Renal Flashcards
Renal Trauma Grading
- Haematuria, no parenchymal involvement, subcapsular, normal urogram
- Non-expanding, confined to retroperitoneum, < 1cm, no urinary extravasation
- III >1cm involving renal cortex (no urinary extravasation or collecting system involvement)
- Cortex, medullary and collecting system or vascular involvement
- Shattered or an avulsed kidney
Rhabdomyolysis
Assessment
* tender swollen muscles
* elevation of CK
- nearly always > 1,000
- usually > 10,000 -100,000
* in late presentations, serum myoglobin may be normal
* presence of myoglobinuria
- dark red brown urine
- dip stick positive but red cells not seen on microscopy
- may not be present in patients who are severely oliguric / anuric
*risk of renal impairment
- urine myoglobin concentration > 20 000µg/L
- myoglobin clearance rate < 4 mL/min.
- automated immunoassays are becoming more widespread for the measurement of urine myoglobin
- hyperkalaemia
- hypocalcaemia
- most common metabolic abnormality
- usually self limiting
- hyperphosphataemia
- hyperuricaemia
- hypoalbuminaemia
- elevated serum aldolase
Management
* Rx life threatening hyperkalaemia as a priority
* Avoid suxamethonium
Anuric
* haemodialysis
* replace insensible losses and restore euvolaemia only
Oliguric
* urinary output monitoring
* maintenance of high urinary flow
-> 2 mL/kg/hour
*IV fluids
-usually NSaline at 1L/hour for first 4 hours
* mannitol
* CVP monitoring if urine output inadequate following initial fluid loading
-avoid fluid overloading in elderly or those with decreasing urine outputs
* commence dopamine if urine output low despite adequate CVP
* urinary alkalinisation
- aim to maintain urinary pH > 7
- myoglobin has higher renal toxicity at lower pH
- 50 mmol/hour HCO3- in first hour usually required
- beware of worsening hypocalcaemia
- Ca2+cannot be mixed with HCO3- due to precipitate formation
Treat underlying cause
* thermal regulation
* seizure control
* fasciotomy / amputation
* antibiotics
Prognosis
* hospital admission usually required
* exertional rhabdomyloysis without heat stroke usually has a benign course even when CK > 25,000
-suitable for short stay admission
PO4
The normal physiologic blood level of phosphate is 0.8 mmol/L - 1.4 mmol/L.
In view of its vast physiological importance in the body, phosphate homeostasis is very closely regulated in the body, via vitamin D, PTH and the kidneys
Roles:
- Bone Structure
- Cellular processes
- Intergral DNA/RNA component
- 2,3 DPG production
- ATP - energy for cellular functions/transport/metabolism (aerobic and anerobic)
- Buffering
- Bone
- Urine
Hyperphosphataemia
Hyperphosphataemia - serum >1.4 mmol/L.
Chronic > acute
CRF most common cause
Oral sodium phosphate laxatives can cause acute severe hyperphosphataemia, which can be life-threatening.
Acute - usually Asx unless very acute/severe
- Seizures
- CV collpase
- Respiratory depression
Chronic
- See effects of hypocalcemia - Sx/ECG signs
- Metastatic calcification
- Calculus formation
Causes
- XS intake
- PO4 enemas/laxatives
- Iatrogenic
- Dec excretion
- Ac and CRF
- Inc renal tubular reabsorbption
- HypoPTH
- Thyrotxicosis
- XS vitamin D
- Shift intracellular to extracellular
- Metabolic or respiratory acidosis
- Tumour lysis
- Rhabdo
- Spurious
- Paraproteinaemia
- Hyperbilirubinaemia
- Heamolysis
- Hyperlipidaemia
Mx
- Rehydration
- Haemodialysis if not responding to IVF or CRF
- Ca / Mg replacement
- Chronic - decrease dietary intake /PO4 binders/
Hypophosphataemia
Normal: 0.8 mmol/L - 1.5 mmol/L.
Mild hypophosphataemia: 0.6 - 0.8 mmol/L.
Moderate hypophosphataemia: 0.30 - 0.6 mmol/L.
Severe hypophosphataemia: < 0.3 mmol/L.
Causes
- Reduced intake
- Malnutrition
- Malabsorption
- Intracellular shift (redistribution)
- Increased Excretion
Intracellular shift
- the most common cause
- usually
- transient
- normalises when the precipitant is removed
•respiratory alkalosis
- the most common cause
- rarely symptomatic
- phosphofructokinase activation stimulates production of phosphorylated glucose precursors
•catecholamines and beta receptor agonists
- severe pain
- post icrtal
- stimulant use
- e.g. Cushing’s syndrome
•carbohydrate / insulin
- phosphate moves into cells with glucose
- known as the ‘refeeding syndrome’
•rapidly growing leukaemias or lymphomas
-may preferentially consume phosphate
•hungry bone syndrome
- following parathyroidectomy for hyperparathyroidism
- massive uptake of Ca2+ and PO4-in bone
Hypercalcaemia
Increased urinary excretion
- chronic alcoholism
- primary and secondary hyperparathyroidism
- acute volume expansion
- osmotic diuresis
- carbonic anhydrase inhibitors
- malignancy
- transplanted kidneys
- Fanconi’s syndrome
Decreased intestinal absorption
- usually causes total body phosphate depletion
- chronic alcoholism
- chronic severe malnutrition
- malabsorption
- chronic phosphate-binding antacids or sucralfate use
-aluminium hydroxide antacid
Other
- hypothyroidism
- hypomagnesaemia
- hypokalaemia
- theophylline toxicity
- isolated phosphate deficiency is very rare - comorbid conditions nearly always exist
Ca2+
Hypocalacemia
Urine Creatinine Ratio
(70%) Pre-renal >100:1
Normal or (20%) Post-renal 40-100:1
( 10%) Renal <40:1
Low anion gap
Decreased unmeasured anions - albumin or dilution
Increased unmeasured cations - Li, Mg, Paraproteins
Bromide OD (falsely elevated Cl measurements)
RIFLE criteria for AKI
Risk - Creat 1.5x, GFR dec 25%, OU <0.5ml/kg
Injury - Creat 2x, GFR dec 50%, UO <0.5ml/kg
Fiailure - Creat 3x, or > 350, GFR dec 75%, UO <0.3ml/kg
Loss: 4 weeks persistent RF
ESRF > 3 months
Indications for renal replacement
Oliguria<200ml/12h
Anuria <50ml/12h
Serum concentrations
* Urea >35
* K >6.5
* Na <100 or >160
Pulmonary oedema refractory to diuretics
Severe metabolic acidosis
Uraemic syndrome - aterixis, psychosis, myoclonus, sizures, pericarditis)
Over dose with Dialysable toxin (Li, ASA, )
Causes of toxic ATN
