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Introduction: The metabolic syndrome (MS) encompasses many metabolic abnormalities and the insulin resistance is considered as one of the most significant denominators. The chronic kidney disease (CKD) is an emerging health problem but only few patients would reach the end stage renal disease. There exists an increasing strong association between MS and CKD, but up until now the link between MS and CKD is unclear and there are few studies regarding the renal histology in MS. Methods: We describe an acute tubulointerstitial nephritis case, due to both infective and pharmacological aetiology, overlapping relevant histological changes (focal segmental glomerulosclerosis [FSG], hyaline arteriosclerosis) in a patient with MS and previously normal renal function. Despite the severe vascular finding (elevated renal arterial resistive index), the patient recovered a normal renal function. Results: We reviewed the kidney pathological studies in MS and analyzed the principal renal histological images of glomerulomegaly, segmental glomerulosclerosis, and obesity-related glomerulopathy. Conclusion: Despite the strong association, the renal involvement in MS has not been proven. A greater knowledge of the combination of histological renal changes in MS can help to understand the pathophysiological mechanism(s) of MS. [ABSTRACT FROM AUTHOR]

Cirrhosis is frequently associated with sarcopenia, with reported rates of over 80% in patients with decompensated alcohol-related liver disease. Sarcopenia negatively impacts the prognosis of cirrhotic patients and affects the response to treatment of patients with hepatocellular carcinoma (HCC). For these reasons, identifying an easy-to-perform method to assess sarcopenia in is a key element in the optimization of care in this patient population. Assessment of muscle mass by computed tomography is considered the standard of care for the diagnosis of sarcopenia, but exposure to radiation and high costs limit its application in this setting, especially for repeated assessments. We believe that ultrasound, a cheap and harmless technique also used for HCC screening in cirrhotic patients, could have an expanding role in the diagnosis and follow-up of sarcopenia in these patients., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Competing Interests: The Authors do not report any conflict of interest.

Competing Interests: There are no conflicts of interest.

Encapsulating peritoneal sclerosis (EPS) is a rare and life-threatening complication of long-term peritoneal dialysis and until now, there is no established medical treatment for it. Many factors have been incriminated in its pathogenesis but they do not explain all risk conditions. EPS is significantly associated with PD duration, particularly more than 5 years, however the relationship between long-term PD and EPS increased risk is currently unknown. The "two-hit hypothesis" analyzes the relationship between the histological changes Peritoneal Dialysis-induced and intercurrent acute inflammatory episodes, but it does not explain the transition from Sclerosis Simple to EPS. We report our experience and we investigate the predisposing factors. The abdominal cocooning is a pathognomonic finding but it requires further investigations. Probably unidentified factors make some patients more susceptible to developing encapsulating peritoneal sclerosis.

Acute crescentic transformation is a rare but well described event in patients with membranous glomerulonephritis. We report our experience with a 66-year-old Caucasian man presented for rapid decline in renal function. For nearly 10 years, he was suffering from hypertension and mixed sensori-motor polyneuropathy. He performed therapy with prednisone and azathioprine, suspended 1 year before presentation. Moreover, six months before presentation, laboratory tests showed a serum creatinine concentration 220 mol/L and a 24-h protein excretion 0,75 g/d. The physical examination showed oedema and severe hypertension; the 24-h protein excretion was 1,1 gr/d and creatinine concentration was 550.8 mol/L; ANCA and other immunological tests were negative. There was no evidence of SLE, infection or malignancy. The kidney biopsy highlighted a membranous GN with crescentic overlap. The patient was treated with steroid and cyclophosphamide. Because there was no sign of improvement after 2 months, we stopped the cyclophosphamide therapy and the patient started chronic haemodialysis treatment. Unlike membranous nephropathy, patients with superimposed crescentic glomerulonephritis appear to have a more aggressive clinical course. The importance of recognizing this group of patients with membranous nephropathy and crescentic glomerulonephritis is that immunosuppressive therapy may ameliorate the progression of renal damage and in some cases early treatment was associated with useful recovery of renal function.