OBJECTIVE Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes. RESEARCH DESIGN AND METHODS Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to <75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c <7.5% (58 mmol/mol) or ≥7.5%. RESULTS Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c <7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia. CONCLUSIONS Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.

Introduction. Acute or recurrent pancreatitis may be a complication of primary hyperparathyroidism and patients with previous episodes of pancreatitis may develop secondary diabetes mellitus. Case report. We describe the clinical case of a 52-year old Caucasian man diagnosed with chronic recurrent pancreatitis in 2007. The first episode of acute pancreatitis occurred in 2002, followed by another 4 episodes in 2004 and 2007. In 2004, papilosfincterectomy was implemented with a stent mount that was removed one month later. In 2005, the patient underwent a surgical intervention for the diagnosis of chronic lithiasis, and cholecystectomy was performed. Additional investigations on the etiology of recurrent chronic pancreatitis, initially diagnosed as idiopathic, revealed elevated values of total serum calcium, serum parathormone, and the presence of a parathyroid adenoma in the right lower pole of the thyroid. In September 2007, parathyroidectomy was performed with a favorable evolution and the remission of the acute pancreatitis episodes. The patient had not had any family history of diabetes; in 2017 he was diagnosed with diabetes. Conclusion. In cases of recurrent pancreatitis, screening for hyperparathyroidism is recommended. Metabolic evaluation is required, because the risk of developing diabetes in patients with recurrent pancreatitis is high.

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Insulinoma are insulin-secreting tumors of pancreatic origin that generates hypoglycemia by excessive secretion of insulin. Insulinoma is a rare disease ant the most tumors are benign, solitary and occur at intrapancreatic sites. Case report. A 42-year old Caucasian women was hospitalized at the “Prof. N.C. Paulescu” National Institute of Diabetes, Nutrition and Metabolic Diseases Bucharest in April 2019 after an episode of hypoglycaemia remitted after intravenous glucose administration. Patient accused for about two weeks anxiety phenomena. At the time of admission in the hospital the patient was conscious in a good general condition. Paraclinical investigations revealed basal blood glucose 29 mg/dl, fasting insulin serum 87.7 µU/ml and pancreatic C-peptide-7.90 ng/ml. During hospitalization under strict glycaemic monitoring, the patient presented frequent asymptomatic hypoglycemic episodes that was remitted after intravenous glucose administration. Nuclear magnetic resonance highlighted a nodular lesion of the pancreas and in May 2019 the tumor resection was practiced. After surgery the blood glucose ranged between 86 mg/dl and 116 mg/dl. To mention that patient has a family history of diabetes and she’s obese. Conclusion. This case suggests that lack symptoms of hypoglycaemia may be present in patients with insulinoma. Diagnostic of insulinoma requires high clinical suspicions, accurate biochemical investigations and imaging techniques for the localization of the tumor and may represent a challenge in certain situations.