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This document provides information on glomerulonephritis (GN), including its presentation, causes, types, investigations, management, and details on specific types like minimal change disease, focal segmental glomerulosclerosis, membranous GN, and rapidly progressive GN. GN is inflammation of the glomeruli that can cause nephrotic or nephritic syndrome. It has primary and secondary causes and is investigated via blood tests, urine tests, imaging and renal biopsy. Management involves treating the underlying cause, controlling blood pressure and cholesterol, and immunosuppression.
This document provides information on glomerulonephritis (GN), including its presentation, causes, types, investigations, management, and details on specific types like minimal change disease, focal segmental glomerulosclerosis, membranous GN, and rapidly progressive GN. GN is inflammation of the glomeruli that can cause nephrotic or nephritic syndrome. It has primary and secondary causes and is investigated via blood tests, urine tests, imaging and renal biopsy. Management involves treating the underlying cause, controlling blood pressure and cholesterol, and immunosuppression.
This document provides information on glomerulonephritis (GN), including its presentation, causes, types, investigations, management, and details on specific types like minimal change disease, focal segmental glomerulosclerosis, membranous GN, and rapidly progressive GN. GN is inflammation of the glomeruli that can cause nephrotic or nephritic syndrome. It has primary and secondary causes and is investigated via blood tests, urine tests, imaging and renal biopsy. Management involves treating the underlying cause, controlling blood pressure and cholesterol, and immunosuppression.
>10mmol/l) is often present 4. Oliguria Causes Primary Causes Secondary Causes Nephrotic Sydrome: Nephrotic Sydrome: Membranous nephropathy SLE(class V nephritis) Minimal Change Diabetes FSGS Amyloid Mesangiocapillary GN Hepatitis B/C
Nephritic Syndrome: Nephritic Syndrome:
IgA nephropathy Post-streptococcal Mesangiocapillary GN Vasculitis SLE Anti-GBM disease cryoglobulinemia Types
Minimal change nephropathy
Focal segmental glomerulosclerosis Membranous glomerulonephritis Mesangiocapillary glomerulonephritis IgA nephropathy Post-streptococcal glomerulonephritis Henoch-Schonlein Purpura Anti-glomerular basement membrane disease Rapidly Progressive GN Minimal Change Nephropathy Reversible effacement of podocytes foot processes Presents with proteinuria or nephrotic syndrome Treatment: remits with high dose corticosteroid therapy (1mg/kg prednisolone for 6 weeks) Some patients who respond incompletely or relapse frequently need maintenance corticosteroids, cytotoxic therapy or other agents Focal Segmental Glomerulosclerosis Can occur in all age groups Primary FSGS: cause unknown Present with massive proteinuria and nephrotic syndrome Sclerosis in segments of the glomeruli Secondary FSGS: Present with less proteinuria and sclerosis The focal scarring may reflect healing of previous focal glomerular injury such as HUS, cholesterol embolism or vasculitis. Other secondary causes-HIV, podocyte toxins and massive obesity. Treatment: high dose corticosteroid therapy(0.5-2mg/kg/day) but most patients show little or no response Immunosuppressive drugs e.g ciclosporin used but efficacy uncertain Progression to CKD is common in patients who don’t respond to steroids and the disease frequently recurs after renal transplantation Membranous Glomerulonephritis Most common cause of nephrotic syndrome in adults Caused by autoantibodies directed at antigens expressed on the surface of podocytes Biopsy: diffusely thickened GBM with IgG and C3 deposits in immunofluroscence 1/3 patients with idiopathic membranous glomerulonephritis undergo spontaneous remission, 1/3 remain in a nephrotic state and 1/3 go on to develop CKD Treatment: treat underling cause Give ACE-I and diuretics Short-term treatment with high dose corticosteroids and cyclophosphamide may improve the nephrotic syndrome and long term prognosis Mesangiocapillary Glomerulonephritis Two types: immune complex mediated and complement mediated Increase in mesangial cellularity with thickening of glomerular capillary walls and subendothelial deposition of immune complexes and complements Causes: hepatitis C, SLE, monoclonal gammopathy and abnormalities in complement pathway Presents with proteinuria and hematuria Biopsy: double contouring of the capillary walls(tram-tracks) and thickened capillary basement membrane Treatment: treat underlying cause. Give ACEI/ARB to all. Immunosuppression with steroids and cyclophosphamide if rapid progression of disease IgA Nephropathy One of the most common types of GN Presents with hematuria, hypertension and proteinuria In many cases there is slowly progressive loss of renal function leading to ESRD A particular hallmark in some individuals is acute self-limiting exacerbations, often with gross haematuria, in association with minor respiratory infections. There is increased IgA which forms immune complexes and deposits in mesangial cells IF shows IgA and C3 deposits and mesangial proliferation in renal biopsy The latency from clinical infection to nephritis is short Treatment: BP control with ACE-I Immunosuppressant may slow decline in renal function in those with nephritic presentation The management of less acute disease is largely directed towards the control of BP in an attempt to prevent or retard progressive renal disease Henoch-Schonlein Purpura Characterised by systemic vasculitis that often arises in response to an infectious trigger. Presents with purpuric rash on extensor surfaces(mostly legs), flitting polyarthritis, abdominal pain and nephritis GN is usually indicated by hematuria Diagnosis is confirmed with + IF for IgA and C3 in skin/renal biopsy Treatment: same as IgA nephropathy Prognosis is good with spontaneous resolution but some develop ESRD Systemic Lupus Erythematous 1/3 patients with SLE will have evidence of renal disease with vascular, glomerular and tubulointerstitial damage Requires early treatment Antiglomerular Basement Membrane Disease(Goodpasture’s disease) Caused by autoantibodies(IgG) to type IV collagen, an essential component of GBM. Type IV collagen is also found in lungs and pulmonary hemorrhage can occur especially in smokers. Present with hematuria/nephritic syndrome AKI may occur within days of onset of symptoms Treatment: plasma exchange, steroids and cytotoxics If started early, full recovery is possible and relapses are rare Case
20year old male presents with
hematuria and puffiness of face, eyes and trunk. On examination he was found to be hypertensive(170/100) with scrotal swelling. The patient gives a history of pyoderma 5 weeks ago. Post-streptococcal GN
More common in children than adults
Occurs 1-12 weeks after a sore throat or skin infection. A streptococcal antigen is deposited on the glomerulus, causing a host reaction and immune complex formation Molecular mimicry also occurs Presents as nephritic syndrome(↓ GFR, proteinuria, hematuria and oliguria) Treatment: improves spontaneously within 10-14days supportive (>95% patients renal function recovers)-fluid and salt restriction with hypotensive agents. Rapidly progressive glomerulonephritis Also known as crescentic glomerulonephritis Rapid loss of renal function over days to weeks. Most aggressive GN, potential to cause ESRD over days. Classified into 3 categories: 1. Immune complex disease e.g post-infections, SLE, IgA/HSP 2. Pauci-immune disease 3. Anti GBM disease e.g Goodpasture’s disease Clinical presentation: AKI with systemic features(fever, myalgia, weight loss, hemoptysis). Pulmonary hemorrahge is the commonest cause of death Renal biopsy shows crescentric lesions Treatment: aggressive immunesuppression with high dose IV steroids and cyclophosphamide + plasma exchange Investigations for GN Management