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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.
Labels: health tips, disease condition

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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 check behind the
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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 conse
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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
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