Renal - Week 3 Flashcards

Question

what needs to be assessed in patients needing a transplant

Answer 1

Age important (biological vs chronological!) - frailty Primary cause of renal failure e.g. polycystic kidneys versus conditions which can recur in a Tx (e.g. aHUS, FSGS) Comorbid disease e.g. cardiovascular disease (IHD, PVD), diabetes etc History of infections History of tumours (need tumour free period) Urological disease e.g. bladder dysfunction Additional investigations: CARDIAC - exercise ECG, myocardial perfusion studies Angiography (need decent vessels for the anastomosis) Urodynamic studies Tumour markers, imaging etc

Answer 2

``` Cadaveric Tx (commonest) e.g. subarachnoid haemorrhage • DCD = donated after cardiac death • DBD = donation after brain death Living related donor Tx • Sibling, spouse, altruistic Typically a kidney Tx ``` Live donation lasts longer than cadaveric

Answer 3

Blood group (ABO) compatible (RIE now has an ABO incompatible programme) Immunological ‘X-match negative’ • Take serum from the recipient and donor lymphocytes • Add a complement e.g. vital dye which will enter killed cells and turn them a colour if they are matched to recipient antibodies

Answer 4

If a person is exposed to a foreign HLA molecule, they can produce an HLA antibody against this e.g. patient is A1, A24 and with exposure to A31 generating an anti-A31 antibody Approximately 30% patients on renal waiting list have anti-HLA antibodies The ‘specificity’ of these antibodies has to be defined (e.g. A31, B8, DR3 etc) Highly sensitised patients exhibit high levels of cytotoxic Abs to many HLA antigens that may be derived from: • Previous transfusions (WBC filtered) • Pregnancies • Previous Transplantation

Answer 5

HLA antibody status requires careful consideration - make a successful X-match less likely (long wait for Tx) - can lead to antibody mediated rejection - Consider desensitisation/antibody removal or paired exchange Tx

Answer 6

Hyperacute rejection (should not happen) Acute rejection Chronic rejection

Answer 7

put beads with selected class I or II antigens into a well incubate this with patient serum wash incubate with PE conjugated anti-human IgG wash and then scan them. you can derive a graph from this to show how many antibodies they have to certain molecules

Answer 8

Occurs when the Tx carries antigens to which the recipient is already sensitised Cytotoxic antibodies bind endothelial cells and induces complement activation, platelet aggregation and intravascular thrombus formation The Tx is often destroyed ‘on the operating table ``` Features: • Rise in creatinine (often only indication) • Reduced urine output • Tender transplant • Fever Exclude: • Dehydration (clinical examination, BP, weight) • Renal obstruction (ultrasound) • Vascular catastrophe (Doppler) • Drug toxicity (tacrolimus levels) ```

Answer 9

``` High dose methyl prednisolone (anti-inflammatory, kills lymphocyte etc) Change to more potent immunosuppressive agent or an increased dose ‘Anti-T cell’ antibody (increased risk of infection, tumours) Plasma exchange (severe acute Ab mediated rejection) ```

Answer 10

Features: • Progressive renal dysfunction • Interstitial fibrosis and vascular disease on renal biopsy Need to exclude: • Recurrent disease (membranous, MCGN) • Obstruction (ultrasound) • Renal artery stenosis (Doppler of renal artery +/- MRI angiography)

Answer 11

* Artery stenosis * Recurrent crescentic nephritis * Recurrent diabetic neuropathy * Interstitial fibrosis * Vasculopathy – can cause narrowed lumen of arteries

Answer 12

Multifactorial: immune and non-immune mechanisms: Increased HLA mismatch (1-2-1 vs 0-0-1) Previous acute rejection Poor drug compliance (low tacrolimus levels) Prolonged cold ischaemia time of kidney prior to surgery (CIT of living donor << cadaveric donor)

Answer 13

``` Delayed graft function Cytomegalovirus (CMV) infection Age of donor and ‘donor disease’ Poor blood pressure control Proteinuria ```

Answer 14

No specific treatment available Most patients will eventually require dialysis and potentially a further Tx Optimise immunosuppression Proactive treatment of BP, lipids, proteinuria etc

Answer 15

Bacteria urinary tract infection, chest infection prophylactic cotrimoxazole Viral CMV, herpes virus, parvo virus, BK virus (causes renal dysfunction) prophylactic valgancyclovir if recipent CMV –ve and donor CMV +ve TB (may require prophylactic treatment)

Answer 16

Incidence of all cancers increased Skin cancers common (UV block, avoid sun, skin surveillance) Post Tx Lymphoproliferative Disorder (PTLD) – secondary to infection with Epstein Barr virus (reduce immunosuppression, may need chemotherapy)

Answer 17

Calcineurin inhibitors are nephrotoxic! Plasma levels of tacrolimus are measured regularly Increased risk of diabetes (steroids and tacrolimus) Hypertension (steroids and CNI) Osteoporosis (steroids)

Answer 18

any of the following: * Increase in serum creatinine by > 26.5 μmols/L in 48 hours or, * Increase in serum creatinine by > 1.5x baseline creatinine within last 7 days or * Urine volume < 0.5ml/kg/hr for 6 hours

Answer 19

* Increased length of stay in hospital * Increased morbidity * Increased hospital & post-discharge mortality * Very costly (~£500 million/annum)

Answer 20

PRE-RENAL reduced real or ‘effective’ blood volume - Hypovolaemia e.g. bleeding, 3rd space fluid losses, over-enthusiastic diuretic therapy! - Hypotension e.g. septic/cardiogenic shock, liver failure - Reduced renal blood supply secondary to severe renovascular disease (±ACEI), dissection of the abdominal aorta etc

Answer 21

RENAL glomerulus, tubules and interstitium • Acute tubular injury – Commonest cause of AKI in hospitals and can complicate everything previously discussed! – Tubular toxins, eg gentamicin, cisplatinum, NSAIDs, radio-contrast dye – Severe prolonged hypotension (sepsis, MI) – Renal hypoperfusion e.g. elderly patient on ACEI, diuretic who has D&V – Initial oliguria then may exhibit polyuric recovery phase (watch electrolytes) ``` Tubulointerstitial causes Acute allergic interstitial nephritis DRUG-RELATED e.g. PPIs, (omeprazole) antibiotics, diuretics, NSAIDs May have an eosinophilia (no rash) Often respond well to steroids ``` Examples of cresentic RPGN (rapidly progressing glomerular nephritis) Goodpasture’s syndrome: anti-GBM Ab Wegener’s granulomatosis: PR3 Ab Microscopic polyarteritis (MPA): MPO Ab SLE: Anti-nuclear Ab (ANA), anti-dsDNA Abs Vascular causes Haemolytic uraemic syndrome (HUS) E coli related (E coli O157) Familial cases (genetic aetiology) * Acute tubular injury - may follow severe hypotension * Rhabdomyolysis - crush injury or low lie on the floor * Contrast nephropathy * Interstitial nephritis - drugs e.g. penicillin, NSAIDs * Systemic vasculitis * Myeloma - tumour of plasma cells * Haemolytic uraemic syndrome - E. Coli O157 infection

Answer 22

POST-RENAL obstruction – multiple levels (e.g. ureter, bladder etc) - Note that bilateral obstruction OR obstruction of a single kidney (transplant) is required in order to result in AKI Causes include: Prostate – hypertrophy (common), cancer Bladder lesions - tumour Ureter - calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour Myeloma – proliferation of B cells in the bone marrow – these make a single antibody called a paraprotein which can precipitate and completely obstruct the lumen Hydronephrosis – very dilated due to an obstruction All patients with significant renal injury MUST have an ultrasound to exclude or demonstrate obstruction to the renal tract

Answer 23

* Take a clinical history * Perform a clinical examination * Request appropriate investigations * Clinical history in AKI * Renal history – pre-existing renal disease, diabetes, family history * Urine volume - ?acute oliguria * Drug history – ? New drugs, nephrotoxic drugs (NSAIDs, ACEI, antibiotics) * Systemic symptoms – diarrhoea, rashes etc

Answer 24

Fluid status (JVP, postural BP) ?dehydrated ?evidence of infection ?rash, joint pathology Arterial bruits ?underlying renovascular disease Palpable bladder (obstruction) Check drug chart!

Answer 25

``` Urine dipstick – simple BUT important (blood, protein) Urine culture Renal Ultrasound - if obstructed then decompress Renal biopsy (AKI and normal sized kidneys) Angiography ± intervention ```

Answer 26

FBC, blood film, clotting screen Biochemistry including Ca2+, PO42- LFTs and albumin Creatinine kinase (rhabdomyolysis) - black urine Blood cultures Virology and serology e.g Hep B, ASOT

Answer 27

``` IgGs and serum electrophoresis (myeloma) Complement levels (SLE, post strep GN) Autoantibodies e.g. - Anti-nuclear factor (ANA) - SLE - Anti-neutrophil Ab (ANCA) - vasculitis - Anti-GBM Ab - Goodpasture’s syndrome, ```

Answer 28

Urine: Bence Jones protein = light chains (myeloma) Chest X ray (cardiac size, pulmonary oedema or haemorrhage) ECG especially if hyperkalaemia

Answer 29

Optimise fluid balance and circulation Stop exacerbating factors e.g. nephrotoxic drugs (check drug charts) Appropriate prescribing (check BNF, discuss with pharmacist) e.g. opiates accumulate in AKI Supportive treatment e.g. dialysis, nutrition

Answer 30

``` Obstruction - drain renal tract Sepsis - effective antibiotics Rapidly progressing glomerular nephritis RPGN e.g. SLE (systemic lupus erythematosus) - immunosuppression Goodpasture’s syndrome - Plasma exchange Compartment syndrome - fasciotomy ```

Answer 31

``` Severe ‘uraemia’: - no prospect of immediate improvement - uraemic encephalopathy or seizures - uraemic pericarditis Hyperkalaemia unresponsive to medical treatment (>6.5) ``` ``` Fluid overload, especially pulmonary oedema, resistant to treatment with diuretics/fluid restriction Severe acidosis (results in myocardial depression and hypotension) ```

Answer 32

Vascular access related complications - Pneumothorax Infection Bleeding Anticoagulation required which may be problematic in patients with bleeding. Hypotension may be troublesome in some patients (sepsis, IHD, diabetes)

Answer 33

* 500 mL 0.9% sodium chloride or plasmalyte over 15 minutes * Reasonable to repeat if no response * Do not give more than 2000 mL as resuscitation fluid without senior input

Answer 34

* ACE inhibitors and angiotensin receptor blockers * Blood pressure lowering drugs * Diuretics * Non-steroidal anti-inflammatory drugs (NSAIDs) * Radiocontrast agents

Answer 35

(for those >6.5 mmol/L) • IV calcium salts if ECG abnormal • Lasts around 30 minutes * Insulin/glucose and nebulized salbutamol * Push potassium into cells * Lasts around 4-6 hours * Treat underlying cause * Need to get kidneys working to excrete potassium

Answer 36

• Dipstick urinalysis * Serum anti-neutrophil cytoplasmic antibodies * Often present with coincident infection * Tissue diagnosis * Kidney most common * Lung * Nerve

Answer 37

``` • Glucocorticoids • Oral prednisolone • Plasma Exchange • Significant renal disease and/or pulmonary haemorrhage ``` • Cyclophosphamide/Rituximab

Answer 38

* Needs to block both kidneys to cause AKI * Some people have a single kidney * In women can be due to pelvis cancer-cervical, ovarian * Bladder tumours can also occlude ureteric orifice * Blood clot in bladder

Answer 39

• 2+ or more implies intrinsic renal disease and very unlikely to be explained by asymptomatic infection o The correct response to a finding of proteinuria is NOT to send an MSU “to exclude infection” • Quantify: albumin/creatinine ratio (timed collection rarely helpful) • Test kidney renal function, consider systemic diseases • NEVER ignore/dismiss it

Answer 40

• Albumin/creatinine ratio (mg/mmol) can be performed on small urine sample taken at any time of day • ACR x 10 approximates to mg/24 hours (eg in renal disease 100 reflects c 1g/24h) • Normal ACR (eg) less than 3.5 o 3.5 – 30 microalbuminuria o > 30 (macro)albuminuria

Answer 41

* plasma/serum creatinine * estimated GFR: MDRD formula (sex, age, race, creatinine) * creatinine clearance * isotope GFR (usually 51Cr EDTA)

Answer 42

due to mutation in podocyte-specific gene eg nephrin

Answer 43

The presence of blood and protein in the urine implies glomerular disease and an urgent need to test excretory kidney function, consider systemic diseases such (eg vasculitis, lupus)

Answer 44

* In diabetes mellitus, microalbuminuria is the earliest clinical feature of diabetic nephropathy; may initially be intermittent * In hypertension, albuminuria suggests a primary renal cause * In all patients, including in the absence of diabetes or hypertension, albuminuria carries prognostic significance Albuminuria is a potent, independent cardiovascular risk factor in both diabetic and non-diabetic populations. Aggressive management of cardiovascular risk is indicated.

Answer 45

* Clinical syndrome comprising oedema, heavy proteinuria, hypoalbuminaemia * Not included in the definition but often clinically important are thrombotic risk, propensity to infection and (often severe) hyperlipidaemia * May or may not be associated with impairment of excretory kidney function * Dominant symptoms often severe lethargy, reduced exercise tolerance, nausea, loss of appetite * Causes include glomerulonephritis, diabetes, infections (hepatitis B/C, malaria, HIV), amyloid

Answer 46

Haematuria, whether visible (macroscopic) or non-visible (microscopic) can be a sign of a serious systemic disease for which diagnosis and treatment is very urgent, whether or not there is also albuminuria don’t dismiss haematuria as “probably due to urine infection” without considering other possibilities: history, examination, investigations, possible specialist referral

Answer 47

(may present with proteinuria and/or haematuria) • Rare genetic/developmental disorders • Diabetes mellitus • Vascular disease/ischaemia/age • Inflammation of blood vessels “vasculitis isolated or as part of a systemic disease • Inflammation of glomerulus itself (“glomerulonephritis”, various types) • Deposition diseases eg amyloid,myeloma Anything which damages blood vessels

Renal - Week 3 Flashcards

(72 cards)