Renal

Question 1

Define AKI

Answer 1

Acute reduction in renal function following an insult to the kidneys.

Question 2

What are the pre-renal causes of an AKI?

Answer 2

Hypotension from sepsis or hypovolaemia from blood loss

Renal artery stenosis

Question 3

What are the renal causes of an AKI?

Answer 3

(1) Vasculitis – affects the vessels
* Small vessel (microangiopathic) = HUS, TTP, DIC, GPA, eGPA
o HUS (E. coli toxin 0157; triad S/S: MAHA, thrombocytopenia, AKI)
o TTP (pentad S/S: MAHA, thrombocytopenia, AKI, neurological impairment, fever)
* Large vessel (obstructive) = renal artery/vein thrombosis/embolus
(2) Glomerulonephritis – affects the glomerulus (i.e. membranous, membranoproliferative, etc.)
* Most common in children -> minimal change disease -> 2/3 relapse; 1/3 complete recovery
* Most common in adults -> membranous glomerulonephritis
(3) ATN – affects the tubules (i.e. post-hypovolaemia, rhabdomyolysis)
(4) AIN / interstitial nephritis – affects the surrounding tissue; 4-7 days after exposure
* S/S: rash, fever, eosinophilia (± sterile pyuria, white cell casts), nephrotic syndrome
* Drugs = 75% (NSAIDs, penicillin, sulfa-drugs, PPIs, ciprofloxacin, allopurinol, furosemide)
* I.E. CAP treated with amoxicillin returns with fever, rash and arthralgia with rising creatinine

Question 4

What are the post-renal causes of an AKI?

Answer 4

This is where there is an obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function.

Classify as luminal, mural, extra-mural

Question 5

Who is at an increased risk of AKI?

Answer 5

Risk factors for AKI include:
* chronic kidney disease
* other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
* history of acute kidney injury
* use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
* use of iodinated contrast agents within the past week
* age 65 years or over
* oliguria (urine output less than 0.5 ml/kg/hour)
* neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer

Question 6

What are the symptoms and signs of a AKI?

Answer 6

• reduced urine output
• pulmonary and peripheral oedema
• arrhythmias (secondary to changes in potassium and acid-base balance)
• features of uraemia (for example, pericarditis or encephalopathy)

Question 7

What ix results would be expected in an AKI?

Answer 7

Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
* a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
* a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
* a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.

Question 8

How do we stage an AKI?

Answer 8

Question 9

How should we manage an AKI?

Answer 9

Supportive
* Review medications
* Hyperkalaemia also needs prompt treatment to avoid arrhythmias which may potentially be life-threatening.
-Stabilisation of the cardiac membrane: 10ml 10% Intravenous calcium gluconate
-Short-term shift in potassium from extracellular to intracellular fluid compartment: Combined insulin/dextrose infusion or Nebulised salbutamol
-Removal of potassium from the body: Calcium resonium (orally or enema) or Loop diuretics or Dialysis

• Specialist input from a nephrologist is required for cases where the cause is not known or where the AKI is severe.
• All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist

Question 10

What are the indications of dialysis?

Answer 10

•  Refractory hyperkalaemia [K+ >6.5]
•  Refractory fluid overload
•  Metabolic acidosis [pH <7.1]
•  Uraemic symptoms (encephalopathy, nausea, pruritis, malaise, pericarditis)
•  CKD stage 5 (GFR <15mL/min) / often planning starts <20 and dialysis starts <12

Question 11

What RRT is used on ITU?

Answer 11

haemofiltration (uses ultrafiltration and subsequent convection to remove solutes)

Question 12

What is this?

Answer 12

Vascath (central venous catheter) for haemofiltration

Question 13

What is the first line for RRT? What are the complications?

Answer 13

peritoneal dialysis (APD- automated peritoneal dialysis [done overnight by machine] or CAPD- Continuous ambulatory peritoneal dialysis [pt. operated in day])

Cx: infection (CoNS (S. epidermidis) > other gram +ve (S. aureus) > gram -ve)

Question 14

Answer 14

Tenckhoff catheter

Question 15

What is the second line for RRT? What are the complications

Answer 15

haemodialysis [1st line if IBD]; AV fistula made 4-6 weeks before HD commences

Before a fistula can be formed, you can use a Tesio line (a type of central line)
* Cx (AV fistula): thrombosis, stenosis, infection, bleeding, aneurysm, steal syndrome
* Cx (Tesio): sepsis, peritonitis, DIC, fluid overload, DDS
o DDS = Dialysis Disequilibrium Syndrome = cerebral oedema

Question 16

Answer 16

AV fistula

Question 17

What is this? Describe the entry points?

Answer 17

Tessio Line

Tesio line = central line to Internal Jugular and RA, tunnelled under skin and has 2 lumens entering skin
* Central line entry points:
o Internal jugular vein 2 lumens = Tesio line
o Subclavian vein 3 lumens = Swan-Gantz line
o Femoral vein

Question 18

How is haemodialysis carried out?

Answer 18

 3x/week, for 4 hours per session
 Uses diffusion and oncotic pressures to remove excess solutes

Question 19

What is the 3rd line of RRT?

Answer 19

Transplant

Question 20

What is scar C?

Answer 20

Rutherford Morisson scar from renal transplant

Question 21

What medication needs to be given with a transplant?

Answer 21

Immunosuppression mx = calcineurin inhibitors, anti-proliferative (MMF/azathioprine), steroids

Question 22

What are the types of transplant rejection? What are the RFs? How should they be managed?

Answer 22

 Rejection = immune-mediated organ dysfunction; mx: depends on type of rejection:
* Hyperacute (<24hrs) = ABs in recipient serum attack donor ABO/HLA; mx: explantation
o RFs: previous blood transfusion, previous transplant, multiple pregnancies
* Acute (<6m):
o Antibody-mediated (weeks-months)  mx: IVIG, plasmapheresis, anti-CD20, anti-C5
o T-cell-mediated (weeks-months; most common) mx: steroids, OKT3, ATG
* Chronic (>6m) = unknown aetiology – mx: needs to go back on dialysis

Question 23

What should be done in transplant failure?

Answer 23

organ fails to function (not immune-mediated); mx: dialyse patient and wait

Question 24

What HLAs need to matched before transplanting?

Answer 24

DR > B > A

Question 25

How do we estimate kidney function?

Answer 25

Serum creatinine may not provide an accurate estimate of renal function due to differences in muscle. For this reason, formulas were developed to help estimate the glomerular filtration rate (estimated GFR or eGFR). The most commonly used formula is the Modification of Diet in Renal Disease (MDRD) equation, which uses the following variables: * serum creatinine * age * gender * ethnicity Factors which may affect the result pregnancy muscle mass (e.g. amputees, body-builders) eating red meat 12 hours prior to the sample being taken

Question 26

How do we classify CKD?

Answer 26

Question 27

When do we refer CKD to a nephrologist?

Answer 27

o In CKD, a referral (routine) to a nephrologist can take place if… * eGFR <30mL/min/1.73m2 * eGFR decrease >25% or >15mL/min/1.73m2 in 12 months

Question 28

What are the causes of CKD?

Answer 28

diabetic nephropathy chronic glomerulonephritis chronic pyelonephritis hypertension adult polycystic kidney disease

Question 29

What is the presentation of CKD?

Answer 29

Chronic kidney disease is usually asymptomatic and is generally diagnosed following abnormal urea and electrolyte results. However, some patients with undetected late-stage disease may become symptomatic. Possible features include: oedema: e.g. ankle swelling, weight gain polyuria lethargy pruritus (secondary to uraemia) anorexia, which may result in weight loss insomnia nausea and vomiting hypertension

Question 30

What are the consequences of CKD?

Answer 30

Question 31

What is the management of CKD?

Answer 31

 Diet: * Reduce dietary PO42-, Na+, K+, fluid restrict * Avoid ETOH, too much tea/coffee, processed food, chocolate, bananas  PO4^-2 binders * Aluminium-based binders (less commonly used) * Calcium-based binders (SE: hypercalcaemia, vascular calcification) * Sevelamar (non-calcium-based binder) o More commonly used o Binds to dietary phosphate and prevents absorption o Reduces uric acid levels and improves lipid levels in those with CKD  Vitamin D: alfacalcidol, calcitriol  Parathyroidectomy (rarely)

Question 32

What antihypertensives are used in CKD?

Answer 32

ACEi + Furosemide With ACEi, NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs). A rise greater than this may indicate underlying renovascular disease.

Question 33

How do we manage anaemia in CKD?

Answer 33

Management the 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dl determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA). Many patients, especially those on haemodialysis, will require IV iron ESAs such as erythropoietin and darbepoetin should be used in those 'who are likely to benefit in terms of quality of life and physical function'

Question 34

Define anti-glomerular basement membrane disease

Answer 34

Anti-glomerular basement membrane (GBM) disease (previously known as Goodpasture's syndrome) is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

Question 35

What serology would be expected in Anti-GBM disease?

Answer 35

It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen

Question 36

What serology would be expected in Anti-GBM disease?

Answer 36

It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen

Question 37

Who is Anti-GBM disease seen in?

Answer 37

Goodpasture's syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.

Question 38

What is the presentation of anti-GBM disease?

Answer 38

Goodpasture's syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.

Question 38

What is the presentation of anti-GBM disease?

Answer 38

* pulmonary haemorrhage * rapidly progressive glomerulonephritis * this typically results in a rapid onset acute kidney injury * nephritis → proteinuria + haematuriaGoodpasture's syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.

Question 39

What are the ix for Anti-GBM disease?

Answer 39

renal biopsy: linear IgG deposits along the basement membrane raised transfer factor secondary to pulmonary haemorrhages

Question 40

What is the management of anti-GBM disease?

Answer 40

plasma exchange (plasmapheresis) steroids cyclophosphamide

Question 41

What increases the likelihood of pulmonary haemorrhage from anti-GBM disease?

Answer 41

One of the main complications is pulmonary haemorrhage. Factors that increase the likelihood of this include: * smoking * lower respiratory tract infection * pulmonary oedema * inhalation of hydrocarbons * young males

Question 42

Define Alport's syndrome.

Answer 42

It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).

Question 43

How is Alport's syndrome inherited? Who is it worse in?

Answer 43

Alport's syndrome is usually inherited in an X-linked dominant pattern*. The disease is more severe in males with females rarely developing renal failure.

Question 44

Why would an Alport's patient have a failing renal transplant?

Answer 44

This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture's syndrome like picture.

Question 45

How does alport's syndrome present?

Answer 45

Alport's syndrome usually presents in childhood. The following features may be seen: * microscopic haematuria * progressive renal failure * bilateral sensorineural deafness * lenticonus: protrusion of the lens surface into the anterior chamber * retinitis pigmentosa * renal biopsy: splitting of lamina densa seen on electron microscopy