Renal Flashcards
What is AKI
Acute drop in kidney function
Diagnosed by measuring serum creatinine
Increased morbidity and mortality
What is the NICE criteria for AKI
Rise in creatinine in .25 micromol/L in 48 hrs
Rise in creatinine of > 50% in 7 days
Urine output of < 0.5 ml/kg/hr for > 6 hrs
What are the risk factors for AKI
Consider in anyone with an acute illness or having surgery
CKD
Heart failure
Diabetes
Liver disease
Sepsis
> 65
Cognitive impairment
Nephrotoxic drugs (NSAISs, ACE inhibitors, antibiotics)
Use of contrast
What are the pre-renal causes of AKI
Most common cause of AKI
Due to inadequate blood supply to kidneys
Dehydration
Hypotension (shock)
Heart failure
What are the renal causes of AKI
Glomerulonephritis
Intestinal nephritis
Acute tubular necrosis
What are the post-renal causes of AKI
Obstruction of outflow of urine (backpressure to kidneys, obstructive uropathy)
Kidney stones
Masses
Ureter/urethral strictures
Enlarged prostate/prostate cancer
What investigations are needed for AKI
Urinalysis (leukocytes and nitrates, proteins, blood, glucose)
Ultrasound of urinary tract
What is the management for AKI
Avoid/stop nephrotoxic drugs
Adequate fluid intake/fluid rehydration
Relieve obstruction
May need dialysis
What are the indications for renal replacement therapy
Hyperkalaemia due to medical therapy
Metabolic acidosis due to medical therapy
Fluid overload due to diuretics
Uraemic pericarditis
Uraemic encephalopathy (vomiting, confusion, drowsiness, reduced consciousness)
Intoxications (lithium, methanol)
What are the complications of AKI
Hyperkalaemia
Fluid overload
Heart failure
Pulmonary oedema
Metabolic acidosis
Uraemia (encephalopathy, pericarditis)
What is CKD
Chronic reduction in kidney function
Usually permanent and progressive
What are the causes of CKD
Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications (NSAIDs, PPIs, lithium)
What are the risk factors for CKD
Increasing age
Hypertension
Diabetes
Smoking
Nephrotoxic drugs
How might CKD present
Usually asymptomatic
Pruritus
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
What investigations are needed in CKD
U&Es (measure eGFR, 2 tests 3 months apart)
Proteinuria (urine albumin:creatinine, > 3 mg/mmol is significant)
Haematuria (urine dip, investigate for malignancy)
Renal ultrasound (if have accelerated CKD, haematuria, family history of polycystic kidney disease, evidence of obstruction)
What are the stages of CKD
G score (based on eGFR):
- G1: > 90
- G2: 60 - 89
- G3: 45 - 59
- G4: 15 - 29
- G5: < 15 (end stage renal failure)
A score (based on albumin:creatine):
- A1: < 3 mg/mmol
- A2: 3 - 30 mg/mmol
- A3: > 30 mg/mmol
Need to have at least eGFR < 60 or proteinuria to have CKD
What are the complications of CKD
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis-related problems
Hyperparathyroidism
Hypertension
Malnutrition
Dyslipidaemia
What are the NICE guidelines for referral to a specialist in CKD
eGFR < 30
ACR > 70 mg/mmol
Accelerated progression (eGFR decrease by 15 (or 25%) in 1 year)
Uncontrolled hypertension (despite using > 4 antihypertensives)
What is the management for CKD
Treat underlying cause
Slow progression (optimise diabetes/hypertension, treat glomerulonephritis, monitor bloods)
Reduce risk of cardiovascular disease (statins, control BP, improve diabetic control, lifestyle modifications)
Reduce risk of complications (exercise, weight loss, smoking cessation, reduce salt, atorvastatin)
Treat complications
How is hypertension treated in CKD
ACE inhibitors (1st line for CKD)
Target < 140/90
Monitor serum potassium (CKD and ACE inhibitors cause hyperkalaemia)
What is anaemia of CKD
CKD causes from in EPO
Management: exogenous EPO, blood transfusions
Treat iron deficiency before giving EPO
What is renal bone disease
Features: osteomalacia, osteoporosis, osteosclerosis
X-ray changes (‘rugger jersey spine’
Management: vit D supplements, low phosphate diet, bisphosphonates
What are the indications for acute dialysis
AEIOU
Acidosis (severe and not responding to treatment)
Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
Intoxication (overdose)
Oedema (severe and unresponsive pulmonary oedema)
Uraemia (seizures, reduced consciousness)
What are the indications for long term dialysis
End stage renal disease (CKD stage 5)
If any of the acute indications continue long term
What are the options for maintenance dialysis
Continuous ambulatory peritoneal dialysis
Automated peritoneal dialysis
Haemodialysis
What is peritoneal dialysis
Use peritoneal membrane as filtration membrane
Dialysis solution (dextrose) added to peritoneal cavity
Ultrafiltration occurs from blood
Involves a tenckhoff catheter
Continuous ambulatory peritoneal dialysis/automated dialysis
Complications: bacterial peritonitis, peritoneal sclerosis, ultrafiltration failure, weight gain, psychological effects, hydrothorax
What is haemodialysis
Usually 4 hours 3 days a week
Tunnelled cuffed catheter/arterio-venous fistula
What are the features of nephritic syndrome
Haematuria
Oliguria
Proteinuria < 3.5 g/24 hrs
Fluid retention
Hypertension
What are the features of nephrotic syndrome
Peripheral oedema
Proteinuria
Serum albumin < 30
Hypercholesterolaemia
Frothy urine
Complication: higher risk of infection, VTE, progression to CKD, hypertension, hyperlipidaemia
What is glomerulonephritis
Conditions that cause inflammation of/around glomerulus and nephrons
What are the types of glomerulonephritis
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
IgA nephropathy
Post-streptococcal glomerulonephritis
Mesangiocapillary glomerulonephritis
Rapid progressive glomerulonephritis
Goodpasture syndrome
What is the general management for glomerulonephritis
Immunosuppression (steroids)
Blood pressure control (ACE inhibitors or ARBs)
What is IgA nephropathy
Berger’s disease
Most common cause of primary glomerulonephritis
Present in 20s
Membranous glomerulonephritis
Most common type of glomerulonephritis
Peaks in 20s and 60s
Get IgG and complement deposits on basement membrane
70% idiopathic
Can be secondary to: malignancy, rheumatoid disorders, drugs (NSAIDs)
What is post-streptococcal glomerulonephritis
Usually under 30s (often children 3 - 12)
1 - 3 weeks after streptococcal infection
Usually make full recover
What is Goodpasture syndrome
Anti-GBM antibodies attack glomerulus and pulmonary basement membranes
Get: glomerulonephritis, pulmonary haemorrhage
What is rapidly progressive glomerulonephritis
See ‘crescentic glomerulonephritis’ on histology
Very acute illness
Responds well to treatment
Often secondary to Goodpasture syndrome
What is diabetic nephropathy
Most common cause of glomerular pathology or CKD
Chronically high levels of glucose passing through glomerulus (get glomerular scarring)
Have proteinuria
What investigations are needed for diabetic nephropathy
Diabetic patients should regularly be screened for nephropathy with albumin:creatinine and U&Es
What is the management for diabetic nephropathy
Optimise blood sugar levels and blood pressure (ACE inhibitors)
What is interstitial kidney disease
Inflammation of the space between cells and tubules in the kidney
What is acute interstitial nephritis
On presentation: AKI, hypertension, features of hypersensitivity reaction (rash, fever, eosinophilia)
Acute inflammation of tubules and interstitium
Usually due to hypersensitivity to drugs/infection
Management: treat underlying cause, steroids
What is chronic tubulointerstitial nephritis
Chronic inflammation of tubules and interstitium
Present with CKD
Management: treat underlying cause, steroids
What is acute tubular necrosis
Necrosis of epithelial cells of renal tubules
Most common cause of AKI
Damage due to ischaemia/toxins
Reversible (epithelial cells can regenerate, 7-12 days to recovery)
What are the causes of acute tubular necrosis
Ischaemia: shock, sepsis, dehydration
Toxins: contrast, gentamycin, NSAIDs
What investigation is needed for acute tubular necrosis
Urinalysis (‘muddy brown casts’)
What is the management for acute tubular necrosis
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
What is renal tubular acidosis
Metabolic acidosis due to pathology in renal tubule
Tubules: maintain normal pH
4 types
What is type 1 renal tubular acidosis
Pathology in distal tubule (unable to excrete H+)
Causes: genetic, SLE, Sjogren’s syndrome, primary biliary cirrhosis, hyperthyroidism, sickle cell anaemia, Marfan’s syndrome
Presentation: failure to thrive in children, hyperventilation (compensate for metabolic acidosis), CKD, bone disease
Treatment: oral bicarbonates (correct electrolyte imbalance)
Complications: hypokalaemia, metabolic acidosis, high urinary pH
What is type 2 renal tubular acidosis
Pathology in proximal tubule (unable to reabsorb HCO3-)
Causes: Fanconi’s syndrome
Treatment: oral bicarbonates
Complications: hypokalaemia, metabolic acidosis, high urinary pH
What is type 3 renal tubular acidosis
Pathology in proximal and distal tubule (combination of types 1 and 2)
Very rare
What is type 4 renal tubular acidosis
Due to reduced aldosterone
Causes: adrenal insufficiency, medications (ACE inhibitors, spironolactone), SLE, diabetes, HIV
Treatment: fludrocortisone, sodium bicarbonate
Complications: hyperkalaemia, high chloride, metabolic acidosis, low urinary pH
What is haemolytic uraemic syndrome
Thrombosis in small blood vessels throughout body
Usually triggered by shiga toxin (E coli 0157)
Clots: consume platelets, cut up RBCs as they pass
How might haemolytic uraemic syndrome present
Classic triad: haemolytic anaemia, AKI, thrombocytopenia
Initially get GI symptoms (bloody diarrhoea)
Around day 5, develop HUS: reduced urine output, haematuria, abdominal pain, lethargy and irritability, confusion, hypertension, bruising
What is the management for haemolytic uraemic syndrome
Supportive management: antihypertensives, blood transfusion, dialysis
10% mortality
What is rhabdomyolysis
Skeletal muscle breaks down, releases breakdown products into blood
Apoptosis of myocytes releases: myoglobin (nephrotoxic), potassium, phosphate, creatine kinase
What are the causes of rhabdomyolysis
(Anything that causes significant damage to muscle cells)
Prolonged immobility
Rigorous exercise
Crush injuries
Seizures
How might rhabdomyolysis present
Muscle aches and pains
Oedema
Fatigue
Constipation
Red-brown urine
What investigations are needed for rhabdomyolysis
Creatinine kinase (rises for around 12 hours, remains elevated for 1-3 days, increased risk of AKI)
Urine dipstick
U&Es
ECG
What is the management for rhabdomyolysis
IV fluids (rehydration, filtration of breakdown products)
IV sodium bicarbonate (reduces toxicity of myoglobin)
IV mannitol (increases GFR, flush out breakdown products, reduces oedema)
Treat complications
What are the causes of hyperkalaemia
Conditions: AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome
Medications: aldosterone antagonists (spironolactone), ACE inhibitors, ARBs, NSAIDs, potassium supplements
What investigations are needed for hyperkalaemia
U&Es
ECG
What is the management for hyperkalaemia
Close ECG monitoring
Insulin and dextrose infusion
Calcium gluconate (stabilises cardiac muscles)
Nebulised salbutamol
Oral calcium resonium
Sodium bicarbonate
Dialysis
What is polycystic kidney disease
Kidney function impaired
Also get hepatic cysts and cerebral aneurysms
Can be autosomal dominant or autosomal recessive
How is polycystic kidney disease diagnosed
Ultrasound
Genetic testing (autosomal dominant PKD-1/PKD-2,
Give an overview of autosomal dominant polycystic kidney disease
Extra-renal manifestations: cerebral aneurysms, hepatic/splenic/pancreatic/ovarian cysts, mitral regurge, colonic diverticula, aortic root dilation
Complications: chronic loin pain, hypertension, cardiovascular disease, gross haematuria, renal stones, end-stage renal failure
Give an overview of autosomal recessive polycystic kidney disease
Rarer, more severe
Often presents with pregnancy (oligohydramnios)
Features: underdevelopment of lungs (respiratory failure just after birth), dysmorphic features (underdeveloped ear cartilage, low set ears, flat nasal bridge)
What is the management for polycystic kidney disease
Tolvaptan (vasopressin receptor antagonist, slows development of cysts)
Supportive: antihypertensives, analgesia, antibiotics, dialysis, renal transplant
Other steps: genetic counselling, avoid contact sports, regular ultrasounds, regular bloods, regular BP monitoring, MR angiogram
