An 84-year-old man with a personal history of allergy to procaine and streptomycin, who had undergone surgery for a left hip replacement and bilateral inguinal hernia. In August 2010, he was diagnosed with RP and treatment with prednisone 30 mg/day was indicated. The patient was independent for activities of daily living and had no cognitive impairment.
At the time of consulting the Nephrology Department (8 months after the diagnosis of RP), he was on therapy with prednisone 5 mg, omeprazole 20 mg/day, enalapril 5 mg every 12 hours, levothyroxine 25 mg/day, chlorthalidone 12.5 mg/day.
The patient was admitted to the Nephrology Department for an increase in volume in the lower limbs and in the abdominal-scrotal region of four days' duration. On interrogation, he only reported a slight decrease in the diuresis rhythm and nocturia at one time.
Physical examination revealed a blood pressure of 150/80 mmHg, heart rate of 80 bpm, globular abdomen with dullness in the mesogastrium and oedema with pitting in the lower limbs, the rest of the examination being unremarkable.
Blood tests on admission showed: creatinine: 0.8 mg/dl; cholesterol: 354 mg/dl; triglycerides: 104 mg/dl; albumin: 2.2 g/dl; total protein: 5 mg/dl. Blood count and coagulation were normal. Serology for hepatitis B, C and human immunodeficiency virus: negative. In the immunological study, antinuclear antibodies and anti-neutrophil 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.
Tumour markers (carcinoembryonic antigen [CEA], CA19-9, alpha-fetoprotein and prostate-specific antigen [PSA]) were within normal values. CA125 was 136 IU/ml (normal value: 0-35).
The 24-hour urine protein quantification was 9.51 g/24h. Creatinine clearance was 77 ml/min. Urine electrophoresis also ruled out the presence of monoclonal peaks and Bence-Jones proteinuria was negative.
Chest X-ray showed a right pleural effusion.
In the renal ultrasound, the kidneys were 11 cm in size and there was no lithiasis or dilatation.
An abdominal CT scan was performed, which revealed a 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.
In the presence of florid nephrotic syndrome, a percutaneous ultrasound-guided renal biopsy was performed with the following findings: "5 glomeruli per slice plane, all with the usual histological characteristics. Immunofluorescence was negative for the markers studied (IgG, IgA, IgM and C3). The interstitium, tubules and vascular component were free of lesions. The final diagnosis was minimal change nephropathy (MCN).
Based on the biopsy findings, the prednisone dose was increased to 1 mg/kg/day. One month later, the clinical and biochemical remission of the nephrotic syndrome was confirmed at the outpatient clinic, and a tapering prednisone regimen was indicated.
Seven months later, when the patient was on maintenance therapy with prednisone 5 mg/day, a relapse of the nephrotic syndrome was observed, which made it necessary to increase the prednisone dose to 50 mg/day. After the nephrotic syndrome disappeared, prednisone was tapered to a dose of 2.5 mg/day.
One month after maintaining prednisone at a dose of 2.5 mg/dl, the patient consulted his general practitioner for oedema. Laboratory tests showed the appearance of proteinuria of 1.66 g/day, so it was decided to increase the prednisone dose to 10 mg/day, and the proteinuria disappeared. At the last nephrology review, on maintenance with prednisone 10 mg/day, the patient was asymptomatic and without proteinuria.

