My Nephrology

• 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

• 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

• Commonest primary glomerular disease
• Abnormally glycosylated IgA deposits in the mesangium
• Mesangial cell proliferation = glomerulosclerosis and tubular scarring
• Haematuria, proteinuria, hypertension, renal impairment

• 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

• When kidney damage causes:
• Proteinuria
• Hypoalbuminaemia
• Hyperlipidaemia
• Oedema

• When kidney disorder causes:
• Haematuria (with RBC casts)
• Proteinuria
• Hypertension
• Uremia with oligouremia

• Acute presentation, with a normal GFR but nephrotic syndrome and oedema
• No abnormalities found in light microscopy
• Ideopathic podocyte fusion occurs

• Rapidly progressing glomerulonephritides
• Group of conditions with common histology; crescent formation and acute severe damage
• Examples include Goodpastures, Wegener's

• 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

• Hypertension
• Haematuria
• Renal impairement
• Nephrotic syndrome
• Nephritic syndrome

• 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

Decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatining

• Polyuric phase for 2-3 days (>6litres daily)
• 'Low quality' urine; tubules cannot concentrate
• Low K, Ca, Ma content

• Bloods: Urea, creatinine, CK, LDH (just raised urea = dehydration)
• Clinical assessment of fluid status
• Urinalysis
• Renal US
• GN screen (including Bence-jones)

• 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?

• Hyperkalaemia a result of kidney injury
• Insulin/dextrose therapy activates Na/K pumps
• Causes potassium uptake into cells

• 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

• 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)

• Haemo: Hypotension, hypoxia, air embolism, disequilibrium (sudden creatinine/urea loss), allergy
• Peritoneal: Fluid retention/overload, fibrosis, hypertension

• CFs: Increased creatinine, tenderness, haematuria
• Investigations: U+Es, FBCs, US, Urinalysis, biopsy, Ig levels

• Hyperfiltration in early diabetes
• Mesangial cell hyperplasia (=glomerulosclerosis)
• Loss of podocytes

• Intensive plasma glucose control to reduce CV risk
• Hypertension control, especially with RAAS inhibitors
• RRT if ESRD occurs
• Transplantation only provides temporary improvement

• 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

• Hypertension, carotid/femoral bruits and proteinuria
• CTA, MRA, CO2 angiography, biopsy

• Interventional radiology of severe (uncontrollable BP, pulmonary oedema)
• BP control (3 or more hypertensives)
• Risk factor control

• Also called 'clear cell carcinoma'
• An adenocarcinoma, arising from proximal convoluted tubule
• Commonly metastasises along veins to the IVC

• Smoking
• Polycystic kidney disease
• Horseshoe kidney
• Von-Hippel Lindau

• Loin pain
• Mass felt
• Frank haematuria
• Paraneoplastic syndromes (hypercalcaemia, hypertension, polycythaemia)

• Differentiate from spleen mass (ballotable, resonant, doesn't move on respiration)
• FBC, U&Es, LFTs
• CT and US
• Biopsy

• Slow growing
• Vast majority are primary adenocarcinoma, in peripherals
• Gleason grading and TNM classification

• Increasing age
• Genetics (hereditary prostate cancer 1)
• Ethnicity; black>white>others
• Environmental/occupational
• Hormones (androgen production)
• STIs
• Diet

• Many cases are asymptomatic
• Usually presents early
• Painful/slow micturation and retention
• UTI
• Haematuria
• Bone pain

• PR
• Raised PSA level; protease in semen/plasma. Tissue not tumour specific
• Trans-rectal US guided biopsy

• 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

• Watchful waiting
• Active surveillance
• Radiotherapy (with/without LHRH analogue)
• Radical prostatectomy
• Orchidectomy

• Smoking
• Increasing age
• Occupation (especially working with rubbers)
• Schistosomiasis (or other chronic infections)

• Transitional cell carcinoma; transitional epithelium found in the urinary tract
• 75% are superficial, 25% are invasive

• Frank haematuria/microscopic haematuria
• Flexible cytoscopy
• Endoscopic resection (if confined), trans-urethral resection, intravesical BCG immunotherapy, cystectomy/radiotherapy

• Scrotal US/CT
• Alpha fetoprotein
• Beta hCG
• LDH

• 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

• Colicky pain, in loin or lateral abdomen
• Sepsis
• Mimics: appendicitis, gallstones, diverticulitis and especially AAA

• 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

• 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.

• Treatment: Conservatively. Lithotripsy. Endoscopy. Open surgery/laparoscopy
• Factors: Size, site, symptoms, depth, density