A 60-year-old man with a history of type 2 DM of more than 20 years of evolution, initially treated with antidiabetic drugs and in the last 5 years with insulin, with poor metabolic control.
Non-proliferative diabetic retinopathy.
Ex-smoker 30 cigarettes/day for 5 years.
The patient came to the emergency department complaining of generalized edema of one month of evolution, dyspnea on medium exertion and nocturia of 2-3 times.
On physical examination, the patient was in good general condition, conscious and oriented.
Blood pressure was 160/110 mmHg, heart rate was 80 beats/min. Jugular engorgement.
cardiac arrest.
Pulmonary auscultation revealed minimal crackles in the lung bases.
Oedemas with fovea to the knee; the rest of the examination was normal.
Blood analysis revealed glucose 200 mg/dl; urea 52 mg/dl; creatinine 144 mg/dl; ferritin 41dl proteins 1,2 mg phosphorus/dl; cholesterol 313 mg/dl; triglycerides 144 mg/dl; albumin 1,9 g.
Hemoglobin was 11.6 g/dl, hematocrit 3 and all other hemogram and coagulation tests were normal.
Thyroid hormones, serology of virus (HIV, hepatitis By C virus), and PSA were normal.
Hemoglobin A1c was 8.3%.
The immunological study, including immunoglobulins, complement, rheumatoid factor, ASLO, ANA, anti-DNA, ANCA and C-reactive protein, was also normal.
The urine systematic showed proteins +++, blood +, glucose ++, negative nitrites.
The 24-hour urine proteinuria was 10 g.
In urine electrophoresis, proteinuria was non-selective and Bence-Jones proteinuria was negative.
The chest X-ray showed cardiomegaly and signs of venocapilar hypertension grade II.
Abdominal ultrasound showed a normal morphology of the right kidney of 12 cm; the left kidney was 15 cm, with dilatation of the excretory system.
Depletive treatment was initiated with diuretics, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (AIIRAs), statins, low molecular weight heparin, and improved glycaemic control was recommended.
Due to left kidney hydronephrosis caused by pyeloureteral junction syndrome, a pyeloplasty was performed and percutaneous nephrostomy was placed in the left kidney.
In spite of these measures, the patient required new hospital admissions due to haemodialysis to initiate the nephrotic syndrome, with an increase in plasma creatinine to 2.5-3 mg/dl and persistence of nephrotic proteinuria, which is the reason for the program
Although the initial suspicion was DN, the patient on hemodialysis persisted with poor volumetric control and biochemical parameters of activity of nephrotic syndrome perform renal biopsy to rule out associated glomerulopathy.
Biopsy findings were: 12 glomeruli per cutting plane, five of them completely sclerosed.
All glomeruli studied showed mesangial expansion with formation of acellular nodules (Kinmelstein-Wilson).
Immunofluorescence was negative.
Moderate fibrosis with tubular focalization was observed in the interstice.
The vascular component showed a remarkable hyaline of its wall, being the final pathological diagnosis compatible with a diffuse nodular glomerulus, with morphological substrate of diabetic disease.
