Renal

Question 1

Definition of CKD

Answer 1

ACR>3 with any eGFR
EGFR <60 on 2 occasions 3 months apart
Structural kidney disease even if normal egfr.

Question 2

What is the most common cause of end stage renal disease in the UK

Answer 2

diabetes (20% of those on dialysis)

Question 3

Causes of visible and non visable haematuria

Answer 3

Cancer - bladder, kidney, endometrial, prostate
UTI
renal causes - kidney stones, glumerulonephritis, IgA nephropathy, PKD (bleeding into cyst).
BPH or prostatitis
Trauma/exercise induced nephropathy.
Renal infarct (rare). TB rare.
Uncontrolled anticoagulation
Red coloured urine with drugs (rifampicin), rhabdo, foods (beetroot).

Question 4

How to investigate non visible haematuria

Answer 4

If occurring with UTI and resolves with treatment - do nothing.
If positive dipstick without UTI or persisting after treatment
1. if >65Yo and raised WCC or dysuria - refer 2ww
2. If not meeting above criteria, do BP renal function ACR and renal USS.
- refer to urology if symptomatic or more than 40YO or abnormal invx.

Question 5

What are the chances of someone with non visible haematuria having cancer?

Answer 5

Not very much! if NVH alone in someone over 65YO, only 1.6% will have cancer.
If NVH over 65YO plus raised WCC or dysuria, this goes up to 3% which meets threshold for further invx (cancer pathway).

Question 6

What medication should be offered in CKD as primary prevention of CVD

Answer 6

Atorvastatin 20mg should be offered.

ACEi or ARB should be used if CKD and evidence of kidney damage (this is generally to help the kidney) - raised ACR

Question 7

When should you follow CKD guidance for choice of antihypertensive and when should you use normal guidance

Answer 7

First choice drug for CKD is determined by ACR.
If ACR is less than 30, use normal hypertesion guidance eg CCB if older than 55YO
If ACR is more than 30, use ACEi or ARB first line.

In CKD target blood pressure is 140/90 if ACR is less than 70 and 130/80 if ACR if more than 70 (worse renal function needs better blood pressure control).

Question 7

When should you refer those with CKD into secondary care?

Answer 7

• 5yr risk of needing RRT of >5% using 4 variable kidney failure risk equation
• ACR of 70mg/mmol or more unless known to be caused by diabetes and being appropriately treated
• ACR >30 with haematuria
• sustained decrease in eGFR of 25% or more (and change of eGFR category) in prev 12 months.
• sustained decreased in eGFR of 15 or more per year.
• hypertension that remains poorly controlled despite use of 4 antihypertensive drugs
• known or suspected rare or genetic causes of CKD
• suspected renal artery stenosis

Question 8

What is renal artery stenosis

Answer 8

Progressive narrowing of renal artery - blood downstream of narrowing is at lower pressure. Kidney senses this, raises BP via RAAS - therefore vicious cycle of high blood pressure.
Over time kidney will atrophy.
Can cause AKI/acute renal failure if bilateral.
Causes of renal artery stenosis is atherosclerosis, or renal fibromuscular dysplasia (classically develops in young women).

Symptoms will be from htn - headache, blurry vision.
Diagnosis - lab tests, imaging, gold standard renal arteriography.
Treatment - manage htn. balloon angioplasty to open artery, may need stent, or can do bypass graft. May remove stenosed kidney.

Question 9

Presentation of nephrotic syndrome

Answer 9

often present with peripehral or periorbital oedema

will have protein in the urine

Question 10

Presetnation of nephritic synrome

Answer 10

Haematuria

Question 11

Definition of AKI

Answer 11

increase in creat of >26.5micromol/l within 48hrs OR 1.5 x baseline creatinine in 7 days OR urine output <0.5ml/kg/h for 6hrs.

Then staging of AKI depending on how bad within that. Stage 3 is worst, all 3s. Creat 3x baseline or >354micromol/l, or <0.3ml/kg/hr for 12hrs.

Question 12

Causes of renal failure.

Answer 12

Pre renal - reduced blood flow - cardiac failure, hypovolaemia, hypotension, renal artery stenosis

Renal - nephritis

Post-renal - urinary tract obstruction - stones, BPH, tumour.

AKI often as part of another illness (sepsis, decompensated heart failure, ESRD), triggered by certain drugs.

Question 13

Who to always think about AKI in

Answer 13

Old people with comorbidities, especially during intercurrent illness.

Those with CKD - deterioration may be due to AKI rather than progression of CKD

Nephron harming drugs - diuretics, ACEi/ARBs, NSAIDS - remember DAMN-glif drugs.

Question 14

What about sick day rules?

Answer 14

Some evidence doesnt actually prevent harms (risks with stopping drugs too)

Need to be actual acute illness of vomiting or diarrhoea, fevers, sweats or shakes, to count!

More important is getting people to understand the importance of maintaining good fluid intake at times of intercurrent illness.

Question 15

What to do if bloods flag up AKI

Answer 15

AKI stage 1
- if stable clinical context - repeat U&E and rv in <72hrs
- if acute illness, repeat and clinical rv in 24hrs

AKI stage 2
- If stable, repeat and clinical rv in 24hrs
- if acute illness, repeat and review in 6hrs.

AKI stage 3
- if stable, repeat and rv in 6hrs
- if acute illness, admit immediately.

If AKI confirmed on repeat testing, consider causes
- sepsis
- hypotension
- hypovolaemia
- known heart failure? (change in meds, over diuresis, illness)
- known CKD
- intrinsic kidney disease - dip urine - if negative likely to be pre renal or drug cause.
- urinary tract obstruction - stones, blocked catheter, pelvic mass, prostatic enlargement.
- hypercalcaemia.

Also medication review
Also fluid status

Question 16

Drugs that can exacerbate AKI

Answer 16

Diuretics
NSAIDS
ACEi/ARBs

Drugs that accumulate in renal impairment - metformin.

Question 17

Which groups are commonly at highest risk of AKI

Answer 17

Frail elderly
those on potentailly nephrotoxic drugs
those with comorbidities - heart liver diabetics malignancy.
renal comorbidities
fluid losses ++ (gastroenteritis)
recent iodinated contrast.

Question 18

When to immediately admit with AKI q

Answer 18

AKI stage 3
or metabolic disturbance - fluid overload, pulmonary oedema, hyperkalaemia, metabolic acidosis, uraemia or complications of uraemia eg pericarditis, encephalopathy.

Question 19

How to identify cause of AKI

Answer 19

Urinalysis - if haematuria and proteinuria in absence of UTI/trauma in catheterisation, consider possibility of nephritis.

US - not needed if cause found. However if no cause found, need to US renal tract in 24hrs (likely need admission to do this). If obstruction suspected need US within 6 hours and stenting within 12hrs.

Question 20

Follow up after episode of AKI

Answer 20

clinical review at 3 months after AKI - lifestyle advice, medication review, plan for ongoing blood monitoring.

Need to monitor for 3 years after AKI even if bloods return to baseline.

This is because these patient will be higher risk of developing CKD.

Periodic eGFR and ACR.

Question 21

renal function monitoring when starting ACEi/ARBs

Answer 21

Measure renal function at baseline before starting and before any dose increase. Then at 2 weeks after starting or dose increase.

Question 22

renal function monitoring when starting spironoloactone or eplerenone

Answer 22

U&E at baseline, at 1 wk, monthly for 3 months then 3 monthly for 1 yr then 4 monthly thereafter.

So patients going onto spironolactone need to know this!!

Question 23

What to do if worsening renal function on ACEI/ARB

Answer 23

try to continue if strong indication for drug (CHF MI CKD with albuminaemia).

If creat rise 15-30% - assess, if BP <120, reduce or stop other antihtn drugs, assess fluid status, continue ACEi/ARB and repeat U&E in 1-2wks.

If creat rises >30%, as above plan but recheck bloods 5-7d. If not improved, need to stop ACEi/ARB, or reduce to lower tolerated dose, then recheck U&E in 5 more days to ensure resolution.
May need alternative antihtn.
Get nephrology advice.
Discuss with HF team if indication was HF.

Question 24

Management of hyperkalaemia

Answer 24

Manage in primary care only if asymptomatic and no acute kidney injury and only mild hyperkalaemia (or moderate if you have access to ECG and it is normal!) if moderate K6.0-6.9, do ECG. If any ECG abnormalities, admit for IP treatment and cardiac monitoring If severe >7.0 - admit

Question 25

ECG changes in hyperkalaemia

Answer 25

bradycardia, diminished P waves, prolonged PR, wide QRS, tented T waves.

Question 26

mx of hyperkalaemia in community (if mild or mod with a normal ECG)

Answer 26

repeat U&E in 3 days if mild or 1 day if moderate. Review patient and medications, stop causitive agents If on ACEi/ARB/MRA, halve dose and recheck in 1wk, review ongoing use. If CKD or HF, consider discussing with specialist team. Minimal evicence for low K diet if no CKD. Loop diuretic may help if passing urine, not dehydrated and renal function preserved. Need to monitor U&E with this.

Question 27

Drugs that can cause hyperkalaemia

Answer 27

ACEI/ARBs Spironolactone/eplerenone Amiloride (K sparing diuretic) NSAIDs Macrogols Non selective beta blockers trimethoprim/co-trimoxazole digoxin toxicity LoSalt in diet.

Question 28

Causes of hyperkalaemia

Answer 28

Drugs see prev card. Spurious result - delayed processing, cold weather, sample problem Extreme exercise/crush/cold - all cause rhabdo Excessive dietary potassium - fruit veg processed food - especially problem if CKD. Tumour lysis syndrome Addisons disease Risk factors -renal impairment, diabetes, HF, low serum bicarb.

Question 29

Electrolyte disturbance in addisons disease

Answer 29

Low sodium High potassium

Question 30

What common medical conditions can contribute to AKI

Answer 30

Constipation - due to reduced gut excretion of potassium Poor controlled diabetes.

Question 31

How to prevent hyperkalaemia

Answer 31

In CKD/HF or diabetes, monitor U&E 2-4 times yearly due to their increased risk of AKI Sick day rules Monitor bloods more frequently if intercurrent illness, prev AKI or prev hyperK Caution using trimethoprim in these patients. Note hyperK increases risk of hospitalisation, prolonged stay and death.

Question 32

Two types of PCKD

Answer 32

Autosomal dominant type Autosomal recessive type - normally diagnosed around birth.

Question 33

AD PCKD

Answer 33

commonest inherited renal disease one of commonest forms of ESRD. Problem is increased destruction of renal parenchyma by multiple cysts. Often results in ESRD by age 50, but variation between people.

Question 34

Features of polycystic kidney disease

Answer 34

Renal manifestations - declining renal function - anaemia - secondary hyperparathyroidism - metabolic bone disease - inadequate nutrition - increased CVD risk - acute and chronic pain - cyst infections - renal stones Extra renal manifestations - hepatic cysts (90% people >35YO but rarely affects LFTs) - 20% get polycystic liver disease (may cause pain, early satiety, GORD, portal htn, ascites and pleural effusions if severe). - pancreatic cysts - intracranial aneurysms - 20% affected if Fhx aneurysm so do MRI screening for aneurysm if this is the case. If no Fhx, rate is twice that of normal population. - abdominal hernias - cardiac valve lesions - usually asymptomatic, no screening.

Question 35

How does autosomal dominant PCKD present

Answer 35

May be incidental finding or may present clinically Clinically most common presentations include renal cysts or extra renal manifestation. Maybe stones, frank haematuria, abdo pain. High blood pressure common in PCKD. If considering cysts, USS first line. MRI may be used if <40YO as can pick up smaller cysts.

Question 36

Inheritence of PCKD

Answer 36

Autosomal dominant type - but up to 25% have no fhx. Genetic referal indicated for those affected. PKCD 1 genes on chromosome 16 = 80% - more severe, ESRD at age 58 on average PKCD 2 genes on chromosome 4 = 15% - less severe, ESRD at age 79 on average.

Question 37

Management of AD PCKD

Answer 37

No treatment will stop disease. Aiming to slow progression Long term specialist follow up Lifestyle - diet, limit salt, high water intake. Maintain optimal weight. Regular CV exercise. No smoking. Limit NSAID use. TREAT HYPERTENSION - helps renal and CV outcomes. Strict BP control <110/75 if under 50 and eGFR>60. ACEi first line. Statin if CKD present (eGFR<60) Tolvaptan (vasopressin V2 receptor antagonists) = slows cyst progression. Therefore disease modifying. - side effects thirst, polydipsia, polyuria, nocturia. Only px by specialists. Dialysis /transplant if ESRD.

Question 38

Pathophysiology of nephrotic syndrome

Answer 38

problem is increased glomerular permeability, albumin and other plasma proteins escape into urine. plasma albumin drops, oedema develops due to osmotic pressures. Prothrombotic state is multifactorial!

Question 39

Presentation of nephrotic syndrome

Answer 39

Oedema - may be in limbs, but commonly periorbital, especially noticed in the morning, or including ascites or pleural effusions. (think about in new onset oedema!) Other symptoms may be foamy urine, dyspnoea, fatigue. Other symptoms may relate to consequences of nephrotic syndrome of thrombosis or hypertension.

Question 40

first investigation in possible nephrotic syndrome

Answer 40

urine dip - will show 3+ protein. then need to refer to secondary care who will look for complications, determine which type of nephrotic syndrome they have, ascertain underlying disease if one present.

Question 41

Criteria for nephrotic syndrome

Answer 41

Proteinuria (cut off based on lab) Clinical evidence of peripheral oedema AND severe hyperlipidaemia urgently refer to secondary care - should be seen within 2 weeks - so need to call team to make sure this happens!

Question 42

Common causes of nephrotic syndrome

Answer 42

membranous nephropathy 30% (more common white) focal segmental glomerulosclerosis 30% (more common black) minimal change disease 15% IgA nephropathy 15% 10% due to other causes including diabetes, SLE, amyloidosis, cancer, drugs, infx, congen - all rare! But 80% of nephrotic syndrome is idiopathic - unknwon cause!

Question 43

Complications of nephrotic disease

Answer 43

Increased thromboembolic risk - venous and rarely arterial too - up to 25% people with nephrotic syndrome Increased susceptibility to infections (cellulitis, pneumonia, peritonitis) - as losing good proteins Acute or chronic renal failure hyperlipidaemia

Question 44

treatment of nephrotic syndrome

Answer 44

all in secondary care usually sodium and fluid restriction and diuretics ACEi Consider prophylactic anticoagulation on individual basis. Immune suppressive therapy - steroids or other agents depending on cause .

Question 45

Referral for suspected renal cancer

Answer 45

Refer people using a suspected cancer pathway referral for renal cancer if they are aged 45 years and over and have: Unexplained visible haematuria without urinary tract infection, or Visible haematuria that persists or recurs after successful treatment of urinary tract infection.