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FLASHCARDS from MEDED lectures COPY > renal > Flashcards

renal Flashcards

1
Q

What is the function of the kidney?

A
  • •Regulation of blood volume
  • •Regulation of blood pressure
  • •Acid-base balance
  • •Electrolyte balance
  • •Production of Red blood cells
  • •Synthesis of Vitamin D – Bone metabolism
  • •Excretion of water-soluble waste products – Filter
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2
Q

What are the different stages of AKI?

A

Stage 1: creatinine rise of 1.5x compared to baseline or urine output <0.5 ml/kg/hour for 6 hours.

Stage 2: creatinine rise of 2x compared to baseline or urine output <0.5 ml/kg/hour for 12 hours.

Stage 3: creatinine rise of 3x

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3
Q

How does the patient present in AKI?

A

Symptoms

  • •Depends on underlying CAUSE
  • •Oliguria/anuria
  • •NOTE: abrupt anuria suggests post-renal obstruction
  • •Nausea/vomiting
  • •Dehydration
  • •Confusion

Signs

  • •Hypertension
  • •Distended bladder
  • •Dehydration - postural hypotension
  • •Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
  • •Pallor, rash, bruising (vascular disease)
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4
Q

What is the mechanism behind pre renal failure?

What are the complication?

A

Due to Renal Hypoperfusion, most common causes are hypotension due to sepsis and hypovolaemia from fluid loss.

No blood to kidney = no pee = AKI

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5
Q

Haemolytic uraemic syndome

What is it charactrised by?

What is the pathophysiology

WHat infection precedes it usually

What is the treatment

A

What is it charactrised by?

  1. Progressive renal failure - Kidneys
  2. Microangiopathic haemolytic anaemia (MAHA) – Blood
  3. ↓ Platelets - Blood

What is the pathophysiology?

  1. Gastroenteritis (E.coli 90%) -> toxin
  2. Endothelial damage
  3. Thrombosis, platelet consumption + fibrin strand deposition → ↓ Platelets
  4. Destruction of RBCs – schistocytes, ↓ Hb

What infection precedes it usually?

E coli

What is the treatment?

Mainly supportive

  • dialysis
  • NO antibiotics
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6
Q

How do treat Diabetic nephropathy?

A
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7
Q

What is the spectrum of Glomerulonephritis?

Name one important fact about them and where thy are on the spectrum

A

NEPHROTIC:

Primary:

Minimal change disease- in children - treat with corticosteoids

Membranous Nephropathy/Glomerulonephritis- commonest type in adults- subepithelial immune complex deposits

Focal segmental glomerulosclerosis- sclerosing of glomeruli in segments- IgM and complement deposition

Membranoproliferative glomerulonephritis- really rare

Secondary to Systemic Disease

  1. DM- 5 stages, Stage 1 hyperfiltration, Stage 2 silent, Stage 3 microalbuminuria, Stage 4 persistant protenuria with hypertension, Stage 5 end stage renal disease
  2. SLE- SOAP BRAIN MD
  3. Amyloidosis

Nephritic

  • IgA Nephropathy / Berger’s Disease- commonest -macroscopic haematuria few days after Upper respiratory tract infecton- IgA & C3 depostition
  • Post-streptococcal glomerulonephritis- 1-2 weeks after sore throat or skin infection- common in children
  • Crescentic/ Rapidly progressive glomerulonephritis
    • Type 1: Anti-GBM- Goodpasture syndrome- Anti GBM antibodies against type 4 collagen- affects long and kidney
    • Type 2- Immune complex deposition
    • Type 3 Pauci immune
  • Thin BM Disease - Autosomal dominant- thinning GBM by mutatio of type 4 collagen alpha 4 chain
  • Alport’s Syndrome- X- linked recessive 4 collagen alpha 5 chain, EAR sensory neural deafness, EYE, lense dislocation - cataract
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8
Q

TTP

What are t?

What is the pathophysiology?

What is the pentad?

A

What is it?

What is the pathophysiology?

  • Deficiency of protease (ADAMTS13) that cleaves cleave vWF à
  • Large vWF multimers form à
  • Platelet aggregation & fibrin deposition
  • Microthrombi

What is the pentad?

ADAMTS-13

NO Antibody
Decreased platelet
AKI
MAHA
Temperature
Swinging CNS (Seizures, hemiparesis, ↓ consciousness,↓ vision)
13- (von willebrandt 13 letters- so can’t break that down)

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9
Q

how do you approach an AKI

A
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10
Q

What does this ECG show?

How would you treat this

A
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11
Q

GLomerulonephritis table MEDED- less extensive than other flashcards

A
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12
Q

Fill in the table

A
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13
Q

What are causes of an AKI? annotate the diagram

A
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14
Q

What could causes these findings on a urine dip?

A
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15
Q

What are the differences between nephrotic and nephritis syndrome

A
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16
Q

What is this?

A

Polycystic ovary syndrome

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17
Q

SBA1

A

A

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18
Q

SBA 2

A

E

Diclofenac is a strong non-steroidal anti-inflammatory drug (NSAID) that is usually prescribed for muscular injury and renal colic. NSAIDs inhibit the production of prostaglandins, which are essential in maintaining renal perfusion. NSAIDs are therefore nephrotoxic and should be avoided in patients with known renal disease and in those at risk of renal disease, e.g. elderly people. Long-term use of NSAIDs may lead to analgesic nephropathy and chronic renal failure.

Analgesic nephropathy is injury to the kidneys caused by analgesic medications such as aspirin, phenacetin, and paracetamol. The term usually refers to damage induced by excessive use of combinations of these medications, especially combinations that include phenacetin. It may also be used to describe kidney injury from any single analgesic medication.

The specific kidney injuries induced by analgesics are renal papillary necrosis and chronic interstitial nephritis. They appear to result from decreased blood flow to the kidney, rapid consumption of antioxidants, and subsequent oxidative damage to the kidney. This kidney damage may lead to progressive chronic kidney failure, abnormal urinalysis results, high blood pressure, and anemia. A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease.

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19
Q

SBA3

A

D

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20
Q

SBA 3

A

E

Goodpasture’s syndrome is a rare condition in which autoantibodies are formed against the glomerular basement membrane and the alveolar membrane. The antibodies trigger a type II hypersensitivity reaction that causes renal failure, pulmonary haemorrhage and haemoptysis. The condition is usually diagnosed by the detection of anti-glomerular basement membrane antibody (anti- GBM) in the serum and via renal biopsy. The biopsy often shows focal or diffuse crescentic glomerulonephritis. Immunofluorescence may demonstrate linear deposition of IgG antibodies and complement (C3) on the glomerular basement membrane. Goodpasture’s syndrome is usually treated aggressively with plasmapheresis, corticosteroids and immunosuppression.

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21
Q
A

B.

Membranous glomerulonephritis is the most common cause of nephrotic syndrome in adults. In this condition, immune complexes are formed when circulating antibodies bind to basement membrane antigens or antigens deposited in the glomerulus from the circulation. The immune complexes activate an immunological response that involves the complement cascade. This response damages the glomerular basement membrane, making it more leaky to protein

Rapidly progressive glomerulonephritis – aka crescentic glomerulonephritis

3 main cause

  • Immune complex-associated (SLE, IgA, post-infectious glomerulonephritis)
  • Anti-GBM disease
  • Pauci-immune crescentic glomerulonephritis (ANCA)
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22
Q

What is the triad of the nephrotic syndrome?

What are other symptoms

A
  1. proteinuria
  2. low serum albumine
  3. oedema

Liver tries to increase the production of albumin and at the same time produces more lipids (hyperlipidaemia)

loss of antithrombin 3 and hypogammaglobuliaemia leads to hypercoagulable state

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23
Q

What are common condition in adult and child that lead to a nephrotic syndrome

A

adults: membranous glomerulonephritis OR DM

children; minimal change glomerulonephritis

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24
Q

What is the nephritic syndrome triad

A
  1. Haematuria
  2. hypertenison
  3. oedema

CAST cells prove haematuria is glomerular

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25
Q

What are investigation and management of Glomerulonephritis?

A

Investigations:

  • Bloods – FBC, U&Es, CRP, Complement, Autoantibodies
  • Urine
  • Imaging – renal US +/- renal biopsy

Management:

  • Refer specialist
  • BP management – <130/80
  • ACE-I or ARB – reduce proteinuria and preserve renal function
  • Steroids/immunosuppression
  • Treat underlying cause
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26
Q

What is the most common renal cause of AKI?

A

acute tubular necrosis

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27
Q

What can renal tubular injury be due to?

A

ischaemia

nephrotoxic agents

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28
Q

What are exogenous and endogenous causes of acute tubular necrosis?

A

Exogenous:

  • Drugs: NSAIDs, Aminoglycosides, amphotericin b, contrast media, calcineurin inhibitors, cisplatin etc.

Endogenous:

  • myoglobinaemia (rhabdomyolysis),
  • haemaglobinuria
  • crystals
  • myeloma
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29
Q

What is rhabdomyolysis?

What is the pathophysiology

What is the presentation

What are the investiagtions

A

What is rhabdomyolysis?

Skeletal muscle death

What is the pathophysiology

release of myoglobin, potassium and creatinine kinase (CK), obstruction of renal tubules - acute tubular necrosis

What is the presentation?

Muscle pain and swelling, dark urine (myoglobin)

What are the investiagtions

•Hyperkalaemia, High CK

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30
Q

What is the pathophysiology of Acute tubular necrosis due to ischaemia?

What are the 3 phases?

A

What is the pathophysiology of Acute tubular necrosis due to ischaemia?

  1. Ischaemia >
  2. Tubular cell injury >
  3. Necrosis >
  4. Obstruction of tubule by debris >
  5. ↓GFR

What are the 3 phases?

3 phases:

  1. INITIATION –acute ↓ GFR + ↑ Cr + ↑urea
  2. MAINTENANCE – sustained ↓ GFR (~1-2w) à Cr + urea ↑
  3. RECOVERY – tubular function regenerates à ↑urine volume + gradual ↓ urea + Cr
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31
Q

What cancer can cause acute tubular necrosis?

What is the pathophysiology?

What are the clinical features?

A

What cancer can cause acute tubular necrosis?

Malignant disease of bone marrow plasma cells which results in a clonal expansion of plasma cells - monoclonal paraprotein production

What is the pathophysiology?

free light chains of paraproteins precipitate in kidneys > inflammation

What are the clinical features?

CRAB

Calcium – HIGH

Renal failure (acute or chronic) - ↑ urea ↑ Cr

Why? Hypercalcaemia, paraprotein deposition

Anaemia

Bone – osteolytic bone lesions – pain, fracture (risk cord compression)

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32
Q

What are some nephrotoxic agents?

A

Examples:

  • Analgesics e.g. NSAIDS
  • Antibiotics e.g. aminoglycosides – gentamicin, streptomycin

•Contrast agents

  • Anaesthetic agents
  • Chemotherapeutic agents

•ACE-I and ARBs

•Immunosuppressants e.g. ciclosporin, MTX

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33
Q

What can cause interstial nephritis?

A
  • Drugs
  • Infections
  • Immune disorders e.g. SLE
  • Lymphoma
  • Tumor lysis syndrome following chemo
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34
Q

What are post renal causes of AKI?

A

Luminal: Stones, clots

Mural: Malignancy (e.g. uteric, prostate, bladder), BPH,

strictures

Extrinsic compression: Retroperitoneal fibrosis

35
Q

What is the management of AKI?

A

General

  • Assess volume status + Aim for euvolaemia
  • Stop nephrotoxic drugs (ACEi, ARBs, gentamicin, stop metformin if eGFR <30)
  • Monitoring + Nutrition

Treat underlying cause

  • Pre-renal: Correct volume depletion with appropriate fluids, antibiotics (IF sepsis), inotropes (IF signs of shock)
  • Post-renal: Catheterise + imaging of renal tract (CTKUB) + urology + reversal
  • Intrinsic renal: Refer early to nephrology

Manage complications

  • Hyperkalaemia:
  • Pulmonary oedema
  • Uraemia
  • Acidemia

Renal replacement therapy – haemodialysis and haemofiltration if any complications are refractory to medical Mx

36
Q

What are risk factors for CKD?

A
  1. DM
  2. HTN
  3. CVS
  4. Structural renal disease
  5. multisystem disorders involving kidney
  6. FHx
  7. recurrent UTI
  8. vesicoureteric reflux
37
Q

How long does a loss of kidney need to be going on to be chronic?

A

3 months

38
Q

What are the 2 most common causes of CKD?
What are other causes of CKD?

A
  1. Diabetes
  2. Hypertension
  3. Artherosclerosis
  4. Chronic glorulonephritis
  5. infective or obstructive uropathy
  6. adult polycystic kidney disease (most common inherited cause)
39
Q

What are signs and symptoms of CKD?

A

ASYMPTOMATIC unless really severe- usually incidental

SEVERE symtoms:

  • Anorexia
  • Nausea and vomiting
  • Fatigue
  • Pruritus
  • Peripheral oedema
  • Muscle cramps
  • Pulmonary oedema
  • Sexual dysfunction is common

Signs:

rarely any signs!

But if really bad can show signs complications:

  1. Anaemia: conjunctival pallor
  2. Uraemia: skin pigemnetation, excoriation
  3. Bone disease: renal bone disease
  4. peripheral vascular disease
  5. hypertension
  6. peripheral oedema
40
Q

What are the consequences of CKD

A
  1. Progressive failure of homeostatic function
    - Acidosis
    - Hyperkalaemia
  2. Progressive failure of hormonal function
    - Anaemia
    - Renal Bone Disease - Osteomalacia
  3. Cardiovascular disease
    - Vascular calcification
    - Uraemic cardiomyopathy
  4. Uraemia and Death
41
Q

What investigations do you do in CKD?

A
  • Bloods: ↓Hb (normocytic anaemia); U&Es (↑urea/Cr), glucose (DM), eGFR, ↓Ca2+, ↑PO43−, ↑ALP (in renal osteodystrophy) ↑PTH if severe CKD
  • Urine: dipstick, MC&S, Protein:Cr ratio
  • Imaging: USS to check size/anatomy/cortico-medullarly differentiation and eliminate obstruction – in CKD kidneys are small (<9cm) but may be enlarged in infiltrative disorders
  • CXR: Pericardial effusion or pulmonary oedema
  • Histology: consisted renal biopsy if rapidly progressing or unclear cause (C/I for small kidneys)
42
Q

Management of CKD

A

1) Limiting progression/ complications
* BP: target <130/80 ( <125/75 is diabetic)
* Tight glucose control in DM
* Decrease CVS risk ( stop smoking, lose weight etc)
* Diet: multidisciplinary team: moderate protein, restrict K+, avoid high phosphate foods.
* Reneal osteodystrophy:
* •Calcichew - Ca supplement

  • Calcium acetate - phosphate binders
  • Cinacalcet (calcimimetic) – reduce PTH levels

2) Symptom control
* •Anaemia: Human EPO might be required
* Acidosis: Consider sodium bicarbonate supplements for patients with low serum bicarbonate.
* Oedema: loop diuretics, restriction of fluids
3) Preparation for Renal Replacement Therapy

  • Haemodialysis – Vascular Access required
  • Transplantation – Gold standard treatment, Major surgery and long term immunosuppression.
43
Q
A
44
Q

What is the most common cause of a UTI?

What other oragnism can cause it?

A

MOST COMMON: E coli

other causative organism:

  • Staphylococcus saprophyticus
  • Proteus mirabilis
  • Enterococci

Atypical organisms that can cause UTI (usually in immunocompromised individuals):

  • Klebsiella
  • Candida albicans
  • Pseudomonas aeruginosa
45
Q

What are the different sub classifications of UTI’s

A
  • Lower UTI - affecting the urethra (urethritis), bladder (cystitis) or prostate
  • Upper UTI - affecting the renal pelvis (pyelonephritis)
46
Q

What are the risk factors for UTI

A
  • FEMALE
  • Sexual intercourse
  • Exposure to spermicide
  • Pregnancy
  • Menopause
  • Immunosuppression
  • Catheterisation
  • Urinary tract obstruction
  • Urinary tract malformation
47
Q

How many GP consultations are for UTI?

A

1-3%

48
Q

Sign and symptoms of a cystitis?

A
  • Frequency
  • Urgency
  • Dysuria
  • Haematuria
49
Q

What are signs and symptoms of Prostatitis?

A
  • Suprapubic pain
  • Flu-like symptoms
  • Low backache
  • Few urinary symptoms
50
Q

What are signs and symtoms of acute pyelonephritis?

A
  • High fever
  • Rigors
  • Vomiting
  • Loin pain and tenderness
  • Oliguria (if AKI)
51
Q

What are in general signs and symptoms of a UTI

A

Fever

Abdominal or loin tenderness

Foul-smelling urine

Distended bladder (occasionally)

Enlarged prostate (if prostatitis)

52
Q

What are investigations and management of UTI?

A

Investigations

  • Urine dipstick (presence of nitrites)
  • MSU for urine MCS
    • Microscopy: WBC presence (pyuria)
    • Culture: provide colony forming unit
    • Sensitivity
  • Bloods: FBC, U&E, CRP
  • If complicated UTI - Renal USS/IV urography

Management – Follow local guidance

  • Uncomplicated: Cefalexin 500mg PO BD 3/7 OR Nitrofurantoin 50mg PO QDS 7/7
    • If pregnant + BF: Cefalexin; Co-amoxiclav 62
  • Male: 7/7 course of Cefalexin OR ciprofloxacin 500mg PO BD 14/7 (if suspicion of prostatits)
  • Pyelonephritis/urosepsis: Co-amoxiclav 1.2mg IV ± amikaxin (CXH/HH) or gentamicin (SMH) first 1-2/7
53
Q

What is important to rule out in patients with UTI?

A

other vaginal infections (chlamidya trachomatis)

sterile pyuria

Urogenital tract pathology

54
Q

Polycystic Kidney Disease

Definition

History

Examination

Investigation

A

Definition: fluid filled cysts grow on the kidney, 10% of ESRF

  • Autosomal dominant inheritance, onset at 30-60 years
    • :1000 (85% of PKD1 Chr16, 15% PKD2 Chr4)

History: clinically silent for many years!

  • Acute loin pain, stone formation, abdominal discomfort
  • Sx of renal failure
  • FHx of SAH (berry aneurysms)

Examination: HTN, renal enalregment, abdominal pain ± haematuria

Investigations: Haematuria, raised Hb, deranged U&E, abdominal USS, MRI angiography IF +ve 1st-degree SAH + ADPKD

55
Q

What is PKD assosiated with (polycystic kidney disease)?

A

berry aneurysm in the circle of Willis

56
Q

What is a renal carcinoma?

What is the triad?

What are other symptoms?

What are the risk factors?

What are the investigations?

A

What is a renal carcinoma? Neoplasm Arising from the renal parenchyma/cortex

What is the triad? haematuria, loin pain, abdominal mass

What are other symptoms? PUO, night sweats, rarely polycythemia

if invades the left renal vein compresses left testicular vein = varicocele

What are the risk factors?

  • Age
  • Smoking
  • Obesity
  • HTN
  • Dialysis (15%)
  • certain inherited syndromes (von Hippel-Lindau, tuberous sclerosis, familial papillary renal cell carcinoma)

What are the investigations?

  • Increased BP (renin)
  • Polycythaemia or IDA (bleeding cysts)
  • ALP (bone mets)
  • RBCs in urine,
  • Cannon ball metastasis
  • filling defect ± calcification (CT/MRI intravenous urogram IVU)
57
Q

Renal artery stenosis

Causes

Clues

Investigation

A

Causes: Atherosclerosis (80%), fibromuscular dysplasia (10%, young F)

Clues:

  • ↑ ↑ ↑ BP refractory to Tx (1-5% of HTN)
  • Worsening renal function after ACEi/ARB in bilateral RAS
  • Flash pulmonary oedema (sudden onset, without LV impairment on echo)
  • Abdominal ± carotid or femoral bruits, weak leg pulses

Investigation:

  • Ultrasound measurement of kidney size (affected size is smaller)
  • CT Angiogram or MR Angiography: risk of contrast nephrotoxicity
  • Digital Subtraction Renal Angiography = GOLD STANDARD (but invasive
58
Q

Why do get hypertension in renal artery stenosis?

A
  • Renal hypoperfusion (due to the stenosis) stimulates the renin-angiotensin system leading to increased angiotensin II and increased aldosterone
  • This leads to increased blood pressure
  • The high blood pressure leads to fibrosis, glomerulosclerosis and renal failure
59
Q

What drug should you not give someone with renal artery stenosis?

Why not?

A

What drug should you not give someone with renal artery stenosis? ACE INHIBITORS

Why not?

ACEi remove the efferent arterial tone - causing hypoperfusion and a sharp reduction in GFR

60
Q

What are signs of someone with reanl artery stenosis?

A
  • Hypertension
  • Signs of renal failure in advanced bilateral disease
  • Renal artery bruits
61
Q

Someone comes in with 2/7 dysuria + frequency + offensive urine

WHat investigation would you like to do?

A

MSU for MCS

62
Q

someone comes in with Severe loin pain, vomiting & Haematuria on the dipstick

What investigation would you like to do?

A

Non-contrast CT-KUB – most sensitive

63
Q

Someone comes in with Recurrent UTI, FTT, baby FHx of vesico-ureteric reflux

What investigation would you like to do?

A

USS of renal tract

64
Q

Someone has just returned from India and has had weight loss, night sweats

On the Urine dipstick there is blood and leukocytes

The urine sample does not grow anything

What investigations would you like to do

A

3 early morning urine samples for Microscopy, culture, ZN staining

65
Q

Someone has had kidney Transplant (4/12 ago) and his renal function has worsened over 2/52

He also complains of pain around the area

What investigation would you like to do?

A

Renal biopsy

66
Q

What are the different types of stones compositions and what is the most commone

A
  • _Calcium phosphate and calcium oxalat_e (common) – radiopaque
  • Magnesium ammonium phosphate (struvite), staghorn calculus - associated with urea-splitting bacteria (10-15%); klebsiella
  • Urate (uric acid)- associated with gout, small bowel disease, tumour lysis syndrome – Radiolucent (Mx: K+ citrate alkalise stone)
  • Cysteine – semi opaque
67
Q

How do you treat a ureteric stone?

A
68
Q

Someone presents with

Muddy brown cast + high creatinine

High urine sodium, low urine osmolality

Low urine:serum urea ratio

Low urine:plasma osmolarity ratio

What is your top differential for this?

A

Acute tubular necrosis

69
Q

Someone presents with

Unwell after ACEi

Bilateral renal bruits, Hx of IHD

What is your top differential for this?

A

Pre-renal acute renal failure 2° renal artery stenosis

70
Q

Someone presents with

Esoinophilic cast, urine dip: protein+blood

Old man, CAP, penicillin Tx, dysuria, back pain

What is your top differential for this?

A

Acute interstitial nephritis

71
Q

Someone presents with

Bladder palpable up to umbilicus + unable to pass urine + man

What is your top differential for this?

A

Post-renal AKI 2° to prostatic hypertrophy

72
Q

Someone presents with

D&V + high urea + creatinine + K+

Normocytic anaemia + fractionate RBC (film)

Escherichia coli O157:H7 stool

What is your top differential for this?

A

Haemolytic uraemic syndrome

73
Q

Someone presents with

HUS + Fever + neurological manifestations

What is your top differential for this?

A

TTP

74
Q

Someone presents with

24 years of rheumatoid + develop peripheral oedema

Proteinuria 3+ urine – cause?

What is your top differential for this?

A

Amyloidosis

75
Q

Someone presents with

Bone pain, lethargy, poor renal function

Monoclonal band on serum electrophoresis

Monoclonal globulin protein in urine

What is your top differential for this?

A

Multiple myeloma

76
Q

Someone presents with

Crohn’s, poor renal function, proteinuria

Stain +ve with congo red – renal Biopsy

What is your top differential for this?

A

Amyloid A amyloidosis

77
Q

Someone presents with

T1DM albuminuria, previous dipstick normal

What is your top differential for this?

A

Diabetic microalbuminuria

78
Q

Someone presents with

Collapse following stroke: High urea + creatinine, K+, High CK, urine dark red

What is your top differential for this?

A

Rhabdomyolysis

79
Q

Someone presents with

4M, facial swelling, 3+ proteinuria, low albumin

What is your top differential for this?

A

Minimal change glomerulonephritis

Electron microscopy: Fusion of podocytes

80
Q

Someone presents with

25M, facial swelling, 3+ proteinuria, low albumin

What is your top differential for this?

A

Membranous glomerulonephritis

81
Q

Someone presents with

+ve anti-GDM antibodies

What is your top differential for this?

A

Goodpasture’s syndrome

82
Q

Someone presents with

7M 2/7 after URTI hematuria, flank pain

Biopsy: Proliferative glomerulonephritis with antibody deposition

What is your top differential for this?

A

IgA nephropathy (Berger’s disease)

83
Q

Someone presents with

15F, 2/52 post-tonsilitis, dark urine, puffy

High titres of anti-streptolysin O antibody

What is your top differential for this?

A

Post-strep glomerulonephritis

FLASHCARDS from MEDED lectures COPY (35 decks)

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