A 51-year-old man presented with nephrology consultation for proteinuria in nephrotic range (12.7 g) and elevated serum creatinine (1.65 mg/dl).
She reported lower limb edema and foamy urine.
She had a history of obesity and systemic arterial hypertension diagnosed seven years before and managed with slow-release nifedipine, enalapril and clonidine.
On physical examination, the patient was in good general condition, with a temperature of 36°C, blood pressure of 150/100 mm Hg, respiratory rate of 15 per minute, heart rate of 70 per minute and grade II edema of 84 kg.
The rest of the examination showed no positive findings.
Paraclinical tests are summarized in Table 1.
Renal ultrasound revealed increased cortical echogenicity, preserving the corticomedullary relationship, and normal size and renal contours.
1.
Glomerular disease, nephrotic-nephritic syndrome, uncontrolled systemic arterial hypertension, obesity and stage 3 chronic kidney disease were considered as presumptive diagnoses.
Antihypertensive therapy was readjusted providing greater antiproteinase effect, hypoproteic tests with 0.8 g protein per kg of weight per day (one gram more protein per gram of proteinuria), oral hypolipidemic diets were ordered.
In view of the findings, percutaneous renal biopsy was performed, showing the presence of stenosis of the basal tubular lumen; showing a total number of 39 (11morphous membranes with a negative membrane (50%); fibrosis+; segmental artery stenosis+; pink cell proliferation).
Immunofluorescence revealed: IgG (++) in the basal capillary membrane and tubular basement membrane; IgA, trace or negative in the basal capillary membrane; cylinders (++); IgM, trace in the basal tubular membrane.
There were no other positive findings.
Diffuse thickening of the basal capillary membrane with presence of doubles and interposition of the mesangium was found in the electronic contour.
No deposits were found with characteristics of complexes in any location.
The mesangium matrix was expanded.
There were large masses of organized deposits of appearance.
flar, arranged at random, located mainly in the mesangium and intramedullary, measuring less than 25 nm.
Pathological examination revealed glomeru-lonephritis fantasy and chronic tubulointerstitial nephritis.
1.
established the first case of a patient with persistent nephrotic syndrome with intense proteinuria. Despite the findings of tubulointerstitial nephritis associated with chronic corticosteroid therapy and previous history of cyclophosphamide/kg of glomerulonephritis diary response.
Response was null and a second attempt with mycophenolate mofetil was also unsuccessful.
Therefore, the decision was made to intensify the control of the progression factors of renal disease.
During follow-up, her clinical evolution was characterized by difficulty in controlling blood pressure levels, persistent obesity, persistently elevated proteinuria in nephrotic range, difficult control of dyslipidemia and slow but progressive renal impairment.
After three years of follow-up, the patient was admitted to the emergency room for uremia and hypervolemia, creatinine levels of 12 mg/dl and BUN of 96 mg/dl, and urgent hemodialysis was initiated.
Two months later he was transferred to a chronic peritoneal dialysis program, in which he remains today.
