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Background: In 2013, the British Columbia (BC) Childhood Nephrotic Syndrome Clinical Pathway (CNSCP) was developed to standardize the care of children with nephrotic syndrome (NS). In BC, children access nephrology care at BC Children's Hospital (BCCH) and multiple regional clinics.

Objective: The primary objective was to compare induction therapy and clinical outcomes between BCCH and regional clinics since implementation of the CNSCP.

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Background: Lupus podocytopathy (LP) is a non-immune complex-mediated glomerular lesion in systemic lupus erythematosus (SLE), characterized by the diffuse effacement of podocyte processes without immune complex deposition or with only mesangial immune complex deposition. LP is a rare cause of nephrotic syndrome in SLE patients with implications for prognosis and treatment.

Case Report: We present the case of a 28-year-old woman with a medical history of type 1 diabetes mellitus (T1DM) who presented with lower limb edema, dyspnea, hypercholesterolemia, with nephrotic range proteinuria, without acute kidney injury, and laboratory findings compatible with auto-immune hemolytic anemia.

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Tripartite motif-containing 8 (TRIM8) gene mutations are associated with autosomal dominantly inherited neurorenal syndrome. The kidney manifestations range from nephrotic range proteinuria to nephrotic syndrome and kidney failure. The histopathology has been focal segmental glomerulosclerosis (FSGS) in all reported cases.

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Background: This study aimed to evaluate the response to therapy and outcome with long-term daily mycophenolate mofetil (MMF) and high-dose alternate-day steroids (HADS) in children with dense deposit disease (DDD).

Methods: Children with DDD who received long-term MMF (1200 mg/m/day) and HADS (1.5-2 mg/kg AD) with slow tapering were retrospectively evaluated for their clinico-pathological presentation, response to therapy (complete, partial, no remission) and outcome (patient and renal survival).

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Introduction: Experts have cautioned that assessment of proteinuria using urine protein-to-creatinine ratios (UPCRs) are not valid during acute kidney injury (AKI) because reduced urine creatinine in the denominator may artificially inflate the ratio. However, there is little empiric data assessing this theoretical concern.

Methods: Here, we retrospectively examined changes in UPCRs measured during episodes of severe AKI and assessed whether the magnitude and direction of these changes associate with how the serum creatinine level is changing at the time of UPCR collection.

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