Background Various risk factors have been identified for the new-onset or rapid deterioration of chronic kidney disease. However, it is thought that many risk factors that have not yet been clarified remain. Methods Based on the results of specific annual health checkups at Tama City (n = 18,383) in 2017 and 2018, we analyzed the factors that cause new-onset chronic kidney disease and the risk factors that rapidly worsen renal function. For new-onset chronic kidney disease, proteinuria and estimated glomerular filtration rate < 60 mL/min/1.73m2 were examined separately. Rapid deterioration of renal function was defined as an estimated glomerular filtration rate of ≥ 25% lower than the previous year. Results Multivariate analysis showed that, in addition to age and impaired glucose tolerance, anemia, and atrial fibrillation were risk factors for the new appearance of proteinuria. Risk factors for a decrease in estimated glomerular filtration rate < 60 mL/min/1.73m2 were age and hyperuricemia. Age, systolic hypertension, urinary protein and urinary occult blood, high triglycerides, and anemia were significant risk factors for the rapid deterioration of renal function in patients with chronic kidney disease stage 3 or later. Conclusions From the results of specific annual health checkups at Tama City, atrial fibrillation, anemia, and hyperuricemia were identified as risk factors for new-onset chronic kidney disease over a short period of 1 year. Anemia was also a factor for the rapid deterioration of kidney function in subjects with renal dysfunction.
Nephrotic syndrome is sometimes refractory; however, it is rarely accompanied by acute pancreatitis. A 47-year-old Japanese woman complaining of limb edema was diagnosed with nephrotic syndrome. Blood and urine examinations suggested minimal change nephrotic syndrome (MCNS), and pulse intravenous methylprednisolone was administered, followed by oral prednisolone. Although proteinuria improved, the patient's condition remained unchanged, and diuresis was insufficient. As in patients with other nephrotic syndromes, this patient showed significant dyslipidemia. Atorvastatin was started for remarkable dyslipidemia since her admission, but her low-density lipoprotein cholesterol (LDL-C) level did not improve significantly. During the clinical course, she developed acute pancreatitis, and large-volume fluid replacement was performed. Although diuretic levels were increased in response to the increased fluid volume, diuresis was not enough, and lung edema developed. Extracorporeal ultrafiltration was started to ameliorate the lung edema. With the onset of pancreatitis, oral intake, including atorvastatin, was discontinued, and prednisolone was administered intravenously. To treat the high-LDL cholesterolemia, 140 mg of evolocumab was injected subcutaneously. Nausea slightly decreased on the following day, and the administration of 150 mg cyclosporine was initiated. LDL-C levels, proteinuria, and renal function promptly ameliorated. The results of a renal biopsy suggested MCNS. On the 44th day of hospitalization, she had complete remission. Evolocumab is potentially effective for severe nephrotic syndrome with uncontrollable dyslipidemia.
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