Renal Flashcards
Risk factors for diabetic nephropathy
- Poor diabetic control
- Long duration of diabetes
- Presence of other microvascular complications
- Ethnicity
- Family history
Management of diabetic nephropathy
- Good glycaemic control
- Blood pressure control - ACE inhibitors + ARBs
- Dietary changes e.g. weight loss
Clinical features of IgA nephropathy
- Young men typically affected
- Flares triggered by URTIs - usually 1-2 days after symptoms
- Haematuria
- Loin pain
- Oedema in the hands and feet
- Dark urine
- Hypertension
- Henoch-Schonlein purpura
Investigation results in IgA nephropathy
- Increased mesangial matrix and cells
- IgA deposition in the epithelium
Management of IgA nephropathy
- Blood pressure control with ACE inhibitors
Clinical features of post-streptococcal glomerulonephritis
- Symptoms occur 10-14 days after streptococcal infection (e.g. strep throat, skin infection)
- Most commonly affects children and young adults
- Haematuria
- Oliguria
- Oedema
- Hypertension
- Fluid retention
- Malaise
Investigation results in post-strep GN
- Urine microscopy: Red cell casts and dysmorphic red cells
- Bloods: positive Anti-Streptolysin test, low C3 and C4 levels
- Renal biopsy: cresenteric lesions with diffuse proliferation of cells and immune deposits
Management of post-strep GN
- Usually none required
- Can provide supportive management
Clinical features of small vessel vasculitis
- Typically affects middle-aged people
- Typically affects Caucasians
- Visible haematuria
- Foamy urine
- Hypertension
- Decreased kidney function
- Other symptoms based on body systems affected
Management of small vessel vasculitis
- Corticosteroids
- Cyclophosphamide
- Rituximab
- Plasmapheresis
Clinical features of Anti-GBM/Goodpasture’s disease
- Haematuria +/- proteinuria
- Lung haemorrhage
- Systemic symptoms e.g. weight loss, fever, malaise
- Arthralgia
Investigation results in anti-GBM disease
- Urine microscopy: characteristic red cell casts and dysmorphic red cells
- Anti-GBM antibody present
- Renal biopsy: cresenteric nephritis
- EM: linear IgG deposits on the GBM
Management of anti-GBM disease
- Glucocorticoids
- Cyclophosphamide
- Plasma exchange
Clinical features of Henoch-Schonlein purpura
- Most commonly affects children
- Characteristic petechial rash on the buttocks and lower legs
- Abdominal pain
- Arthralgia
- Renal disease - haematuria +/- proteinuria
- Often preceded by an infection
Investigation results in Henoch-Schonlein purpura
- Renal biopsy: mesangial IGA deposition that are indistinguishable from IgA nephropathy
Causes of nephritic syndrome
- IgA nephropathy
- Post-streptococcal glomerulonephritis
- Small vessel vasculitis
- Anti-GBM disease
Causes of nephrotic syndrome
- Minimal Change Disease
- FSGS
- Membranous nephropathy
Triad of symptoms seen in nephrotic syndrome
- Oedema
- Proteinuria
- Hypoalbuminaemia
Clinical features of minimal change disease
- Typically affects children
- Proteinuria
- Widespread oedema e.g. peri-orbital
- Impaired kidney function
- Hypoalbuminaemia
- Associated with atopy, drugs (e.g. NSAIDs), haematological malignancies
Investigation results in minimal change disease
- Renal biopsy: normal
- EM: fusion of foot processes
Management of minimal change disease
- High-dose corticosteroids e.g. 6 weeks PO prednisolone
Causes of secondary FSGS
- Healing of previous local glomerular injury e.g. HUS, cholesterol embolism, vasculitis
- HIV
- Sickle cell disease
- Heroin
- Morbid obesity
- Chronic hypertension
- Renal disease
Clinical features of FSGS
- Can occur in any age group
- More common in people of West African descent
- Proteinuria
- Oedema
- Hypoalbuminaemia
- Hyperlipidaemia
- Kidney failure
Investigation results in FSGS
- Renal biopsy: partial sclerosis seen in some glomeruli. May stain positive for C3 and IgM deposits on immunofluorescence.
- EM: podocyte foot process fusion
Management of FSGS
- Primary: high dose glucocorticoids
- Secondary: treat underling cause and reduce proteinuria with ACE inhibitors
Clinical features of membranous nephropathy
- Age between 30-50
- Caucasian
- Proteinuria
- Oedema
- Hypoalbuminaemia
- Kidney failure
Investigation results in membranous nephropathy
- Renal biopsy: segmental scars
- Silver staining: GBM spikes
Prognosis of membranous nephropathy
- 1/3rd will progress to end stage renal disease
- 1/3rd will remain stable
- 1/3rd will resolve spontaneously
Management of membranous nephropathy
- High dose glucocorticoids and immunosuppressants
Investigation specific for amyloidosis
- Congo red staining - apple-green colour under polarised light
Inheritance mode of polycystic kidney disease
Autosomal dominant
Clinical features of adult polycystic kidney disease
- Asymptomatic
- Hypertension
- Haematuria
- Abdominal pain
- Uni- or bilateral palpable kidneys
- Hepatic cysts
- Increased risk of subarachnoid haemorrhage
- Increased risk of renal stones
- Increased risk of UTIs
Most common mutation in adult PKD
PKD1 (85%)
other 15% are PKD2
Diagnostic investigation for adult PKD
- Renal US, using the following criteria:
15-39: at least 3 uni or bilateral cysts
40-59: at least 2 cysts in each kidney
60+: at least 4 cysts in each kidney
Management of PKD
- Hypertension control with ACE inhibitors or ARBs
- Dialysis
- Renal transplant
- ADH receptor antagonists (Tolvaptan) used to slow rate of cyst growth and eGFR loss
Inheritance pattern of Alport’s syndrome
X-linked
Clinical features of Alport’s syndrome
Typically, progressive symptoms develop in the teenage years and progress to ESRD in their 20s:
- Haematuria
- Proteinuria
- Renal failure
- Sensorineural deafness
- Ocular abnormalities
Renal biopsy result in Alport’s syndrome
- Thin or thick, split and degenerating GBM
Management of Alport’s syndrome
- ACE inhibitors
- Dialysis
Causes of acute interstitial nephritis
- Allergic e.g. NSAIDs, antibiotics, PPIs, mesalazine
- Immune
- Infective e.g. acute bacterial pyelonephritis, TB
- Toxins e.g. myeloma light chains, mushrooms
Clinical features of acute interstitial nephritis
- Electrolyte abnormalities
- Moderate proteinuria
- Varying degrees of renal impairment
- Preserved urinary output e.g. polyuria, nocturia
- May have signs of a generalised hypersensitivity reaction e.g. fever, rash
Investigation results in acute interstitial nephritis
Urine dipstick:
- No/minimal protein
- No/minimal blood
- White cells and white cell casts
Bloods:
- Raised eosinophil count
Renal biopsy:
- Acute inflammation with infiltration of polymorphonuclear leucocytes and lymphocytes (+/- eosinophils) +/- granulomas
Management of acute interstitial nephritis
- Withdrawal/treatment of precipitating factors
- High dose prednisolone
Causes of chronic interstitial nephritis
- AIN
- Glomerulonephritis
- Immune/inflammatory disorders e.g. sarcoidosis, SLE, Sjogren’s syndrome
- Toxins e.g. lead
- Drugs e.g. Lithium, cyclosporin
- Severe pyelonephritis
- Congenital abnormalities e.g. VUR
- Metabolic disorders e.g. calcium phosphate crystallisation, hypokalemia, hyperoxaluria
Clinical features of chronic interstitial nephritis
- CKD
- Hypertension
- Renal hypoplasia
Clinical features of salt-losing nephropathy
- Hypotension
- Polyuria
- Features of sodium and water depletion
Investigation results in chronic interstitial nephritis
- Non-specific urinalysis abnormalities
Management of chronic interstitial nephritis
- Supportive management
Causes of rhabdomyolysis
- Pressure
- Crush injury
- Ischaemic injury
- Drugs e.g. statin
- Extreme exercise
Investigation results in rhabdomyolysis
- Increased urinary myoglobin
- Increased serum potassium
- Increased serum phosphate
- Decreased serum calcium
- Increased creatinine kinase
- Increased LDH
Management options for rhabdomyolysis
- Emergency treatment of hyperkalemia
- Preventative treatment e.g. fluids
- Sodium bicarbonate
- Dialysis
- Muscle compartment pressures and fasciotomy if required
Causes of renal artery stenosis
- Atherosclerosis
- Fibromuscular dysplasia
- Vasculitis
- Thromboembolism
- Aneurysms
Clinical features of renal artery stenosis
- Hypertension
- Acute pulmonary oedema
- Progressive renal failure
- Deterioration in renal function with ACE inhibitors or ARBs
- Clinical evidence of peripheral vascular disease
Features on examination when make a diagnosis of renal artery stenosis more likely
- Severe, recent onset or difficult to control hypertension
- Asymmetrical kidneys on US
- Recurrent flash pulmonary oedema
- Lower limb peripheral vascular disease present
- Renal function deteriorates with ACE inhibitors or ARBs
Blood test results in renal artery stenosis
- Impaired renal function
- Elevated plasma renin
- Hypokalemia
Imaging to consider in renal artery stenosis
- CT/MR angiography
Management of renal artery stenosis
Anti-hypertensives
Indications for surgical intervention (angioplasty or stenting) in renal artery stenosis
- Patients <40
- Blood pressure not controlled with anti-hypertensive medication
- History of flash pulmonary oedema
- Malignant hypertension
- Deteriorating renal function
Complications of renal artery angioplasty/stenting
- Renal artery occlusion
- Renal infarction
- Atheroembolism
Clinical features of acute renal infarction
- Acute onset loin pain
- Non-visible haematuria
- Severe hypertension
- AK and anuria (in bilateral obstruction)
- Signs of widespread vascular disease
Investigations and results in acute renal infarction
- Bloods: Increased LDH and CRP
- CT scan
Management of acute renal infarction
- Mostly supportive
- Anticoagulants if source identified
- Stenting if presents early enough
Most common infective causes of HUS
- E. Coli
- Shigella dysenteriae
Management of HUS
- Renal replacement therapy as required
Clinical features of cholesterol emboli
- Renal impairment
- Haematuria
- Proteinuria
- Eosinophilia with inflammatory features
- Widespread atheromatous disease with recent intervention or surgery, or anticoagulant/thrombolytic treatment
Management of a cholesterol emboli
No specific management available
Define AKI
Increase in serum creatinine >26.5 within 48 hours
OR
Increase in >1.5x baseline within 7 days
OR
Decrease in urine volume <0.5ml/kg/hr for >6 hours
Causes of AKI
Pre-renal:
- Hypotension
- Sepsis
- Hypovolaemia e.g. vomiting, diarrhoea, burns, haemorrhage
- Dehydration
- Organ failure
- Drugs e.g. ACE inhibitors, NSAIDs
- Liver disease
- Cardiac failure
Renal:
- Glomerulonephritis
- Interstitial nephritis
- Acute tubular necrosis (from prolonged pre-renal causes)
- CKD
- Renovascular disease
Post-renal:
- Obstruction
- Neurological conditions
- Intra-renal cysts
Investigations to consider in a patient with suspected AKI
- Routine bloods
- Urinalysis
- Renal US
- CXR
- Cultures
Examination/investigation results which would suggest a pre-renal cause of AKI
- Hypotension
- Tachycardia
- Weight loss
- Dry mucous membranes
- Increased skin turgor
- JVP not visible
- LOW urinary sodium
- High urea: creatinine ratio
Examination/investigation results which would suggest a renal cause of AKI
- Hypertension
- Oedema
- Purpuric rash
- Uveitis, arthritis
- HIGH urinary sodium
- Inappropriately dilute urine
- Urinalysis: blood and protein (or none in ATN)
Management principles in AKI
- Control of fluid intake - just replace predicted losses
- Monitor and correct hypokalemia
1) Immediate ECG
2) IV calcium gluconate
3) Inhaled salbutamol, IV glucose + IV insulin, IV sodium bicarbonate
4) IV furosemide and normal saline - Monitor for and correct acidosis - sodium bicarbonate
- Monitor for and treat pulmonary oedema - dialysis
- STOP ACE inhibitors and NSAIDs
- Treat primary cause
- Haemodialysis if indicated
Indications for haemodialysis in AKI
- Pulmonary oedema (URGENT)
- Severe hyperkalemia despite medical management
- Symptomatic or poor biochemical results
- Pericarditis
- Need for high fluid intakes during oliguria.
