Renal Function Tests Tute Flashcards
What causes a change in creatinine levels?
Increased
- Impaired renal function (acute or chronic failure)
- Lrge muscle mass or recent large protein (meat) meal
- Drugs that interfere with tubule handling of creatinine
Decreased
- Low muscle mass
- Pregnant women with an increase GFR
- Early increase in GFR in diabetic nephropathy
What causes altered urea?
Increased
- Impaired renal function (renal failure)
- Volume depletion (increased reabsorption of urea)
- High protein diet
- Upper GIT bleed (protein load/hypovolaemia)
- Catabolic states (sepsis and steroid therapy)
Decreased urea
- Reduced protein intake
- Malabsorption
- Liver disease (unable to general urea)
Causes of proteinuria
Benign: transient, fever, exercise, orthostatic
Glomerular: glomerulonephritis (nephritic or nephrotic syndrome), diebetes
Tubular: damage to the tubules - tubulointerstitial nephritis, acute tubular necrosis usually less than 3.5g/day
Overflow: ie in patients with multiple myeloma, myoglobin in rhabdomyolysis.
Causes of hyponatraemia
- Renal or GIT sodium and water losses (ADH increase) and patients are hypovolaemic
- Water excess due to: inappropriate ADH secretion, primary polydipsia (decreased ADH), low diet solute (decrease ADH) and patients are euvolaemia
- Reduced tissue perfusion including advanced cirrhosis and heart failure with fluid retention and patients are hypervolaemic.
Useful tests for hyponatraemia
Measure osmolality!
- High: suggests another osmotically active substance is in the blood (check glucose)
- Normal: think pseudohyponatremia (measure proteins and lipis)
-
Low: true hyponatremia
- Assess fluid status
- Measure urine sodium and osmolality
Presentation of hyponatraemia
People can be acutely hyponatremix and symptomatic (nausea, drowsiness, vomiting, confusion, seizures, coma) or chronically hyponatremic (heart failure) and be relatively asymptomatic. It is a rapid change in sodium that can be paritcularly dangerous.
Causes of hypernatraemia
Almost always due to a problem with water balance. Hypernatraemia willnot develop unless there is an impaired thirst mechanism or difficulties with access tow ater. Dehydration until proven otherwise! Other causes include:
- Osmotic diuresis (uncontrolled diabetics) - is a cause of dehydration
- Diabetes insipidus - central or neurogenic
- Consider too much salt
Diabetes insipidus presentation
Inability of the kidneys to concentrate the urine, resulting in polyuria. Patient has intense thirst and polydipsia. Patients can drink lots of water, thereby preventing hypernatremia - when they cannot they become hypernatemic.
- Central diabetes insipidus: caused by deficiency in ADH production due to lesions in the hypothalamus or pituitary
- Nephrogenic diabetes insipidus: due to an abnormal renal response to ADH
Causes of hypokalaemia
- Artefactual - sample taken from drip arm
- Decreased K+ intake. Oral rarely, inadequate K+ management in IV fluids more commonly.
- Depletion of total body potassium secondary to excessive renal or gastrointestinal losses.
* *Renal losses** - spot urine- Diuretics
- Mineralocorticoid excess
- Shift of potassium into the cells
- Metabolic alkalosis
- Glucose/insulin
- Catecholamines
- Salbutamol
- Anabolic state: B12 or folic acid (red cell production), GM-CSF (white cell production), total parenteral nutrition
- Hypothermia
Clinical presentation of hypokalaemia
Mild
- Asymptomatic
Moderate
- muscle weakness
- fatigue
- parasthesia
- constipation
Severe
- Weakness of respiratory muscles and respiratory failure
- Patients with cardiac disease are at an increased risk of ventricular arrhythmias
ECG changes from hypokalaemia
- Flattened or inverted t waves
- a U wave
- ST depression
- a wide PR interval
Investigations for hypokalaemia
- Acid base balance
- Spot K+ urine test
- Follow up with ABG if needed
Clinical presentation of hyperkalaemia
Symptoms are common, may have:
- Paraesthesia
- Cramps
- Severe muscle weakness
- Paralysis
- Cardiac arrhythmia: bradyarrhythmias and sudden death
Causes of hyperkalaemia
- Artefactual
- Acute or chronic renal impairment
- Drug related: ACE inhibitors, ATR blocker, spironolactone, NSAIDs
- Acute shifts of potassium out of the cell into the extracellular fluid with acid base disturvances
- Decreased K+ secretion
- Primary hypoaldosteronism
- Secondary hypoaldosteronism
- Resistance to aldosterone
Metabolic acidosis
pH <7.35, and HCO3- <22mmol/L
Clinically, patients with a severe metabolic acidosis exhibit a marked increased in ventilation due to both increased respiratory rate and increased depth of respitation.
