An 84-year-old man with a history of allergy to procaine and streptomycin underwent left hip replacement surgery and bilateral inguinal hernia.
In August 2010, she was diagnosed with RP and was treated with prednisone 30 mg/day.
The patient was independent for activities of daily living and had no cognitive impairment.
At the time of consultation with the Nephrology Department (8 months after RP), the patient was on prednisone 5 mg diagnosed, enalapril 20 mg/day, enalapril 5 mg every 12 hours, levothyroxine 25 mg.
The patient was admitted to the Nephrology Department due to an increase in volume in the lower limbs and in the abdomino-caudal region of four days of evolution.
The patient only reported a slight decrease in the rate of diuresis and nocturia at one time.
Physical examination revealed blood pressure of 150 mmHg, heart rate of 80 bpm, globulous abdomen with mesogastric tenderness and edema with fovea in the lower limbs examination.
Blood analysis at admission showed: creatinine: 0.8 mg/dl; cholesterol: 354 mg/dl; triglycerides: 104 mg/dl; albumin: 2.2 g/dl; total proteins: 5 mg/dl. Blood count was normal.
Serology of hepatitis B, C and human immunodeficiency virus: negative.
In the immunological study, antinuclear antibodies and antineutrophil cytoplasmic antibodies were negative, and complement was normal.
IgG was 450 mg/dl (normal range: 751-1560) and IgM and IgA were normal.
Blood electrophoresis showed a percentage decrease in albumin without monoclonal peaks.
The tumour markers (an anticancer agent), CA19-9, afetoprotein and pro-specific antigen [PSA]) were within normal limits.
CA 125 of 136 IU/ml (normal value: 0-35).
The 24-hour urine protein quantification was 9.51 g/24 h.
Creatinine clearance of 77 ml/min. Urine electrophoresis also ruled out the presence of monoclonal peaks, with negative Bence-Jones proteinuria.
The chest X-ray showed a right pleural effusion.
On renal ultrasound the kidneys were 11 cm in size and there was no stone or dilatation.
Abdominal computed tomography revealed thickening of the gastric folds.
For this reason a gastroscopy was requested, which confirmed the existence of a thickened pyloric fold, but without evidence of malignancy in the anatomopathological study.
Due to the presence of a florid nephrotic syndrome, an ultrasound-guided percutaneous renal biopsy was performed with the following findings: «5 glomeruli by cutting plane, all of them with usual histological characteristics.
Immunofluorescence was negative for the markers studied (IgG, IgA, IgM and C3).
There were no lesions in either interstice, tubules or vascular component.'
The final diagnosis was minimal change nephropathy (MCN).
The biopsy findings increased the prednisone dose to 1 mg/kg/day.
One month later, clinical and biochemical nephrotic syndrome remission was confirmed in the outpatient clinic and a descending prednisone regimen was indicated.
Seven months later, when the patient was on maintenance therapy with prednisone 5 mg/day, there was a relapse of nephrotic syndrome that continued to increase the prednisone dose to 50 mg/day.
After achieving the disappearance of the nephrotic syndrome, a descending prednisone regimen was indicated until reaching a dose of 2.5 mg/day.
One month after maintaining prednisone at a dose of 2.5 mg/dl, the patient consulted with his primary care physician for edema.
The laboratory tests showed proteinuria of 1.66 g/day, so it was decided to increase the dose of prednisone to 10 mg/day, achieving the disappearance of proteinuria.
In the last review of Nephrology, maintained with prednisone 10 mg/day, the patient is asymptomatic and without proteinuria.
