A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively.
The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 51 years old. 
The concentration of creatinine is 2.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.57 m * 1.57 m) = 19.879 kg/m^2.The patient's BMI is 19.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 49.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 49.0 * 1) / (2.0 * 72) = 30.285 mL/min. Hence, the patient's creatinine clearance is 30.285 mL/min.