Sieged Kidneys.

To the Editor, A 20-year-old male was admitted to the nephrology outpatient clinic due to swelling of legs, abdominal distention, and dyspnea. His medical history was remarkable for steroid-resistant focal segmental glomerulosclerosis due to podocin mutation. His sister also had the same renal disease, and after a period of peritoneal dialysis treatment for a while, she received a kidney transplant from her mother. Neither recent trauma nor operation history was present. He had recevied methylprednisolone, cyclosporin, and tacrolimus in the past, and current therapy consisted of dual renin angiotensin inhibition, statin, and proton-pump inhibitor. On physical examination, arterial pressure was 140/80 mm Hg, heart rate 89/min, also bilateral crackles at lower lobes of lungs, bilateral pretibial edema, and ambiguous costovertebral angle tenderness were present. Routine laboratory findings were as 24 h proteinuria 11.8 g/d, serum albumin 1.44 g/dL, total protein 4.44 g/dL, creatinine 0.85 mg/dL, and low-density lipoprotein was 230 mg/dL. Thoracoabdominal computed tomography revealed bilateral pleural and perirenal effusion without any evidence of hydronephrosis (Figures 1 and 2). Intravenous loop diuretic therapy concurrently with albumin infusion was initiated. He is still under follow-up but refusing any further interventions and potential immunsuppression.Figure 1: Thoracoabdominal computed tomography, transverse scan, Right perirenal fluid ~7 cm, left perirenal fluid ~4 cm thick, which compresses the kidney parenchyma.Figure 2: Thoracoabdominal computed tomography, coronal scan, bilateral perirenal effusion.Perinephric collections may be composed of lymph, hematoma, pus, urine, as well as fluid accumulations of different characteristics. Vascularization is very intense in the perirenal region and sodium/water retention, veno-occlusive situations are thought to be mostly responsible forthis entity. Nephrotic syndrome, postoperative lymphoceles (post-renal transplant), pulmonary hypertension-Eisenmenger syndrome, lymphangiomatosis, and Page kidney are the main nontraumatic etiologies for peri-renal fluid collection. However, peri-renal effusion in bilateral nature is not experienced frequently, especially during systemical disorders. Fluid accumulation can happen in any body cavities: peritoneal, pleural - in nephrotic syndrome and very rarely renal subcapsular area. Glomerulonephritis-associated perirenal effusion has a few examples in the literature. Wani et al described a teenager with focal segmental glomerulosclerosis (FSGS) with the initial signs of massive unilateral renal subcapsular effusion and hypertension treated with cyclophosphamide and enalapril.[1] Kumar et al reported a 21-year-old female presenting with bilateral massive renal subcapsular collections and after renal biopsy diagnosis was FSGS-not otherwise specified. The fluid collection did not decreased with steroids and so fenestration was performed.[2] Yalcin et al reported a patient with FSGS presenting as nephrotic syndrome. Intense subcapsular fluid collection was treated completely with the immunsuppresion of cyclophosphamide, and steroids.[3] Aliasgari et al reported a 27-year-old patient with membranoproliferative glomerulonephritis presenting with perirenal effusion initially.[4] Treatment of subcapsular effusion in nephrotic syndrome is achieved best by treating the underlying kidney disease and draining the subcapsular fluid if necessary. Therefore, in patients with glomerulonephritis and flank pain, subcapsular fluid accumulation should be considered. Both systemic immunsupression and drainage seem to be efficient in approach to perirenal fluid collection regarding to the systemic conditions. Diuretics also can be used but watching over the risk of effective volume decrease, especially in nephrotic sydnrome. It seems quite interesting that reported cases with glomerulonephritis in the literature were generally young and the association with FSGS was more prominent. Written informed consent was obtained from the patient. Conflict of interest: None declared.