Nephrological Conditions Flashcards
What does the glomerular filtration barrier consist of?
- Endothelial cells of the glomerular capillaries
- Glomerular basement membrane (GBM)
- Podocytes - epithelial cells of bowmann’s capsule
What is Glomerulonephritis (GN) and RF (6) ?
- Term used to describe numerous conditions that involve:
- inflammation or damage to glomeruli
- presents with proteinuria, haematuria or both
- Diagnosed on renal biopsy
- Causes CKD
- Can progress to renal failure (Except minimal change disease)
RF
- Fx, HLA-DR7, children, younger adults, infection, autoimmunity
Pathophysiology of GN
(1. ) Inflammatory condition where immune-mediated damage varies according to GN type
(2. ) Staphy-GN shows deposits of IgA and C3
(3. ) Post-strepto, SLE, IgA nephropathy show antigens trapped within GBM
(4. ) These cause activation of inflamma pathways that causes proliferation & sclerosis of glomerular
(5. ) Damaged glomeruli causes: leaky, high BP, decline renal function, GBM breakdown
(6. ) This leads to the retention of uremic toxins –> progression to CKD & ESRD with their associated CDV
Classification of GN (4).
GN can be presented in 4 ways:
(1. ) Nephrotic Syndrome: proteinuria, oedema (due to podocyte pathology)
(2. ) Acute Nephritic Syndrome: Haematuria, HTN (due to inflammation damage). Most serious and potentially devastating
(3. ) Asymptomatic urinary abnormalities
(4. ) CKD
Presentation of GN
GN does not usually cause any noticeable Sx, found incidentally
Severe GN
- Haematuria
- Oedema/Fluid retention (nephrotic syndrome)
- Foamy urine
- High BP
- Haemoptysis
Ix of GN (6)
Assess damage and potential cause
(1. ) Blood + cultures
- Creatinine, FBC, U&E, LFT, CRP, Glucose, Lipid profile
(2. ) Immunological
- Autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM etc)
- Complements profile (C3, C4)
- Hepatitis screen
(3. ) Myeloma screen (Bence-Jones protein urine)
(4. ) Urinalysis: proteinuria, RBC casts
(5. ) Imaging
- KUB US: check kidney size, any blockages etc
- CXR
(6.) **Renal biopsy: Required for diagnosis***
Mx of GN
- Mild cases may not be treated
- Diet: less salt to reduce strain on kidneys
- Manage BP: ACEi
- Immunosuppression: If there are problems with immune system
- Refer to nephrologist
Complications of GN
- ESRF, CKD
- HTN
- High cholesterol
- Blood clots - DVT, PE
- Damage to other organs
Pathophysiology of Acute Nephritic Syndrome
- Inflammation that damages the GBM causing haematuria & RBC casts in urine
- This can lead to renal failure
Clinical features of Acute Nephritic Syndrome
- Haematuria
- Proteinuria (mild)
- Oliguria (Reduced U/O)
- Oedema
- HTN
- Uraemic Sx (anorexia, pruritus, lethargy, nausea).
- AKI i.e. rapid deteriorating renal function
Ix of Acute Nephritic Syndrome (5)
(1. ) Urinalysis
- Red cell cast is Dx of ANS*
- Can be used to rule out infections, WBC present? etc.
(2.) Blood: Presence of creatinine? indicates kidneys aren’t filtering
(3. ) Evidence of: HTN / fluid overload
- LVH: Can indicated fluid overload and HTN
- Crepitation in lungs
- raised JVP
- Fundoscopy: retina bleeding due to high BP
(4. ) Imaging: CT or US: can show a blockage or inflammation of the kidneys or urinary tract.
(5. ) Note: Renal biopsy is not always performed in ANS unless tx is failing of Dx is needed.
Aetiology of Acute Nephritic Syndrome (5.)
(1. ) IgA nephropathy (most common GN cause), type 3 hypersensitivity.
(2. ) Post-streptococcal GN
(3. ) Anti-GBM disease/Goodpastures disease
(4. ) ANCA associated vasculitis
(5. ) Multisystem systemic diseases e.g. SLE, systemic sclerosis
Mx of Acute Nephritic Syndrome
(1. ) Steriods, immunosuppressants
(2. ) If IgA GN: ACEi, ARBS (focus on reducing proteinuria by reducing BP)
(3. ) If strep GN: Abx
(4. ) If anti-GBM: plasma exchange to remove antibody
Pathophysiology of Nephrotic Syndrome
(1. ) Immune-mediated injury to podocytes, so proteins pass through tubule (proteinuria).
(2. ) Loss of proteins (hypoalbuminemia) means loss of oncotic pressure in vessels, so fluid remains in interstitial space (oedema).
(3. ) Antithrombin III proteins may also be lost, so pt’s acquire a hypercoagulable state (thrombosis risk).
(4. ) Immunoglobulin proteins are also lost so inc risk of infection
(5. ) Lipids are lost which gives urine ‘frothy, foamy’ and fatty casts.
Aetiology of Nephrotic Syndrome (primary and secondary causes)
Primary Causes i.e. Podocyte damage
- Minimal change disease
- Membranous nephropathy, glomerulonephritis
- Focal segmental glomerulonephritis
Secondary causes
- Diabetic neuropathy (most common)
- SLE
- Amyloid
- Infections
- Drugs - gold, penicillamine
- Malignancy
