Nephrology Flashcards
(143 cards)
1
Q
What is ADPKD?
A
Inherited renal disorder characterised by continuous formation and growth of cysts in the kidneys leading to progressive renal impairment due to destruction of nephrons leading to end stage kidney disease
2
Q
Epidemiology of ADPKD?
A
ADPKD is the most common genetic kidney disorder in adults
Prevalence is approximately 1:1000
Men and women are affected equally, and it occurs in patients of all ethnicities
It is responsible for up to 10% of end-stage renal disease
Approximately 85% of patients have PKD1 mutations and 15% have PKD2 mutations
Around 15% of patients with ADPKD have no family history of the condition (for example due to de novo mutations)
3
Q
Aetiology of ADPKD?
A
The PKD genes cause mutations in polycystin 1 and 2, which lead to cyst formation and expansion
PKD1 is located on chromosome 16, and PKD2 is located on chromosome 4
Disease is typically more severe with PKD1 mutations
4
Q
Signs and symptoms of ADPKD?
A
Flank pain; may be secondary to cyst haemorrhage, infection or UTI
Haematuria
Fever and systemic illness
Polyuria
Nocturia
CKD; lethargy, peripheral oedema, pruritis
Bilateral large masses in the flanks (palpable enlarged kidneys)
Hepatomegaly (up to 70% have liver cysts)
Hypertension
Splenomegaly is rarer (5% have splenic cysts)
5
Q
Differentials for ADPKD?
A
Simple renal cysts
Acquired cystic kidney disease
ARPKD
Tuberous sclerosis
Von Hippel- Lindau disease
Medullary cystic kidney disease
6
Q
Investigations to diagnose ADPKD?
A
Urine dip; haematuria, proteinuria
Urine ACR
Urine MC&S
FBC, U+E, bone profile, LFT
USS kidney, CT/ MRI of kidney, MRI head, abdominal USS
Echocardiogram
Genetic testing
Renal testing
7
Q
Management of ADPKD?
A
Conservative management;
Screening of at risk adults
BP monitoring
Avoid contact sports
Reduce CVD risk; smoking cessation, healthy diet and exercise
Avoid nephrotoxic drugs
Avoid oestrogen; promote growth of hepatic cysts
Serial USS
Medical management;
Tolvaptan
Antihypertensive; aim below 130/80
Antibiotics
Surgical management;
Cyst drainage
Nephrectomy
If ESRF; renal replacement therapy
Drainage/ resection of liver cysts
Clipping/ coiling of intracranial aneurysm
8
Q
Complications of ADPKD?
A
Cyst haemorrhage
Cyst infection
Recurrent UTI
Renal stones
Liver cysts
Pancreatic cysts
Seminal vesicle cyst
Arachnoid membrane cyst
Intracranial aneurysm Aneurysm
Cardiovascular valvular disease
Chronic pain
End stage renal disease
9
Q
Features of liver cysts in ADPKD?
A
80% of patients have liver cysts by the age of 30
These increase with age, especially in women
20% of patients will develop symptoms
These include abdominal and back pain, abdominal distension, early satiety and gastro-oesophageal reflux
Liver cysts may also rupture, bleed or become infected
Treatment options include aspiration and sclerotherapy or fenestration of cysts
In some cases liver resection is indicated for symptomatic relief
10
Q
Aetiology of haematuria?
A
Trauma (including catheterisation)
Infection - either acute urinary tract infection or chronic, e.g. urogenital tuberculosis
Glomerulonephritis e.g. IgA nephropathy, anti-glomerular basement membrane disease
Urinary tract stones
Malignancy
Benign prostatic hyperplasia (in a minority of patients)
Iatrogenic (e.g. after radiotherapy for prostate cancer)
Medications (e.g. hemorrhagic cystitis secondary to cyclophosphamide)
Coagulopathies (e.g. haemophilia)
Renal infarction (e.g. due to a cardiac embolism or in situ thrombosis)
11
Q
Aetiology of haemoglobinuria?
A
Autoimmune haemolytic anaemia
Transfusion reactions
Microangiopathic haemolytic anaemia
Paroxysmal nocturnal haemoglobinuria
Sickle cell disease
Infections (e.g. malaria)
Drug-induced haemolytic anaemia (e.g. methyldopa)
Metallic heart valves
12
Q
Aetiology of myoglobinuria?
A
Rhabdomyolysis
Excessive physical exertion
Compartment syndrome
Hyperthermia
Myositis (e.g. viral, autoimmune)
Prolonged seizures
13
Q
Aetiology of proteinuria?
A
Chronic kidney disease
Nephrotic syndrome
Glomerulonephritis
Malignant hypertension
Pyelonephritis
Amyloidosis
Diabetes
Heart failure
Infective endocarditis
Eclampsia
Pregnancy
Intense exercise
Fever
Urinary tract infection
Orthostatic proteinuria (a benign condition where there is increased protein excretion when upright only)
Medications (e.g. aminoglycosides, NSAIDs)
14
Q
Aetiology of pyruia?
A
Urinary tract infection (UTI)
Sterile pyuria refers to high white cells in urine with a negative urine culture:
Recently treated UTI
Genitourinary tuberculosis
Interstitial nephritis
Urinary tract stones
Renal papillary necrosis (e.g. due to diabetes, sickle cell disease)
Malignancy
Interstitial cystitis
Chlamydial urethritis
15
Q
Aetiology of glycosuria?
A
Diabetes
Impaired glucose tolerance
Excessive sugar intake
Severe illness
Thyrotoxicosis
Cushing’s syndrome
Acromegaly
Other causes include:
Pregnancy (especially if gestational diabetes present)
Fanconi’s syndrome
Renal glycosuria (rare genetic condition)
Treatment with sodium-glucose co-transporter-2 (SGLT2) inhibitors
16
Q
Aetiology of ketonuria?
A
Poorly controlled or decompensated diabetes
Low carbohydrate diets
Starvation
Alcohol excess
Hyperthyroidism
Pregnancy
Prolonged vomiting
False positives may occur with some medications (e.g. captopril, levodopa)
17
Q
What is acute tubular necrosis?
A
Renal tubular epithelial cells are damaged due to nephrotoxic agents or ischaemic insult
18
Q
Epidemiology of acute tubular necrosis?
A
Leading cause of intrinsic AKI
Seen in acutely ill patients and is a poor prognostic factor
19
Q
Risk factors for acute tubular necrosis?
A
Hypovolaemia
Older age
Chronic kidney disease
Recent use of nephrotoxic drugs
20
Q
Aetiology of acute tubular necrosis?
A
Ischaemic causes;
Hypovolaemia
Diarrhoea and/or vomiting
Haemorrhage
Dehydration
Burns
Renal losses (diuretics, osmotic diuresis)
Third-spacing (e.g. severe pancreatitis)
Systemic vasodilation
Anaphylaxis
Septic shock (also has toxic effects on the kidneys)
Surgery, due to a combination of:
Fluid losses
Haemodynamic changes under anaesthesia
Interruption of renal perfusion e.g. supra-aortic clamping in abdominal aortic aneurysm surgery
Nephrotoxic;
Aminoglycoside antibiotics (e.g. gentamicin)
Antifungals (e.g. amphotericin)
Chemotherapy agents (e.g. cisplatin)
Antivirals (e.g. tenofovir)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Contrast agents
Myoglobin (rhabdomyolysis)
Haemoglobin (intravascular haemolysis, e.g. transfusion reactions, autoimmune haemolytic anaemia)
21
Q
Signs and symptoms of acute tubular necrosis?
A
Dehydration
Nausea
Vomiting
Lethargy and malaise
Nausea and vomiting
Oliguria or anuria (polyuria may be seen in the recovery phase)
Confusion
Drowsiness
Peripheral oedema
22
Q
Differentials for acute tubular necrosis?
A
Pre-renal AKI
Acute interstitial nephritis
Post renal AKI
23
Q
Investigations to diagnose acute tubular necrosis?
A
Urine microscopy shows muddy brown granular casts and renal tubular epithelial cells
Urinary sodium is key to differentiating pre-renal AKI from ATN - sodium is low in pre-renal AKI and high in ATN (usually > 40 mmol/L)
Urine osmolality is low as urine concentrating capacity is impaired (< 450 mOsmol/kg)
Urine dip may be falsely positive for blood if there is myoglobinuria or haemoglobinuria
Blood gas to assess for acidosis and hyperkalaemia that may complicate AKI
ECG looking for hyperkalaemic changes
Bloods
U&Es to confirm renal impairment and assess electrolytes
Urea:creatinine ratio is low in ATN as water, sodium and urea are not retained unlike in pre-renal AKI
Full blood count may show anaemia in some causes of ATN (e.g. haemorrhage, haemolysis); there may be a leukocytosis in sepsis
Creatine kinase if rhabdomyolysis is suspected
Liver function tests may show a concurrent ischaemic liver injury
Bone profile may be abnormal e.g. hypercalcaemia causing dehydration
CRP may be raised in some causes of ATN e.g. sepsis
Blood cultures should be sent in suspected sepsis
Coagulation screen may show a prolonged aPTT due to platelet dysfunction secondary to uraemia
USS KUB
Renal biopsy
24
Q
Management of acute tubular necrosis?
A
Stop nephrotoxic drugs, fluid balance monitoring
Medical;
IV fluids to correct hypovolaemia and/or hypotension
Blood products are preferred in haemorrhage
Medical management may be required for the underlying cause (e.g. antibiotics in sepsis)
Vasopressors may be used with fluids in patients with shock
Interventional;
Dialysis
25
Prognosis of acute tubular necrosis?
Poor prognostic factor with mortality rate of 50%
Patients who are septic/ require dialysis
If survived 5% require renal replacement therapy
26
What is acute interstitial nephritis?
Cause of intrinsic AKI where there is acute tubulo-interstitial inflammation
Classical triad of hypersensitivity with fever, macular/ maculopapular rash and eosinophilia
27
Epidemiology of acute interstitial nephritis?
Up to 20% of AKI cases and 1% of end-stage renal disease are due to acute interstitial nephritis
70% of cases are secondary to medication, most commonly antibiotics, NSAIDs, PPI
28
Aetiology of acute interstitial nephritis?
Medications;
Beta-lactams
Cephalosporins
Fluoroquinolones
Non-steroidal anti-inflammatory drugs (NSAIDs)
Diuretics
Rifampicin
Allopurinol
PPIs
Immune checkpoint inhibitors
Ranitidine
Warfarin
Phenytoin
Autoimmune;
Sjogren syndrome
Systemic lupus erythematosus (SLE)
Sarcoidosis
Tubulo-interstitial nephritis with uveitis (TINU)
Infections:
Bacterial (Mycobacteria, Streptococcus)
Viral (HIV, influenza)
Fungal (cryptococcus, histoplasmosis)
Parasitic (hydatid, ascaris)
Rickettsial
Malignancies:
Leukaemia
Lymphoma
Myeloma
29
Signs and symptoms of acute interstitial nephritis?
Rash - typically macular or maculopapular and fleeting
Fevers, usually low-grade
Oliguria
Flank pain or a sensation of fullness
Arthralgia
Peripheral oedema (especially in NSAID-induced AIN where a concurrent nephrotic syndrome may be seen)
Examination is often normal
30
Differentials for acute interstitial nephritis?
Pre-renal AKI
Acute tubular necrosis
Glomerulonephritis
Cholesterol embolism
Post renal AKI
31
Investigations to diagnose acute interstitial nephritis?
Urine microscopy shows pyuria and white cell casts; proteinuria may be present but is usually mild
Urine culture is negative (i.e. sterile pyuria)
Blood gas to assess for acidosis and hyperkalaemia that may complicate AKI
ECG looking for hyperkalaemic changes
Bloods;
FBC, U+E, Autoimmune screen, ANA, ANCA, anti-dsDNA, complement
Imaging;
Renal US
Renal biopsy; inflammatory infiltrate in the interstitium and tubules with eosinophils, lymphocytes and plasma cells
32
Management of acute interstitial nephritis?
Conservative:
Identification of the causative medication and stopping it is key to managing drug-induced AIN
Supportive management with monitoring of renal function, electrolytes and fluid balance
Salt and fluid restriction may be required
Refer to specialist renal services - urgent review may be required for patients who have not responded within a week of stopping the causative medication
Medical:
Steroids are indicated for AIN secondary to an autoimmune condition (e.g. SLE, TINU, sarcoidosis)
A short course of oral prednisolone (e.g. 40 mg OD for 2 weeks, then tapered over 4-6 weeks) may be considered in drug-induced AIN also (there is some evidence that this may increase the rate and extent of renal recovery)
Diuretics (e.g. furosemide) may be required if there is significant fluid overload
Interventional:
In AKI with complications (e.g. refractory fluid overload or uraemia), dialysis may be required
33
Prognosis of acute interstitial nephritis?
Renal impairment is common due to tubulo-intersitial fibrosis resulting from AIN
40-60% of patients go on to develop chronic kidney disease (CKD)
End-stage renal disease may occur, with AIN accounting for 1% of cases
Recurrence of AIN occurs in a minority of patients but is associated with worsening renal impairment and a poorer prognosis
Hypertension may develop secondary to renal impairment - patients should have blood pressure monitored annually after recovery as well as annual U&Es and urinalysis looking for CKD
Poor prognostic factors include delayed diagnosis, delayed steroid treatment and longer duration of taking causative medications
34
What is AKI?
Decline in renal function that happens rapidly (over hours to days). It is diagnosed based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria as below:
Increase in serum creatinine by >26.5 mmol/l within 48 h, or
Increase in serum creatinine > 1.5x the baseline within the last 7 days, or
Urine output < 0.5 ml/kg/h for 6 hours
35
Risk factors for AKI?
Patients with CKD
Elderly patients
Previous AKI
Malignancy
Medical conditions increasing risk of urinary obstruction (e.g. benign prostatic hyperplasia)
Cognitive impairment and disability (may be reliant on others for fluid intake)
Recent use of medications such as NSAIDs or ACE inhibitors
Recent administration of iodine-containing contrast media
36
Epidemiology of AKI?
20% of patients admitted to hospital with upto 50% in critical care
It is a marker of severe illness, with a 90-day mortality rate of approximately 25%.
37
Aetiology of AKI?
Pre-renal causes are the most common, and occur due to decreased renal perfusion e.g. due to:
Hypovolaemia (e.g. dehydration, haemorrhage, gastrointestinal losses, burns)
Renovascular disease (e.g. renal artery stenosis)
Medications reducing blood pressure or renal blood flow (e.g. NSAIDs, ACE inhibitors, ARBs, diuretics)
Hypotension due to reduced cardiac output (e.g. heart failure, sepsis)
Renal causes occur due to structural damage to the kidneys, which may affect:
The glomeruli (e.g. acute glomerulonephritis, nephrotic syndrome)
The tubules (e.g. acute tubular necrosis due to ischaemia or toxins, rhabdomyolysis)
The interstitium (e.g. acute interstitial nephritis secondary to drugs)
The renal vessels (e.g. renal vein thrombosis, vasculitis)
Post-renal causes involve obstructed to urinary flow anywhere along the urinary tract, which may be:
Luminal (e.g. ureteric stones or a blocked catheter)
Intramural (e.g. urethral or ureteric strictures, ureteric carcinomas)
Due to external compression (e.g. an abdominal or pelvic tumour, benign prostatic hyperplasia)
38
Classification of AKI?
Stage 1 - any of:
Creatinine rise of 26 micromol/L or more within 48 hours
Creatinine rise to 1.5-1.99x baseline within 7 days
Urine output < 0.5 mL/kg/hour for more than 6 hours
Stage 2 - any of:
Creatinine rise to 2-2.99x baseline within 7 days
Urine output < than 0.5 mL/kg/hour for more than 12 hours
Stage 3 - any of:
Creatinine rise to 3x baseline or higher within 7 days
Creatinine rise to 354 micromol/L or more with either
Acute rise of 26 micromol/L or more within 48 hours or
50% or more rise within 7 days
Urine output < than 0.3 mL/kg/hour for 24 hours
Anuria for 12 hours
39
Signs and symptoms of AKI?
Symptoms may be seen especially in severe cases where uraemia occurs, and include:
Nausea and vomiting
Fatigue
Confusion
Anorexia
Pruritus
On examination, look for:
Hypertension (a complication of AKI)
Bladder distension due to urinary retention
Hypotension and dehydration (in many pre-renal causes)
Signs of fluid overload (e.g. raised jugular venous pressure, pulmonary and peripheral oedema) as a complication of AKI
Signs related to the underlying cause (e.g., fevers in sepsis, rashes in vasculitis)
Pericardial rub (in uraemic pericarditis)
40
Investigations to diagnose AKI?
Urinalysis - urine dip may show blood and protein in glomerular disease, increased white blood cells may suggest infection or interstitial nephritis
ECG to screen for complications of hyperkalaemia
Blood gas to look for acidosis as a complication of AKI, allows rapid potassium measurement
Bloods;
U+E, FBC,LFT, clotting, bone profile, creatinine kinase, CRP
Acute renal screen;
ANA
Double-stranded DNA
Anti-nuclear cytoplasmic antibodies
Anti-GBM antibodies
Erythrocyte sedimentation rate
Serum immunoglobulins
Serum electrophoresis
Serum free light chains
Complement levels (C3 and C4)
HIV screening
Hepatitis B and C serology
Bladder scan
USS KUB
41
Investigations included in an acute renal screen?
ANA
Double-stranded DNA
Anti-nuclear cytoplasmic antibodies
Anti-GBM antibodies
Erythrocyte sedimentation rate
Serum immunoglobulins
Serum electrophoresis
Serum free light chains
Complement levels (C3 and C4)
HIV screening
Hepatitis B and C serology
42
Management of AKI?
IV fluid resuscitation
Fluid balance and catheterise
Suspend nephrotoxic drugs
Screen for complications of AKI (e.g. hyperkalaemia, acidosis, pulmonary oedema) and instigate treatment promptly
Involve the renal team early in severe or complicated AKIs, where the cause is unclear or where a renal cause is suspected
The following should prompt referral for consideration of renal replacement therapy with dialysis or haemofiltration;
Acidosis (severe metabolic acidosis with pH of <7.20)
Electrolyte imbalance (resistant hyperkalaemia)
Intoxication (AKI secondary to certain drugs or poisons)
Oedema (refractory pulmonary oedema)
Uraemia (uraemic encephalopathy or pericarditis)
43
What is ant glomerular basement membrane disease?
Autoimmune pulmonary-renal syndrome characterised by anti-GBM antibodies, rapidly progressive glomerulonephritis and pulmonary haemorrhage
44
Epidemiology of anti- GBM disease?
Anti-GBM disease is rare, causing 1-2% of cases of rapidly progressive glomerulonephritis
Approximately 3x as many men as women are affected
There is a bimodal age distribution with two peaks of cases in 20-30 year olds and 60-70 year olds
45
Pathophysiology of anti-GMB disease?
IgG antibodies directed against non-collagenous domain of the 3 chain of type IV collagen
These antigens are present on the glomerular basement membrane and alveolar basement membrane in the lungs
A type II hypersensitivity reaction occurs (IgG or IgM antibody-mediated cytotoxic reaction), with subsequent inflammation
A rapidly progressive glomerulonephritis occurs in the kidneys
A necrotising haemorrhagic interstitial pneumonitis occurs in the lungs
46
Risk factors for anti-GBM disease?
HLA-DRB1 gene
Smoking
Exposure to hydrocarbons, metal dust, organic solvents
Infection
Alemtuzumab
Alport syndrome
Post renal transplant
47
Signs and symptoms of anti-GBM disease?
Symptoms;
Haematuria (may be visible)
Cough +/- haemoptysis
Chest pain
Dyspnoea
Lethargy
Weight loss
Anorexia
Weight loss
Myalgia
Arthralgia
Signs;
Hypertension
Oliguria/anuria
Tachynpoea; increased work of breathing
Crackles heard in the lower zones of the lungs
Cyanosis
Pallor (due to anaemia)
Fever
48
Differentials for anti- GBM disease?
Granulomatosis with polyangiitis
Microscopic polyangiitis
SLE
Cryoglobulinaemia
49
Investigations to diagnose anti-GBM disease?
Urinalysis to confirm haematuria and proteinuria
Protein:creatinine ratio to quantify proteinuria
Venous blood gas to rapidly measure potassium and assess for metabolic acidosis secondary to acute kidney injury
Bloods;
FBC, U+E, LFT, bone profile, coagulation screen, CRP, group and save, anti-GBM antibodies, ANA, ENA, dsDNA, ANCA, cryoglobulins
Serum protein electrophoresis, serum free light chains, complement levels, viral screen
Renal USS
CXR
CT chest
Renal biopsy; gold standard for diagnosis, demonstrating linear IgG deposition along the basement membrane
50
Management of anti-GMB disease?
Monitor FBC, U+E, anti- GBM titres
High dose steroids, cyclophosphamides to suppress antibody production
Alternative to cyclophosphamide; rituximab. mycophenolate
Initially pulsed methylprednisolone is given, then stepped down to oral prednisolone and weaned
Cyclophosphamide is continued for around 2-3 months
Steroids are continued for around 6 months
Interventional therapy;
Plasma exchange
IVIG
Renal transplant
51
Prognosis of anti- GBM disease?
If untreated it is fatal
Respiratory failure secondary to pulmonary haemorrhage is the commonest cause of death
With aggressive treatment, survival at one year is approximately 70-90%
Poor prognostic factors;
Requiring dialysis at presentation
More likely to develop end stage renal failure, older age, higher creatinine at presentation, oliguria
52
Antibodies in goodpastures syndrome?
Anti-glomerular basement membrane antibodies against type 4 collagen found within glomerular and alveolar basement membranes
53
Antibodies in Granulomatosis with polyangiitis (Wegener's)?
Cytoplasmic anti-neutrophil cytoplasmic antibodies
54
Antibodies in churg- stauss syndrome?
Peri-nuclear anti-neutrophil cytoplasmic antibodies
55
Antibodies in SLE?
Antinuclear antibody,
Double-stranded DNA
Anti-smith antibody are more specific
56
Antibodies in rheumatoid arthritis?
Rheumatoid factor
Anti-Cyclic Citrullinated Peptide (anti-CCP) is more specific
57
What is CKD?
Abnormal kidney function for over 3 months with implications on health
A GFR below 60 ml/min/1.73m2 is considered significantly abnormal kidney function.
Examples of abnormal kidney structure include:
Urinary albumin:creatinine ratio > 3 mg/mmol
Urinary sediment abnormalities e.g. haematuria, pyuria or casts
Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders
Histological abnormalities e.g. glomerulosclerosis, tubular atrophy
Structural abnormalities e.g. polycystic kidneys or reflux nephropathy
Previous renal transplant
58
Epidemiology of CKD?
Estimated global prevalence of 9%
Diabetes is the commonest cause accounting for upto 50% of cases
Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension
59
Risk factors for CKD?
Family history of CKD
Black or Hispanic ethnicity
History of acute kidney injury (AKI)
Older age
60
Aetiology of CKD?
Diseases causing intrinsic kidney damage:
Diabetes
Hypertension
Glomerulonephritis, which may be primary or secondary
Conditions causing urinary tract obstruction:
Recurrent urolithiasis
Structural abnormalities (e.g. ureteropelvic junction obstruction)
External compression (e.g. from a pelvic mass)
Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)
Iatrogenic causes:
Radiotherapy
Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs
Renal involvement secondary to multisystem diseases:
HIV
Myeloma
Vasculitis
Systemic lupus erythematosus (lupus nephritis)
Amyloidosis
Genetic kidney diseases
Autosomal dominant polycystic kidney disease (ADPKD)
Alport's syndrome
Tuberous sclerosis
Cystinosis
Recurrent urinary tract infections
Often secondary to vesico-ureteric reflux or other anatomical defects
Leads to chronic pyelonephritis which may lead to end-stage renal disease
61
Symptoms of CKD?
Lethargy
Anorexia
Headaches
Weight loss (or gain due to fluid overload)
Nausea and vomiting
Itching (uraemic pruritus)
Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)
Muscle cramps, especially at night
Bone pain (due to renal osteodystrophy)
Taste changes
Cognitive impairment
Urinary symptoms:
Polyuria or oliguria may occur
Nocturia
Frothy urine (due to proteinuria)
62
Signs of CKD?
Hypertension
Pallor (due to anaemia)
Abnormal fluid status
Fluid overload with peripheral and/or pulmonary oedema
Dehydration
Cachexia
Ammonia-like smelling breath due to uraemia
Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis
Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)
Patients on renal replacement therapy may have additional signs such as:
Arteriovenous fistula (AVF)
Peritoneal dialysis catheter
Renal transplant scar (usually right iliac fossa)
Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism
63
Differentials for CKD?
AKI
False positive eGFR
False positive ACR; menstruation, strenuous exercise, orthostatic proteinuria, UTI
64
Investigations for CKD?
Bedside tests;
Urine dipstick; haematuria, proteinuria
ACR
Bloods;
U+E, FBC, LFT, Bone profile, HbA1c, Bicarbonate, Lipid profile, clotting screen, parathyroid hormone, HIV, hepatitis B and hepatitis C
Antibodies;
Antinuclear antibodies
ANCA antibodies
dsDNA antibodies
Anti-GBM antibodies
Serum complement
Imaging;
Renal tract USS
CT KUB
CT/ MRI angiography
Special tests;
Renal biopsy
65
Management of CKD?
Lifestyle advice should be provided, including:
Smoking cessation
Moderating alcohol intake
Maintaining a healthy weight with regular exercise
Maintaining a healthy diet
Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies
Optimise diabetes
Stop nephrotoxic drugs
BP control;
Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol
Aim for < 130/80 if ACR is > 70 mg/mmol
Consider statin and antiplatelet prophylaxis
Annual influenza vaccine
5 yearly pneumococcal vaccine
Renal replacement therpay
66
Indications for renal replacement therapy?
eGFR approximately 5-7 ml/min/1.73m_
Symptomatic uraemia affecting quality of life
Refractory fluid overload
Refractory biochemical abnormalities
Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)
Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism
67
Complications of CKD?
Anaemia
Mineral and bone disorder
CVD risk
Uraemia
Metabolic acidosis
Fluid overload
Malnutrition
AKI
Increased risk of malignancy
Hypertension
Reduced quality of life
68
What is diabetic nephropathy?
Kidney damage due to long standing hyperglycaemia characterised by albuminuria, impaired renal function
69
Risk factors for diabetic nephropathy?
Hypertension
Higher waist circumference
Diabetic retinopathy
Male gender
Smoking
South Asian ethnicity
Dyslipidemia
70
Epidemiology of diabetic nephropathy?
Diabetes is the most common cause of CKD and ESRF
1 in 3 people with diabetes develop diabetic nephropathy
71
Pathophysiology of diabetic nephropathy
The pathophysiology of diabetic nephropathy involves uncontrolled hyperglycaemia initially leading to glomerular hyperfiltration
This is followed by metabolic, inflammatory and haemodynamic changes which lead to glomerulosclerosis, interstitial fibrosis and tubular atrophy
Kidneys initially increase in size although they may later atrophy as CKD progresses
Basement membrane damage is a key feature that manifests clinically with albuminuria and proteinuria
72
Classification of diabetic nephropathy?
Class I; Mild or nonspecific changes on light microscopy; glomerular basement membrane thickening on electron microscopy
Class II; Diffuse mesangial expansion
Class III; Nodular sclerosis (Kimmelstiel-Wilson lesions)
Class IV; Advanced diabetic glomerulosclerosis affecting more than 50% of glomeruli
73
Signs and symptoms of diabetic nephropathy?
Fatigue
Anorexia
Weight loss
Nausea and vomiting
Taste disturbance
Itch
Breathlessness
Sleep disturbance
Bone pain
Foamy urine due to proteinuria
Polyuria or oliguria
Hypertension
Peripheral and/or pulmonary oedema
Encephalopathy
Cachexia
Pallor
Uraemic odour
74
Differentials for diabetic nephopathy?
Atherosclerotic renal artery stenosis
Multiple myeloma
75
What is fibromuscular dysplasia?
Non-atherosclerotic, non-inflammatory arterial diseases. These primarily involve the renal and carotid arteries but may affect any vascular bed.
76
Epidemiology of fibromuscular dysplasia?
Affects women with peak incidence at 30 to 50 years
77
Aetiology of FMD?
various hormonal and mechanical factors postulated to play a role.
no definitive cause has been identified
78
Signs and symptoms of FMD?
Renal Artery FMD: Most commonly presents as reno-vascular hypertension. Multifocal stenoses with a 'string-of-beads' appearance are detected on angiography in over 80% of these cases.
Carotid/Cervico-cranial FMD: Presents with symptoms related to cerebral ischemia or complications such as dissection. Symptoms can include headaches, neurological deficits, or symptoms of Horner's syndrome (ptosis, miosis, anhidrosis).
79
Complications of FMD?
Arterial dissection, presenting as severe headache or neck pain.
Horner's syndrome due to carotid dissection.
Stroke due to embolic disease or arterial dissection.
Intracerebral aneurysms, which increase the risk of subarachnoid or intracerebral haemorrhage.
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Differentials for FMD?
Atherosclerosis
Vasculitides; Takayasu arteritis
Aneurysmal disease
Coarctation of aorta
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Investigations to diagnose FMD?
Gold standard; catheter angiography
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Management of of FMD?
Antihypertensive therapy: For reno-vascular hypertension.
Percutaneous angioplasty: For severe stenoses, especially in renal artery FMD.
Reconstructive surgery: In cases with complex FMD that extends to segmental arteries.
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What is glomerulonephritis?
Nephritic syndrome presents with renal impairment, haematuria and non-nephrotic-range proteinuria (+/++ on the urine dipstick). There may be oliguria, with water retention and HTN.
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Causes of nephritic syndrome?
SLE
HSP
Anti-GBM disease (also known as Goodpasture's disease)
RPGN
Post-infectious GN, eg. streptococcal, infective endocarditis
Alport syndrome
IgA nephropathy (also known as Berger's disease)
MPGN
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Investigations to diagnose nephric syndrome?
Urine dipstick
Urine micsrocopy, looking for red-cell casts
Urine PCR
FBC, U&Es, LFT, bone profile, CRP, ESR
Nephritic screen: ANA (inc. dsDNA), ANCA, anti-GBM, C3/C4
USS kidneys, ureters and bladder (KUB)
Kidney biopsy
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What is IgA nephropathy?
A type of GN characterised by IgA deposition in the mesangium.
This is the most common type of GN worldwide.
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Pathophysiology of IgA nephropathy?
Increased propensity to form IgA immune complexes that are lodged in the mesangium of the glomerulus
IgA deposition combined with activation of the complement pathway and cytokine release leads to glomerular injury
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Presentation of IgA nephropathy?
Many patients are asymptomatic and are identified due to an incidental finding of microscopic haematuria or proteinuria (usually mild)
Most commonly, patients present with visible haematuria
This usually occurs 12-72 hours after an upper respiratory tract or gastrointestinal infection
It is typically self-limiting within a few days
Haematuria typically recurs with subsequent infections
Loin pain (either unilateral or bilateral) may accompany episodes of haematuria
Signs include:
Hypertension
Oedema and frothy urine in patients presenting with nephrotic syndrome (approximately 5% of cases)
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Associations of IgA nephropathy?
HSP/IgA vasculitis, chronic liver disease, inflammatory bowel disease (IBD) and skin and joint disorders, eg. psoriasis
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Investigations to diagnose IgA nephropathy?
Urinalysis; blood and protein
Urine microscopy
The gold-standard method for diagnosis is renal biopsy:
This shows diffuse mesiangial IgA immune complex deposition
Serum IgA is elevated in approximately 50% of patients
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Management of IgA nephropathy?
Dietary salt restriction
Treatment of proteinuria (>0.5 g/day) with an ACE-i/ARB
Treatment of HTN
Corticosteroids
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What is post streptococcal glomerulonephritis?
Immune-complex-mediated GN that can occur 1–3 weeks after a streptococcal upper respiratory-tract infection
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Aetiology of PSGN?
Group A beta haemolytic streptococci
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Presentation of PSGN?
Sudden onset haematuria, oliguria, HTN
Oedema
1-3 weeks post infection
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Investigations to diagnose PSGN?
Urinalysis, MC&S
FBC, U+E, immunoglobulins, complement, autoantibodies
The gold-standard method for diagnosis in adults is a renal biopsy: the classical finding is subepithelial 'humps' on electron microscopy
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Aetiology of infection associated glomerulonephritis?
Bacterial; streptococcus, staphylococcus, pneumococcal
Viral; hepatitis B, EBV, CMV, influenza, mumps, rubella
Fungal; candida
Parasitic; malaria, toxoplasmosis, schistosomiasis
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Causes of membranoproliferative glomerulonephritis?
Hepatitis C
Mixed cryoglobulinaemia
Monoclonal gammopathies
due to immune complex deposition and complement activation
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Investigations to diagnose membranoproliferative
Urinalysis
MC&S
Acute renal screen
The gold-standard method for diagnosis in adults is a renal biopsy: the classical finding is a 'double contour' of the basement membrane
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Management of membranoproliferative glomerulonephritis?
Dietary salt restriction
Treatment of proteinuria (>0.5 g/d) with ACE-i/ARB
Treatment of HTN
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Prognosis of membranoproliferative glomerulonephritis?
Around 50% of patients progress to ESKD by 10 years
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Types of ANCA?
cANCA is named as such for producing cytoplasmic staining patterns
cANCA reacts with anti-proteinase-3 (PR3) antigens in the cytoplasm of the neutrophils
pANCA is so called for producing perinuclear staining patterns
pANCA reacts with myeloperoxidase (MPO) in the lysosomes of monocytes
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Differentials for IgA nephropathy?
Secondary IgA nephropathy
Liver cirrhosis
Coeliac disease
HIV associated
Post- streptococcal glomerulonephritis
Henoch schonlein purpura
Lupus nephritis
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What is nephritic syndrome?
Nephritic syndrome refers to a collection of signs and symptoms that occur due to renal inflammation (nephritis), specifically glomerular inflammation (glomerulonephritis).
The key features are haematuria, proteinuria (usually non-nephrotic range i.e. < 3.5 grams/day), hypertension, oliguria and oedema.
Hypertension, haematuria, proteinuria `
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Aetiology of nephritic syndrome?
Lupus nephritis
Henoch-Schonlein purpura
Post-infectious glomerulonephritis (GN), for example:
Post-streptococcal GN
Other bacteria e.g. pneumococcal pneumonia
Viral infections e.g. hepatitis B
Parasitic infections e.g. malaria
Anti-glomerular basement membrane (anti-GBM) disease
IgA nephropathy
Membranoproliferative glomerulonephritis (MPGN)
Infective endocarditis
ANCA-associated vasculitides e.g.
Granulomatosis with Polyangiitis (GPA)
Microscopic Polyangiitis (MPA)
Eosinophilic Granulomatosis with Polyangiitis (EGPA)
Cryoglobulinaemia
Genetic causes e.g. Alport syndrome
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Presentation of nephritic syndrome?
Haematuria (often microscopic but may be macroscopic) - "cola-coloured" brown urine is typical
Hypertension (may cause symptoms of headache and blurred vision)
Non-nephrotic range proteinuria
Peripheral and pulmonary oedema
Oliguria
Uraemic symptoms due to renal impairment, for example:
Anorexia
Nausea
Fatigue
Pruritus
Lethargy
Alopecia, rashes and arthralgia in systemic lupus erythematosus
Haemoptysis and dyspnoea in anti-GBM disease
Purpuric rash, arthritis and abdominal pain in Henoch-Schonlein purpura
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Differentials for nephritic syndrome?
Nephrotic syndrome
UTI
Malignancy
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Investigations to diagnose nephritic syndrome?
Urine dip
Urine microscopy and culture
Urine PCR
Blood gas
Bloods;
FBC, U+E, LFT, CRP, ESR, Coagulation screen, anti- GBM antibodies, ANCA, complement
Renal USS
CXR
Echocardiogram
Renal biopsy
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Management of nephritic syndrome?
Stop any causative medications
Fluid and salt restriction may be advised to help control hypertension and oedema
A low potassium diet may be required in patients with hyperkalaemia
Medical;
Immunosuppression
Antihypertensive
Diuretics
Plasmapheresis
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Complications of nephritic syndrome?
Acute renal failure
Hypertension induced heart failure
Hyperkalaemia
Uraemia
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What is nephrotic syndrome?
Excessive loss of protein in the urine leading to hypoalbuminaemia, peripheral oedema, hyperlipidaemia, abnormal coagulation and immunodeficiency
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Aetiology of nephrotic syndrome?
Minimal change disease causes the majority of cases of nephrotic syndrome in young children
It is usually idiopathic but may rarely be associated with lymphoma or NSAID use
Glomeruli are normal under light microscopy
Electron microscopy shows diffuse effacement of the podocyte food processes
Steroid responsiveness is characteristic
Focal segmental glomerulosclerosis may be primary or secondary to conditions including HIV, extensive nephron loss or drugs (e.g. heroin)
Biopsy shows sclerosis of segments of the glomerular tuft, only affecting some glomeruli
Membranous nephropathy is the leading cause of nephrotic syndrome in older people
Biopsy shows thickening of the glomerular basement membrane without cellular proliferation
A classic "spike and dome" appearance is described where subepithelial immune deposits are interspersed with new basement membrane growth
Most cases are primary; usually associated with PLA2R antibodies
Others may be secondary to malignancy, infections, autoimmune disease or drugs
Membranoproliferative glomerulonephritis is also referred to as membranoproliferative glomerulonephritis
It can present with nephrotic or nephritic syndrome
It may be idiopathic or secondary to infections such as hepatitis C or systemic lupus erythematosus
Diabetic nephropathy may affect patients with longstanding type 1 or 2 diabetes
It tends to be a progression from microalbuminuria, especially if untreated
Patients are at risk of end-stage renal disease
Biopsy shows thickening of the glomerular basement membrane, mesangial expansion and Kimmelstiel-Wilson nodules
Amyloidosis, especially AA amyloid due to chronic inflammation
AL amyloid (due to light chain deposition) and hereditary amyloidosis can also cause nephropathy
On biopsy, amyloid deposits stain with Congo red and display apple green birefringence under polarized light
Multiple myeloma can present with a variety of renal manifestations, with proteinuria and renal insufficiency the most common
Nephrotic syndrome occurs in a minority of cases and may be due to a number of underlying mechanisms
Lupus nephritis i.e. renal involvement due to systemic lupus erythematosus
Class V (membranous lupus nephritis) is the most likely to cause nephrotic syndrome
This is characterised histologically by subepithelial immune complex deposition
Medications are a rarer cause of nephrotic syndrome, including:
Bisphosphonates
NSAIDs
D-penicillamine
Probenecid
Tolbutamide
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Presentation of nephrotic syndrome?
Frothy urine due to proteinuria
Swelling of the face and body
Weight gain due to fluid retention
Fatigue
Lethargy
Anorexia
Signs include:
Oedema - typically peripheral and periorbital
Muehrcke's lines refers to paired white transverse lines across the nails that may occur secondary to hypoalbuminemia
Signs of hyperlipidaemia such as xanthelasma (yellow plaques over the eyelids)
Signs of pleural effusion e.g. dull bases to percussion with decreased air entry
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Differentials for nephrotic syndrome?
Heart failure
Cirrhosis
CKD
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Investigations to diagnose nephrotic syndrome?
Urine dip
Urine PCR
Baseline bloods
CXR
USS KUB
Renal biopsy
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Management of nephrotic syndrome?
Conservative:
Restrict salt intake to <2g/day
Fluid restriction to <1.5L/day
Weight should be monitored, with a target of 1-2 kg weight loss per day until the patient reaches their predicted "dry weight" (i.e. weight when not oedematous)
Dietary changes (e.g. avoiding a high protein diet, limiting fat intake) may be advised and dietician input may be indicated
Mechanical thromboprophylaxis (TEDS) to reduce risk of venous thromboembolism
Medical;
Corticosteroids, ciclosporin, cyclophosphamide, mycophenolate mofetil or rituximab
Diuretics
Statin
Renal replacement therapy
116
Complications of nephrotic syndrome?
Increased risk of infection
VTE
Hyperlipidaemia
AKI
CKD
Medication side effects
Hypothyroidism
Vit D deficiency
Anaemia
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Prognosis of nephrotic syndrome?
Prognosis varies between subtypes, for example minimal change disease rarely progresses to end-stage renal failure (1% of cases), whereas 50% of patients with FSGS will do over 5-10 years.
Mortality has been greatly reduced with the use of steroids and immunosuppression.
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What is pyelonephritis?
Infection of renal pelvis and parenchyma typically caused by bacteria due to ascending lower UTI
119
Risk factors for pyelonephritis?
Pregnancy
Immunosuppression or immunocompromise (e.g. diabetes, long-term steroid use)
Structural abnormalities affecting urinary flow (e.g. neuropathic bladder, obstruction due to benign prostatic hyperplasia)
Structural renal abnormalities such as polycystic kidney disease or horseshoe kidney
Vescio-ureteric reflux
Catheterisation or other indwelling foreign bodies (e.g. ureteric stents, nephrostomies)
Renal stones
Extremes of age (infancy and elderly patients)
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Epidemiology of pyelonephritis?
1 in 830 people
Women are 6 times more affected than man
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Aetiology of pyelonephritis?
Gram negative bacteria; E.coli
Klebsiella, proteus mirabilis, pseudomonas, enterobacter
Gram positive species
Fungal; candida albicans, aspergillosis
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Symptoms of pyelonephritis?
Fevers
Flank pain (usually unilateral)
Nausea and vomiting
Myalgia
Lethargy
Anorexia
Lower urinary tract symptoms: Urinary frequency, Urgency, Dysuria
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Signs of pyelonephritis?
Renal angle tenderness
Haematuria
Suprapubic tenderness (without guarding)
Rigors
Sweating
Signs of dehydration (e.g. dry mucous membranes, tachycardia, cool peripheries)
Signs of sepsis (e.g. hypotension, tachypnoea, impaired level of consciousness)
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Differentials for pyelonephritis?
Lower UTI
Bowel obstruction
PID
Shingles
Ruptured abdominal aortic aneurysm
125
Investigations to diagnose pyelonephritis?
Urine dipstick
Urine culture
Pregnancy test
Blood gas
Bloods; FBC, U+E, CRP, Coagulation screen, blood cultures
Renal USS
Non contrast CT KUB
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Management of pyelonephritis?
Uncomplicated pyelonephritis in low-risk patients may be treated in the community with oral antibiotics
Patients should be safety netted to seek medical help e.g. if becoming more unwell, not improving within 48 hours of taking antibiotics
Indications to refer a patient to hospital include:
Signs of sepsis
Significant dehydration
Unable to take oral fluids and medications due to vomiting
Pregnancy
High risk of complications due to immunosuppression or underlying urinary tract disease
Renal impairment (either acute or chronic)
Recurrent pyelonephritis
Not responding to oral antibiotics
Oral cephalexin for 7-10 days is first-line in the community
IV options include ceftriaxone, ciprofloxacin or co-amoxiclav
Oral trimethoprim or ciprofloxacin may be used if penicillin allergy
Antibiotic choice should be targeted once urine culture and sensitivity results are available
IV fluids
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Complications of pyelonephritis?
Pyonephritis
Pyonephrosis
Perinephric abscess
Sepsis
Renal scarring
Emphysematous pyelonephritis
Renal abscess
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Prognosis of pyelonephritits?
The majority of patients respond to antibiotics and recover completely within a few weeks
Patients at higher risk of complications include the elderly, patients immunosuppressed e.g. due to diabetes, those with urinary tract abnormalities or obstruction
Preterm labour is a risk of pyelonephritis in pregnant women
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What is rapidly progressive glomerulonephritis?
Acute and severe development of renal impairment with cresents and vascular lesions seen on biopsy
"Crescents" refer to proliferation of epithelial cells in Bowman's space which occur due to injury of the glomerular capillary wall causing rupture of the glomerular basement membrane
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Epidemiology of rapidly progressive glomerulonephritis?
2 per million
More common in 4th and 7th decade of life
More common in white ethnicity
The most common subtype is pauci-immune complex glomerulonephritis (commonly ANCA-associated)
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Types of rapidly progressive glomerulonephritis?
Type I - Anti-Glomerular Basement Membrane (GBM) disease;
Linear staining on immunofluorescence of IgG deposits along the basement membrane
Patients may have a pulmonary-renal syndrome due to anti-GBM antibodies targeting the alveolar basement membrane, causing pulmonary haemorrhage
Type I is the most aggressive form of RPGN
Type II - Immune complex disease;
Granular staining on immunofluorescence due to immune complex deposition
Causes include:
Post-streptococcal glomerulonephritis
Lupus nephritis
IgA nephropathy
Henoch-Schonlein purpura
Cryoglobulinaemia
Membranoproliferative glomerulonephritis (MPGN)
Type III - Pauci-immune disease;
No (or scanty) staining of immunoglobulin or complement deposition
Majority are ANCA-associated:
Granulomatosis with Polyangiitis (GPA)
Microscopic Polyangiitis (MPA)
Eosinophilic Granulomatosis with Polyangiitis (EGPA)
Approximately 15% are ANCA negative
May be medication induced (e.g. rifampicin, hydralazine, penicillamine)
Type III is the most common form of RPGN
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Presentation of rapidly progressive glomerulonephritis?
Oliguria
Haematuria (may be macroscopic or microscopic)
Frothy urine due to proteinuria
Peripheral oedema
Hypertension
Fatigue
Anorexia
Nausea and vomiting
Fevers
Night sweats
Weight loss
Mucosal ulceration (e.g. systemic lupus erythematosus)
Shortness of breath, haemoptysis (e.g. anti-GBM disease, GPA, MPA)
Sinusitis, necrosis of nasal cartilage (e.g. GPA)
Abdominal pain (e.g. EGPA, MPA)
Purpuric rashes or ulceration (e.g. cryoglobulinaemia)
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Differentials for rapidly progressive glomerulonephritis?
Prerenal AKI
Acute tubular necrosis
Acute interstitial nephritis
Post renal AKI
Thrombotic microangiopathy
134
Investigations to diagnose rapidly progressive glomerulonephritis?
Urine dip
Urine microscopy
Urine protein; creatinine ratio
Blood gas
Bloods; FBC, U+E, LFT, CRP, ESR, coagulation, antibodies, viral serology
Renal USS, CXR
Renal biopsy - definitive diagnostic test
Widespread crescents in >50% of glomeruli, immunofluoresence confirms type
Parietal epithelial cells that form the cellular crescents may transform to become fibrocellular and fibrous crescents - these are irreversible (cellular crescents may recover)
135
Management of rapidly progressive glomerulonephritis?
Discontinue causative medication, salt and fluid restriction
Immunosuppression, corticosteroids, rituximab
Plasmapheresis
Renal replacement therapy
136
Complications of rapidly progressive glomerulonephritis?
Renal failure
Hypertension
Hyperkalaemia
Peripheral/ pulmonary oedema
Complications of immunosuppression
137
Prognosis of rapidly progressive glomerulonephritis?
Mortality rate of 80% in pauci-immune RPGN
Aggressive immunosuppression improves survival to 75% at 5 years
Approximately 25% of patients progress to end-stage renal failure
Poor prognostic factors include more severe renal failure at presentation, requiring dialysis at presentation, older age and pulmonary haemorrhage
Relapse in 40 % of patients
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What is haemodialysis?
Haemodialysis refers to the process of filtering blood across a semipermeable membrane
Water is removed from the patient's plasma via ultrafiltration (how much is removed is calculated for individual patients based on their dry weight)
Solutes are drawn across the membrane also down a diffusion gradient
This removes toxins such as urea, normalises electrolyte levels and corrects acidosis
The majority of patients attend a dialysis centre to receive haemodialysis, usually 3 days a week for around 4 hours per session
In some cases, patients will do haemodialysis at home
Patients need a form of vascular access that can provide a flow rate of at least 200 ml/min of blood, which will be one of the following:
An arteriovenous (AV) fistula
An artery and vein are joined surgically, usually the radial artery and cephalic vein
This increases the flow rate of blood as capillaries are bypassed
An AV fistula needs to be created at least 4-8 weeks prior to use to give it time to mature
During dialysis, blood is removed and returned via two needles inserted into the venous side of the fistula
An arteriovenous graft
An alternative when creating an AV fistula is difficult anatomically or in arterial disease
A synthetic or natural graft is used to join an artery and vein
This is more likely to clot or stenose than an AV fistula
Tunnelled vascular catheters
Usually inserted into the internal jugular vein
Wider bore access than a normal central line
Tunnelling under the skin reduces infection risk
May be used temporarily whilst an AV fistula matures or if a fistula or graft has failed
Can also provide semipermanent access if a fistula or graft are not suitable
Non-tunnelled vascular catheters
Temporary access only so often used in emergencies
Internal jugular catheters may stay in for 2-3 weeks
Femoral lines need removal within a week due to a higher risk of infection
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What is peritoneal dialysis?
Peritoneal dialysis involves using the patient's own peritoneal membrane for filtration
A peritoneal catheter is placed through which dialysate fluid is introduced into the abdominal cavity
The fluid is then left for 1-4 hours in the abdomen whilst toxins and excess fluid diffuse into the dialysate fluid
The fluid is then drained out via the peritoneal catheter and discarded
Each cycle of this is called an "exchange"
The major benefit of peritoneal dialysis is that it can be carried out at home without having to regularly attend a dialysis centre
There are two main ways of carrying out peritoneal dialysis:
Continuous Ambulatory Peritoneal Dialysis (CAPD) involves dialysate remaining in the peritoneal cavity continuously
Patients undergo 3-5 exchanges per day
Automated Peritoneal Dialysis (APD) involves a machine performing exchanges overnight
Dialysate may be drained or can stay in the peritoneal cavity during the day to maximise effectiveness
Some people on APD also need to do a CAPD exchange once per day
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Indications to start dialysis?
eGFR of 5-7 ml/min/1.73m2
Symptoms of uraemia (e.g. malaise, nausea, pruritus)
Fluid overload refractory to medical treatment
Resistant hyperkalaemia
Resistant acidosis
141
Complications of haemodialysis?
Hypotension
Muscle cramps
Arrhythmia
Dialysis disequilibrium syndrome refers to acute cerebral oedema due to rapid extraction of osmotically active substances
AV fistula complications; bleeding, aneurysm, ischaemic steal syndrome, thrombosis, stenosis, high output heart failure, air embolism, increased risk of infection, infective endocarditis, heparin induced thrombocytopenia , vascular calcification, malnutrition, psychological impacts
142
Complications of peritoneal dialysis?
Peritoneal dialysis
Sclerosis encapsulating peritonitis
Local infection
Peri-catheter leaks
Catheter obstruction/ compression
Volume overload
Hyperglycaemia
Hernia
Back pain
Weight gain
Back pain
Malnutrition
Psychosocial impact
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