Class I-IV (increasing severity) and Class V (membranous)
• DIFFUSE, PROLIFERATIVE GLOMERULONEPHRITIS = most common renal complication of SLE
• SLE causes nephritic > nephrotic (V) disease

89
Q

what is the WHO classification of Lupus Nephritis

A
  • class I: normal kidney
  • class II: mesangial glomerulonephritis
  • class III: focal (and segmental) proliferative glomerulonephritis
  • class IV: diffuse proliferative glomerulonephritis
  • class V: diffuse membranous glomerulonephritis
  • class VI: sclerosing glomerulonephritis

Class IV (diffuse proliferative glomerulonephritis) is the most common and severe form.

90
Q

how would you treat Lupus Nephritis

A

Acute = IV Steroids + Cyclophosphamide/Mycophenolate

91
Q

what is the definition of CKD

A

Impaired renal function for >3 months based on abnormal structure/function. Or, GFR < 60 for >3 months without evidence of kidney damage. 5 stage classification. Symptoms usually only occur once stage 4 is reached (GFR <30). End-stage renal failure (ESRF) = GFR < 15 or need for Renal Replacement Therapy.

92
Q

Describe the classifications of CKD in term of GFR, from G1-G5

A 
G1 - >90
G2 - 60-89 
G3a - 45-59 
G3b - 30 - 44 
G4 - 15-29 
G5 - <15
93
Q

How could you classify the Albumin Creatinine Ratio in CKD?

A

A1 - <3
A2 - 3-30
A3 - >30

94
Q

what are some common causes of CKD

A
  1. Endocrine: Diabetic Nephropathy (T2&raquo_space; T1) (40% of cases)
  2. Renal: Chronic Glomerulonephritis (IgA Nephropathy = commonest)
  3. Unknown
  4. Vascular: HTN or Renovascular Disease
  5. Infectious: Pyelonephritis
  6. Mechanical: Reflux Nephropathy
95
Q

What drug could cause hypertrophy of the gums? What would this indicate?

A

Cyclosporin

Renal Transplant

96
Q

Give four complications of CKD

A

Anaemia of Chronic Disease
Mineral Bone Disease
Hyperparathyroidism
Hypertension

97
Q

What is the link between Hypertension and CKD?

A

Chronic raised BP causes Nephrosclerosis

Renal Artery Stenosis causes Hypertension (investigate with Magnetic Resonant Angiogram)

98
Q

How may CKD present?

A
  • vague symptoms like fatigue, malaise, anorexia, weakness
  • swelling of face and legs
  • breathlessness due to pulmonary odema
  • pruritis, lethargy, cramps and headaches due to raised urea
  • insomnia
  • polyurea
  • sexual dysfunction
  • predisposing factors often present
  • usually picked up incidentally by urine dips
99
Q

How is CKD investigated?

A
  • urine dip
  • 24 hr urine collection/ spot urine collection to look at ACR
  • bloods: u&e, alk phos, parathyroid hormone, plasma glucose and HbA1c, serum ablumin, lipid screen (usually high), FBC (normocytic anaemia), anti nuclear antibodies, c ANCA and p ANCA, anti GMB if no clear cause
  • ECG and echo as heart failure is often a differential and LVH often occurs due to fluid overload
  • Renal USS if suspect APCKD, obsutruction, haematuria, low GFR
  • renal biopsy when indicated
100
Q

When should a renal biopsy be done in someone with CKD

A

Progressive disease, nephrotic syndrome, systemic disease, AKI without recovery, unknown cause

101
Q

When should the GP refer someone with CKD to a nephrologist?

A
  • When reach stage 4
  • ACR>70 mg/mmol unless due to DM
  • ACR >30 with haematuria
  • eGFR decrease by 15% in 12 months
  • high BP poorly controlled despite >4 antihypertensives at theraputic dose
  • known or suspected rare or genetic cause of CKD
102
Q

What treatment is given in CKD to slow disease progression

A
  • ACEi or ARB (not both) and check K+ before and 2 weeks after starting treatment
  • Good glyaemic control
  • lifestyle advice
  • Avoid NSAIDS, nephrotoxic drugs and K+ sparing diuretics (amiloride and spironolactone)
  • Adjust doses of renal metabolised/ excreted drugs
103
Q

What treatments are given for CKD complications?

A
  • odema: furosemide/ bumetanide, restrict sodium and fluid intake
  • Anaemia: ferrous sulphate or IV iron then EPO if not work
  • Acidosis: sodium bicarb supplements
  • high phosphate and K+: reduce in diet (refer to dietician), calcium acetate works as phosphate binder
  • hyperparathyoidism/ hypocalcaemia: give adcal D3/ alphacalciferol
  • CVD: anti platelets (aspirin) and statin
104
Q

what is Renal Osteodystrophy

A

A bone disease caused by failure of renal calcium and phosphate homeostasis

105
Q

what is the conservative management of renal replacement therapy

A

Dietary restriction: K, PO4, Na, H2O

Blood Pressure Control

  • Strict fluid balance
  • ACE-i/ARBs
  • Β blockers, vasodilators,
  • Anaemia = EPO or Fe, Folate, Vit B12
  • Bone disease = Phosphate-binders, Vit D supplements
106
Q

When should dialysis be started in Acute Kidney Injury?

A
  • Refractory fluid overload
  • Severe hyperkalaemia (>6.5) or ECG changes
  • Severe metabolic acidosis (pH < 7.2)
  • Uraemia: pericarditis or encephalitis
  • Drug overdose (BLAST)
    o Barbiturates
    o Lithium
    o Alcohol (including ethylene alcohol)
    o Salicylates (aspirin)
    o Theophylline
107
Q

When should dialysis be started in end-stage Chronic Kidney Disease

A

Absolute Indications
• Uraemic pericarditis, pleuritis, encephalopathy

Common Indications
• Refractory fluid overload
• Refractory hyperkalaemia, acidosis, hyperphosphataemia
• Uraemic Symptoms
o Mild cognitive impairment
o Declining nutritional status
o Fatigue and malaise
108
Q

When does a pt with CKD need specialist renal care? (7)

A
  • GFR > 30 with or without diabetes
  • ACR 70 or more unless diabetes
  • ACR 30 or more with haematuria
  • sustained decrease in GFR or 25% or more
  • Hypertension which remains poorly controlled despite 4 drugs at theraputic doses
  • known or suspected rare or genetic causes of CKD
  • Suspected renal artery stenosis
  • outflow obstruction should go to urology
109
Q

Describe how youd undertake a fluid assessment?

A

look at tongue, JVP, skin turgor, HR, BP, cap refill, pulmonary odema, peripheral odema

110
Q

Give adv and dis avd of haemodialysis

A

Disadv: need to go in hospital 4x 3 hrs a week, need access with central line or fistula, diet restrictions
Adv: can sometimes be done at home, other hrs of week they can do as please, can remove fluid at same time,

111
Q

What are the two types of peritoneal dialysis

A

APD: nightime bags
CAPD: continuous bags
The more concentrated the bags the more fluid is removed

112
Q

What are contraindications of peritoneal dialysis

A

IBD, adhesions due to previous abdo surgery, massive central obesity or very little abdofat

113
Q

What 3 drugs does everyone go on after renal transplant

A

Tacrolimus, azathioprine and cyclosporin
Most also go on mycophenolate and prednisolone. Also need contraception for 1st year and need to monitor U&E, dipstick, PTH, lipids, glucose and screen for malignancies.

114
Q

What are the advantages of renal transplant

A

no diet restriction, normal life afterwards

115
Q

What are the complications of haemo and peritoneal dialysis?

A

peritoneal: peritonitis, thickening of peritoneum leading to small bowel obstruction (encapsulating peritoneal sclerosis) or access failure
Haemo: fistula clotting, SVC obstuction, endocarditis, line sepsis, access failure, shock

116
Q

Give 3 complications of renal transplants

A

infections, rejection, obstuction, thrombosis, delayed graft function, donor derived infections

117
Q

Describe the genetics of APCKD

A 
Autosomal Dominant
Type 1 (85%) - Mutation on Chromosome 16 
Type 2 (15%) - Mutation on Chromosome 4, slower course, reaches end stage renal failure sooner
118
Q

Give 4 clinical presentations of APCKD

A

Loin Pain
Visible Haematuria
Renal Calculi
High BP

119
Q

Name three disease associations of APCKD

A

Mitral Valve Prolapse
Ovarian Cysts
SAH

120
Q

How would you diagnose APCKD?

A

Family History and USS (although cysts aren’t usually visible until after the age of 30)

121
Q

How would you treat APCKD?

A 
Controlling BP (NOT with CCB though)
Tolvaptan (ADH antagonist) may slow growth
122
Q

Describe four reasons why someone may have Anaemia of Chronic Disease in CKD

A

Reduced Erythropoietin production
Absolute Iron Deficiency (Malnutrition)
Functional Iron Deficiency (Inflammation)
Bone Marrow Supression from Uraemia

123
Q

How would you manage ACD in CKD?

A 
Replace any Haematinics that need replacing
Give ESA (Erythropoietin Stimulating Agent)
124
Q

What is AV Fistula Steal Syndrome?

A

Reduced oxygenation of tissue distal to the fistula due ot mixing of oxygenated and deoxygenated blood

taz- year 3 med (10 decks)

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