An 11-year-old girl was admitted to our hospital with microscopic hematuria and nephrotic-range proteinuria detected by school urinary screening. The patient did not have any characteristic features of Fabry’s disease such as angiokeratoma or neuralgia. On admission, her physical examination was unremarkable (body weight 47.4 kg, body height 157.3 cm), and her blood pressure normal (106/60 mmHg). Laboratory investigations revealed hypoproteinemia (serum total protein 5.6 g/dL, serum albumin 2.9 g/dL, serum IgG 318 mg/dL). All other biochemical investigations were within normal limits: blood urea nitrogen 8 mg/dL, serum creatinine 0.43 mg/dL, IgA 111 mg/dL, C3 140 mg/dL (normal 84 – 151 mg/dL), C4 26 mg/dL (normal 17 – 40 mg/dL). Anti-hepatitis B surface antigen, anti-hepatitis C antibody, and anti-nuclear antibody were negative. Urinalysis findings were 3+ for occult blood and 3+ for the dipstick protein reaction; her 24-hour urine protein excretion was 2.5 g. Light microscopy analysis of the initial renal biopsy specimen revealed diffuse mesangial proliferative glomerulonephritis with fibrocellular crescents in 4 of 13 glomeruli (a). Immunofluorescence revealed granular deposits of IgA (3+) and C3 (1+) in the mesangial areas (b), and electron microscopy revealed paramesangial electron-dense deposits. Based on these findings, a diagnosis of severe IgA nephropathy was made. The patient was treated intravenously with three courses of methylprednisolone (20 mg/kg/day) pulse therapy (MPT), followed by 2 years of alternate-day prednisolone (initially 1 mg/kg and then tapered gradually) combined with an angiotensin receptor blocker (telmisartan 1 mg/kg/day). In addition, a tonsillectomy was performed 3 months after MPT. However, microscopic hematuria and mild proteinuria persisted.
At the age of 13 years, the patient was re-admitted for a second renal biopsy to assess the therapeutic effect. All laboratory investigations were within normal limits: serum total protein 6.3 g/dL, serum albumin 4.0 g/dL, blood urea nitrogen 12 mg/dL, serum creatinine 0.44 mg/dL, IgA 108 mg/dL, C3 96 mg/dL, C4 26 mg/dL. Urinalysis revealed a 2+ value for occult blood and a dipstick protein reaction of 2+; the 24-hour urine protein excretion was 0.5 g. Light microscopy analysis of the second renal biopsy specimen revealed focal segmental mesangial proliferative glomerulonephritis. Immunofluorescence revealed granular deposits of IgA (2+) and C3 (1+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. After the second renal biopsy, the patient was additionally treated with three courses of MPT, and her microscopic hematuria disappeared within 6 months.
At the age of 15 years, she was admitted for a third renal biopsy. On admission, her physical examination was unremarkable (body weight 55.9 kg, body height 165 cm), and her blood pressure normal (102/70 mmHg). Laboratory investigations were all within normal limits: serum total protein 6.6 g/dL, serum albumin 4.2 g/dL, blood urea nitrogen 11 mg/dL, serum creatinine 0.48 mg/dL, IgA 135 mg/dL, C3 121 mg/dL, C4 25 mg/dL. Urinalysis was negative for occult blood and the dipstick protein reaction was 2+; her 24-hour urine protein excretion was 0.7 g. Light microscopy analysis of the third renal biopsy specimen revealed minor glomerular abnormalities (a). Immunofluorescence revealed granular deposits of IgA (2+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. In addition, numerous myelin-like bodies were first observed in podocytes (b). Low serum α-galactosidase A activity (13.8 Agal U, cut-off value < 20) and increased GL3 excretion in the urine (0.54 mg/mgCr, control 0.1 – 0.4) were also observed. On the basis of these findings, a final diagnosis of concomitant IgA nephropathy (healing stage) and subclinical Fabry’s disease was made.
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 female, which means that the gender coefficient is 0.85.
The patient is 15 years old. 
The concentration of creatinine is 0.48 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 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 55.9 kg. The patient's bmi is therefore 55.9 kg / (1.65 m * 1.65 m) = 20.533 kg/m^2.The patient's BMI is 20.5, 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 55.9 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 15) * 55.9 * 0.85) / (0.48 * 72) = 171.857 mL/min. Hence, the patient's creatinine clearance is 171.857 mL/min.