Glomerulonephritis Flashcards
Definition
Glomerular injury, most often, not always inflammatory in nature. May involve all or part of glomerular apparatus.
Commonest causes of end stage renal
- Diabetes
- Hypertension
- GN
Etiology (8)
- Infections (group A beta-haemolytic Streptococcus, respiratory and GI infections, hepatitis B and C, endocarditis, HIV, toxaemia, syphilis, schistosomiasis, malaria, and leprosy)
- Systemic inflammatory conditions such as vasculitides (SLE, rheumatoid arthritis, and antiglomerulobasement disease, Wegener’s granulomatosis, microscopic polyarteritis nodosa, cryoglobulinaemia, Henoch-Schonlein purpura, scleroderma, and haemolytic uraemic syndrome)
- Drugs (penicillamine, gold sodium thiomalate, NSAIDs, captopril, heroin, mitomycin C, and ciclosporin)
- Metabolic disorders (diabetes mellitus, hypertension, thyroiditis)
- Malignancy (lung and colorectal cancer, melanoma, and Hodgkin’s lymphoma)
- Hereditary disorders (Fabry’s disease, Alport’s syndrome, thin basement membrane disease, and nail-patella syndrome)
- Deposition diseases (amyloidosis and light chain deposition disease).
- Idiopathic
Primary GN->causes
Primary disease: the pathological glomerular injury is limited to the kidney and not part of a systemic disease manifestation. The injury may or may not be idiopathic. Any systemic symptoms are a result of renal injury.
Post-infectious GN
IgA nephropathy
Anti-glomerular basement membrane (anti-GBM) GN
Idiopathic crescentic GN
Focal segmental glomerulsclerosis
Rapidly progressive.
Secondary disease->causes
Secondary disease: renal pathology in this group is a result of systemic disease such as vasculitis, which also has other organ involvement.
SLE Henoch-Schonlein purpura Wegener's granulomatosis Microscopic polyangiitis Cryoglobulinaemia Thrombotic microangiopathies Deposition diseases (amyloidosis, light chain deposition disease) Malignancies (Hodgkin's lymphoma, lung and colorectal cancer).
Nephrotic diseases
Nephrotic syndrome (nephrotic-range proteinuria, hypoalbuminaemia, hyperlipidaemia, and oedema)
Deposition diseases
Minimal change disease (number 1 cause in children)
Focal and segmental glomerulosclerosis (second most common cause in children)
Membranous nephropathy
Membranoproliferative GN.
Neprhitic diseases
Nephritic syndrome (haematuria, sub-nephrotic-range proteinuria, and HTN)
IgA nephropathy Postinfectious GN Rapidly progressive GN Vasculitis Anti-GBM GN.
Risk factors
Strong
group A beta-haemolytic Streptococcus respiratory infections GI infections hepatitis B hepatitis C infective endocarditis HIV SLE systemic vasculitis Hodgkin's lymphoma lung cancer colorectal cancer non-Hodgkin's lymphoma leukaemia thymoma haemolytic uraemic syndrome drugs
Clinical presentation
haematuria (common) oedema (common) hypertension (common) oliguria (common) anorexia (common) nausea (common) malaise (common) weight loss (common) fever (common) skin rash (common) arthralgia (common) haemoptysis (common) abdominal pain (common) sore throat (common)
First investigations and interpretations
FBE->normocytic, normochronic
UEC-> +Cr
LFTs->may be + if cause hepatitis/HIV/medications
Albumin->low in nephrotic
24 urine protein
Lipids->hyperlipidemia in neprhotic
Kidney USS may be warranted in some instances
Management in mild
May need salt and water restriction Daily weight Monitor BP, fluid input and output Phenoxymethylpenicillin Regular paracetamol if in pain
Management in moderate
moderate-severe disease Salt/water restriction Monitor BP ACE inhibitors and/or angiotensin-II receptor antagonists Phenoxymethylpenicillin Furosemide -->with nephrotic syndrome= prednisolone
Management with anti-GBM
Methylprednisilone
Cyclophosphamide
Electrophoresis
Phenoxymethylpenicillin
Management with immune complex
Methylprednisilone
Cyclophosphamide
Phenoxymethylpenicillin
Patient instructions
- Adhere strictly to diet and medication regimens to avoid long-term consequences
- Diet should be low in salt, water, and fat. Protein restriction, if advised, should be done cautiously to avoid malnutrition.
- Frequent follow-ups will be required to achieve aggressive BP goals and to monitor disease progression by protein in urine and renal functions (every 3-6 months, then less frequently)
Mechanism of Focal segmental glomerulosclerosis
Hyalinosis: amorphous plasma protein deposition--> obliterates capillary lumen \+injury of vessel wall--> focal glomerulosclerosis
Sclerosis: accumulation of collagen
seen +in diabetic nephroscleorsis
obliteraion of capillary lumen
Mechanism of BM thickening
+Protein synthesis
Deposition->immune complexes, amyloid
Progression of injury to glomerulosclerosis
Reduction in renal mass due to injury
- Systemic HTN->mesangial mass/ECcoagulation
- Glomerular hypertrophy->endothelial injury= + permeability to proteins, podocytes cant proliferate following injury->proteinuria.
