Week 8: Renal disease (1) (renal function tests and electrolyte balance) Flashcards
renal function tests
bloods
urine
imaging
blood tests
- FBC – Anaemia, infection, allergic reactions,
- Haematinics – Iron/Folate/B12 deficiency
- U&Es – Potassium, Urea, Creatinine, Bicarbonate
- Bone profile – Calcium, Phosphate, PTH, Alkaline Phosphatase
- CRP – Infection/Inflammation
- HbA1c – Diabetic control
- ABG/VBG
urine
- Urine Dipstick – Infection (leukocytes, nitrites); Glomerular pathology (blood, protein)
- Urine Protein: Creatinine Ratio – Quantifies the amount of all protein in the urine
- Urine Albumin:Creatinine Ratio – Quantifies just albumin (good for diagnosing and monitoring diabetic nephropathy)
- Urine microscopy, culture and sensitivity
imaging
US KUB (kidneys, ureters and bladder)
- look for peri-nephric collections
- size of kidneys
- corticomedullary differentiation
- hydronephrosis
ABG results
the anion gap
useful in working out what could be causing acidosis
high anion gap
acidosis due to increased acid
normal anion gap
acidosis due tor educed alkali
Diabetes insipidus
Differential- psychogenic polydipsia (mental illness and developmental disability)
Presentation
- Dilute urine (osmolality <300)
- Polydipsia and polyuria
- Impaired release of ADH (cranial DI)
Causes
- Impaired release:Cranial DI
- Trauma/post op tumours
- Cerebral sarcoid/TB infections (menin/encep)
- Cerebral vasculitis (SLE/Wegeners)
- Resistance to ADH: Nephrogenic DI
- Congenital, drugs (lithium, amphotericin, demeclocycline), hypokalaemia, hypercalcaemia, tubulointerstitial disease
Treatment: generally- free water
types of hypernatremia
-
Hypovolaemic high Na
- Renal free water losses (osmotic diuresis(NG feed etc), loop diuretics, intrinsic renal disease)
-
Euvolemic High Na
- Renal losses (diabetes insipidus, hypodipsia - dehydration)
-
Hypervolaemia High Na (sodium Gains)
- Primary hyperaldosteronism, Cushing’s syndrome, hypertonic dialysis, hypertonic sodium bicarbonate, sodium chloride tablets
hypernatraemia impact on body
- Causes cellular dehydration (osmotic drag)
- Creates vascular shear stress (bleeding and thrombosis)
presentations of hypernatremia
- Thirst
- Apathy
- Irritability
- Weakness
- Confusion
- Reduced consciousness
- Seizures
- Hyperreflexia
- Spasticity
- Coma
Change in sodium is rarely a change in sodium conc, usually a change in
water
causes of hypernatraemia
- Think of water- less water to sodium (not really about sodium)
-
Causes
- Osmotic diuresis (e.g. uncontrolled diabetes)- excreting too much water
- Fluid loss without replacement (sweating, burns, vomiting)
- Diabetes insipidus (suspect of lots of dilute urine produced)
- Incorrect intravenous fluid replacement
- Primary aldosteronism
hyponatraemia impact on the body
causes cellular swelling
symptoms of hyponatraemia
- Decreases perception
- Gait disturbance
- Yawning
- Nausea
- Reversible ataxia
- Headache
- Apathy
- Confusion
- Seizures
- Coma
causes of hyponatreamia
- Pseudohyponatremia
- High lipids
- Myeloma
- Hyperglycaemia
- Uraemia
- Hypovolaemic hyponatremia
- Euvolemic hyponatremia
- SIADH
- Hypervolemic hyponatremia
causes of hyponatraemia
- Pseudohyponatremia
- High lipids
- Myeloma
- Hyperglycaemia
- Uraemia
- Hypovolaemic hyponatremia
- Euvolemic hyponatremia
- SIADH
- Hypervolemic hyponatremia
investigations for hyponatraemia
- Plasma osmolality (if normal or raised then pseudohyponatremia)
- Hypokalaemia/hypomagnesemia potentiates ADH release
- Urine sodium (if <20 then non-renal salt losses, if >40 then SiADH) (diuretics may confound)
- TSH
- 9am cortisol
- Calcium
- Albumin
- Glucose
- LFT
- CT head
- CT chest- SIADH
Risk of correcting hyponatraemia quickly
Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis.
- Aim to correct <12 mmol/L/day
treatment of hyponatraemia
- Acute (tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy)
- If acute hyponatraemia (within 48 hours) and symptomatic – Give 3% hypertonic saline IV boluses +/- Furosemide Chronic
- If chronic (>48 hours) and symptomatic – hypertonic saline boluses if having seizures.
- Otherwise isotonic saline and furosemide – aim to correct 8mmol/L in 24 hours
- If chronic and asymptomatic – water restriction, stop offending drug, if dehydrated – restore volume, if overloaded – Na and water restriction and diuretics
causes of euvolemic hyponatraemia
normal sodium stores and a total body excess of free water
causes:
- Hypothyroidism
- Primary polydipsia (if urine osmolality <200)
- Glucocorticoid deficiency- adrenal insufficiency
- SIADH
SIADH
- Low serum osmolality
- Inappropriately concentrated urine – Urine osmolality >100
- Urine Na >20
- Clinical euvolaemia
- Not on diuretics
- Diagnosis of elimination – normal renal, thyroid, adrenal function
Management of SIADH
- Fluid restrict <800ml/day.
- PO sodium chloride
- May give furosemide
- Demeclocycline induces diabetes insipidus (reversing ADH effect), alternatively Tolvaptan
causes of hypovolaemic hyponatraemia
- Renal loss (urine Na+ >20 mmol/L)
- Diuretics (thiazides), osmotic diuresis (glucose, urea in recovering ATN), Addison’s disease (mineralocorticoid deficiency)
- Non renal loss (urine Na <20mmol/L)
- Diarrhoea, vomiting, sweating, third space losses (burns, bowel obstruction, pancreatitis)
treatment of hypovolaemic hyponatraemia
- IV fluids (0.9% NaCl at 1-3ml/kg/hour
- Give K if necessary
hypervolemic hyponatraemia
This increase in total body water is greater than the total body sodium level, resulting in edema.
Causes
- CCF
- Nephrotic syndrome
- Liver cirrhosis
Treatment
- Fluid restriction and consider furosemide
cause sof hyperkalaemia
- CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)
- Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/B- blockers)
- Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use
- Rarer – Hyperkaliaemic periodic paralysis, Gordon’s syndrome
- Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis
ECG changes in hyperkalaemia
- Tented T waves
- Prolonged QRS
- Slurring of ST segment
- Loss of P waves
- Asystole
treatment of hyperkalaemia
- 10mls of 10% calcium gluconate over 5-10 minutes
- Stabilises myocardium to prevent arrhythmias
- IV fast acting insulin (actrapid)
- With 10 units IV glucose/dextrose 50% 50mls
- Shifting potassium back into the intracellular space
-
Calcium resonium
- 15-45g orally or rectally
- Eliminating potassium from body
-
Furosemide
- Eliminating potassium from the body
-
Dialysis
- Eliminating potassium from the body
Hyporeninaemic hypoaldosteronism (Type IV renal tubular acidosis)
- Hypochloraemic acidosis in about 50%
- hyperkalaemia
- Often hypertensive with increased extra-cellular fluid volume (renin often down regulated by fluid overload
Risk factors
- Increased age
- Reduced eGFR
- Diabetes nephropathy
- Nephritis
- TIN/sickle cells
- NSAIDs CNI
- Lupus nephritis
symptoms of hypokalaemia
- Fatigue
- Constipation
- Proximal muscle weakness
- Paralysis
- Cardiac arrhythmias
- Worsened glucose control in diabetics
- Hypertension
ECG treatment in hypokalaemia
- Small T waves
- U wave (after T)
- Increased PR interval
causes of hypokalaemia
- Pseudohypokalaemia – acute leukaemia
- Extra-renal losses - Inadequate PO intake, Gut losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)
- Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)
- Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)
- Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),
- Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.
treatment of hypokalaemia
- Replace magnesium
- Oral K replacement
- IV K replacement (Usually in 0.9% NaCl - avoid in dextrose as induces further hypokalaemia)