Kidney disease in patients with obesity: It is not always obesity-related glomerulopathy alone.

OBJECTIVE: Patients with obesity are at risk for chronic kidney disease. The aim is to characterize the spectrum of kidney disease in these patients, which may be related to obesity, termed obesity-related glomerulopathy (ORG), or may have other diseases secondary to associated or unassociated medical conditions. METHODS: Native kidney biopsies from 2000 to 2012 were retrospectively reviewed from all patients with body mass index >30kg/m2. Glomerular diameter was measured using a standard micrometer and clinicopathologic characteristics were analyzed. RESULTS: 4% (287) of all biopsies were obtained from patients with obesity (mean: weight 122kg, BMI 40.4±7.35kg/m2) for proteinuria in 93% and renal insufficiency in 53%. Frequent associated factors were abnormal glucose metabolism (31%), hypertension (60%), and obstructive sleep apnea (9%). Typical lesions of ORG were seen in 41% of cases and additional diseases in the rest. Glomerulomegaly, glomerular diameter >180µm, was present in 84% of cases (mean 224µm) vs normal size in 11% (mean 157µm), but was not increased with higher magnitude of obesity. Proteinuria was highest in patients with idiopathic FSGS (mean 8g/24h) and immune complex diseases (mean 7.4g/24h) and was mainly subnephrotic in obesity-related FSGS and tubulo-interstitial diseases. Creatinine levels were highest in tubulointerstitial diseases (mean 8.4mg/dL) and progressive diabetic nephropathy (mean 2.5mg/dL). CONCLUSIONS: Diverse kidney pathology superimposed on ORG is present in patients with obesity with varied clinical renal disease, some of which may be amenable for therapy. Kidney biopsy will assist in delineating these lesions for appropriate management and prognosis.

Bortezomib therapy for nephrotic syndrome due to idiopathic membranous nephropathy.

Idiopathic membranous nephropathy is a common cause of nephrotic syndrome in adults. The nephrotic syndrome due to idiopathic membranous nephropathy is often resistant to glucocorticosteroids and requires an alkylating agent such as chlorambucil or cyclophosphamide to induce remission. Recent studies illustrate that antibodies against the autoantigen M-type phospholipase A2 receptor contribute to a vast majority but not all cases of idiopathic membranous nephropathy. Herein, we report a patient with nephrotic syndrome due to membranous nephropathy that was resistant to 6 months of therapy with ramipril and high-dose glucocorticosteroids but responded to a single cycle of bortezomib infusion.