r e n a l

Question 1

what are the pre renal causes of AKI

Answer 1

Shock - dehydration, hypovolaemia
 RAS
 Hepatorenal syn.

Question 2

what are the renal causes of AKI

Answer 2

Glomerulonephritis
 Acute Tubular Necrosis
 Interstitial disease

Question 3

what are the post renal causes of AKI

Answer 3

1. Diseases of renal papillae, pelvis, ureters, bladder or urethra.

SNIPPIN

 Stone
 Neoplasm
 Inflammation: stricture
 Prostatic hypertrophy
 Posterior urethral valves
 Infection: TB, schisto
 Neuro: post-op, neuropathy

Question 4

what are the presentations relating to AKI

Answer 4

Uraemia / Azotaemia
 Acidosis
 Hyperkalaemia
 Fluid overload
 Oedema, inc. pulmonary  ↑BP(or↓)
 S3 gallop
 ↑ JVP

Question 5

how would you assess for AKI clinically

Answer 5

1. Acute or chronic?
 Can’t tell for sure: Rx as acute
 Chronic features
 Hx of comorbidity: DM, HTN
 Long duration of symptoms
 Previously abnormal bloods (GP records)
2. Volume depleted?
 Postural hypotension
 ↓ JVP
 ↑ pulse
 Poor skin turgor, dry mucus membranes
3. GU tract obstruction?
 Suprapubic discomfort
 Palpable bladder
 Enlarged prostate
 Catheter
 Complete anuria (rare in ARF)
4. Rare cause?
 Assoc.  ̄c proteinuria ± haematuria
 Vasculitis: rash, arthralgia, nosebleed

Question 6

what are the investigations required in AKI

Answer 6

Bloods: FBC, U+E, LFT, glucose, clotting, Ca, ESR
 ABG: hypoxia (oedema), acidosis, ↑K+
 GN screen: if cause unclear. f blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA,
C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
 Urine: dip, MCS, chemistry (U+E, PCR, osmolality, BJP)
 ECG: hyperkalaemia
 CXR: pulmonary oedema
 Renal US: Renal size, hydronephrosis

Question 7

describe how AKI is classified

Answer 7

RIFLE = 3 grades of AKI and 2 outcomes
Classification determined by worst criteria

table

Question 8

in pre renal failure what is happens to osmolality and sodium

Answer 8

in pre-renal failure, urine is concentrated and Na is reabsorbed = increase osmolality, Na less than 20mM

Question 9

what is the general management for AKI

Answer 9

 Identify and Rx pre-renal or post-renal causes
 Urgent US
 Rx exacerbating factors: e.g. sepsis
 Give PPIs
 Stop nephrotoxins: NSAIDs, ACEi, gent, vanc
 Stop metformin if Cr > 150mM

Question 10

What are the features to be monitored in AKI

Answer 10

Catheterise and monitor UO
 Consider CVP
 Fluid balance  Wt.

Question 11

what are the ECG changes seen in hyperkalamia

Answer 11

ECG Features (in order)
 Peaked T waves
 Flattened P waves
 ↑ PR interval
 Widened QRS
 Sine-wave pattern → VF

Question 12

how do you treat hyperkalaemia

Answer 12

10ml 10% calcium gluconate
 100ml 20% glucose + 10u insulin (Actrapid)  Salbutamol 5mg nebulizer
 Calcium resonium 15g PO or 30g PR
 Haemofiltration (usually needed if anuric)

Question 13

how do you treat pulmonary oedema

Answer 13

Sit up and give high-flow O2
 Morphine 2.5mg IV (± metoclopramide 10mg IV)
 Frusemide 120-250mg IV over 1h
 GTN spray ± ISMN IVI (unless SBP <100)
 If no response consider:
 CPAP
 Haemofiltration / haemodialysis ± venesection

Question 14

what are the indications for acute dialysis (in AKI)

Answer 14

1. Persistent hyperkalaemia (>7mM)
2. Refractory pulmonary oedema
3. Symptomatic uraemia: encephalopathy, pericarditis 4. Severe metabolic acidosis (pH <7.2)
   reabsorbed → ↑osmolality, Na <20mM
4. Poisoning (e.g. aspirin)

Question 15

what are the life threatening complications in AKI

Answer 15

Hyperkalaemia

Pulmonary oedema

Question 16

how do you manage acute renal failure

Answer 16

refer to notes

1. A-E
2. life threatening complications
3. shock or dehydration
4. monitor
5. look for evidence of post renal causes
6. hx and lx
7. manage sepsis
8. further management

Question 17

what are the features of chronic renal disease?

Answer 17

Kidney damage ≥3mo indicated by ↓ function
 Symptoms usually only occur by stage 4 (GFR<30)
 ESRF is stage 5 or need for RRT

Question 18

how is CKD classified

Answer 18

based on eGFR
stage 1 = Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)

stage 2 = 60-90ml/min if kidney tests are normal, no CKD
stage 3a = 45-59ml/min
stage 3b = 30-44ml/min
stage 4 = 15- 29ml/min
stage 5 = less than 15 ml/ min = dialysis or kidney transplant needed

Question 19

what are the common causes of CKD

Answer 19

Common
 DM
 HTN = Chronic raised BP causing nephrosclerosis.

Other
 RAS
 GN
 Polycystic disease
 Drugs: e.g. analgesic nephropathy 
 Pyelonephritis: usually 2O to VUR 
 SLE
 Myeloma and amyloidosis

Question 20

describe the inheritance pattern for adult polycystic disease and chr affected by type 1 and 2

Answer 20

2 Types (both are autosomal dominant)
 Type 1 (85%; PKD1 mutation on Chromosome 16)
 Type 2 (15%; PKD2 mutation on Chromosome 4)

Question 21

what are sx seen in APKD

Answer 21

size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic

Question 22

what are the factors affecting anaemia in chronic kidney disease

Answer 22

Decreased production of erythropoietin from the kidney
Absolute iron deficiency (poor absorption and malnutrition)
Functional iron deficiency (inflammation, infection) Blood loss
Shortened Red Blood Cell survival
Bone marrow suppression from uraemia Medication induced
Deficiency of Vit B12 and folate

Question 23

in CKD, mineral bone disease leads

Answer 23

CKD leads to
Increased Fibroblast Growth Factor-23 Increased Alkaline Phosphatase and PTH Increase Phosphate
Decreased Serum Calcium
decreased 1,25 - vitamin D

Question 24

describe tertiary hypothyroidism in CKD

Answer 24

Occurs when PTH release continues despite raised serum Calcium levels (independently)
• As a result of parathyroid gland nodular hyperplasia
• Consequence of advanced CKD

Question 25

how is anaemia of CKD managed

Answer 25

Measure haematinics – Vitamin B12, Folate, Ferritin, Iron, Transferrin Saturation, CHr If deficient in any of above – replace this first • IV Iron may be better tolerated than PO Discuss with renal team regarding starting ESA aim for Hb 100-120

Question 26

describe management of ADPKD

Answer 26

Control BP  As per CKD management  Tolvaptan (Vasopression receptor-2 antagonist) is available for some patients to slow progression of CKD.  Genetic counselling and testing

Question 27

how id ADKPD DX

Answer 27

Family history is KEY | USS

Question 28

describe the pathophysiology and investigations for HTN nephropathy and treatment

Answer 28

Chronic raised BP causing nephrosclerosis. Investigations to identify if primary or secondary HTN (based on clinical findings and index of suspicion):  24 hour Urinary metanephrines (Phaeochromocytoma)  Aldosterone: Renin ratio (Primary aldosteronism)  Cortisol & Dexamethasone suppression test (Cushing’s syndrome)  TSH (hyperthyroidism)  MRA (Renal artery stenosis) Treatment Anti-hypertensives (see ABCD guidelines)

Question 29

in CKD what are questions to ask

Answer 29

``` past UTI HTN, DM FH DH sx ```

Question 30

what are the investigations in CKD

Answer 30

BLOOD = ↓Hb, U+E, ESR, glucose, ↓Ca/↑PO4, ↑ALP, ↑PTH  Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep  Film: burr cells Urine: dip, MCS, PCR, BJP Imaging  CXR: cardiomegaly, pleural/pericardial effusion, oedema  AXR: calcification from stones  Renal US  Usually small (<9cm)  May be large: polycystic, amyloid  Bone X-rays: renal osteodystrophy (pseudofractures)  CT KUB: e.g. cortical scarring from pyelonephritis renal biopsy if cause unclear and size normal

Question 31

what are the complications of CKD

Answer 31

CRF HEALS ``` Cardiovascular disease  Renal osteodystrophy  Fluid (oedema)  HTN, Hypothyroidism secondary and tertiary  Electrolyte disturbances: K, H  Anaemia  Leg restlessness  Sensory neuropathy ```

Question 32

describe the features our renal osteodystrophy

Answer 32

osteoporosis: ↓ bone density |  Osteomalacia: ↓ mineralisation of osteoid (matrix)

Question 33

describe the mechanism of renal osteodystrophy

Answer 33

↓ 1α-hydroxylase → ↓ vit D activation → ↓ Ca → ↑ PTH  Phosphate retention → ↓ Ca and ↑ PTH (directly)  ↑ PTH → activation of osteoclasts ± osteoblasts  Also acidosis → bone resorption

Question 34

describe the management of CKD

Answer 34

MDT focused general = rx reversible causes stop nephrotoxic drugs lifestyle = exercise, healthy weight, stop smoking, Na, fluid and PO4 restriction CV risk = statins, low dose aspirin, manage DM HTN = target 140/90 and 130/80 if DM. in DM kidney disease give ACEi/ARB ACEi/ ARB = reduce proteinuria Oedema = furesomide Bone disease = phosphate binders = sevelamar. vit D analogues - alfacalcidiol. Ca supplements Anaemia = exclude IDA and ACD. EPO to raise Hb to 11g/dl (higher thrombosis risk) Restless legs = clonazepam ``` Refer for fistula o Venous mapping  Refer for PD tube insertion  Work-up for transplant o Further tests o Refer to Transplant work-up clinic ```

Question 35

describe RRT options

Answer 35

H.D P.D kidney transplant

Question 36

diabetic nephropathy is the biggest cause of...

Answer 36

ESKD

Question 37

describe the pathology of diabetic nephropathy

Answer 37

Hyperglycaemia → renal hyperperfusion → hypertrophy and ↑ renal size  Hypertrophy and metabolic defects inc. ROS production → glomerulosclerosis and nephron loss  Nephron loss → RAS activation → HTN

Question 38

clinically, what are the progression of diabetic nephropathy

Answer 38

Microalbuminuria (30-300mg/d or albumin:creatinine >3)  Strong independent RF for CV disease  Progresses to proteinuria (albuminuria >300mg/d)  Diabetic retinopathy usually co-exists and HTN is common

Question 39

describe screening for diabetic nephropathy

Answer 39

T2DMs should be screened for micrroalbuminuria 6 monthly

Question 40

how is diabetic nephropahty managed

Answer 40

Good glycaemic control delays onset and progression BP target 130/80 Start ACEi/ARB even if normotensive Stop smoking Combined kidney pancreas Tx possible in selected pts

Question 41

renal transplant is the treatment of choice in ...

Answer 41

ESRF

Question 42

what factors needs to be checked/ or assessed before renal transplant

Answer 42

Virology status: CMV, HCV, HBV, HIV, VZV, EBV  CVD  TB  ABO and HLA haplotype

Question 43

what are the contraindications to renal transplant

Answer 43

Active infection  Cancer  Severe HD or other co-morbidity

Question 44

what are the types of renal graft?

Answer 44

cadaveric: brainstem death ̄c CV support  Non-heart beating donor: no active circulation  Live-related = Optimal surgical timing + HLA-matched + Improved graft survival  Live unrelated

Question 45

what immunosuppression is required in renal transplant pre and post op

Answer 45

``` pre = campath/alemtuzumab post = pred short term and tacrolimus/ciclosporin long term ```

Question 46

what is the prognosis for cadaveric renal allografts

Answer 46

15 years

Question 47

what are the complications of renal transplant

Answer 47

``` Post-op  Bleeding  Graft thrombosis  Infection  Urinary leaks Hyperacute rejection (minutes)  ABO incompatibility  Thrombosis and SIRS ``` Acute Rejection (<6mo)  ↑ing Cr (± fever and graft pain)  Cell-mediated response  Responsive to immunosuppression Chronic Rejection (>6mo)  Interstitial fibrosis + tubular atrophy  Gradual ↑ in Cr and proteinuria  Not responsive to immunosuppression Ciclosporin / tacrolimus nephrotoxicity  Acute: reversible afferent arteriole constriction → ↓GFR  Chronic: tubular atrophy and fibrosis ↓ Immune Function  ↑ risk of infection: opportunists, fungi, warts  ↑ risk of malignancy: BCC, SCC, lymphoma (EBV) Cardiovascular Disease  Hypertension and atherosclerosis

Question 48

what are differentials for raising Cr in Tx pt

Answer 48

Rejection  Obstruction  ATN  Drug toxicity

Question 49

what are the causes of hyperkalaemia

Answer 49

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

Question 50

what does each drug used in hyperkalaemia do?

Answer 50

Treatment of hyperkalaemia involves: 1. Stabilizing the myocardium to prevent arrhythmias  10mls of 10% Calcium Gluconate over 5-10 minutes 2. shifting potassium into 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

Question 51

what are sx of hypokalaemia

Answer 51

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

Question 52

what are the causes of hypokalaemia

Answer 52

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.

Question 53

what are the ECG changes seen in hypokalaemia

Answer 53

ECG Changes  Small T waves  U wave (after T)  Increased PR interval

Question 54

what are the rx of AKI

Answer 54

``` Diabetes  CKD  IHD/CCF/CVD  Any major medical co-morbidity  Elderly >75  Sepsis  Medications – ACEi, ARBs, NSAIDs, Antibiotics ```

Question 55

how is hypokalaemia treated

Answer 55

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