Genitourinary Flashcards
Define AKI
Rapid decline in renal excretory function over hours or days recognised by a rise in urea and creatinine
What is the KDIGO grading for AKI?
Stage 1 - Increase by >/=1.5 but < 2 X baseline creatinine or an increase >26micromol/L in 48 hours
Stage 2 - Serum creatinine > 2 - 2.9 X baseline
Stage 3 - Serum creatinine > 3 X baseline or > 354 micromols/L
Give some examples of causes of pre-renal, renal and post-renal disease?
Pre-renal: Circulatory failure and hypo perfusion (Renal artery stenosis, hypovolaemia due to blood loss or inadequate fluids, cirrhosis or heart failure)
Renal: Gentamicin, ischaemic ATN, nephrotoxic ATN, glomerulonephritis, interstitial nephritis
Post-renal: Renal papillary necrosis, LN compression, prostate Ca, cervical Ca, urethral strictures, kidney stones
What are the absolute indications for dialysis?
Refractory potassium >/=6.5
Refractory pulmonary oedema
What are some management options in patients with anaemia in CKD?
Darbepoietin alfa - EPO
Alfacalcidol - Inc vit D to inc Ca
Phosphate binders (due to hyperphosphataemia)
Cincacalcet - to reduce PTH due to 2ndary HPTH
How would you classify CKD?
Stage 1 - > 90ml/min/1.73m^2 (normal or increased eGFR with evidence of some renal damage)
Stage 2 - 60-89 (slight decrease in eGFR with other evidence of kidney damage)
Stage 3 - 30-59 (moderate kidney disease)
Stage 4 - 15-29 (severe renal disease)
Stage 5 - < 15 (established renal failure)
What are some complications of CKD?
Anaemia
Renal bone disease (renal osteodystrophy)
CVD
Peripheral neuropathy
What characterises nephrItic syndrome?
GMB damage
HTN
Protein and blood in urine
Rapidly declining kidney function
Urinary sediment shows RED CELL CASTS, leucocytes, sub-nephrotic range proteinuria and dysmorphic red cells.
What triad characterises nephrOtic syndrome?
Proteinuria >3g/day Serum albumin < 25g/L Peripheral oedema Dyslipidaemia Loss of Ig - risk of infections. Loss of antithrombin III - risk of VTE
What is IgA nephropathy?
AKA Berger’s disease
Mesangial cell disease
Presents in 20s
Heavy proteinuria, visible haematura. HTN
Precipitated by synpharyngitis (upper respiratory tract infection)
May be secondary to coeliac or cirrhosis
What is the most common GN?
FSGN commonets in adults
Membranous
Mostly idiopathic, 10% secondary to malignancy
Nephrotic syndrome
Anti-phospholipase A2 receptor
Prone to thrombosis due to loss of anti-thrombin III in urine
IgG complexes and complement depositions on GBM
What is the commonest GN in children?
Minimal change disease I
Nephrotic syndrome
Fusion of foot processes
What causes rapidly progressive GN/ crescentic GN?
Lupus nephritis
HSP nephritis
ANCA vasculitis
Good pastures syndrome (anti-GBM)
What is transplant rejection?
When the body recognises cell surface proteins as ‘non-self’, blood group incompatibility, HLA incompatibility. T cell mediated or antibody mediated rejection.
How can you prevent transplant rejection?
Immunosuppression: Basiliximab - anti-IL-2 Tacrolimus - Calcineurin inhibitor Mycophenolate mofetil - inhibits T and B cell proliferation ± steroids - azathioprine, cyclosporin
What are the indications for renal replacement therapy?
AEIOU
Acidosis - severe and not responding to treatment
Electrolyte imbalance - severe and nor responding hypERkalaemia
Intoxication - overdose
Oedema - severe and not responding pulmonary oedema
Uraemia - seizures, reduced consciousness, uraemic pericarditis, encephalopathy
What symptoms characterise uraemic syndrome?
Itch, metallic taste, vomiting, restless legs, anorexia , weight loss
How does haemo-dialysis work?
Diffusion and pressure
Diffusion of solutes into dialyte solution - K and Urea
Filtration of fluid by hydrostatic pressure
What are some complications of haemodialysis?
Crash 'acute hypotension' Access problems Fatigue Air embolism Blood loss Hypokalaemia Cramps
How does Peritoneal dialysis work?
Diffusion and osmotic filtration
Uses the peritoneum to filter fluid. Dialysis solution is put into the peritoneum, it is high in glucose, it absorbs waste and extra fluid and then is removed.
Called Exchange
What are some complications of peritoneal dialysis?
Infections - peritonitis Development or worsening control of diabetes Hernia, dislodged catheter Encapsulating peritoneal sclerosis Hypoalbuminaemia Psychological effects
What other treatment would you need to give if a patient with kidney failure who is receiving dialysis?
Anaemia - EPO and iron
Renal bone disease - Phosphate binders, Vit D
Neuropathy
Endocrine
What are the types of Adult polycystic kidney disease?
PKD 1 - on chromosome 16 - rapidly progressive and leads to ESRD
PKD - on chromosome 4 - slowly progresses and will not usually reach ESRD
What causes PKD?
Polycyctins are over expressed in cysts
They are found in the renal tubular epithelium
They usually regulate IC calcium
Cysts gradually enlarge - increased pressure - normal kidney tissue replaced, kidney volume increased. eGFR drops.
How can PKD present?
Loin pain, HTN, impaired renal function, haematuria
Extra-renal:
Hepatic and pancreatic cysts, abdominal hernia, diverticular disease, bronchiectasis, LVH
What drug could you give in PKD before you eventually need to start RRT?
Tolvaptan - Vasopressin V2 receptor antagonist to increase urine output by blocking reabsorption of water
SE - hepatotoxic (monitor LFTs), hypernatraemia
What is Alport’s syndrome?
X-linked. Collagen 4 abnormalities
Deafness, eye problems and renal failure.
microscopic proteinuria, haematuria and ESRF
Sensorineural hearing loss in late childhood.
90% on dialysis or transplant by 40
What disease is due to alpha galactosidase 4 deficiency?
Fabry’s disease. X-linked
Accumulation of Gb3 in glomeruli and podocytes - proteinuria and ESRD
Check alpha-gal4 activity in leukocytes and renal biopsy for inclusion bodies of gb3
Replace enzyme
How might renal artery stenosis present?
Resistant to treatment
Flash pulmonary oedema
Worsened renal function with ACEi/ARB in bilateral stenosis
Increased bp
Give the pathogenesis of renovascular disease.
Progressive narrowing of the renal artery with atheroma
20% stenosis - GFR falls but oxygenation of cortex and medulla maintained
Stenosis at 70% and there is cortical hypoxia - microvascular damage and inflammation and oxidative pathways
Parenchymal inflammation and fibrosis progresses and becomes irreversible.
Give statin
AVOID ACEi/ARB
What is amyloidosis?
Nephrotic syndrome
A group of disorders characterised by EC deposits of insoluble proteins in abnormal fibrillar form and are resistant to degradation
8-10nm linear aggregated fibrils
What is primary amyloidosis?
AL amyloidosis.
Ig fragments from haematological conditions such as myeloma or monoclonal gammopathy of undetermined significance
Light chain can break off or bone marrow can produce excess light chain.
What organs can be damaged in AL amyloidosis? (amyloid light chain)
GI- malabsorption, hepatomegaly, N&V, diarrhoea
Purpura
Renal - proteinuria (frothy urine) and nephrotic syndrome
CV - restrictive cardiomyopathy, arrhythmias
Carpal tunnel and peripheral and autonomic neuropathy
What is secondary amyloidosis?
AA amyloid. Serum amyloid precursor protein
An acute phase reactant protein raised in chronic inflammation or infection - Crohns, RA, TB
Hepatospenomegaly, nephrotic syndrome
What is systemic lupus erythromatous?
A multisystem, inflammatory AI connective tissue disease where autoantibodies are formed agains a variety of autoantigens causing tissue damage.
What immunology is involved in SLE?
>95% ANA positive high dsDNA - renal involvement C3 and C4 low Anti-ribosomal - CNS involement Anti-phospholipid antibodies
What symptoms may be seen in SLE?
Butterfly rash, Photosensitive rash
Arthritis, pain and tenderness in prox IPJ, Pericartitis
Reynaud’s
Dry mouth and eyes
Seizures
Haemolytic anaemia, thrombocytopenia, PEs
Miscarriage, pre-eclampsia - antiphospholipid Ab
What treatment is used in mild SLE?
DMARD - Hydroxychloroquine
NSAIDs
Low dose corticosteroids - prednisolone
Aspirin