Renal Flashcards
Definition and detection of AKI
- rise in creatinine from baseline of >50% within 7 days -suspect of oligouria <0.5ml/kg/hr -check creatinine in all ill patients, especially if elderly, or confused -particularly if suspecting sepsis, HF, liver failure, hypotension, dehydration, diabetes -particularly if on nephrotoxic drugs
Nephrotoxic drugs
stop the DAMN drugs Diuretics ACEi and ARBs Metformin- not nephrotoxic, accumulates + causes lactic acidosis NSAIDs
Indications for dialysis in AKI
AEIOU Acidosis pH<7.1 Electrolytes e.g. refractory hyperkalaemia Intoxications e.g. salicylate, lithium Overloaded with fluid Uraemia symptoms e.g. encephalopathy
Emergency treatment of hyperkalaemia
Calcium glauconite to stabilise myocardium- 10ml of 10% slow IV Glucose and insulin IV- 10 units, in 50ml 50% glucose over 15 minutes Salbutamol
Causes of CKD
HIDDEN hypertension Infection e.g. ureteric reflux in children Diabetes Drugs e.g. analgesic nephropathy, NSAIDs, lithium Exotics e.g. SLE Nephritis, Glomerulonephritis
Indications for dialysis in CKD
Progressive decline in renal function <15ml/min Symptomatic uraemia despite conservative treatment Volume overload despite fluid restriction and Diuretics Other- pericarditis, Bone Disease, hyperkalaemia despite treatment
What is CAPD?
Tenckhoff catheter into abdomen Less expensive than haemodialysis More convenient as low tech- holidays Relatively easy to teach May have to stop due to peritonitis Fibrosis may reduce permeability 3 litres of fluid, 4 times a day with 30min exchanges Can cause diaphragm splinting, can’t use in COPD
What is removed in CAPD?
Urea, creatinine, potassium and phosphate pass along their concentration gradient- isotonic fluid Water is removed down an osmotic gradient, by including some bags of hypertonic fluid with a high glucose and polymer gradient
Peritoneal dialysis peritonitis
Cloudy effluent- urgent MC&S and culture from ‘first cloudy bag’ Abdominal pain +/- fever Exit site infection (take swab) If I’ll, take blood cultures Gram +ve staph or strep- intraperitoneal vancomycin Gram -ve or pseudomonas- IV ciprofloxacin Uncertain- use both
Questions to ask in CKD?
What are your energy levels like? Do you get breathless? Do you suffer from itching? (Hyperphosphataemia/ hyperuracaemia) Do you have joint pain/ gout? Do you get numb or tingling feet?
Three causes of fatigue in CKD
Anaemia- normochromic normocytic Anaemia of chronic disease Solute retention- many retained solutes are cerebral depressants Psychosocial- loss of employment, feeling trapped by chronic disease
Three causes of breathlessness in CKD
Anaemia, fluid overload, heart failure (CAD and hypertension are common)
Peripheral neuropathy in CKD
Retention of beta-2-microglobulin leading to amyloidosis of peripheral nerves Underlying diabetes is a common cause of CKD and causes neuropathy
Features of CKD
BIG BEAN Breathless Itching Gout Bone pain Energy levels low Ankle swelling/ anaemia Neuropathy
4 features of renal bone disease
Osteoporosis
hyperparathyroidism
osteomalacia
osteosclerosis
Features of renal bone disease
Often assymptomatic
low back pain/ vertebral crush fracture
brachydactyly (short stubby fingers)
osteolysis of terminal phalanges tuft (acronecrosis)
Features of nephrotic Syndrome?
Proteinuria >3g per 24hrs, makes urine frothy
hypoalbuminaemia <30g/dl
oedema (loss of protein on optic pressure allows salt and water into extra cellular space; increased salt and water retention by Kidney)
hypercholesterolaemia as Liver makes more cholesterol-linked to compensatory increase in albumin synthesis
Loss of antithrombin 3- increased thrombin activity- hypercoagulable
Main cause of nephrotic Syndrome in children
Minimal change disease
Idiopathic, steroid responsive
doesnt progress to CKD
Main causes of nephrotic Syndrome in adults
- glomerulosclerosis especially due to diabetes
- membranous Glomerulonephritis- usually idiopathic.
Treatment of nephrotic syndrome
Oedema- Diuretics and salt retention
minimal change Glomerulonephritis- steroids +/- cyclophosphamide
ACEi reduces protein excretion- lowers glomerular filtration pressure
anticoagulation
statins
Features of nephritic syndrome
HOST
Hypertension
Oliguria
Smoky Brown haematuria with red cell casts
Trace of oedema
Causes of acute nephritis
post streptococcal
IgA nephropathy- post strep
vasculitis e.g. SLE
Investigations in nephritic symdrome
Throat swab, ASO titres, 24hr urinary protein
Urea
Excreted mainly by kidneys
large renal reserve- rises late in disease
rise with: dehydration, HF, Diuretics, high protein diet, GI bleed, catabolic states (trauma, infection, fever)
low in: liver disease, over hydration
Creatinine
levels vary depending on muscle mass
low in- elderly
high- young athletes
rise late in renal decline
CKD stages
Blood test acute vs chronic renal failure
Normochromic, normocytic anaemia
hypocalcaemia
hyperphosphataemia
Prevent renal bone disease
Dietary phosphate restriction
phosphate binders
alphacalcidol to correct activated vitamin D deficiency
calcium supplements
How do you monitor renal bone disease?
Causes of hyperkalaemia
The hyperkalemia MACHINE
Medications – ACE Inhibitors, NSAIDS, potassium-sparing diuretics
Acidosis – Metabolic and respiratory
Cellular destruction – burns, traumatic injury, hemolysis
Hypoaldosteronism – Addison’s
Intake- excessive
Nephrons- renal failure
Excretion – Impaired
How do ACEi cause acute renal failure?
pre-renal
efferent Arterial vasodilation, reducing GFR
How do NSAIDs cause acute renal failure
Prerenal- inhibition of prostaglandin mediated affording arteriole vasodilation
renal- direct nephrotoxic
Early complications of ATN
hyponatremia
hypokalaemia
hypovolaemia
CKD stages
