Renal Flashcards
Pre-renal constitutes what percentage of AKIs?
What are the most common causes of pre-renal AKI?
40-70%
- Most cases are fluid loss causing hypotension and hypovolaemia.
No blood flow to kidney, no urination = AKI
- Hypovolaemia- Renal loss from diuretic overuse
- Systemic vasodilation- sepsis
- Decreased cardiac output- HF/ MI
Give an example of intrinsic renal damage for the following anatomical locations:
- Tubular
- Glomerular
- Interstitial
- Vascular
- Acute tubular necrosis- ischaemia, drugs, toxins
- Glomerulonephritis: post infection and other causes
- Interstitial nephritis: drugs, infections, infiltration
- Vessel obstruction: Thrombosis, vasculitis, haemolytic microangiopathy
What are the 3 characteristic features of Haemolytic Ureamic syndrome.
What is the most common cause of HUS?
Microangiopathy characterised by
- Progressive renal failure
- Microangiopathic haemolytic anaemia
- Low platelets.
E. Coli, particularly children <5. Most common cause of renal failure in children.
Give 4 pathophysiological stages of Haemolytic Uraemic Syndrome.
- Gastroenteritis (E. Coli 90%)- toxin production
- Endothelial damage
- Thrombosis, platelet consumption + fibrin strand deposition.
- Destruction of RBCs = schistocytes, low Hb.
Give 2 symptoms and 3 investigation findings of Haemolytic Uraemic Syndrome
Symptoms: Abdominal pain, bloody diarrhoea
Investigation: Low Hb, Low platelet, haematuria/ proteinuria.
What is the pentad of features for Thrombotic Thrombocytopenic purpura?
Give 4 other symptoms.
- Thrombocytopenia
- Haemolytic anaemia
- Uraemia
- Neurological signs
- Fever
Other symptoms are seizures, hemiparesis, reduced consciousness, reduced vision.
What is the genetic mutation in Thrombotic Thrombocytopenic Purpura?
What is the pathophysiology caused by this gene mutation?
- Deficiency of von Willebrand Factor cleaving protease- ADAMTS13 in endothelial cells
- Leads to increased vWF multimers promoting platelet activation and aggregation in circulation.
- Also promotes fibrin deposition.
Give two ways in which glomerular inflammation is caused and how they present.
- Loss of barrier function: proteinuria, haematuria
- Loss of filtering capacity: Reduced excretion > accumulation of waste products
What is the triad of nephrotic syndrome?
What happens to serum lipid level?
What happens to Antithrombin 3?
Give two examples of an underlying cause for nephrotic syndrome.
Give 1 peripheral stigmata of low albumin.
-Proteinuria >3.5g/24hrs.
- Low Serum albumin <25 g/L
- Oedema
NB: liver compensates for hypoalbuminaemia by causing hyperlipidaemia (>10 mmol/L)
- Reduced anti-thrombin 3 production. Can cause hypercoagulable state.
Break down of selectivity for glomerular filtration- protein leak. Loss of podocytes. E.g.
- Minimal change glomerulonephritis- children < 5 years
- Membranous glomerulonephritis/ Diabetes - adults.
Leukonychia is peripheral stigmata of hypoalbuminaemia.
What is the triad of Nephritic syndrome? What happens to urine level?
What is pathophysiology of nephritic syndrome?
- Hypertension
- Haematuria ( + white cells in urine, plus sediment)
- Oedema (+ Oliguria <400 L/day)
+ granular casts- inflammatory cells.
Immune complexes lodge in capillaries, launch immune response against capillary. White cell recruitment- inflammation, cell breakdown. Allows white and red blood cells to leave bowman’s capsule alongside protein.
More severe glomerular damage than nephrotic syndrome.
Give two common primary causes of nephrotic syndrome.
Give 3 common secondary causes of nephrotic syndrome.
Primary:
- Membranous glomerulonephritis - immune complex mediated.
- Minimal change disease- children, glomeruli look normal under microscopy. Most common cause of nephrotic syndrome in children.
Secondary:
- Diabetes, SLE, Amyloid.
Give 1 common primary cause of nephritic syndrome.
Give 3 common secondary causes of nephritic syndrome
Primary:
- IgA nephropathy.
Secondary:
- Post streptococcal infection, SLE, anti-GBM disease (affects alveolar basement membrane also- lung haemorrhage)
What is IgA nephropathy?
What is anti-GBM (Goodpasture’s)?
What is Henoch Schonlein purpura?
What is Pauci-immune?
- IgA nephropathy: days after URTI, increase in IgA immune complex formation. Episodic haematuria.
- Anti-GBM: Auto Ab to type IV collagen (GBM and lung). Haematuria and haemoptysis.
- HSP: Systemic variant IgA, causes purpuric rash- systemic involvement
- Pauci-immune: ANCA associated antibodies bound to neutrophils, activation in glomerulus.
Give 5 blood tests for glomerulonephritis.
Give 1 other bedside test.
Give 2 further investigations.
- FBC, U&E, CRP, complement, autoantibodies.
- Also test urine.
- Renal US, +/- renal biopsy.
Give two medications used to preserve proteinuria and renal function in glomerulonephritis.
Give two other medications used in treatment of glomerulonephritis.
- ACEi or ARB.
- Steroids.
- Immunosuppressants.
What are the 3 stages of acute tubular necrosis due to ischaemia?
- Initiation: acute low GFR, high Creatinine, high urea.
- Maintenance- sustained low GFR, raised creatinine and urea.
- Recovery- tubular function regenerates, increased urine volume and gradual decreased urea and creatinine.
How does myeloma cause acute tubular necrosis?
What are the 4 clinical features of acute tubular necrosis due to myeloma?
- Malignant bone marrow plasma cells increases plasma cell clones- leads to monoclonal paraprotein production.
- Hypercalcaemia and paraprotein deposition causes inflammation and renal failure.
CRAB
- Calcium- high
- Renal failure
- Anaemia: BM infiltration by plasma cells, anaemia of chronic disease, decreased EPO secondary to renal failure.
- Bone- osteolytic bone lesions- pain, fracture, risk of cord compression
List 5 exogenous nephrotoxic agents.
- NSAIDs
- ACE inhibitors and ARBs
- aminoglycosides- e.g. gentamicin, streptomycin
- Contrast agents
- Immunosuppresants e.g. ciclosporin
List 4 endogenous nephrotoxic agents.
- Myoglobin (rhabdomyolysis), haemoglobinuria, crystals, myeloma paraprotein.
Explain the pathophysiology of rhabdomyolysis leading to acute tubular necrosis.
Give two symptoms of rhabdomyolysis and 2 investigative blood tests.
- Skeletal muscle breakdown
- Release of myoglobin, potassium and creatine kinase (CK).
- Obstruction of renal tubules.
- Muscle pain/ swelling, dark urine (myoglobinuria)
- Potassium , creatine kinase test.
Which test measures proteinuria?
Urine ACR/ PCR
- Albumin/ creatinine ratio - 30-300 is normal
- Protein/ creatinine ratio
What are the 4 main complications of AKI and how are they managed?
- Hyperkalaemia: calcium gluconate IV, dextrose, insulin, nebulised salbutamol.
- Pulmonary oedema: sit up, high flow oxygen, venous vasodilator
- Uraemia: dialysis if severe complication
- Acidaemia: IV sodium bicarbonate via central line infusion.
Give 6 causes of chronic kidney disease.
How long is required to be chronic?
- Diabetes
- Hypertension
- Atherosclerosis
- Chronic glomerulonephritis
- Infective or obstructive uropathy
- Adult polycystic kidney disease. commonest inherited cause of CKD
> 3 months
What is the pathophysiology of diabetic nephropathy
- Glycation of efferent arteriole
- Outflow obstruction
- Increased pressure within glomerulus
- Hyperfiltration
- glomerulosclerosis
- Reduced blood filtration/ GFR.
