14 - Renal Medicine Flashcards
What are the different ways that renal disease can present?
1. Asymptomatic: non visible haematuria, asymptomatic proteinuria, abnormal eGFR, HTN, electrolyte abnormalities
2. Renal tract symptoms: urinary symptoms, loin poin, visible haematuria, nephrotic syndrome, symptomatic CKD
3. Systemic disorder with renal involvement: DM, sickle cell, SLE, infection, malignancy, pregnancy, drugs
How do you take a renal history?
- If being dialysed ask them what mode, what access and when they were last dialysed
- Important to ask if NSAIDs being taken OTC
How do you perform a renal examination on a patient?
https: //www.youtube.com/watch?v=PPhwQgsebKY
- General inspection
- Hands
- Arms
- Face
- Chest
- Abdomen
- Legs and Sacrum
- Further tests
What are some of the different modes of renal replacement therapy?
- APD (Automated peritoneal dialysis via peritoneal catheter)
- CAPD (Continuous ambulatory peritoneal dialysis)
- Assisted PD (Can perform at home with help of district nurses)
- UHD (Unit based haemodialysis)
- HHM (Home haemodialysis)
What are the different ways of access for dialysis? (both peritoneal and haemodialysis)
- PD catheter
- AV fistula
- Tunelled (Perm-Cath)
- Non-Tunelled (Vas-Cath)
What are some signs on examination of advanced renal disease?
- Brown nails
- Yellow brown uraemic skin
- Uraemic frost from sweat on skin
- Hyperreflexia
- Pericardial rub
What are some different renal function tests?
Bloods: FBC, U+Es, bone profile, CRP, HbA1c
Urine: dipstick, protein-creatinine ratio, albumin-creatnine ration, urine culture
Imaging: US KUB
How does a metabolic alkalosis show on a VBG and what are some causes of this?
- GI losses: vomiting and diarrhoea
- Renal losses: primary hyperaldosteronisms, diuretics
- Intracellular shift: hypokalaemia
How does a metabolic acidosis show on VBG and how can you work out the cause?
Anion Gap!!!!
Na - (Cl + HCO3)
Normal is 8-12
What is the cause of the derangment of this patients blood gas?
What are some of the symptoms of hypernatraemia and what is the number one cause of this electrolyte abnormality?
Thirst, irritability, weakness, confusion, seizures, hyperreflexia, spasticity, coma
Usually due to dehydration which causes cellular dehydration and vascular shear stress so bleeding and thrombosis
What are some causes of hypovolemic, euvolemic and hypervolemic hypernatraemia?
Hypovolemic: vomiting, diarrhoea, diuretics, osmotic diuresis
Euvolemic: diabetes insipidus, hypodipsia, inadequate water intake, heatstroke
Hypervolemic: hypertonic dialysis, sodium bicarbonate administration, hypertonic saline administration, hyperaldosteronism, Cushing’s
What are some causes of central and nephrogenic diabetes insipidus?
Central (impaired release of ADH)
- Trauma
- Tumours
- Cerebral sarcoid/TB
- Infection e.g meningitis
- Cerebral vasculitis e.g SLE
Nephrogenic: (resistance to ADH)
- Congenital
- Drugs (lithium, amphotericin)
- Hypokalaemia
- Hypercalcaemia
How is hypernatraemia managed?
Free water
What are some of the symptoms of hyponatraemia?
- Headache
- Decreased perception
- Confusion
- Seizures
- Gait disturbance
- Reversible ataxia
- Nausea
What is pseudohyponatraemia?
- Sodium <135 but with a normal serum osmolality
- Due to either high lipids, myeloma, hyperglycaemia, uraemia
What are some causes of hypovolemic, euvolemic and hypervolemic hyponatraemia?
Hypovolemic: diuretics (thiazides), osmotic diuresis, Addison’s disease due to mineralcorticoid deficiency, diarrhoea
Euvolemic: Hypothyroidism, Glucocorticoid deficiency, SIADH
Hypervolemic: CCF, nephrotic syndrome, liver cirrhosis, renal failure
What are some investigations you should do when a patient has hyponatraemia?
- Plasma osmolality: rule out pseudohyponatraemia
- K+ and Mg2+: hypoK and hypoMg can potentiate ADH release
- Urine Na: if <20 then non-renal salt losses, if >40 then SIADH
- TSH and 9am Cortisol
- Calcium, Albumin, Glucose, LFTs
- CT head if suspect SIADH
How do you diagnose SIADH?
- Hyponatraemia with low serum osmolality
- Urine osmolality >100 with urine Na>20
- Euvolemia
- Not on diuretics
PROCESS OF ELIMINATION: normal renal, thyroid and adrenal function
What are some causes of SIADH?
- Malignancy
- Meningitis
- Subarachnoid haemorraghe
- Drugs e.g SSRIs, morphine, amitriptylline
- Hypothyroidism
What is the management for SIADH?
- Fluid restrict: <800mls day
- Furosemide
- Demelocycline or Tolvaptan to induce ADH release (can reverse too far to DI)
- PO NaCl
What is the management of hypovolemic and hypervolemic hyponatraemia?
Hypovolaemic: (renal or GI losses of Na) IV fluids 0.9% NaCl at 1-3ml/kg/hr and add K+ if needed
Hypervolaemic: (increased water lowering Na) fluid restrict and consider furosemide
Why should you not correct hyponatraemia rapdily?
Risk of central pontine myelinolysis, correct by <12 mmol/day
How should acute and chronic hyponatraemia be managed?
Acute and Symptomatic (<48hours)
- 3% HYPERTONIC SALINE BOLUSES +/- Furosemide)
Chronic and Symptomatic (>48 hours)
- If seizures hypertonic saline boluses
- Otherwise isotonic saline and furosemide
Chronic and Asymptomatic
- Water restriction
- Stop offending drug
- If dehydrated give water
- If fluid overloaded give water restriction, furosemide and Na
What drugs can cause hyperkalaemia?
- ACEi/ARBs
- Spironolactone
- Amiloride
- NSAIDs
- Heparin
- Trimethoprim
- Betablockers
What are some causes of hyperkalaemia?
- CKD/AKI
- Drugs (ACEi, spironolactone, NSAIDs, etc)
- Hypoaldosteronism
- Addison’s disease
- Rhabdomyolysis
- Metabolic acidosis e.g DKA
- Hyperkalaemic periodic paralysis
What are some causes of artifact hyperkalaemia?
- Haemolysis
- Raised WCC
- Raised platelets
What can hyperkalaemia do to the pH of the blood?
Metabolic acidosis
When is a patient having Type IV RTA and what are some common causes of this?
Due to issue with distal tubule not being able to respond to aldosterone
- Hyperkalemia
- Hypochloraemic metabolic acidosis
- HTN
Causes: hyporeinaemic hypoaldosteronism, diabetic nephropathy, hypertension, NSAIDs, lupus nephritis
How is hyperkalaemia due to type 4 RTA treated?
- Low K diet
- Fluid restrict
- Loop diuretic if overloaded
What are some ECG changes with hyperkalaemia?
- Tented T’s
- Prolonged QRS
- Slurring ST segment
- Loss of p waves
- Sine then asytole
What is the first investigation you should do when a patient has hyperkalaemia on their blood results?
- VBG to check correct
- ECG to look for changes
How is hyperkalaemia with ECG changes treated?
Stabilise myocardium to prevent arrhythmias: 10mls of 10% Calcium Gluconate over 5-10 minutes
Shift potassium back into extracellular space: IV fast acting insulin with glucose or Salbutamol neb
Eliminate potassium from body: Calcium resonium
Dialysis: if treatment resistant
What are some of the symptoms of hypokalaemia?
- Fatigue
- Constipation
- Proximal muscle weakness
- Poor glucose control
- Cardiac arrhythmias
What are some of the causes of hypokalaemia?
- Poor intake
- Gut losses e.g vomiting, NG losses, ileostomy
- Drugs e.g alpha blockers, beta agonists, insullin, theophylline
- Refeeding syndrome
- Conn’s syndrome (Primary hyperaldosteronism)
- Cushing’s syndrome
- Diuretics
- Hypomagnesiumaemia
What are some ECG changes with hypokalaemia?
- Small T waves
- U wave after T
- Increased PR interval
HypoK is <3.5 but do not see ECG changed until moderately low <2.5-2.9
How is hypokalaemia managed?
- Replace Mg
- Oral K replacement
- IV replacement in 0.9% NaCl NOT dextrose
When is long term dialysis started?
When needed to manage the symptoms of renal failure. eGFR usually <10-15. Used as a bridge to transplantation
- Inability to control fluid status e.g pulmonary oedema
- Inability to control VP
- Acid-base or electrolyte abnormalities
- Cognitive impairment
How does peritoneal dialysis work to filter the blood?
- Peritoneal membrane acts as dialysis membrane
- Catheter inserted into peritoneal cavity and dialysate fluid is infused.
This fluid has a high osmotic gradient due to addition of glucose, which pulls water from the patient into the fluid
- Solutes (urea, creatinine, electrolytes) move from blood across peritoneal membrane into dialysate fluid
- Continuous process with intermittent drainage and refilling of peritoneal cavity
What are the different types of peritoneal dialysis?
- Automated PD: Automatic cycler machine at night over 10hours with 10-12L exchanged. Leaves daytime free
- Continuous Ambulatory PD: 4-5 dialysis exchanges a day at regular intervals of 2L.
- Assisted Automated PD: healthcare assistants visit the patient’s home to set up machine for night
What are the advantages of peritoneal dialysis?
- Increase QOL as home based
- Good if patient still got some residual renal function
- Regime individualised to patient rather than HD clinics
- Lower risk of HepC
- No anticoagulation needed
What are the disadvantages of peritoneal dialysis?
- Patient needs to learn technique
- Unsuitable if patient has stoma or previous GI surgery
- Risk of peritonitis
- Hernia
- Hydrothorax
- Leaks
- Catheter site infection
- Loss of membrane function over time
How does haemodialysis work to filter the blood long term?
Blood pumped from patient into machine where it is passed over a semi-permeable membrane containing dialysis fluid flowing in the opposite direction
Solutes diffuse across down concentration gradient. Excess fluid diffuses down hydrostatic gradient (not osmotic like PD)
Access usually via AV fistula due to risk of infection with central venous dialysis catheters
What are the different types of HD?
- Unit based
- Home based: training offered so can do more frequently
- Nocturnal
- CRRT: used in ITU/HDU
What are the advantages of haemodialysis?
- More efficient form of dialysis
- Unit based so support from staff
What are the disadvantages of haemodialysis?
- Risk of bleeding due to heparin
- Infection
- Hypotension
- Anaemia
- AVF steal syndrome
- SVCO from central lines
- Time consuming
How does haemofiltration work and when is it used?
- Used in critical care patient’s BP is too low for haemodialysis
- Waste is replaced with volume of clean fluid before (pre-dilution) or after (post dilution) the membrane
What are the advantages and disadvantages of a renal transplant for ESRF?
Advantages
- Near normal lifestyle
- Better mortality/morbidity
Disadvantages:
- Lifelong medication
- Risk of rejection
- Risk of malignancies over time
- Risk of infection and immunosuppression
- Long waiting times
- Need to fufill certain criteria
What are some contraindications for kidney transplantation?
- Active infection or malignancy
- Severe heart or lung disease
- Reversible renal disease
- Uncontrolled substance abuse
- Non-adherance to treatment
- Short life expectancy
What are the different types of renal graft?
Deceased Donor:
- Long waiting list
- Survival of kidney and patient lower than living
Living Related Donors
- Best possible transplant option as higher compatibility as time to HLA march
- Only takes few months
Living Unrelated Donor:
- Also a best option
- 4 types: live-donor paired exchange, live-donor/deceased-donor exchange, live-donor chain, altruistic donation
How is long term rejection of a renal graft avoided?
Maintenance of immunosuppression therapy
Steroids: prednisolone or prednisone
Calcineurin Inhibitors: tacrolimus, cyclosporin
Antimetabolites: mycophenolate, azathioprin
T cell regulation: belatacept, belimumab
What is the long term care a patient needs following a renal transplant?
- For first 6 months review every few times a month
- Monitor GFR, CNI levels, proteinuria, Ca, PO4, PTH, lipids and glucose
- Screen for infections
- Vaccinations (not live or attentuared)
- Check for CVD and bone mineral disease
- Annual skin checks for skin cancer
- Contraception for first year then counsel about pregnancy
What infections are common following a renal transplant?
<4 weeks: nosocomial or from donor
1-12 months: activation of latent infections or opportunistic infections e.g CMV and Pneumocystitis Jirovecci
After 12 months: community acquired
What malignancies should you screen for after a renal transplant?
- Skin
- Cervix
- Prostate
- Renal and urothelial
- Liver
- Colorectal
- Lymphoproliferative disorder (especially if have EBV)
What is the prognosis following a renal transplant?
How do you carry out a fluid assessment on a patient?
- Hands: temp, cap refill, turgor
- Pulse and blood pressure
- JVP
- Face: eyes sunken and dry mouth
- Chest: heart sounds, lung bases, resp rate
- Abdomen: ascites
- Oedema
What are some signs on examination of CKD?
- Oedema
- Uraemic breath
- Pericardial rub
- Pulmonary oedema
- Palpable kidneys
- Uraemic yellow skin
What are some of the causes of sterile pyuria?
- TB
- Recently treated UTI
- Appendicitis
- Chlamydia
- Calculi
- Pregnancy
- Recent catheter
How does urinary tract tuberculosis present?
- Dysuria
- Frequency
- Suprapubic pain
- Sterile pyuria
- Negative culture
How does diabetic nephropathy develop?
- Hyperglycaemia leads to hyperfiltration and capillary hypertension as RAAS is activated due to less Na getting to macula densa
2. GBM thickens
3. Mesangial proliferation
4. Glomerulosclerosis
Prolonged exposure to high levels of glucose damages the delicate blood vessels in the glomeruli.
The damage to the glomeruli can result in increased pressure within the kidneys, leading to hyperfiltration.
The damaged glomeruli may become more permeable, allowing essential proteins, such as albumin, to leak into the urine. The presence of proteins in the urine is a sign of kidney damage and is known as proteinuria.
Inflammation and Fibrosis: The chronic exposure to high glucose levels and the leakage of proteins trigger inflammatory responses in the kidneys. Over time, this inflammation contributes to the development of fibrosis (the formation of scar tissue) in the kidney tissue.
Progression to Nephropathy: As diabetic nephropathy progresses, the kidneys’ ability to filter waste and fluids declines, leading to a gradual decline in kidney function.
Hypertension (High Blood Pressure): Diabetes can also contribute to hypertension, and high blood pressure, in turn, can worsen kidney damage. It creates a vicious cycle where kidney damage contributes to high blood pressure, and high blood pressure further damages the kidneys.
How is diabetic nephropathy diagnosed?
- Screening for microalbuminuria using albustix annually
- Dipstick for overt proteinuria
- ACR ratio in urine by sending off
How is diabetic nephropathy treated once microalbuminamia has developed?
Need to stop proteinuria developing as this is irreversible:
- Strict HbA1c control <6.5%
- Tight blood pressure contol using ACEi/ARB
- Statins
What diuretics work in each part of the kidney tubule?
What are some nephrotoxic drugs?
- NSAIDs
- Rifampacin
- Valproate
- PPIs
- Furosemide
- Thiazides
- ACEi/ARB
- Lithium
- Gentamicin and Tobramycin
How may a patient with ADPKD present?
- Asymptomatic
- Abdominal discomfort due to pressure
- Haematuria from haemoraghe into cyst
- Hypertension
- Renal calculi
What are some examples of loop diuretics, what is their action, when are they given and what are some common side effects?
Furosemide and Bumetanide
- Block Na/K/Cl transporter
- Fluid overload
- HypoNa, HypoK, Diuresis, Dehydration
What are some examples of thiazide/thiazide like diuretics, what is their action, when are they given and what are some common side effects?
Bendroflumethiazide and Indapamide
- Block NaCl channel in DCT
- Hypertension and fluid overload
- Cause HypoNa and Hypo K and Hyper GLUC
What are some examples of K sparing diuretics, what is their action, when are they given and what are some common side effects?
Amiloride and Spironolactone
Can cause hyperK and gynacoemastia
What are some examples of carbonic anhydrase inhibitors what is their action, when are they given and what are some common side effects?
Acetazolamide
- Used for glaucoma and benign intracranial HTN
- Flushing, metabolic acidosis, agranulocytosis
What are some of the side effects of steroids and what are some medications you should give alongside steroids?
- Hyperglycaemia
- Raised white cells
- Cushing’s
- Osteoporosis
- Glaucoma
- Muscle wasting
- Skin thinning
