Skip to main content

Glomerulonephritis

  • Background

    Definition and classification

    • Inflammation of the glomeruli.
    • This page discusses primary glomerulonephritides, but glomerular disease can also be secondary to diabetes and multi-system autoimmune or infiltrative diseases.
    • Can be classified by whether they typically present with nephrotic syndrome – minimal change disease, membranous GN, membranoproliferative GN, FSGS – or haematuria/nephritic syndrome – IgA nephropathy, post-streptococcal GN, rapidly progressive GN. However, presentation is often non-specific and asymptomatic.

    Presentation

    • Can be an incidental finding in an asymptomatic individual e.g. with hypertension, proteinuria or haematuria on dipstick, abnormal renal function test, anaemia.
    • Symptomatic presentations include oedema (nephrotic syndrome), frank haematuria, or generally unwell (uraemia, anaemia).

    Management

    • See chronic kidney disease (CKD) and/or acute kidney injury (AKI) for general management of renal impairment. BP control (SBP <130) and ACEi/ARB therapy (esp. if proteinuric) is particularly important.
    • The sections below outline which types of GN may benefit from immunosuppression.
  • Minimal change disease

    Pathophysiology and epidemiology

    • Pathology: podocyte effacement seen on electron microscopy.
    • Commonest cause (90%) of nephrotic syndrome in children.
    • Causes: idiopathic, Hodgkin's lymphoma, NSAIDs, lithium.

    Management and prognosis

    • Usually responds to corticosteroids, especially in kids (90%). 2nd line cyclophosphamide or calcineurin inhibitors (tacrolimus, ciclosporin).
    • Although relapses are common, long-term prognosis is good.
  • Membranous glomerulonephritis

    Pathophysiology and epidemiology

    Diffuse thickening of glomerular basement membrane, due to:

    • Autoimmune reaction to phospholipase A2 receptor (PLA2R) or other podocyte autoantigens.
    • Cancer: lung, prostate, Hodgkin's.
    • Infection: HBV, HCV, TB, malaria.
    • Drugs: NSAIDs, anti-malarials, gold, penicillamine.
    • SLE

    Commoner in adults.

    Management and prognosis

    • Untreated, 50% self-resolve and 50% progress to end-stage kidney disease.
    • Given potential for resolution, only treat in severe nephrotic syndrome, with corticosteroids plus cyclophosphamide.
  • Membranoproliferative glomerulonephritis

    Aka mesangiocapillary glomerulonephritis.

    Pathophysiology and epidemiology

    • Mesangial proliferation (capillary smooth muscle cell proliferation) and thickened glomerular basement membrane.
    • Causes: idiopathic, SLE, HBV/HCV, monoclonal gammopathy, lymphoma.
    • Relatively uncommon. Usually occurs in children or young adults.

    Presentation and prognosis

    • Presents with nephrotic (50%) or nephritic (30%) syndrome, or sometimes just isolated protein- and haematuria.
    • 50% develop end-stage kidney disease in 10 years.
  • Focal and segmental glomerulosclerosis (FSGS)

    Pathophysiology

    • Accumulation of type 4 collagen (sclerosis) in parts (segmental) of some (focal) glomeruli.
    • Typically leads to nephrotic syndrome.
    • Causes: idiopathic, cancer, HIV, obesity.

    Management and prognosis

    • 50% respond to corticosteroids.
    • Further immunosuppression (ciclosporin, cyclophosphamide, MMF, or rituximab) may be beneficial in steroid-resistant FSGS, but many progress to end-stage kidney disease.
  • IgA nephropathy

    Aka Berger's disease.

    Pathophysiology and epidemiology

    • A type of mesangial proliferative nephritis, involving glomerular IgA deposition.
    • Commonest type of glomerulonephritis worldwide.
    • Henoch-Schonlein purpura is sometimes considered a systemic form, as it causes renal IgA deposition.

    Presentation

    • Around 50% present with visible haematuria in the days following an URTI, which is thought to trigger the disease. Flank pain may be present.
    • Remainder mostly present with incidental microscopic haematuria ± proteinuria.
    • Rarely, presents with nephrotic syndrome or rapidly progressive glomerulonephritis (RPGN).

    Management

    Corticosteroids for those with rapidly progressive disease, otherwise benefit is unclear.

  • Post-streptococcal glomerulonephritis

    • Typically 1-2 weeks after pharyngitis or (less commonly) impetigo.
    • Usually presents with haematuria or nephritic syndrome, but can also lead to rapidly progressive glomerulonephritis.

Comments

DISEASE CONDITIONS LIST THAT IMPROVED KNOWLEDGE.

Newborn Baby Assessment

Baby check at birth and 6 weeks  Check notes and get equipment ready:   Measuring tape. Ophthalmoscope Sats probe. In notes, look at full details of pregnancy and birth, including Apgar scores at 1 and 5 minutes. Observation: Colour: pink/red, pale, jaundiced. Any rash? Erythema toxicum is a self-limiting rash of red papules and vesicles, surrounded by red blotches which sometimes give a halo appearance. Usually occurs between 2 days and 2 weeks. Behaviour and mood. Movements. Face: dysmorphism? Head: Feel fontanelle (bulging? sunken?) and sutures. Note that posterior fontanelle closes at 1-2 months, and anterior at 7-19 months. Measure circumference at widest point; take the highest of 3 measurements. Looking for hydrocephalus and microcephaly. Eyes: check red reflex with ophthalmoscope. Feel inside top of mouth with little finger for cleft palate. Also gives you the sucking reflex. Inspect ears to see if they are low-set (below eye level), have any tags or lumps, and ch...

Hypertension (HTN)

Background     Causes Primary causes: Essential HTN (i.e. idiopathic). Commonest cause. Non-pathologically raised during pain or anxiety (including white coat HTN). However, this may suggest underlying problem so consider following up. Kidney diseases (80% of secondary HTN): Chronic kidney disease. Renal artery stenosis: due to atherosclerosis or fibromuscular dysplasia. Latter most commonly occurs in young women, but even then essential HTN is still commoner. Endocrine: Conn's Cushing's Pheochromocytoma Acromegaly Hyperparathyroidism Other: Obstructive sleep apnoea Pregnancy or pre-eclampsia. Coarctation of the aorta. Medication: CE-LESS ('see less'): C yclosporin E strogen (OCP) L iquorice E PO S teroids S ympathomimetics: α-agonists, dopamine agonists, cocaine, amphetamines, and nasal decongestants such as ephedrine. Signs and symptoms Symptoms of HTN itself are rare, and occur only in severe disease. They include heada...

immunization schedule

Infant immunisations  2 months 5-in-1 DTaP/IPV/Hib – diptheria, tetanus, pertussis, polio, Hib – dose 1. Pneumococcal conjugate vaccine (PCV) dose 1. Rotavirus dose 1. Live, oral virus. MenB dose 1. 3 months 5-in-1 dose 2. MenC dose 1. Rotavirus dose 2. 4 months 5-in-1 dose 3. PCV dose 2. MenB dose 2. 12 months MMR dose 1. MenC dose 2 + Hib dose 4 (combined). MenB dose 3. PCV dose 3. Hepatitis B if they have risk factors. Toddler immunisations Flu vaccine Annual, live attenuated nasal spray flu vaccine in September/October at age 2-7. Kids with asthma and other chronic diseases like CF will continue to get this through childhood and beyond. Contraindicated in severe egg allergy, immunosuppression (inc. steroids in past 2 weeks), and severe asthma or active wheeze. Alternative form can be given. Postpone in those with heavy nasal congestion. 3.5 years 4-in-1 DTaP/IPV: dip, tet, pertussis, polio pre-school boost. MMR dose 2. Teenager immunisations 12 years HPV: Girls only. Parental c...