Kidney disease and blood pressure Flashcards
How will glomerular disease present?
Hypertension Incidental microscopic haematuria Incidental proteinuria Nephrotic syndrome Progressive renal impairment AKI
What is nephrotic syndrome?
Heavy proteinuria > 3.5g a day
Hypoalbuminaemia
Oedema
Hyperlipidaemia
Most common cause of GD in children?
Minimal change disease
Why is it called minimal change disease?
Under the microscope the kidney tissue looks normal
What is renal bruits?
Stenosis
Blood investigations in glomerulonephritis?
U+E FBC CRP C3/4 Abs (IgA) RF Anti-NA, anti-dsDNA, ANCA
What are the primary glomerular causes of microscopic haematuria?
IgA nephropathy Alports Thin BM disease Post-infectious GN Membranoproliferative GN
What are the secondary glomerular causes of microscopic haematuria?
Henoch Scorlein Purpura (IgA vasculitis) SLE Haemolytic uraemic syndrome (HUS) ANCA associated vasculitis Sickle nephropathy
Presentation of ANCA associated vasculitis
Rapid decline in renal function
Rapidly progressing glomerulonephritis
Differentials between Henoch Scorlein Purpura and IgA nephropathy?
HSP affects small blood vessels in kidney, skin and gut
HSP is associated with a leucocystoclasic vasculitic rash
Extra-renal symptoms
Biopsy of IgA nephropathy findings?
Mesangial proliferation with IgA deposition
Primary causes of nephrotic syndrome:
Membranous nephropathy
FSGS
MCGN
Minimal change disease
Secondary causes of nephrotic syndrome:
Diabetic nephropathy SLE Amyloidosis Malignancy Drugs
Complications of nephrotic syndrome:
Protein malnutrition Hypovolaemia AKI VTE - risk if albumin <20-25(DVT, PE, Renal vein thrombosis) Infections
Pregnancy associated nephrotic syndrome?
Pre-eclampsia
Which nephrotic syndromes respond well to steroids?
Minimal change disease
Focal segmental glomerulosclerosis
Management of nephrotic syndrome:
Diuretics ACE Anticoagulants Statins Renal biopsy
What is a paraneoplastic nephrotic syndrome of Hodgkin’s syndrome?
Minimal change disease
How will minimal change disease present?
Sudden onset oedema
(Periorbital in children)
(Peripheral in adults)
Drug causes of minimal change disease?
NSAIDs Lithium Pellicinamine Pamidronate Sulfazolizine Immunisations
MCD associated with?
SLE
T1DM
APKD
HIV nephropathy
What sets focal segmental glomerulosclerosis (FSGS) apart from other causes of nephrotic syndrome?
It is a lesion not a disease
Biopsy of FSGS?
Areas of mesangial collapse and sclerosis
Secondary causes of FSGS:
HIV Reflux nephropathy Massive obesity Scarring from previous insult (e.g. IgA, SLE, vasculitis) Heroin
Symptoms of FSGS:
Proteinuria
Hypoalbuminaemia
High cholesterol
VTE risk
Most common cause of primary nephrotic syndrome in adults?
Membranous nephropathy
Pathology of membranous nephropathy
Glomerular BM thickening
Immune deposits in the glomerular BM
Idiopathic membranous nephropathy Ab?
Anti-PLA2
Secondary membranous nephropathy causes?
Hep B Thyroiditis Carcinomas Penicillamine Captopril NSAIDs
Mesangiocapillary glomerulonephritis (MCGN) pathology?
Immune complex deposition
Complement dysregulation
Cryoglobulinaemia pathology?
Circulating complexes that precipitate out in the cold
Associated with rash - livedo reticularis
Arthralgia
Myalgia
Biopsy of cryoglobulinaemia findings?
MCGN
Pulmonary renal syndromes:
Anti-GBM disease
ANCA vasculitis
Lupus with pulmonary haemorrhage
What does GPA stand for in the context of ANCA +ve vasculitis?
Granulomatosis with polyangitis
ANCA +ve vasculitis biopsy findings?
Crescent formation
Rapidly progressing GN
ANCA stands for?
Anti-neutrophil cytoplasmic antibody
Presentation of ANCA +ve vasculitis?
Pulmonary haemorrhage with AKI
Symptoms of ANCA +ve vasculitis?
Joint pains
Rash
Upper respiratory tract symptoms
Nose bleeds
Nephritic syndrome associated diseases:
Post-streptococcal glomerulonephritis (post URTI)
IgA nephropathy
Crescentic, rapid GN - Goodpastures, vasculitis
Membranoproliferative GN
HSP
Rhabdomyolysis (myoglobin)
Pathology of Goodpastures syndrome?
Anti-glomerular BM Abs (crescent formation and rapid GN)
Anti-alveolar BM Abs (pulmonary haemorrhage)
Goodpastures presentation?
Pulmonary haemorrhage and AKI
Presentation of rhabdomyolysis?
Coca-cola coloured urine
What is rheumatoid factor?
Anti-bodies to the Fc portion of IgG (usually IgM)
Cancer test in glomerular disease?
Myeloma screen - Igs, electrophoresis and urine Bence-Jones proteins
Life-threatening complications of glomerular disease?
Hyperkalaemia
Fluid overload
Treatment for hyperkalaemia?
Need to normalise bicarbonate
Calcium gluconate (prevents arrhythmias)
Then dextrose
Then insulin
When are ACE inhibitors contraindicated?
Renal failure Pregnancy/breastfeeding Renal artery stenosis Aortic stenosis (hypotension) High dose diuretic therapy (>80mg furosemide) Hereditary idiopathic angio-oedema
Why are ACE inhibitors contraindicated in renal failure?
They lower the glomerular filtration pressure and thus GFR
How do ACE inhibitors reduce the glomerular filtration pressure?
Vasodilate the efferent artery (angio II normally constricts it)
Side-effects of ACE inhibitors?
Cough
Hyperkalaemia
Angio-oedema (year after starting)
First dose hypotension (especially in those on diuretics)
Step 1 treatment for hypertension?
ACE inhibitor or CCB
Step 2 treatment for hypertension?
ACE + CCB or ACE + Diuretic
Step 3 treatment for hypertension?
ACE + CCB + Diuretic
Step 4 treatment for hypertension and K is < or equal to 4.5?
Add spironolactone
Step 4 treatment for hypertension and K is > 4.5?
Add alpha- or beta-blocker
Which diuretics are potassium sparing and where do they operate?
Thiazides
Distal convoluted tubule blocking the NaCl symporter
Which diuretics are used for reducing fluid overload in heart failure?
Loop diuretics
Common side effects of thiazide diuretics:
Dehydration Postural hypotension Hyponatraemia, hypokalaemia, hypercalcaemia Gout Impaired glucose tolerance Impotence
Rare side effects of thiazide diuretics:
Thrombocytopaenia
Agranulocytosis
Photosensitivity rash
Pancreatitis
Indications for loop diuretics?
Heart failure Resistant hypertension (particularly in patients with renal impairment)
Adverse effects of loop diuretics?
Hypotension
Hyponatraemia, hypokalaemia, hypomagnesaemia
Hypochloraemic alkalosis
Ototoxicity
Hypocalcaemia
Renal impairment (from dehydration + direct toxic effect)
Hyperglycaemia (less common than with thiazides)
Gout
Dietary advice for a patient with chronic kidney disease
Low protein
Low potassium
Low phosphate
Low sodium
Kidney cancer in children?
Wilms’ tumour (abdominal pain and painless haematuria)
Cause fo oxalate nephropathy?
Vitamin C overdose
MACHINE mnemonic for causes of hyperkalaemia:
M - Medications: ACE, NSAIDs A - Acidosis: metabolic and respiratory C - Cellular destruction: burns, traumatic injury H - Hypoaldosteronism, haemolysis I - Intake (excessive) N - Nephrons (renal failure) E - Excretion (impaired)
Hyperkalaemic ECG changes:
Tall tented t waves
Small p waves
Widened QRS leading to sinusoidal pattern and asystole
Why is metabolic acidosis associated with hyperkalaemia?
H and K ions compete for eachother for sodium ions across cell membranes and in the distal tubule
Drug causes of hyperkalaemia:
Potassium sparing diuretics ACE inhibitors Angiotensin 2 receptor blockers Spironolactone Ciclosporin Heparin Beta blockers (can interfere with K transport into cells and can cause hyperkalaemia in renal failure patients - treat with salbutamol)
Disease causes of hyperkalaemia:
Addison’s disease
Rhabdomyolysis
Massive blood transfusion
Drug causes of hypokalaemia:
Beta agonists (temporary) Calcium resonium (temporary) Thiazide diuretics Loop diuretics Acetazolamide
Which type hypersensitivity is Goodpastures syndrome?
Type 2
Does oliguria in acute tubular necrosis respond to IV fluids?
No because the damage is within the kidneys rather than there being fluid depletion
Wilms’ tumour is an example of what?
Nephroblastoma
What is the most common form of AKI?
Acute tubular necrosis
How can a fall cause AKI?
Rhabdomyolysis from the fall (myoglobin release from damaged muscle) causes ischaemia and acute tubular necrosis in the kidney
Diabetic nephropathy histology findings?
Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)
Hyaline arteriosclerosis
BM thickening
What is the histological finding in amyloidosis?
Apple green birefringence in polarised light
What does the histological finding of apple green birefringent crystals in the kidney suggest?
Amyloidosis
When is the histological finding of wire looping of the capillaries in the glomeruli found?
SLE - a diffuse proliferative glomerulonephritis
When is the histological finding of presenting found?
Rapidly progressive glomerulonephritis
Pathophysiology of diabetic nephropathy?
Increase in the glomerular capillary pressure
Glycosylation of the basement membrane
Associations with renal cell carcinoma?
Middle aged man
Smoking
Tubular sclerosis
Von Hippel-Lindau syndrome
Potential endocrine secretions of a renal cell carcinoma?
Erythropoeitin - polycythaemia
Parathyroid hormone - hypercalcaemia
Renin
ACTH
Hepatic paraneoplastic syndrome of renal cell carcinoma?
Stauffer syndrome - cholestastis/hepatosplenomegaly
(thought to be secondary to increased levels of IL-6
What is acute kidney injury?
Syndrome arising from a rapid decline in GFR
Serum creatinine > (or equal to) 26.5 umol/L
OR raise of 1.5 fold or over in 7 days AND urine output <0.5ml/kg/h for 6 hours
KDIGO stage 1 AKI:
Serum creatinine 1.5-1.9 x baseline
KDIGO stage 2 AKI:
Serum creatinine 2.0-2.9 x baseline
KDIGO stage 3 AKI:
Serum creatinine 3 x baseline
Pre-renal causes of AKI:
Hypovolaemia
Cardiac failure
Hepatorenal syndrome
Renal artery causes of AKI:
Renal artery occlusion
Large/medium vessel vasculitis
Small vessel causes of AKI:
Thrombotic microangiopathy
Renal atheroembolism
Small vessel vasculitis
Glomerular disease causes of AKI:
Anti-GBM disease (Goodpastures) Lupus nephritis Post-infective GN Infective endocarditis Membranoproliferative GN Cryoglobulinaemia IgA nephropathy/HSP
Causes of acute tubular necrosis (AKI):
Amphotecerin Aminoglycosides Antiretrovirals Cisplatin Acetaminophen Radiocontrast Organic solvents IV immunoglobulin
Causes of acute interstitial nephritis (AKI):
Drugs
Infection
Systemic disease
Intra-tubular obstruction causes of AKI:
Cast nephropathy
Drugs
Crystalluria
Post-renal obstruction causes of AKI:
Papillary necrosis Tumours Retroperitoneal fibrosis Renal calculi Urinary retention
What can AKI cause?
Hyperkalaemia
ECG change with serum K 5.5-6.5 mmol/l
Peaked T waves
Prolonged PR segment
ECG change with serum K 6.5-8 mmol/l
Loss of P wave
Prolonged QRS
ST elevation
(ectopic beats and escape rhythms)
ECG change with serum K >8 mol/l
Sine wave
Wide QRS
(ventricular fibrillation, asystole, bundle branch blocks, axis deviation, fascicular blocks)
What does the kidney have receptor sites for?
ADH
Aldosterone
ANP
PTH
What doe the kidney produce?
Urine Erythropoetin Prostaglandins Vitamin D Renin (also has a role in gluconeogenesis)
Features of metabolic acidosis?
pH<7.3
Low PaCO2
Normal-high PaO2
Low bicarbonate
Symptoms of metabolic acidosis?
Breathless
Tachypnoea
Nausea
Non-specifically unwell
Features of uraemia?
Waste retention so higher blood levels of: Sulfate Urea Ammonia Creatinine Phosphate
What does uraemia lead to?
Pericarditis
Pleurisy
Encephalopathy, coma, death
RRT may be needed for severe complications of AKI such as…
Life threatening pulmonary oedema Severe metabolic acidosis Severe hyperkalaemia with ECG changes Uraemia pericarditis Uraemic encephalopathy
Bone disease:
High bone turnover due to hyperparathyroidism
OR low bone turnover causing osteoporosis
Vertebral fracture occurs in 21% of harm-dialysis patients
