A 24-year-old male presented with confusion, shortness of breath, and painful calves. It was reported by a friend that he had been lying on the floor for several hours. He was a known intravenous heroin and alcohol abuser. On examination he appeared dehydrated and cold (tem- perature 35°C); his pulse was 75/minute and blood pres- sure 110/70 mmHg. Intravenous injection sites were apparent. His urine was dark coloured. His chest was clear. Arterial blood gases were done in the casualty department and a blood sample was sent to the pathology department and gave the following results (reference ranges are given in brackets): Arterial blood pH PCO₂ PO₂ HCO3- Serum Sodium Potassium Creatinine Calcium Albumin Phosphate Creatine kinase C-reactive protein 7.276 4.82 KPa 12.7 kPa 18.0 mmol/L 138 mmol/L 7.6 mmol/L 236 μmol/L 1.66 mmol/L 32 g/L 2.43 mmol/L >140,000 U/L 73 mg/L (7.35-7.45) (4.7-6.0) (12.0-14.6) (24-29) (135-145) (3.8-5.0) (71-133) (2.10-2.55) (35-50) (0.87-1.45) (55-170) (<10) The patient was considered to have AKI secondary to muscle breakdown (rhabdomyolysis) caused by prolonged limb compression (compartment syndrome). He was started on intravenous normal saline and bicarbonate (forced alkaline diuresis), calcium gluconate, calcium resonium, and dex- trose, and began to feel better within 12 hours. His urine output was poor initially (250 mL output after 5 L infusion) and failed to improve, despite use of the diuretic frusemide. He continued to complain of painful thighs and his calves were swollen, particularly on the left leg. An ultrasound examination found no evidence of deep vein thrombo- sis. He underwent bilateral calf fasciotomies (i.e. surgical procedures in which the fascial compartment around the muscle is cut to reduce pressure) and was subsequently treated with haemofiltration and then haemodialysis. His creatine kinase gradually fell (4,600 U/L by day seven after admission). However, he remained on haemodialysis for nearly a month, by which point his own renal function had recovered. (a) Why did the patient's urine appear dark? (b) Why did he become hypocalcaemic and hyperphos- phataemic?

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A 24-year-old male presented with confusion, shortness of
breath, and painful calves. It was reported by a friend that
he had been lying on the floor for several hours. He was a
known intravenous heroin and alcohol abuser.
On examination he appeared dehydrated and cold (tem-
perature 35°C); his pulse was 75/minute and blood pres-
sure 110/70 mmHg. Intravenous injection sites were
apparent. His urine was dark coloured. His chest was clear.
Arterial blood gases were done in the casualty department
and a blood sample was sent to the pathology department
and gave the following results (reference ranges are given
in brackets):
Arterial blood
pH
PCO₂
PO₂
HCO3-
Serum
Sodium
Potassium
Creatinine
Calcium
Albumin
Phosphate
Creatine kinase
C-reactive protein
7.276
4.82 KPa
12.7 kPa
18.0 mmol/L
138 mmol/L
7.6 mmol/L
236 μmol/L
1.66 mmol/L
32 g/L
2.43 mmol/L
>140,000 U/L
73 mg/L
(7.35-7.45)
(4.7-6.0)
(12.0-14.6)
(24-29)
(135-145)
(3.8-5.0)
(71-133)
(2.10-2.55)
(35-50)
(0.87-1.45)
(55-170)
(<10)
The patient was considered to have AKI secondary to muscle
breakdown (rhabdomyolysis) caused by prolonged limb
compression (compartment syndrome). He was started on
intravenous normal saline and bicarbonate (forced alkaline
diuresis), calcium gluconate, calcium resonium, and dex-
trose, and began to feel better within 12 hours. His urine
output was poor initially (250 mL output after 5 L infusion)
and failed to improve, despite use of the diuretic frusemide.
He continued to complain of painful thighs and his calves
were swollen, particularly on the left leg. An ultrasound
examination found no evidence of deep vein thrombo-
sis. He underwent bilateral calf fasciotomies (i.e. surgical
procedures in which the fascial compartment around the
muscle is cut to reduce pressure) and was subsequently
treated with haemofiltration and then haemodialysis. His
creatine kinase gradually fell (4,600 U/L by day seven after
admission). However, he remained on haemodialysis for
nearly a month, by which point his own renal function had
recovered.
(a) Why did the patient's urine appear dark?
(b) Why did he become hypocalcaemic and hyperphos-
phataemic?
Transcribed Image Text:A 24-year-old male presented with confusion, shortness of breath, and painful calves. It was reported by a friend that he had been lying on the floor for several hours. He was a known intravenous heroin and alcohol abuser. On examination he appeared dehydrated and cold (tem- perature 35°C); his pulse was 75/minute and blood pres- sure 110/70 mmHg. Intravenous injection sites were apparent. His urine was dark coloured. His chest was clear. Arterial blood gases were done in the casualty department and a blood sample was sent to the pathology department and gave the following results (reference ranges are given in brackets): Arterial blood pH PCO₂ PO₂ HCO3- Serum Sodium Potassium Creatinine Calcium Albumin Phosphate Creatine kinase C-reactive protein 7.276 4.82 KPa 12.7 kPa 18.0 mmol/L 138 mmol/L 7.6 mmol/L 236 μmol/L 1.66 mmol/L 32 g/L 2.43 mmol/L >140,000 U/L 73 mg/L (7.35-7.45) (4.7-6.0) (12.0-14.6) (24-29) (135-145) (3.8-5.0) (71-133) (2.10-2.55) (35-50) (0.87-1.45) (55-170) (<10) The patient was considered to have AKI secondary to muscle breakdown (rhabdomyolysis) caused by prolonged limb compression (compartment syndrome). He was started on intravenous normal saline and bicarbonate (forced alkaline diuresis), calcium gluconate, calcium resonium, and dex- trose, and began to feel better within 12 hours. His urine output was poor initially (250 mL output after 5 L infusion) and failed to improve, despite use of the diuretic frusemide. He continued to complain of painful thighs and his calves were swollen, particularly on the left leg. An ultrasound examination found no evidence of deep vein thrombo- sis. He underwent bilateral calf fasciotomies (i.e. surgical procedures in which the fascial compartment around the muscle is cut to reduce pressure) and was subsequently treated with haemofiltration and then haemodialysis. His creatine kinase gradually fell (4,600 U/L by day seven after admission). However, he remained on haemodialysis for nearly a month, by which point his own renal function had recovered. (a) Why did the patient's urine appear dark? (b) Why did he become hypocalcaemic and hyperphos- phataemic?
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