P0452GLYCOSURIA IN MEMBRANOUS NEPHROPATHY: AN UNDERESTIMATED MARKER?. (6th June 2020)

• Record Type: Journal Article
• Authors: Ormonde, Carolina; Laranjinha, Ivo; Gaspar, Augusta; Gonçalves, Margarida; Gil, Célia; Dickson, Jorge; Machado, Domingos
• Is Part Of: Nephrology dialysis transplantation. Volume 35(2020)Supplement 3
• Publication Date: 2020-06-06
• Subjects: Nephrology -- Periodicals; Hemodialysis -- Periodicals; Kidneys -- Transplantation -- Periodicals; Hemodialysis; Kidneys -- Transplantation; Nephrology; Periodicals; 616.61
• DOI: 10.1093/ndt/gfaa142.P0452
• Languages: English
• ISSNs: 0931-0509

Abstract

Abstract: Background and Aims: Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in adults. Some studies have suggested that glycosuria is present in the most severe cases of MN and this finding may be associated with tubular injury caused by the overload of filtered proteins. The aim of this study was to evaluate the association between glycosuria in MN and severity and prognosis of the disease. Method: We conducted a 36-month retrospective cohort study with all patients diagnosed in the last 10 years in our centre with primary MN confirmed by renal biopsy. Data collection was made from patients' charts. Patients were divided in two groups according to their glycosuric status at the diagnosis. Exclusion criteria: patients with diabetes and glucose intolerance, use of SGLT2 inhibitors, transplant kidney patients and secondary MN. Results: We studied 27 patients with primary MN. Four patients (14.8%) presented glycosuria at the time of diagnosis. Glycosuric and non-glycosuric groups had comparable demographic data. We found that glycosuric patients had higher baseline albuminuria (10.7±8.6 vs 4.6±4.1 g/g, p=0.029) and lower estimated glomerular filtration rate (eGFR) (39.2±24.6 vs 75.2±30.7 ml/min/1.73m2, p=0.037). We also found that patients with glycosuria had higher interstitial fibrosis and tubular atrophy (IFTA) (33.8%±21.4 vs 10.7%±17.1, p=0.035) but no differences in the percentage of glomerular sclerosis. There were no differences between groups in serum albumin, haemoglobin or therapy. At the end of the follow-up period there was no difference in eGFR decline rate (ml/min/year), 3-year eGFR, 3-year albuminuria and 3-year chronic kidney disease stage 5D incidence. Conclusion: Prevalence of glycosuria in primary MN is approximately 15%. Its presence at the time of diagnosis was associated with more severe clinical and histological markers: lower eGFR, higher albuminuria and higher IFTA. However, we did not find association between glycosuric status at diagnosis and disease progression. Prospective, bigger and longer studies are needed to evaluate these questions.