105. Acute kidney injury Flashcards

Question

prognosis ATN

Answer 1

The epithelial cells can regenerate, making acute tubular necrosis reversible. Recovery usually takes 1-3 weeks.

Answer 2

Nephrotic syndrome occurs when the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria. It refers to a group of features without specifying the underlying cause. It involves: Proteinuria (more than 3g per 24 hours) Low serum albumin (less than 25g per litre) Peripheral oedema Hypercholesterolaemia

Answer 3

Minimal change disease

Answer 4

Membranous nephropathy

Answer 5

Frothy urine due to excess protein in the urine Generalised oedema due to a combination of a decrease in oncotic pressure from hypoalbuminemia, as well as a primary renal sodium retention

Answer 6

thrombosis, hypertension and high cholesterol relapse

Answer 7

due to loss of proteins that normally prevent blood clotting, and because the liver responds to the low albumin by producing pro-thrombotic proteins.

Answer 8

due to loss of immunoglobulins, complement, and other compounds in the urine. Immunotherapy may exacerbate the infection risk.

Answer 9

Patients become hypoalbuminemic due to the urinary loss of albumin. The liver tries to compensate for this protein loss by increasing the synthesis of albumin, as well as other molecules including lipids. These lipid abnormalities increase the patient’s risk of cardiovascular disease.

Answer 10

oedema proteinuria proteinuria > 3.5 grams/24 hours OR urine ACR > 300 mg/mmol* or PCR > 300g/mol* hypoalbuminaemia serum albumin <2.5 g/dL

Answer 11

24-hour urine collection to quantify proteinuria (gold standard)

Answer 12

proteinuria > 3.5 grams/24 hours OR urine ACR > 300 mg/mmol* OR PCR > 300g/mol*

Answer 13

U&Es albumin lipid profile

Answer 14

Renal biopsy Definitive diagnosis of MCD relies on renal biopsy in adults, with light microscopy typically showing normal glomeruli, and electron microscopy revealing diffuse podocyte foot process effacement. In children, renal biopsy is generally avoided.

Answer 15

Aged < 12 months >10 years Steroid resistant Low serum C3 Clinical evidence of systemic disease e.g. HSP, SLE Concern regarding ciclosporin nephrotoxicity Persistent renal impairment, persistent hypertension or family history of FSGS

Answer 16

High dose steroids (i.e. prednisolone) for 4 weeks (60mg/m2/day) and then gradually weaned over the next 8 weeks Low salt diet Diuretics may be used to treat oedema Albumin infusions may be required in severe hypoalbuminaemia Antibiotic prophylaxis may be given in severe cases

Answer 17

the basement membrane is thickened with subepithelial electron dense deposits. This creates a 'spike and dome' appearance M looks like spike and dome

Answer 18

idiopathic: due to anti-phospholipase A2 antibodies infections: hepatitis B, malaria, syphilis malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia drugs: gold, penicillamine, NSAIDs autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

Answer 19

1. ACEi or ARB (to reduce proteinuria) + ONLY IF SEVERE...immunosuppression

Answer 20

focal and segmental sclerosis and hyalinosis on light microscopy effacement of foot processes on electron microscopy

Answer 21

steroids +/- immunosuppressants

Answer 22

idiopathic secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy HIV heroin Alport's syndrome sickle-cell

Answer 23

Nephritic syndrome refers to a group of features that occur with nephritis: Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible) Oliguria (significantly reduced urine output) Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome) Fluid retention

Answer 24

The most commonly affected age group are children between the ages 5-12years, with an increased risk also present for older adults >60years. Boys appear to be affected twice as commonly as girls.

Answer 25

nephritogenic streptococcal antigens become lodged in glomerular membrane → anti-streptococcal antibodies bind to form immune complexes → activation of complement and inflammation → damage to glomerulus type 3 hypersensitivity

Answer 26

minimal change disease

Answer 27

Post-streptococcal glomerulonephritis

Answer 28

self limiting supportive - monitor BP --> diuretics - monitor oedema --> diuretics Antibiotic therapy should be given if there is any evidence of a persistent streptococcal infection. Early antibiotics reduce the incidence and severity of PSGN.

Answer 29

evidence of infection! - A throat or skin swab for culture should be taken to help confirm the presence of GAS. - Streptozyme test (includes ASO titre) complement - low C3 levels duirng first 2 weeks (as it has been deposited)

Answer 30

subepithelial 'humps' Immunofluorescence: diffuse granular deposits of complement (C3) and immunoglobulin G (IgG).

Answer 31

IgA nephritis (bergers disease)

Answer 32

isolated hematuria, no or minimal proteinuria and normal eGFR - no treatment needed persistent proteinuria above 500 to 1000 mg/day, a normal or only slightly reduced eGFR + ACE inhibitors falling eGFR or not responding to ACEi: + corticosteroids

Answer 33

Age: SG young, IgA teenage Timing of URTI: SG 1-3 weeks ago, IgA days ago Complement levels: SG low Proteinuria: SG has worse Haematuria: IgA has worse

Answer 34

mesangial hypercellularity, positive immunofluorescence for IgA & C3

Answer 35

markers of good prognosis: frank haematuria markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

Answer 36

Goodpasture's disease Polyarteritis nodosum Wegener's granulomatosis (granulomatosis with polyangitis) Microscopic polyangitis

Answer 37

cxr renal biopsy antibodies (c-ANCA, p-ANCA, anti-GBM) angiography

Answer 38

antibodies attack the alpha-3 subunit of type IV collagen found in the basement membrane of the lungs and kidneys. This anti-glomerular basement membrane (anti-GBM) disease leads to small vessel vasculitis in the kidneys and lungs causing bleeding in the lungs and renal failure.

Answer 39

anti-GBM antibody titre renal biopsy (cresenteric glomerulonephritis)

Answer 40

1. intensive plasmapherisis +immunosupression: - prednisolone - cyclophosphamide

Answer 41

patient with no history of lung or renal dysfunction who presents after noticing an abrupt onset of haemoptysis, cough, shortness of breath, peripheral oedema, dark urine and oliguria.

Answer 42

purpura p-anca alveolar haemorrhage mononeuritis glomerulonephritis

Answer 43

p-ANCA antibodies renal biopsy cxr

Answer 44

cyclophospahmide with high dose steroids

Answer 45

saddle nose haemoptysis epistaxis c-anca wegners mononeutiits mononeuritis glomerulonephritis

Answer 46

many diff but cavitating lesions are common

Answer 47

epithelial crescents in bowmans capsule

Answer 48

steroids cyclophosphamide plasma exhcnage

Answer 49

skin - livedo reticularis neuro renal other - ass w hep B, CVS events, HTN

Answer 50

resp inc asthma ENT NO bleeding NO RENAL

Answer 51

Brown/black casts → ATN Red casts → glomerulonephritis White casts → acute interstitial nephritis

Answer 52

fever, rash, arthralgia eosinophilia mild renal impairment hypertension

Answer 53

bloods: eosinophilia urinalysis: sterile pyuria white cell casts

Answer 54

Tubulointerstitial nephritis with uveitis Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.

Answer 55

Membranous nephropathy is frequently associated with malignancy making this the most likely diagnosis.

Answer 56

Rhabdomyolysis is caused by skeletal muscle breakdown. This causes the release of intracellular contents such as myoglobin and potassium into the blood stream. Excess myoglobin can precipitate in the glomerulus causing renal obstruction, direct nephrotoxicity and acute kidney injury.

Answer 57

dark urine, generalised weakness and myalgia.

Answer 58

acute kidney injury with disproportionately raised creatinine elevated creatine kinase (CK) myoglobinuria hypocalcaemia (myoglobin binds calcium) elevated phosphate (released from myocytes) hyperkalaemia (may develop before renal failure) metabolic acidosis

Answer 59

seizure collapse/coma (e.g. elderly patients collapses at home, found 8 hours later) Ischaemia: embolism, surgery ecstasy crush injury McArdle's syndrome drugs: statins (especially if co-prescribed with clarithromycin)

Answer 60

A creatine kinase >5x the normal range is typically diagnostic.

Answer 61

IV fluids to maintain good urine output Correction of electrolyte disturbances urinary alkalinization is sometimes used

Answer 62

Hyperkalaemia (liberated from the damaged muscle) Hyperphosphatemia (liberated from the damaged muscle) Hyperuricaemia (liberated from damaged muscle) Hypocalcaemia (calcium is taken into the damaged muscle by several mechanisms).

Answer 63

SLE is characterised by anti-nuclear antibodies (ANA). These are autoantibodies against proteins within the cell nucleus. These antibodies generate a chronic inflammatory response, leading to the condition’s features.

Answer 64

Hair loss Mouth ulcers Fatigue Fever Photosensitive malar rash Lymphadenopathy Shortness of breath Pleuritic chest pain Weight loss Splenomegaly Arthralgia (joint pain) Non-erosive arthritis Myalgia (muscle pain) Raynaud’s phenomenon Oedema (due to nephritis)

Answer 65

triggered or worsened by sunlight.

Answer 66

Autoantibodies ANA - 85% will have positive - other things can make it positive Anti-dsDNA - 50% will have positive - specific Full blood count may show anaemia of chronic disease, low white cell count and low platelets CRP and ESR may be raised with active inflammation C3 and C4 levels may be decreased in active disease Urinalysis and urine protein:creatinine ratio shows proteinuria in lupus nephritis Renal biopsy may be used to investigate for lupus nephritis

Answer 67

- CVS disease - Infection (from disease and immunosupp drugs) - Anaemia of chronic disease - pericarditis - pleuritis - lupus nephritis - neuropsychiatiric (optic neuritis, transverse myelitis, psychosis) - recurrent miscarriage - VTE - due to antiphospholipid secondary to SLE

Answer 68

First-line options include: Hydroxychloroquine NSAIDs Steroids (e.g., prednisolone) Treatment options for resistant or more severe SLE include: DMARDs (e.g., methotrexate, mycophenolate mofetil or cyclophosphamide) Biologic therapies Biological therapies include: Rituximab (a monoclonal antibody that targets the CD20 protein on the surface of B cells) Belimumab (a monoclonal antibody that targets B-cell activating factor)

Answer 69

Purpura (100%) Joint pain (75%) usually knees and ankles Abdominal pain (50%) Renal involvement (50%) - microscopic or macroscopic haematuria and proteinuria, oedema

Answer 70

URTI 1-3 weeks prior, streptococcus

Answer 71

type 3 - immune complex mediated

Answer 72

To rule out other things: - Sepsis : blood culture, CRP - Thromboytopaenia (inc leukaemia) : coagulation studies - Other vasculidities: Autoantibody screen: antinuclear antibodies, antineutrophil cytoplasmic antibodies, and complement levels To help support HSP diagnosis - ESR raised in 75% of patients - Serum IgA may be high To test for complications: - urinalysis : haematuria, proteinuria - Serum creatinine and electrolyte levels Elevated creatinine indicates renal impairment or renal failure Electrolyte abnormalities may occur in patients with severe gastrointestinal symptoms. - blood pressure If non-typical presentation : - skin/renal biopsy for confirmation of diagnosis If severe abdo pain: - abdo USS

Answer 73

Supportive (fluid, rest, symptomatic relief) - paracetamol (avoid ibruprofen if abdo pain) - steroids may be used in severe cases Monitoring - 6 months periodic urinalysis and BP monitoring - abnormlaity on urinalysis --> test serum cretainine - if persistent - refer to nephrologist

Answer 74

- 6 months periodic urinalysis and BP monitoring - abnormlaity on urinalysis --> test serum cretainine - if persistent - refer to nephrologist

Answer 75

The most common cause is a toxin produced by the e. coli 0157 bacteria, called the shiga toxin. Shigella also produces this toxin. The use of antibiotics and anti-motility medications such as loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS.

Answer 76

Reduced urine output Haematuria or dark brown urine Abdominal pain Lethargy and irritability Confusion Oedema Hypertension Bruising

Answer 77

supportive - antihypertensive - blood transfusion - dialysis HUS is a medical emergency and has a 10% mortality. It needs to be managed by experienced paediatricians under the guidance of a renal specialist. The condition is self limiting and supportive management is the mainstay of treatment: Urgent referral to the paediatric renal unit for renal dialysis if required Antihypertensives if required Careful maintenance of fluid balance Blood transfusions if required 70 to 80% of patients make a full recovery.

105. Acute kidney injury Flashcards

(102 cards)