Glomerulonephritis

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Slide 1 : Glomerulonephritis most important group of generalised parenchymal diseases classification is difficult - a mix of clinical and pathological descriptions clinical features morphology (eg various histology patterns) pathogenetic mechanisms (eg anti gbm disease) aetiology can be primary or secondary
Slide 2 : Major Clinical Manifestations of Glomerular Diseases Acute nephritic syndrome The nephrotic syndrome Persistent urinary abnormalities with few or no symptoms Chronic glomerulonephritis
Slide 3 : Characteristics of common glomerular diseases at presentation
Slide 4 : Outcome of Glomerulonephritis
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Slide 7 : Acute Nephritic Syndrome Syndrome characterised in typical cases by: haematuria oliguria oedema hypertension reduced GFR proteinuria fluid overload
Slide 8 : Clinical Features of the Acute Nephritic Syndrome haematuria is usually macroscopic with pink or brown urine (like coca cola) oliguria may be overlooked or absent in milder cases oedema is usually mild and is often just peri-orbital- weight gain may be detected hypertension common and associated with raised urea and creatinine proteinuria is variable but usually less than in the nephrotic syndrome
Slide 9 : Aetiology of the Nephritic Syndrome Most common cause is acute post infectious glomerulonephritis group A beta haemolytic streptococci of certain serotypes important in NZ IgA disease and Henoch-Schonlein purpura, crescentic glomerulonephritis and SLE can also present in this way
Slide 10 : Management issues in the nephritic syndrome Appropriate investigations: skin and throat swabs,strep serology, complement, urea, creatinine electrolytes, urinalysis and CXR BP, urine output and daily weight fluid and diet management treat hypertension and fluid overload treat infection
Slide 11 : Complications of the Nephritic Syndrome Hypertensive encephalopathy (seizures, coma) Heart Failure (pulmonary oedema) Uraemia requiring dialysis
Slide 12 : Prognosis in the Nephritic Syndrome More than 95% of children make a complete recovery Chronic renal impairment in the longer term is uncommon in children Bad prognostic features include severe renal impairment at presentation and continuing heavy proteinuria and hypertension Adults more likely to have long term sequellae than children
Slide 13 : The Nephrotic Syndrome Is not a disease but a group of signs and symptoms seen in patients with heavy proteinuria presents with oedema proteinuria usually > 3.5g / 24hrs (>0.05g / kg / 24hrs in children) serum albumin < 30g/l other features: hyperlipidaemia, and hypercoaguable state
Slide 14 : Pathophysiology proteinuria: due to an increase in glomerular permeability hypoalbuminuria: occurs when liver synthesis cannot keep up with urine losses oedema mechanism is complex and still in dispute: primary salt and water retention associated with reduced renal function as well as reduced plasma oncotic pressure are primary factors (overfill and underfill) minimal change disease fits the underfill theory best hyperlipidaemia: increased liver synthesis hypercoagulation: increased fibrinogen and loss of antithrombin III
Slide 15 : Nephrotic syndrome biopsy histology in adults at different ages
Slide 16 : Primary glomerular diseases commonly causing the nephrotic syndrome minimal change disease focal and segmental glomerulosclerosis membranous glomerulonephritis proliferative glomerulonephritis (various histology and less common cause) membranoproliferative (mesangiocapillary) focal proliferative diffuse proliferative mesangial proliferative
Slide 17 : Other causes of the nephrotic syndrome 1 Systemic diseases diabetes mellitus amyloidosis SLE and other connective tissue diseases HIV/Aids nephrotoxins nsaids mercury poisoning penicillamine gold salts
Slide 18 : Other causes of the nephrotic syndrome 2 Allergies bee sting pollens poison ivy Circulatory effects congestive cardiac failure constrictive pericarditis renal vein thrombosis (cause or result?) Neoplastic leukaemia solid tumours
Slide 19 : Management of the nephrotic syndrome Na+< 60 mmol/24 hrs water restriction diuretics (if not volume depleted) reduced protein diet (controversial) treat infections prophylaxis for thrombosis specific therapy corticosteroids immunosuppression
Slide 20 : Specific treatments Minimal change disease prednisone for 16 weeks (p) prednisone and cyclophosphamide ( p+c) FSGS p, p+c, p+cyclosporine(cs) Membranous Ponticelli Regimen p+c
Slide 21 : Other Renal Diseases Interstitial Nephritis Diabetic Nephropathy Microscopic Vasculitis and SLE Gout and the Kidney Polycystic Kidney Disease Myeloma Kidney Alport Syndrome and Thin Membrane Disease Renal cases Illustrations and Photomicrographs with permission from Uptodate: www.uptodate.com
Slide 22 : Interstitial Nephritis A disorder of the interstitium and tubules
Slide 23 : Causes of interstitial nephritis Drugs Infection Autoimmune Metabolic Radiation Neoplastic infiltration Mechanical
Slide 24 : Drug Toxicity (i) hypersensitivity penicillins sulphonamides (cotrimoxazole) rifampicin thiazides frusemide omeprazole
Slide 25 : Drug toxicity (ii) direct toxicity aminoglycosides amphotericin B heavy metals (eg lead, mercury) analgesics (especially NSAIDS)
Slide 26 : Drugs and interstitial nephritis
Slide 27 : Bacterial infection bacterial infection of the renal parenchyma causes interstitial nephritis infection without anatomical abnormality seldom produces permanent damage obstruction (stones, prostate etc) in combination with infection can cause progressive disease tuberculosis causes extensive destruction from granulomata, fibrosis and caseation
Slide 28 : immunological metabolic systemic lupus erythematosus transplant rejection deposition of : calcium salts uric acid
Slide 29 : Infiltration in neoplastic and other diseases lymphoma and leukaemias myeloma Bence-Jones protein (light chains from malignant plasma cell clone) causes interstitial nephritis, tubular obstruction(cast nephropathy) and amyloid deposition called myeloma kidney sarcoidosis
Slide 30 : mechanical causes of interstitial nephritis reflux nephropathy calculi ureteric fibrosis prostatic hypertrophy urethral stenosis tumours
Slide 31 : pathophysiolgical changes in interstitial nephritis hypertension (50%) proteinuria (~1-2 g/24hrs) reduced urinary concentrating ability salt wasting renal tubular acidosis
Slide 32 : Diagnosis and Treatment renal impairment “inactive” urine sediment common (cf nephritis) eosinophils in urine and interstitium in acute hypersensitivity reactions renal biopsy improvement after withdrawal of drugs and toxins use of corticosteroids (prednisone) water and and electrolyte treatment of hypertension
Slide 33 : Primary Renal Disease Leading to Dialysis in NZ (ANZ DATA 2002) diabetes mellitus (mostly niddm) 45% glomerulonephritis 23% hypertension 9% polycystic kidney disease 4% reflux nephropathy 4 % miscellaneous 11% includes interstitial nephritis,medullary cystic disease,congenital diseases,calculi,analgesic nephropathy uncertain diagnosis 4%
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Slide 35 : Diabetic Nephropathy Pathological lesions: diffuse glomerular sclerosis nodular sclerosis (Kimmelstiel -Wilson lesion) arteriolar hyalinisation Associated lesions: Papillary necrosis Pyelonephritis Bladder dysfunction Radio contrast renal failure hyporeninaemic hypoaldosteronism with hyperkalaemia
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Slide 39 : Pathophysiology of Diabetic Nephropathy renal hypertrophy and hyperfiltration microalbuminuria (< 100mg/24hrs and negative to protein test strip-albustix) hypertension hyperfiltration and microalbuminuria can be improved by good diabetic control microalbuminuria is a predictor of diabetic nephropathy and mortality in diabetics - it probably has no predictive value for other renal diseases
Slide 40 : Incidence and Time Course of Diabetic Nephropathy IDDM nephropathy affects about 1/2 of patients after 25 years unusual to get disease in less than 10 years nephropathy almost always associated with retinopathy and other complications proteinuria (> 0.5g/24hrs) leads to renal failure in a mean of 5yrs NIDDM some early onset NIDDM seems to lead to overt nephropathy quicker than IDDM end stage renal disease more common in Maori and Pacific peoples than in Europeans
Slide 41 : Prevention of Renal Failure strict diabetic control from time of diagnosis helpful strict diabetic control after onset of proteinuria does not seem to alter outcome of renal disease meticulous blood pressure control (<120/80) alters rate of decline of renal function ACEi and angiotensin II receptor blockers (AT II RB) have an additional role over and above control of hypertension ACEi & AT II RB have not so far been shown to have a beneficial effect in slowing the decline in renal function in NIDDM but do improve mortality
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Slide 43 : Dialysis for Diabetics survival on dialysis less than non diabetics problems with vascular disease and infection correction of renal failure does not halt progression of other complications myocardial infarction, stroke, blindness, gastroparesis and amputation and soft tissue infection (associated with peripheral neuropathy and peripheral vascular disease) are common hospital costs are an increasing problem some diabetics do very well on dialysis and with transplantation about 5 simultaneous kidney pancreas transplants done in Auckland each year
Slide 44 : Systemic Lupus Erythematosus Diagnosis: clinical presentation - rash, arthralgia, fever, tiredness, anaemia etc hypocomplementaemia - (low C3 and C4) antinuclear antibodies and anti DNA antibodies Treatment: depends on histological severity (WHO class I - V) nearly all get corticosteroids WHO Class IV usually get corticosteroids and cyclophosphamide
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Slide 52 : Systemic Vasculitis refers to classical polyarteritis nodosa, microscopic polyarteritis, Wegener’s granulomatosis, Henoch Schonlein purpura, Churg Strauss vasculitis and some cases of rheumatoid arthritis pauci immune rapidly progressive glomerulonephritis is common presentation - sometimes with lung haemorrhage (not classical Goodpasture’s syndrome) diagnosis has been made easier by anti neutrophil cytoplasmic antibody (ANCA) tests
Slide 53 : ANCA +ve Vasculitis (usually a microscopic polyangiitis) recent identification of the association between antibodies to components of neutrophil cytoplasm and microscopic polyangiitis. PR3 and MPO most common antigens and specific elisa assays for these antigens Wegener’s granulomatosis, microscopic polyarteritis and pulmonary- renal syndrome are the most common clinical syndromes usually respond to prednisone and cyclophosphamide
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Slide 59 : Gout, Uric Acid and Renal Disease uric acid calculi, parenchymal deposits of uric acid and tubular obstruction with urate can cause renal damage an elevated plasma uric acid does not in itself seem to cause renal damage 1/4 of patients with gout get uric acid stones 1/4 of patients with uric acid stones will have gout
Slide 60 : Acute and Chronic urate nephropathy acute nephropathy with overproduction of uric acid and kidney obstruction with uric acid crystals can occur with treatment of malignant disease with cytotoxics, heat stroke and status epilepticus treat with fluids and prophylaxis with allopurinol role of uric acid in chronic renal failure disputed but does occur with some familial disorders association between hyperuricaemia, hypertension vascular disease, hyperlipidaemia and diabetes
Slide 61 : Autosomal Dominant Polycystic Kidney Disease (ADPKD) accounts for 7-10% of people on dialysis 50% of sufferers have renal failure by age 60 cysts may occur in liver and pancreas but do not usually give problems 5-10% have saccular cerebral aneurysms a family history of subarachnoid haemorrhage justifies MRA or CT angio common complications include hypertension, pyelonephritis, abdominal pain,haematuria and renal stones
Slide 62 : Pathophysiology and genetics dominant inheritance often obvious from family tree but new mutations do occur mutations of at least 2 genes : PKD-1 on Chr 16 and PKD-2 on Chr 4 abnormal gene products are polycystin 1 and 2 which seem to be involved in cellular signaling cyst cells immature and proliferate and secrete fluid. about 1-2% of nephrons are involved most cases diagnosed by ultrasound
Slide 63 : Treatment of ADPKD No specific treatment Diligent blood pressure control slows decline of renal function ACEi and ATIIRB have no advantages over other agents Extended treatment of UTI necessary Cyst aspiration does not improve kidney function
Slide 64 : Hereditary Nephritis:Alport Syndrome and Thin Membrane Disease Alports syndrome is a disease of collagen type IV that effects the basement membrane of the glomerular capillary as well as causing nerve deafness, eye problems and platelet defects. Phenotype can be quite variable Mutation in COL4A5 gene with X linked 85%, autosomal dominant and recessive forms clinical features of micro haematuria, hypertension proteinuria and renal failure Thin membrane disease another mutation in the same group of genes
Slide 65 : Amyloidosis and Myeloma Kidney amyloid represents a family of proteins which polymerize to produce the beta pleated sheet of amyloid and deposit in tissues AL amyloid (primary amyloid) made from light chains associated with plasma cell disorders, mostly overt myeloma AA amyloid (secondary amyloid) is made from A protein and is an acute phase reactant associated with chronic inflammatory diseases like rheumatoid arthritis and bronchiectasis
Slide 66 : Amyloidosis and myeloma kidney a number of other proteins and familial protein mutations can lead to amyloid a range of clinical presentations with renal, heart, neurological, local deposition and other problems renal failure and nephrotic range proteinuria the most common renal presentation Bence Jones proteinuria (light chains) common in AL amyloid and can cause renal damage. Related renal disorders include light chain deposit disease, cast nephropathy, fibrillary GN and immunotactoid GN
Slide 67 : Renal Quiz 5th year renal organ system 2005
Slide 68 : Renal Quiz 1 a 47 year old male patient presents with renal failure and a serum creatinine of 0.4mmol/l (Ccr 20 ml/min) he has also had an episode of severe haemoptysis but CXR does not suggest tumour or parenchymal lung disease - haemoglobin 88g/l his urine contains 400 rbc/cumm and is 3+ positive on dip stick for protein the kidneys are of normal size and slightly echogenic what are the two most likely diagnoses ?
Slide 69 : Answer Q1 ANCA positive vasculitis (pulmonary renal syndrome) 2. Goodpastures Syndrome (anti gbm antibody disease) (see next two slides)
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Slide 72 : Renal Quiz 3 A 40 year old woman is found to have a serum creatinine of 0.2mmol/l. You want to give her a drug which is excreted by the kidney and you have a table of dose reduction for renal failure which requires you to estimate her creatinine clearance. She has a body mass index of 24 and weighs 50 kg Show the figures you would use in the Cockcroft and Gault estimation of Ccr (mls/min)
Slide 73 : Cockcroft and Gault Estimate of GFR Ccr = (140-age) x Wgt (lean body mass) Scr mmol/l x 815 = (140-40) x 50 0.2 x 815 = 30 ml/min correct for female sex (x 0.85) = 25.5ml/min
Slide 74 : Renal Quiz 4 The same woman does a 24 hour urine which contains 7.34 mmol of creatinine / 24hrs. Her serum creatinine is still 0.2 mmol/l Show the figures you would use to calculate the creatinine clearance
Slide 75 : Ccr formula for question 4 Ccr = 7.34 / 0.2 = litre/24hrs = 7.34/0.2 x 1000/60 x 24 = ml/min = 25.5 ml/sec
Slide 76 : Renal Quiz 5 A 40 year old male is found to have proteinuria of 3.5g /24 hrs he is not diabetic and has no other findings. He feels in good health apart from a little oedema at the end of the day. Serum albumin 32g/l. Estimated Ccr 90ml/min The urine microscopy shows no red or white cells and no bacteria On renal biopsy what are the 3 most likely diagnoses?
Slide 77 : Characteristics of common glomerular diseases at presentation
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Slide 81 : Renal Quiz 6 Name three kinds of renal bone disease
Slide 82 : renal bone disease osteitis fibrosa cystica (PTH effect) osteomalacia (calcitriol deficiency) adynamic aluminium bone disease
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Slide 85 : Renal Quiz Case 7 A 32 year old male visits his family doctor because of tiredness. He has a blood pressure of 123 / 70 , normal pulse and JVP Routine blood tests show a potassium of 2.8 mmol/l,with renal function tests, haematology and other electrolytes normal How would you approach the diagnosis of this problem?
Slide 86 : Causes Of Hypokalaemia inadequate intake extra renal losses (vomiting and diarrhoea) diuretics hypokalaemia with hypertension renovascular primary hyperaldosteronism malignant hypertension licorice hypokalaemia with normal blood pressure Bartter’s syndrome Gitelman’s syndrome distal renal tubular acidosis hypokalaemia due to potassium shifts periodic paralysis
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Slide 88 : Renal Quiz Case 8 A 58 year old male patient has a variety of medical problems including ischaemic heart disease, hypertension, gout, dyslipidaemia and reflux. His therapy includes: atenolol, simvastatin, allopurinol, cilazepril, bendrofluazide and ranitidine. His GP does regular biochemical tests and finds that the serum creatinine has been rising over the last 2 months from 0.12mmol/l to 0.24mmol/l what would you do next?
Slide 89 : Case 8 continued Examination findings: BP140/80, weight unchanged, JVP normal at +2cms, no oedema, no renal bruits, no renal pain or bladder symptoms. Renal U/S normal except for minor increase in parenchymal echogenicity MSU: trace protein, 5 WBC, 2 RBC & no growth on culture
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Slide 92 : Case 9 Renal Quiz A 24 year old male went to a night club and stayed out late drinking. The next morning he did not feel well but took part in a half marathon which he completed in 1hr 24 minutes That evening he had severe pains in his legs and arms and he felt completely exhausted. He noted that his urine was dark brown 2 days later he felt very nauseated and saw his own doctor who noted tender muscles and a normal JVP and blood pressure Creatinine was 0.37 mmol/l. What next?
Slide 93 : Case 9 continued MSU: protein +1, RBC 50, WBC 40, casts, no bacteria Creatine Kinase 30,000 iu (Troponin T normal) urine sodium 58mmol/l urine/plasma creatinine ratio 12 24 hour urine volume 1100mls Calcium 2.2mmol/l Renal biopsy?
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