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
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
3
Q
what OTC medicine is important to ask about in renal patients
A
NSAIDs
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
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
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.
7
Q
what are the acid base disturbances in metabolic acidosis
A
pH low
bicarbonate LOW
pCO2 normal/low
8
Q
what are the acid base disturbances in metabolic alkalosis
A
pH high
bicarbonate HIGH
pCO2 normal
9
Q
what are some causes of metabolic alkalosis
A
GI
- diarrhoea
- vomiting
renal losses
- primary hyperaldosteronism
- tubular transport defects
- diuretics
intracellular shift
- hypokalaemia
10
Q
what is the anion gap used for
A
Can be useful to work out what could be causing the acidosis
11
Q
how do you calculate anion gap
A
Anion Gap = Sodium - (Chloride + Bicarbonate)
[Na+] – ([Cl-]+[HCO3-])
12
Q
what is the normal anion gap
A
8-12mmol/l
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
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
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
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
17
Q
how does Hyponatraemia
present
A
Low Na causes decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy,
confusion, seizures, coma.
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.
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
20
Q
what are some causes of Euvolaemic Hyponatraemia
A
Hypothyroidism, Primary polydipsia – (if urine
osmolality <100)
Glucocorticoid deficiency – adrenal insufficiency, SIADH
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
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
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
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
25
what are some causes of Hyperkalaemia
- 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
26
what are the egg changes for Hyperkalaemia
- Tented T waves
- Prolonged QRS
- Slurring of ST segment
- Loss of P waves
- Asystole
27
how would you treat Hyperkalaemia
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
28
what are the symptoms of Hypokalaemia
Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension
29
what are the causes of Hypokalaemia
- 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.
30
what are the egg changes for Hypokalaemia
- Small T waves
- U wave (after T)
- Increased PR interval
31
what is the treatment of Hypokalaemia
- Replace magnesium
- Oral K replacement
- IV K replacement (Usually in 0.9% NaCl - avoid in dextrose as induces further hypokalaemia)
32
what are some examples, main indications, MOA and common side effects of loop diuretics
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
33
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
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.
34
what are some examples, main indications, MOA and common side effects of K sparing Diuretics
which drug should you take caution prescribing it with
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
35
what are some examples, main indications, MOA and common side effects of Carbonic Anhydrase Inhibitors
eg Acetazolamide, Brinzolamide
main indications- Benign Intracranial hypertension, Glaucoma
MOA- Inhibits carbonic anhydrase
side effects- Flushing, metabolic acidosis, agranulocytosis, liver failure
36
what are some examples, main indications, MOA and common side effects of CORTICOSTERIODS (GLUCOCORTICOID)
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.
37
What is the triad of Diabetes Insipidus?
Polydipsia, Polyuria, Dilute Urine
38
Give two causes of Central DI
TB
| Sarcoidosis
39
Give two causes of Nephrogenic DI
Congenital
Drugs (Lithium, Amphoterecin, Demeclocycline)
40
What three investigation results would prove DI
Serum Osmolality>295
Urine Osmolality<300
Water Deprivation test causes weight loss
41
Using the mnemonic THANKS CYCLE, what drugs contribute to HYPERkalaemia?
```
Trimethoprim
Heparin
ACEI
NSAIDs
K+ Sparing DIuretics
Succinyl Choline
Cyclosporine
```
42
Define AKI
Reduced renal function occurring over hours to days
| A rise in creatinine more than 50% in the last 7 days
43
Give two broad causes of PRE RENAL AKI
Reduced cardiac output
| Reduced circulating volume
44
Give a tubular, glomerular and vascular cause of INTRARENAL AKI
Glomerular - Acute Glomerulonephritis
Tubular - Toxins (endo - myoglobin, exo - aminoglycosides)
Vascular - Vasculitis
45
Give two causes of POSTRENAL AKI
BPH
| Bladder Outflow Obstruction
46
If you thought the AKI might be due to Post Streptococcal Glomerulonephritis, what investigation would you do?
Anti Streptolysins Titre
47
Name would you investigate a suspected AKI
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
48
How do you calculate IV flow rate?
IV Flow Rate = (drop factor * vol)/time
49
What Nephrotoxic agents should you discontinue in an AKI?
```
Aminoglycosides
Vancomycin
Acyclovir
NSAIDs
Cisplatin
Lithium
ACE-I (if RAS)
Cyclosporin
Radiocontrast
```
50
what are some indications for Renal Replacement Therapy in an AKI
- 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
what are the diagnostic criteria of AKI
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
how would you manage AKI
- 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
what is the commonest cause of AKI in children
Hemolytic uremic syndrome (HUS)
54
What are the four characteristics of Nephrotic Syndrome?
Oedema
Proteinuria (>3.5g in 24 hours)
Hypoalbuminaemia (<30)
hyperlipidaemia
55
How does nephrotic syndrome usually present?
- 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
Give 3 secondary causes of nephrotic syndrome?
- diabetes
- lupus nephritis
- myeloma
- amyloid
- pre- eclampsia
57
give 3 primary causes of nephrotic syndrome
- FSGS
- minimal change
- membranous nephropathy
58
What are the classical findings of nephritic syndrome?
- blood and small amounts of protein in urine
- no swelling
- vague symptoms
59
Give primary and secondary causes of nephritic syndrome
primary
- IgA Nephropathy
- Mesangiocapillary GN
secondary
- Post-streptococcal
- Vasculitis
- SLE (other classes)
- Anti-GBM diseases
60
Describe the pathophysiology of Post Streptococcal GN
- 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
What would a serum sample of Post Streptococcal GN show?
Low C3
| Anti Strep Antibodies
62
How would you manage Post Streptococcal GN?
Self Limiting
| ACEI/ARB for proteinuria
63
Describe the pathophysiology of IgA Nephropathy
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
Describe the findings in a serum/urine/biopsy of IgA Nephropathy
Serum - High IgA, Normal C3/C4
Urine - Asymptomatic microhaematuria with intermittent visible
Biopsy - mesangial proliferation + IgA + C3
65
State the three different types of ANCA/Small Vessel Vasculitis
Granulomatosis with Polyangitis
Microscopic Polangitis
Churg Strauss
66
Describe the features of Granulomatosis with Polyangitis
- C-ANCA
| - Pulmonary and Nasopharyngeal involvement (haemoptysis and nasal polyps)
67
Describe the features of Microscopic Polyangitis
P-ANCA
| Mild Respiratory Symptoms
68
Describe the features of Churg Strauss
P-ANCA
| Asthma, Allergic Rhinitis, Peripheral Neuropathy
69
Describe the pathophysiology of Anti GBM disease/ Goodpasture’s Syndrome
Antibodies against type 4 collagen
| Type 4 collagen also lies in Respiratory System therefore haemoptysis
70
What would serum sample/CXR/biopsy of Anti GBM show
Serum - Anti GBM Antibodies
CXR - Pulmonary Infiltrates
Biopsy - Deposition of IgG along basement membrane
71
How would you treat Anti GBM disease?
Plasma Exchange and Immunosupression
72
Describe the pathophysiology of Thin Basement Membrane Disease
Hereditary Abnormalities of Type 4 collagen cauisng microscopic haematuria
Biopsy shows diffuse thinning of GBM
73
What is Alport Syndrome?
X linked abnormalities in Type 4 collagen, also causing hearing loss and eye abnormalities
74
How does the biopsy of Alport and Thin Basement Membrane disease differ
Thin Basement Membrane - Diffuse thinning
| Alport - Alternate thinning and thickening
75
Why should you give LMWH prophylactically in Nephrotic Syndrome?
Low albumin increases VTE risk
| It is an acute phase reactant normally with anticoag properties
76
define Glomerulonephritis
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
what is the pathophysiology of Nephrotic syndrome
Podocyte damage → loss of:
- Albumin → oedema
- IgG/Complement → infection
- AT3, PC, PS → DVT/PE
78
how would you investigate nephrotic syndrome
- Dipstick: protein ++++
- Blood: ↓Albumin, ↑lipids, coagulation tests
- Biopsy: will reveal cause
79
how would you manage nephrotic syndrome
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
what is nephritic syndrome due to and how does it present
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
what is the general treatment of nephritic syndrome
Salt restriction, fluid restriction, loop diuretics, vasodilators
82
what is minimal change nephrotic disease, how does it present and how do you treat
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
what is an example of mixed Nephrotic/Nephritic Syndrome
Membranoproliferative GN (Mesangiocapillary GN)- A mixed nephrotic-nephritic syndrome characterised by both mesangial and endocapillary proliferation
84
how do you manage Membranoproliferative GN
- ACE-i/ARB; Steroids ± Cyclophosphamide if ↓renal function
| - Anti-Complement eculizumab may be trialled
85
how would you manage IgA Nephropathy (Berger’s Disease)
ACE-i/ARB for all patients
| Steroids ± Cyclophosphamide
86
what is Henoch-Schönlein Purpura (IgA Vasculitis): how does it present and how do you treat
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
how would Anti-GBM Disease (Goodpasture’s Syndrome) present and how would you investigate
presents
- haemoptysis
- haematuria/nephritic syndrome
investigations
Renal Biopsy: linear IgG deposits along GBM = pathognomonic
88
what is Lupus Nephritis and how does it present
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
what is the WHO classification of Lupus Nephritis
* 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
how would you treat Lupus Nephritis
Acute = IV Steroids + Cyclophosphamide/Mycophenolate
91
what is the definition of CKD
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
Describe the classifications of CKD in term of GFR, from G1-G5
```
G1 - >90
G2 - 60-89
G3a - 45-59
G3b - 30 - 44
G4 - 15-29
G5 - <15
```
93
How could you classify the Albumin Creatinine Ratio in CKD?
A1 - <3
A2 - 3-30
A3 - >30
94
what are some common causes of CKD
1. Endocrine: Diabetic Nephropathy (T2 >> 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
What drug could cause hypertrophy of the gums? What would this indicate?
Cyclosporin
| Renal Transplant
96
Give four complications of CKD
Anaemia of Chronic Disease
Mineral Bone Disease
Hyperparathyroidism
Hypertension
97
What is the link between Hypertension and CKD?
Chronic raised BP causes Nephrosclerosis
| Renal Artery Stenosis causes Hypertension (investigate with Magnetic Resonant Angiogram)
98
How may CKD present?
- 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
How is CKD investigated?
- 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
When should a renal biopsy be done in someone with CKD
Progressive disease, nephrotic syndrome, systemic disease, AKI without recovery, unknown cause
101
When should the GP refer someone with CKD to a nephrologist?
- 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
What treatment is given in CKD to slow disease progression
- 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
What treatments are given for CKD complications?
- 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
what is Renal Osteodystrophy
A bone disease caused by failure of renal calcium and phosphate homeostasis
105
what is the conservative management of renal replacement therapy
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
When should dialysis be started in Acute Kidney Injury?
- 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
When should dialysis be started in end-stage Chronic Kidney Disease
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
When does a pt with CKD need specialist renal care? (7)
- 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
Describe how youd undertake a fluid assessment?
look at tongue, JVP, skin turgor, HR, BP, cap refill, pulmonary odema, peripheral odema
110
Give adv and dis avd of haemodialysis
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
What are the two types of peritoneal dialysis
APD: nightime bags
CAPD: continuous bags
The more concentrated the bags the more fluid is removed
112
What are contraindications of peritoneal dialysis
IBD, adhesions due to previous abdo surgery, massive central obesity or very little abdofat
113
What 3 drugs does everyone go on after renal transplant
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
What are the advantages of renal transplant
no diet restriction, normal life afterwards
115
What are the complications of haemo and peritoneal dialysis?
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
Give 3 complications of renal transplants
infections, rejection, obstuction, thrombosis, delayed graft function, donor derived infections
117
Describe the genetics of APCKD
```
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
Give 4 clinical presentations of APCKD
Loin Pain
Visible Haematuria
Renal Calculi
High BP
119
Name three disease associations of APCKD
Mitral Valve Prolapse
Ovarian Cysts
SAH
120
How would you diagnose APCKD?
Family History and USS (although cysts aren't usually visible until after the age of 30)
121
How would you treat APCKD?
```
Controlling BP (NOT with CCB though)
Tolvaptan (ADH antagonist) may slow growth
```
122
Describe four reasons why someone may have Anaemia of Chronic Disease in CKD
Reduced Erythropoietin production
Absolute Iron Deficiency (Malnutrition)
Functional Iron Deficiency (Inflammation)
Bone Marrow Supression from Uraemia
123
How would you manage ACD in CKD?
```
Replace any Haematinics that need replacing
Give ESA (Erythropoietin Stimulating Agent)
```
124
What is AV Fistula Steal Syndrome?
Reduced oxygenation of tissue distal to the fistula due ot mixing of oxygenated and deoxygenated blood
