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Final Year > Renal > Flashcards

Renal Flashcards

1
Q

How is AKI diagnosed?

A

Serum creatinine levels

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2
Q

What is the diagnostic criteria for AKI?

A

Rise in creatinine > 25micromol/L in 48h
Rise in creatinine > 50% in 7d
Urine output < 0.5ml/kg/h over 6h

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3
Q

List risk factors for AKI

A

> 65y
Sepsis
CKD
HF
Diabetes
Liver disease
Cognitive impairment- Decreased fluid intake
Medications (NSAIDs, gentamicin, diuretics and ACE-is)
Radiocontrast agents (CT scans)

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4
Q

List pre-renal causes of renal impairment

A

Insufficient blood supply to kidneys reducing filtration of blood
- Dehydration
- Shock (septic or acute blood loss)
- HF

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5
Q

List renal causes of renal impairment

A

Intrinsic disease in kidneys
- Acute tubular necrosis
- Glomerulonephritis
- Acute interstitial nephritis
- HUS
- Rhabdomyolysis

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6
Q

List post-renal causes of renal impairment

A

Obstruction to outflow of urine
- Kidney stones
- Tumours
- Strictures of ureters or urethra
- BPH
- Neurogenic bladder

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7
Q

What is acute tubular necrosis?

A

Damage and death of epithelial cells of renal tubules

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8
Q

What are the causes of acute tubular necrosis?

A

Ischaemia due to hypoperfusion (dehydration, shock, HF)
Nephrotoxins (gentamicin, radiocontrast, cisplatin)

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9
Q

What is seen on urinalysis in acute tubular necrosis?

A

Muddy brown casts
Renal tubular epithelial cells

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10
Q

What is the prognosis of acute tubular necrosis?

A

Epithelial cells regenerate = Reversible
Recovery in 1-3wks

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11
Q

What does urinalysis +ve for protein and blood suggest?

A

Acute nephritis

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12
Q

How to test for obstructive cause of AKI

A

US

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13
Q

Outline management of AKI

A

IV fluids
Withhold meds that worsen condition- NSAIDs, ACE-is
Withhold meds that may accumulate with reduced renal function- Metformin and opiates
Catheter if obstruction
Dialysis if severe

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14
Q

List complications of AKI

A

Fluid overload, HF, pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia (high urea)- Can lead to encephalopathy and pericarditis

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15
Q

Define CKD

A

Chronic reduction in kidney function sustained over 3mths- Permanent and progressive

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16
Q

List causes of CKD

A

Diabetes
HTN
Meds- NSAIDs or lithium
Glomerulonephritis
PKD

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17
Q

Outline presentation of CKD

A

Fatigue
Pallor (anaemia)
Foamy urine (protein)
Nausea
Loss of appetite
Pruritis
Oedema
HTN
Peripheral neuropathy

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18
Q

What is eGFR based on?

A

Serum creatinine
Age
Gender

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19
Q

What is GFR?

A

Rate at which fluid is filtered from blood into Bowman’s capsule

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20
Q

How do you quantify proteinuria?

A

Urine albumin : Creatinine ratio (ACR)

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21
Q

Outline diagnostic criteria of CKD

A

eGFR sustained below 60mL/min/1.73m2
Urine ACR sustained above 3mg/mmol

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22
Q

Outline G score

A

Based on eGFR- Marker of CKD
- G1>90
- G2 60-89
- G3a 45-59
- G3b 30-44

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23
Q

Outline A stage

A

Based on ACR- Marker of CKD
- A1 <3mg/mmol
- A2 3-30mg/mmol
- A3 >30mg/mmol

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24
Q

What is accelerated progression in CKD?

A

Sustained decline in eGFR within 1yr of either 25% or 15mL/min/1.73m2

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25
Q

List complications of CKD

A

Anaemia
Renal bone disease
CVD
Peripheral neuropathy
End stage kidney disease

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26
Q

List criteria for referral to renal specialist

A

eGFR<30mL/min/1.73m2
Urine ACR > 70mg/mmol
Accelerated progression
5yr risk of requiring dialysis >5%
Uncontrolled HTN despite 4+ antihypertensives

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27
Q

List medications that slow disease progression of CKD

A

ACE-i/ARBs
SGLT-2 inhibitor (dapagliflozin)

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28
Q

List medications that reduce the risk of complications of CKD

A

Exercise, maintain healthy weight, avoid smoking
Atorvastatin 20mg for primary prevention CVD

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29
Q

List medications that manage complications of CKD

A

Oral sodium bicarbonate- Metabolic acidosis
Iron and erythropoietin- Anaemia
Vit D, low phosphate diet, phosphate binders- Renal bone disease

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30
Q

Why does anaemia occur in CKD?

A

Kidneys produce EPO (produces RBCs)
CKD= Lower EPO and RBC production
Normocytic, normochromic anaemia

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31
Q

What is renal bone disease?

A

CKD- Mineral bone disorder
High serum phosphate
Low Vit D
Low serum calcium

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32
Q

Why does renal bone disease occur?

A

Reduced phosphate excretion by diseased kidneys results in high serum phosphate
Kidneys metabolise vit D to activate, normally allows calcium absorption in intestines and reabsorbed in kidneys- Responsible for regulating bone turnover and promoting bone reabsorption
Parathyroid glands react to low serum calcium and high serum phosphate by excreting more PTH- Secondary hyperparathyroidism
PTH stimulates osteoclast activity, increasing calcium absorption from bone

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33
Q

Why does osteomalacia occur?

A

Increased turnonver of bones without adequate calcium supply

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34
Q

Why does osteosclerosis occur?

A

Osteoblasts respond by increasing activity to math the osteoclasts, create new tissue in bone
Low calcium level means new bone not properly mineralised

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35
Q

Outline management of renal bone disease

A

Low phosphate diet
Phosphate binders
Active forms of Vit D (alfacalcidol and calcitriol)
Ensuring adequate calcium intake

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36
Q

When are ACE-is offered to patients with CKD?

A

Diabetes + urine ACR >3mg/mmol
HTN + urine ACR >30mg/mmol
All patients with urine ACR >70mg/mmol

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37
Q

What in particular needs monitoring in patients with CKD taking ACE-is?

A

Serum potassium- Risk of hyperkalaemia

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38
Q

What is the criteria for offering SGLT-2 inhibitors to patients with CKD?

A

Dapagliflozin
Offered- Diabetes plus urine ACR >30mg/mmol
Considered- Diabetes plus urine ACR 3-30mg/mmol
Non-diabetic with ACR >22.6mg/mmol

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39
Q

What is a rugger jersey spine?

A

Finding on spinal X-ray involving sclerosis of both ends of each vertebral body (denser white) and osteomalacia in centre (less white)

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40
Q

What is dialysis and when is it used?

A

Performs filtration tasks of kidneys artificially
Used in end-stage renal failure or complications of acute AKI
Removes excess fluids, solutes and waste products

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41
Q

What are the indications for short-term dialysis?

A

A- Acidosis (severe and not responding to treatment)
E- Electrolyte abnormalities (treatment resistant hyperkalaemia)
I- Intoxication
O- Oedema (severe and unresponsive pulmonary oedema)
U- Uraemia symptoms (seizures, reduced consciousness)

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42
Q

Outline haemodialysis

A

4h/d, 3d/wk
Blood taken out of body passed through machine, passes along semipermeable membranes inside machine
Solutes filter out of blood into dialysate and conc. gradient causes water and solutes to leave blood
Anticoagulation with citrate and heparin prevents blood clotting in machine

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43
Q

What are the long term access options for haemodialysis?

A

Tunnelled cuffed catheter (tube in subclavian or jugular vein with tip in SVC or RA)- Has 2 lumens- Red (blood exiting) and blue (blood entering)
Arteriovenous fistula (artificial connection between artery and vein, bypasssing capillary system)- Requires 4-16wks after surgery till it can be used

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44
Q

What are the main complications of a tunnelled cuffed catheter?

A

Infection
Blood clots

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45
Q

What are the main complications of an AV fistula?

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output HF

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46
Q

Where can a fistula be placed for haemodialysis?

A

Radiocephalic- Wrist- Radial artery to cephalic vein
Brachiocephalic- Antecubital fossa- Brachial artery to celhalic vein
Brachiobasilic- Upper arm- Less common

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47
Q

What are the features of a fistula on examination?

A

Check skin integrity
Aneurysms
Palpable thrill (fine vibration over anastomosis)
Machinery murmur on auscultation over fistula

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48
Q

List complications of AV fistulas

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output HF

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49
Q

What is STEAL syndrome?

A

Inadequate blood flow to limb distal to fistula
AV fistula steals blood from rest of limb- Blood diverted away from part of limb it was supposed to supply= Ischaemia

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50
Q

What is high-output HF?

A

Caused by blood flowing quickly from arterial to venous system through AV fistula
Rapid return of blood to heart= Increased pre-load= Hypertrophy of heart muscle and HF

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51
Q

What is a key rule regarding fistulas?

A

Never take blood from a fistula= Risk of damage

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52
Q

Outline the complications of peritoneal dialysis

A

Bacterial peritonitis
Peritoneal sclerosis- Thickening and scarring of peritoneal membrane
Ultrafiltration failure- Dextrose absorbed, reducing filtration gradient= Less effective
Weight gain- Due to absorption of dextrose
Psychosocial impairment

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53
Q

What is peritoneal dialysis?

A

Uses peritoneal membrane to filter blood
Dextrose added to peritoneal cavity
Ultrafiltration occurs from blood, accross peritoneal membrane, into dialysis solution
Dialysis solution replaced, taking away waste products

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54
Q

What is the tube used in peritoneal dialysis called?

A

Tenckhoff catheter

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55
Q

What is continuous ambulatory peritoneal dialysis (CAPD)?

A

Dialysis solution always in peritoneal cavity- Various regimes for changing solution (eg: 2L solution replaced 4x daily)

56
Q

What is automated dialysis?

A

Type of peritoneal dialysis
Machine continuously replaces dialysis fluid for 8-10h overnight

57
Q

What is the potential prognosis of a kidney transplant in end-stage renal failure?

A

10yrs compared to dialysis and significantly improves QoL

58
Q

How is donor matching done?

A

Matched based on human leukocyte antigen (HLA) type A, B and C on Chr 6
Don’t have to fully match, but closer is better

59
Q

Outline the basics of a kidney transplant procedure

A

Leave patient’s kidneys in place
Donor kidney blood vessels anastomosed with pelvic vessels- Usually external iliac vessels
Ureter of donor kidney anastomosed directly with bladder
Donor kidney placed anteriorly in abdomen and can be palpated in iliac fossa area
Hockey stick incision used

60
Q

What is expected post-renal transplant?

A

New kidney will function immediately
Basiliximab- Monoclonal antibody- Targets IL2 receptor on T cells- 2 doses given after surgery to prevent acute rejection
Require life-long immunosuppression- Combination of tacrolimus, mycophenolate, ciclosporin, azathioprine, prednisolone

61
Q

What are the SEs of immunosuppresants?

A

Cause seborrhoeic warts and skin cancers
Tacrolimus- Tremor
Ciclosporin- Gum hypertrophy
Steroids- Features of Cushing’s syndrome

62
Q

List the potential complications of transplant

A

Transplant rejection
Transplant failure
Electrolyte imbalances

63
Q

List complications related to immunosuppressants

A

Ischaemic heart disease
T2D (steroids)
Infections more likely/severe/involve unusual pathogens
Non-Hodgkin lymphoma
Skin cancer (SCC)

64
Q

List unusual infections that can occur secondary to immunosuppressant meds

A

Pneumocystis jiroveci pneumonia (PCP/PJP)
Cytomegalovirus (CMV)
TB

65
Q

What is glomerulonephritis?

A

Inflammation of the glomeruli in the kidneys
Glomerulus= 1st part of nephron- Filters fluid out of capillaries and into renal tubule
Describes pathology that occurs in various diseases- Treat underlying cause

66
Q

What is nephritic syndrome?

A

Group of features that occur with nephritis
Haematuria- Microscopic/macroscopic
Oliguria- Sig. reduced urine output
Proteinuria- But <3g/24h (higher suggests nephrotic syndrome)
Fluid retention

67
Q

What is nephritis?

A

Inflammation of kidneys
Descriptive term, not a diagnosis

68
Q

What are the features of nephrotic syndrome?

A

Proteinuria (>3g/24h)- Frothy urine
Low serum albumin (<25g/l)
Peripheral oedema
Hypercholesterolaemia

69
Q

What is nephrotic syndrome?

A

Basement membrane in glomerulus becomes highly permeable, resulting in significant proteinuria

70
Q

What does nephrotic syndrome predispose patients to?

A

Thrombosis
HTN
High cholesterol

71
Q

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

A

Minimal change disease- Usually idiopathic and treated successfully with steroids

72
Q

What are the main causes of nephrotic syndrome in adults?

A

Membranous nephropathy
Focal segmental glomerulosclerosis

73
Q

What are the less common causes of nephrotic syndrome?

A

Membranoproliferative glomerulonephritis
Henoch-Schonlein Purpura (HSP)
Diabetes
Infection (eg: HIV)

74
Q

Outline IgA nephropathy

A

Most common cause of primary glomerulonephritis
Patient- 20s presenting with haematuria

75
Q

What is seen on histology of IgA nephropathy?

A

IgA deposits and mesangial proliferation (found in centre of gomerulus and help support capillaries)

76
Q

Outline membranous nephropathy

A

Involves deposits of immune complexes in glomerular basement membrane- Causes thickening and malfunctioning of membrane and proteinuria

77
Q

What is seen on histology of membranous nephropathy?

A

IgG and complement deposits on basement membrane

78
Q

What are the causes of membranous nephropathy?

A

Majority idiopathic (70%)
Can be secondary to malignancy/SLE/drugs (eg: NSAIDs)

79
Q

Outline membranoproliferative glomerulonephritis

A

Affects patients <30y
Involves immune complex deposits and mesangial proliferation

80
Q

Outline post-streptococcal glomerulonephritis

A

Affects patients <30y
Presents 1-3wks after streptococcal infection (eg: Tonsillitis/impetigo)
Usually make full recovery

81
Q

Outline rapidly progressive glomerulonephritis

A

Acute severe illness- Responds well to treatment

82
Q

What is seen on histology of rapidly progressive glomerulonephritis?

A

Glomerular crescents

83
Q

What is Goodpasture syndrome?

A

Anti-glomerular basement membrane (anti-GBM) disease
Anti-GBM antibodies attack glomerulus and pulmonary basement membranes

84
Q

What does Goodpasture syndrome cause?

A

Glomerulonephritis
Pulmonary haemorrhage

85
Q

What is the typical presentation of Goodpasture syndrome?

A

Patients in 20s or 60s with acute kidney failure and haemoptysis (coughing up blood)

86
Q

List systemic diseases that can cause glomerulonephritis

A

HSP
Vasculitis (microscopic polyangiitis or granulomatosis with polyangiitis)
Lupus nephritis (associated with SLE)

87
Q

AKI, haemoptysis and anti-GBM antibodies

A

Goodpasture syndrome

88
Q

AKI, haemoptysis and p-ANCA/MPO antibodies

A

Microscopic polyangiitis

89
Q

AKI, haemoptysis, c-ANCA/PR3 antibodies

A

Granulomatosis with polyangiitis

90
Q

Outline management of glomerulonephritis

A

Supportive care (HTN management and dialysis if severe)
Immunosuppression (corticosteroids)

91
Q

What is renal tubular acidosis?

A

Involves metabolic acidosis due to pathology in tubules of kidneys
Tubules balance hydrogen and bicarbonate ions between blood and urine to maintain normal pH

92
Q

Outline Type 1 renal tubular acidosis

A

Distal tubule cannot excrete hydrogen ions
High urinary pH
Low serum potassium
HYPOKALAEMIA

93
Q

Outline type 2 renal tubular acidosis

A

Proximal tubule cannot reabsorb bicarbonate
High urinary pH
Low serum potassium

94
Q

Outline type 4 renal tubular acidosis

A

Low aldosterone/impaired aldosterone function
Low urinary pH
High serum potassium
HYPERKALAEMIA

95
Q

What is the result of type 1 RTA (distal RTA)?

A

High urinary pH due to absence of H+
Metabolic acidosis due to retained H+ in blood
Hypokalaemia due to failure of H+ and potassium exchange (H+/K+ ATPase)

96
Q

What can cause distal RTA (type 1)?

A

Genetic
SLE
Sjogren’s syndrome
PBC
Hyperthyroidism
SCA
Marfans

97
Q

How does type 1 RTA present?

A

Failure to thrive in children
Recurrent UTIs (due to alkaline urine)
Bone disease (rickets or osteomalacia)
Muscle weakness
Arrhythmias (due to hypokalaemia)

98
Q

How is Type 1 RTA managed?

A

Oral bicarbonate- Corrects acidosis and electrolyte imbalances

99
Q

What is the result of Type 2 renal tubular acidosis?

A

High urinary pH due to excess bicarbonate in urine
Metabolic acidosis due to inadequate bicarbonate in blood
Hypokalaemia due to urinary loss of potassium along with bicarbonate

100
Q

What are the key causes of Type 2 renal tubular acidosis?

A

Inherited
Multiple myeloma
Fanconi’s syndrome

101
Q

How is type 2 renal tubular acidosis managed?

A

Oral bicarbonate

102
Q

What is the role of aldosterone?

A

Stimulates sodium reabsorption and potassium and hydrogen ion excretion in distal tubules
Low aldosterone/impaired aldosterone function leads to insufficient potassium and hydrogen excretion

103
Q

What is the role of ammonia?

A

Produced in distal tubules
Balances excretion of hydrogen ions
Is a base and buffers hydrogen ions, preventing urine becoming too acidotic

104
Q

What is the result of type 4 renal tubular acidosis?

A

Hyperkalaemia due to retained potassium in blood
Metabolic acidosis due to retained hydrogen ions in blood
Low urinary pH- Hyperkalaemia suppresses ammonia= Urine acidotic

105
Q

What causes low aldosterone/low aldosterone activity?

A

Adrenal insufficiency
Diabetic nephropathy
Meds (ACE-is, spironolactone, eplerenone)
(Type 4 RTA)

106
Q

Outline management of type 4 renal tubular acidosis

A

Aldosterone deficiency- Fludrocortisone (mineralocorticoid)
Oral bicarbonate
Treatment of hyperkalaemia

107
Q

What is haemolytic uraemic syndrome (HUS)?

A

Thrombosis in small blood vessels throughout body- Triggered by Shiga toxins (E. coli or Shigella)
Most common in children following an episode of gastroenteritis

108
Q

What increases the risk of HUS?

A

Use of antibiotics and antimotility meds (eg: Loperamide) used to treat gastroenteritis

109
Q

Outline the classic triad of HUS

A

Microangiopathic haemolytic anaemia
AKI
Thrombocytopenia (low platelets)

110
Q

Outline management of HUS

A

Stool culture
EMERGENCY- Requires hospital admission and supportive management
Hypovolaemia- IV fluids
Treat HTN
Severe anaemia- Blood transfusion
Severe renal failure- Haemodialysis

111
Q

Outline presentation of HUS

A

Diarrhoea 1st symptom- Turns bloody within 3d- 1wk after diarrhoea onset, features of HUS develop:
Fever
Abdo pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
HTN
Bruising
Jaundice (due to haemolysis)
Confusion

112
Q

What is the result of formation of blood clots in HUS?

A

Blood clots consume platelets, leading to thrombocytopenia
Blood flow through kidney affected by thrombi and damaged RBCs= AKI

113
Q

What is microangiopathic haemolytic anaemia (MAHA)?

A

Occurs in HUS
Destruction of RBCs (haemolysis) due to small vessels- Tiny thrombi partially obstruct small blood vessels and churn RBCs as pass through= Rupture

114
Q

What is rhabdomyolysis?

A

Skeletal muscle breakdown and release into blood:
Myoglobin
Potassium
Phosphate
Creatine kinase

Myocytes undergo apoptosis

115
Q

What is the result of rhabdomyolysis?

A

Potassium- Most immediately dangerous breakdown product- Hyperkalaemia- Cardiac arrhythmias/cardiac arrest
Myoglobin- Toxic to kidneys (AKI)

116
Q

What are the complications of rhabdomyolysis?

A

Compartment syndrome
Disseminated intravascular coagulation

117
Q

List causes of rhabdomyolysis

A

Prolonged immobility- Frail patients who fall and spend time on floor before being found
Extremely rigorous exercise- Beyond person’s fitness level
Crush injuries
Seizures
Statins

118
Q

List signs and symptoms of rhabdomyolysis

A

Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)

119
Q

Outline investigations of rhabdomyolysis

A

Creatine kinase (CK)- >150 U/L- Typically rises in first 12h, remains elevated for 1-3d, then gradually falls- Higher CK = Greater risk of kidney injury
Myoglobinuria- Red-brown- Dip positive for blood
U&Es- AKI and hyperkalaemia
ECGs- Hyperkalaemia

120
Q

Outline management of rhabdomyolysis

A

IV fluids- Corrects hypovolaemia and encourages filtration of breakdown products
Treat complications

121
Q

What is the main complication of hyperkalaemia?

A

Cardiac arrhythmias- VF- Cardiac arrest

122
Q

What are the values of normal serum potassium and hyperkalaemia?

A

Normal- 3.5-5.3
Mild- 5.4-6
Moderate- 6-6.5
Severe- Over 6.5

123
Q

List causes of hyperkalaemia

A

AKI
CKD (stage 4/5)
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome

124
Q

List medications that can cause hyperkalaemia

A

Aldosterone antagonists (spironolactone)
ACE-is (ramipril)
ARBs (candesartan)
NSAIDs (naproxen)

125
Q

What is a cause of falsely elevated potassium (pseudohyperkalaemia)?

A

Haemolysis during sample

126
Q

Outline ECG changes in hyperkalaemia

A

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

127
Q

Outline management of hyperkalaemia <6.5mmol/L w/o ECG changes

A

Treat underlying cause- AKI and stop certain meds

128
Q

When do patients with hyperkalaemia require urgent treatment?

A

ECG changes
Serum potassium >6.5mmol/L

129
Q

Outline mainstay treatment of severe hyperkalaemia

A

Insulin- Drives potassium from ECS to ICS
Dextrose infusion- Prevents hypoglycaemia on insulin
Calcium gluconate- Stabilises cardiac muscle cells and reduces risk of arrhythmias

130
Q

Outline options for lowering serum potassium in hyperkalaemia

A

Nebulised salbutamol- Temporarily drives potassium into cells
Oral calcium resonium- Reduces potassium absorption in GI tract (slow and causes constipation)
Sodium bicarbonate- Used in acidotic patients on renal advice- Drives potassium into cells as corrects acidosis
Haemodialysis- Required in severe/persistent cases

131
Q

What is polycystic kidney disease (PKD)?

A

Genetic condition
Healthy kidney tissue replaced with many fluid-filled cysts
Enlarged kidneys may be palpable on exam
Leads to renal failure

132
Q

What is the inheritance of PKD?

A

Autosomal dominant most common (ADPKD):
PKD1 gene on Chr16 (85% cases)
PKD2 gene on Chr4 (15% cases)

ARPKD

133
Q

List the extra-renal manifestations of ADPKD

A

Cerebral aneurysms
Hepatic/splenic/pancreatic/ovarian/prostatic cysts
Mitral regurgitation
Colonic diverticula

134
Q

List complications of ADPKD

A

Chronic loin/flank pain
HTN
Gross haematuria- Can occur with cyst rupture (usually resolves within a few days)
Recurrent UTIs
renal stones
End-stage renal failure- Mean age 50y

135
Q

Outline autosomal recessive PKD

A

Mutation in Polycystic kidney and hepatic disease 1 (PKHD1) gene on Chr6
More rare and severe than ADPKD
Often picked up on antenatal scans with oligohydramnios (reduced amniotic fluid volume due to reduced urine output)
Oligohydramnios- Leads to underdevelopment of fetal lungs (pulmonary hypoplasia) and resp. failure shortly after birth
May require haemodialysis within 1st few days of life
May have dysmorphic features- Underdeveloped ear cartilage, low-set ears, flat nasal bridge
End-stage renal failure usually occurs before reaching adulthood

136
Q

How is PKD diagnosed?

A

US
Genetic testing

137
Q

Outline management of PKD

A

Tolvaptan- Slow development of cysts and progression of renal failure in autosomal dominant PKD
Antihypertensives (ACE-Is)
Analgesia
ABs (UTIs or cyst infections)
Drainage of symptomatic
Dialysis/renal transplant- End-stage renal failure
Genetic counselling
Avoid contact sports due to risk of cyst rupture
Avoid NSAIDs and anticoagulants
MR angiography- Screen for cerebral aneurysms

Final Year (14 decks)

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