A 62-year-old man, who was admitted to the nephrology service after consulting the emergency department with general malaise associated with bilious vomiting and evening varicella, treated with feline enters the hospital.
diuresis in the last days, without accompanying voiding symptoms.
She did not report taking NSAIDs or other nephrotoxic drugs.
The patient had a history of chronic obstructive pulmonary disease, obstructive sleep apnea syndrome, chronic obstructive pulmonary disease in follow-up by otorhinolaryngology and botulism that required admission to the ICU in 2007.
She had no history of hypertension, diabetes mellitus, dyslipidemia or heart disease.
Physical examination revealed a regular general condition, eupneic at rest, conscious, oriented and cooperative, normohydrated and normal perfusion.
BP was 143/95 mmHg, HR 75 beats/min, temperature 36.5oC and oxygen saturation 97%.
There were no skin or mucosal lesions.
Cardiopulmonary arrest: rhythmic tones without audible murmurs.
Gallbladder mucus without noises.
Abdomen: blade and depressible.
There were no signs of peritoneal irritation.
There were no masses or organomegaly related to fixation.
In the lower extremities he presented edema with fovea to the root of the limbs, without signs of deep vein thrombosis (DVT) or chronic venous insufficiency, with positive pulses.
Neurological examination revealed normoreactive isochoric pupils, normal cranial nerves, and strength and sensitivity preserved by segments.
There were no signs of meningeal irritation.
Blood tests at admission showed: haemoglobin 11 g/dl, haematocrit 34.7%, VCM 92 mEql calcium 9,000 (neutrophil 85%, lymphocytes 9.1%), platelets 213, glucose 107 65 mg/dl
Urine secretion: proteins 100 mg/dl; proteins 300; non-leukocyte negative nitrites.
Chest X-ray showed no signs of condensation or effusion, with normal mediastinum.
A plain abdominal X-ray showed nonspecific meteorism.
Venous acidosis: metabolic acidosis with pH 7.28, total CO2 20 mmol/l, HCO3- 18.8 mmol/l, EB -7.5.
ECG: sinus rhythm at 75 beats/min, normal PR, narrow QRS, without acute changes in repolarization.
Abdominal ultrasound: liver and spleen with no ultrasound abnormalities.
The right kidney was enlarged (15 cm), with loss of corticomedullary differentiation. No dilatation of the excretory pathway was observed.
Left hypoplastic kidney (described in previous studies).
Isotopic renogram with 99mTc-MAG3: functional cancellation of the left kidney.
Severe parenchymal nephropathy of the right kidney.
Immunology: IgG 795 mg/dl, IgA 123 mg/dl, IgM 25.1 mg/dl, C3 133 mg/dl, C4 normal, kappa chain 161 mg/dl, normal lambda.
Autoimmunity: ANA, Ac-anti-DNA and ANCA-c negative, ANCA-p 41U/ml and Ac-anti-MBG 287 U/ml.
Proteinogram normal.
Serology for HBV and HCV negative.
Having these clinical and analytical findings, it was decided to perform a renal biopsy by open lumbotomy, since the patient is a functional mono kidney.
The pathological anatomy describes a total of 49 glomeruli, three of them sclerosed; in the rest there was extensive involvement of the structure with fibrinoid necrosis and extra-cellular and circumferential glomerulus proliferation in 100%.
Small caliber vessels also presented necrotizing vasculitis.
Direct FI study showed linear and diffuse positivity in the glomerular basal membrane with positive IgG, the rest of the antibodies being negative.
In summary, the patient had extracapilary glomerulonephritis with intense involvement of 100% of the glomerulonephritis sampled and typical IF of extracapilary glomerulonephritis type I (anti).
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Since admission the patient required renal replacement therapy.
The patient was treated with conservative treatment with intravenous steroids at doses of 1.5 mg/kg/day, methylprednisolone 500 mg/24 h for 3 days and plasmapheresis (7 sessions).
Cyclophosphamide was discontinued due to thrombopenia.
There was no pulmonary involvement at any time during evolution.
Currently the patient remains on hemodialysis program with arteriovenous fistula as vascular access.
