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Outline the cause of glomerulonephritis
- Causes are related to proteinuria, hypertension and primary disease
- Extrinsic: Antibodies, immune complexes, complement, cytokines, leukocytes (made outwith kidneys)
- Intrinsic: Proteinuria, cytokines, growth factors
- Reduced glomerular function puts increased pressure on remaining glomeruli, accelerating renal failure
Describe the role of different cell types in glomerulonepgritis
- Mesangial cells: Hyperplasia = scarring (glomerulosclerosis) and capillary membrane permeability (leads to haematuria)
- Epithelial cells: Hyperplasia in bowman's capsule causes 'crescent' formation
- Blood endothelium: Ig or complex deposition = vasculitis = focal necrosis
- Tubulointerstitial: Tubular scarring
Outline the pathophysiology and clinical features of IgA nephropathy
- Commonest primary glomerular disease
- Abnormally glycosylated IgA deposits in the mesangium
- Mesangial cell proliferation = glomerulosclerosis and tubular scarring
- Haematuria, proteinuria, hypertension, renal impairment
Outline the pathophysiology of membranous glomerulonephritis
- Commonest cause of nephrotic syndrome in adults
- Immune complex deposition in GBM and mesangium (antigen may be in kidney or ciculation)
- Altered GBM charge affects permeability and activates mesangial cells (= tubule loss/glomerulosclerosis)
- Nephrotic syndrome, hypertension and renal impairement
What is the nephrotic syndrome?
- When kidney damage causes:
What is the nephritic syndrome?
- When kidney disorder causes:
- Haematuria (with RBC casts)
- Uremia with oligouremia
What is 'minimal change disease'
- Acute presentation, with a normal GFR but nephrotic syndrome and oedema
- No abnormalities found in light microscopy
- Ideopathic podocyte fusion occurs
Describe the RPGNs
- Rapidly progressing glomerulonephritides
- Group of conditions with common histology; crescent formation and acute severe damage
- Examples include Goodpastures, Wegener's
Outline the pathogenesis of Wegener's and Goodpastures
- Wegener's: Anti-neutrophil cytoplasm Ig - necrotising granulomas in midline and necrotising vasculitis
- Goodpasture's: Anti-GBM Ig = complex deposition, glomerular destruction and epithelial proliferation = all renal clinical features
What are the common clinical features of glomerulonephritis?
- Renal impairement
- Nephrotic syndrome
- Nephritic syndrome
What lab investiations are useful when diagnosing glomerulonephritis?
- Serum biochemistry: creatinine, albumin
- FBC: Anaemia, Hb
- Ig electro: Monoclonal antibodies (M band)
- Specific Ig: ANCA, RhF, ANA, anti-GBM
- Urine: Proteinuria, microscopy (RBCs)
- Imaging: CXR, renal US
Define 'acute kidney injury'
Decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatining
Outline the production of urea during AKI recovery
- Polyuric phase for 2-3 days (>6litres daily)
- 'Low quality' urine; tubules cannot concentrate
- Low K, Ca, Ma content
How can an underlying diagnosis be reached in known AKI?
- Bloods: Urea, creatinine, CK, LDH (just raised urea = dehydration)
- Clinical assessment of fluid status
- Renal US
- GN screen (including Bence-jones)
Outline the acute management of AKI
- Airway and breathing
- Circulation; assess for shock, hyperkalaemia, pulmondary oedema
- Remove cause, e.g. drugs/sepsis
- Exclude obstruction
- Consider a 'renal' cause; are pre-renal causes sufficient to account for patient's condition?
What is the function of insulin/dextrose therapy in AKI?
- Hyperkalaemia a result of kidney injury
- Insulin/dextrose therapy activates Na/K pumps
- Causes potassium uptake into cells
Outline the pathophysiology of 'salt losing' and 'salt retaining' CKD
- Salt losing: Tubule damage causes inability to concentrate and acidify urine, leading to excessive salt/H2O loss and dehydration/hypotension and acidosis
- Salt retaining: Glomerular damage causes loss of filtration, meaning salt and water retention and so hypertension/oedema
How should progressive CKD be managed?
- Treat underlying cause
- Treat hypertension (especially RAAS inhibition)
- Treat proteinuria (RAAS inhibition helps)
- Stay watchful for anaemia, acidosis, calcium/phosphate levels (EPO, vit D and sodium bicarbonate)
Outline some complications of haemo and peritoneal dialysis
- Haemo: Hypotension, hypoxia, air embolism, disequilibrium (sudden creatinine/urea loss), allergy
- Peritoneal: Fluid retention/overload, fibrosis, hypertension
What are the clinical features and investigations used in assessing chronic transplant rejection?
- CFs: Increased creatinine, tenderness, haematuria
- Investigations: U+Es, FBCs, US, Urinalysis, biopsy, Ig levels
Outline the structural changes which occur in diabetic nephropathy
- Hyperfiltration in early diabetes
- Mesangial cell hyperplasia (=glomerulosclerosis)
- Loss of podocytes
Outline the management of diabetic nephropathy
- Intensive plasma glucose control to reduce CV risk
- Hypertension control, especially with RAAS inhibitors
- RRT if ESRD occurs
- Transplantation only provides temporary improvement
What factors suggests that microalbuminuria is NOT related to diabetes?
- Duration of T1DM less than 10 yrs
- Previously had a documented normal Alb:creat ratio, but rapid proteinuria developed
- Significant haematuria present
- Systemic illness
- Acute GFR loss
What are the clinical features and investigations of renal artery stenosis?
- Hypertension, carotid/femoral bruits and proteinuria
- CTA, MRA, CO2 angiography, biopsy
How should renal artery stenosis be managed?
- Interventional radiology of severe (uncontrollable BP, pulmonary oedema)
- BP control (3 or more hypertensives)
- Risk factor control
Describe kidney cancer
- Also called 'clear cell carcinoma'
- An adenocarcinoma, arising from proximal convoluted tubule
- Commonly metastasises along veins to the IVC
What is the aetiology of kidney cancer?
- Polycystic kidney disease
- Horseshoe kidney
- Von-Hippel Lindau
Outline the common clinical features of kidney cancer
- Loin pain
- Mass felt
- Frank haematuria
- Paraneoplastic syndromes (hypercalcaemia, hypertension, polycythaemia)
How is kidney cancer investigated?
- Differentiate from spleen mass (ballotable, resonant, doesn't move on respiration)
- FBC, U&Es, LFTs
- CT and US
Outline the pathology of prostate cancer
- Slow growing
- Vast majority are primary adenocarcinoma, in peripherals
- Gleason grading and TNM classification
Outline the aetiology of prostate cancer
- Increasing age
- Genetics (hereditary prostate cancer 1)
- Ethnicity; black>white>others
- Hormones (androgen production)
How does prostate cancer commonly present?
- Many cases are asymptomatic
- Usually presents early
- Painful/slow micturation and retention
- Bone pain
How is suspected prostate cancer investigated?
- Raised PSA level; protease in semen/plasma. Tissue not tumour specific
- Trans-rectal US guided biopsy
What important pieces of information should a patient be told if they request a PSA level?
- Test may detect a curable cancer (in 5% of 50-65yo)
- Test may fail to detect some early tumours
- Teset may detect uncurable prostate cancer
- PSA testing and indicated treatment may incur risk while not improving life expectancy
- A biopsy may be required
What methods are used in the management of prostate cancer?
- Watchful waiting
- Active surveillance
- Radiotherapy (with/without LHRH analogue)
- Radical prostatectomy
What is the aetiology of bladder cancer?
- Increasing age
- Occupation (especially working with rubbers)
- Schistosomiasis (or other chronic infections)
Outline the pathology of bladder cancer
- Transitional cell carcinoma; transitional epithelium found in the urinary tract
- 75% are superficial, 25% are invasive
Outline the presentation, diagnosis and management of bladder cancer
- Frank haematuria/microscopic haematuria
- Flexible cytoscopy
- Endoscopic resection (if confined), trans-urethral resection, intravesical BCG immunotherapy, cystectomy/radiotherapy
What investigations are used when investigating suspected testicular cancer?
- Scrotal US/CT
- Alpha fetoprotein
- Beta hCG
Describe the pathgenesis of urinary calculi
- Precipitation occurs due to increased solute:solvent ratio
- Causes of formation include papilla formation, urinary obstruction or UTIs (increase urease production = ph change)
- Calcium oxalate (54%), calcium phosphate (30%), struvite/uric acid
How do urinary calculi present?
- Colicky pain, in loin or lateral abdomen
- Mimics: appendicitis, gallstones, diverticulitis and especially AAA
When does a urinary calculus become an emergency, and how is this managed?
- When calculus passes into ureter, obstructing fluid and leading to infection
- Causes fever, tachycardia, hypotensive/septic shock
- CT and US immediately given
- Renal drained via nephrostomy tube
What investigations are useful when diagnosing a suspected urinary calculus?
- History: Previous kidney stones, fluid intake, dietary change
- Examination: Obs and abdo exam
- Radiology: KUB, IV urography, US, CT KUB
- Bloods: For sepsis/inflammation
- Urinalysis: Dipstick for haematuria, cultures.
How can urinary calculi be managed, and what factors affect this?
- Treatment: Conservatively. Lithotripsy. Endoscopy. Open surgery/laparoscopy
- Factors: Size, site, symptoms, depth, density