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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Focal segmental glomerulosclerosis is a common cause of nephrotic syndrome. Acute inflammatory demyelinating polyneuropathy and focal segmental glomerulosclerosis are autoimmune disorders that may have common pathogenesis. Some literatures suggest IFN-2 as a link between kidney podocytes and peripheral nerve cells. Abnormalities in nephrin have been found in familial and sporadic cases of focal segmental glomerulosclerosis. As per few literature nephrin is also found in neuronal cells. We present an interesting case of focal segmental glomerulosclerosis which coincided with the development of Guillain -Barre – like syndrome.
A 62 years old male patient with no co-morbidities came with edema of bilateral lower limbs and facial puffiness for 2 months. On work up he had serum creatinine 0.6,serum albumin of 2.1,urine albumin creatinine ratio of 9990 mg/gm and 24 hour urinary protein being 4.8gm.Patient was clinically diagnosed as adult onset nephrotic syndrome and renal biopsy was planned. On the day of renal biopsy he had weakness of both lower limbs. The procedure was uneventful. The next day following biopsy he had progressive weakness in all 4 limbs. Neurological examination revealed decreased upper and lower limb deep tendon reflexes. Nerve conduction velocity was performed.
Biopsy revealed focal segmental glomerulosclerosis FSGS-NOS involving 2(15.4%) of the sampled glomeruli. Patient was initiated on tablet prednisolone 80 mg once a day. On the other hand nerve conduction velocity was suggestive of acute inflammatory demyelinating polyneuropathy variant of Guillain-Barre syndrome. Patient was given intravenous immunoglobulin 400mg/kg/day over a period of 5 days. Patient responded well to treatment. His power at the time of discharge improved from 2/5 in lower limbs to 4/5 and 3/5 in upper limbs to 4/5.He was capable of walking with assistance for 10 meters. After 3 weeks the patient’s urine albumin creatinine ratio also showed decremental pattern.
It’s well known that both these condition FSGS and GBS have autoimmune etiology. Our patient’s condition improved on steroids and intravenous immunoglobulin. Previous literatures have reported AIDP association with FSGS, membranous nephropathy and minimal change disease, but the pathogenesis remains under the curtain. In few literature the probable hypothesis is that the GBS autoreactive activated T-cells crosses the damaged blood nerve barrier enhancing cytokine upregulation, macrophage activation and phagocytic attack on the myelin either directly or by proinflammatory mediators. This possibly increases glomerular permeability to albumin by T-cell clones secreting vascular circulating factor in FSGS. The simultaneous occurrence of both these entities is unique reinforcing the fact that they share a common pathogenesis which needs further research.
