Kidney Disease and Renal Failure Flashcards
What are the broad kidney disease syndromes?
Chronic kidney disease, acute kidney injury (AKI), nephritic syndrome, nephrotic syndrome, and rare tubular function disorders.
What are key presentations of kidney disease?
Unexplained impaired kidney function, haematuria/proteinuria, monitoring abnormalities in chronic disease, and rare familial/tubular disorders.
What is serum creatinine used for?
Traditional measure of kidney function.
What factors influence serum creatinine levels?
Gender, ethnicity, age, body mass, diet, exercise.
Why is serum creatinine not ideal in early disease?
It’s not sensitive to small changes in good kidney function.
What is eGFR?
Estimated glomerular filtration rate; a better reflection of kidney function than serum creatinine alone.
What equation is used for eGFR?
CKD-EPI 2009 equation
Why is eGFR more useful than creatinine?
More accurate, especially in low GFR, and recommended by NICE without ethnic correction.
What is the best measure for stable kidney function?
eGFR.
What are common consequences of renal function loss?
Salt/water retention, inability to concentrate/excrete urine, dilutional hyponatraemia, oedema, hypertension.
Why does renal anaemia occur?
Reduced erythropoietin production by kidneys.
Complications of renal anaemia?
Reduced QoL, cognition, exercise capacity, LVH, ↑ CV risk.
How is renal anaemia treated?
Recombinant erythropoietin.
Why does bone disease occur in CKD?
Kidneys can’t activate vitamin D → ↓ calcium absorption → ↑ PTH → bone demineralisation.
How is mineral bone disease treated?
Phosphate restriction and 1α-hydroxylated vitamin D.
What causes hypertension in CKD?
RAS activation, sodium retention, volume expansion, sympathetic activation, endothelial dysfunction.
Why is hypertension problematic in CKD?
Speeds up kidney damage and increases CV risk.
What builds up in renal failure?
Creatinine, nitrogenous waste, urate, phosphate.
What drugs have reduced clearance in CKD?
Opiates, insulin, antibiotics.
Effects of hypokalemia/hyperkalemia?
Muscle dysfunction, arrhythmias.
Effects of hypo/hypernatremia?
Neurological dysfunction.
Effects of hypocalcaemia?
Arrhythmias, spasms, paraesthesia.
Symptoms of acidosis in CKD?
Breathlessness, chest pain, confusion, bone pain.
What defines CKD?
eGFR <60 mL/min/1.73m² or kidney damage ≥3 months.
What are CKD stages based on?
eGFR levels.
How does CKD prevalence change with age?
Increases significantly with age.
What was the cost of CKD in 2009?
£1.4 billion (1.5–2% of NHS budget).
What are dialysis and transplant costs?
£16–24k/yr home dialysis, £20–24k/yr hospital dialysis, £17k 1st yr transplant.
Common systemic causes of CKD?
Diabetes, hypertension.
Vascular causes of CKD?
Atherosclerosis.
What % of diabetics get nephropathy?
~40% of type 1 and 2 diabetics.
What causes renal artery stenosis?
Mostly atheroma, sometimes fibromuscular dysplasia.
What is hydronephrosis?
Fluid-filled cystic kidney cavities due to obstruction.
Most common cause of death in CKD?
Cardiovascular disease.
Why are infections a risk in CKD?
Impaired immune response.
Who manages most CKD patients?
GPs.
When is nephrology referral needed?
Rapid decline, need for transplant, inflammation/genetic cause, uncontrolled BP, children.
How common is AKI in hospital?
~20% of emergency admissions; 0.5% need dialysis.
Is AKI reversible?
Often reversible if treated promptly.
Who is at risk of AKI?
Elderly, diabetics, hypertensives, heart/liver disease, CKD.
What are pre-renal AKI causes?
Perfusion failure (shock, renal artery block).
Intrinsic renal causes of AKI?
Tubular/glomerular/interstitial damage, SLE, myeloma, nephritis.
Post-renal causes of AKI?
Obstruction (stones, BPH, tumours).
Examples of renal tissue damage causes?
Vasculitis, infections (HIV), drugs (NSAIDs, chemo), interstitial nephritis.
Common AKI complications?
Death, infection, oedema, electrolyte imbalances, anaemia, uraemia, chronic kidney disease.
Mortality in stage 3 AKI (UK hospitals)?
36%.
Protein levels in nephritic syndrome?
<3g/24hr or PCR <300–350 mg/mmol.
Clinical features of nephritic syndrome?
Haematuria, HTN, impaired renal function, oedema.
Is nephritic syndrome a medical emergency?
Yes.
Protein levels in nephrotic syndrome?
> 3–3.5g/24hr or PCR >300–350 mg/mmol.
Features of nephrotic syndrome?
Heavy proteinuria, hypoalbuminaemia (<25 g/L), oedema, hyperlipidaemia.
Causes of nephrotic syndrome?
Primary: FSGS, membranous, minimal change.
Secondary: Diabetes, cancers, drugs, infections (HIV/HBV/HCV), SLE, amyloid.
What are the main complications of nephrotic syndrome?
Thrombosis (DVT, PE, renal vein)
Infections
Hyperlipidaemia
Malnutrition
AKI/CKD
General management strategies of nephrotic syndrome?
Diuretics (loop)
Salt restriction
ACEi/ARB to reduce proteinuria
Thrombo-prophylaxis
