["Pediatric inflammatory multisystem syndrome"-Experiences from a Berlin Children's Hospital]. / "Pediatric inflammatory multisystem syndrome" ­ Erfahrungen aus einer Berliner Kinderklinik.

BACKGROUND: Since the beginning of the SARS-CoV­2 pandemic, cases of the hyperinflammatory syndrome pediatric inflammatory multisystem syndrome (PIMS) have been accumulating. The clinical presentation is variable and it occurs 2-6 weeks after infection with SARS-CoV­2. As of today, immunoglobulins and/or steroids as well as ASS are used for medication. METHOD: In our clinic 11 patients presented with PIMS between 06/2020 and 06/2021, whose data were retrospectively collected and analyzed. RESULTS: Of the 11 patients 6 were male, the age distribution ranged from 4-18 years and 7 were overweight or obese. Almost all patients showed gastrointestinal and cardiovascular involvement, 4 had respiratory symptoms, 6 showed signs of nephritis. All showed blood count changes with anemia or leukocytosis and coagulopathy. CRP, ferritin, and soluble IL2 receptor were highly elevated in all patients. Only 2 patients had neither troponin­T nor NT-pro-BNP elevation and 7 patients had impaired left ventricular function. Positive SARS-CoV­2 serology was found in 10, and positive SARS-CoV­2 PCR via nasopharyngeal swabs in 2.All were initially treated with antibiotics, 3 patients required O2 supplementation, 6 required intensive care and 5 required vasoactive agents. All but one patient received immunoglobulins and ASS, 5 received prednisolone. Length of stay ranged from 4-51 days. CONCLUSION: PIMS is a severe acute hyperinflammatory disease, which was secured in 11 patients in our clinic. In some cases, there was a need for intensive care. Under anti-inflammatory therapy there was a good response without exception.

Intrauterine growth retardation aggravates the course of acute mesangioproliferative glomerulonephritis in the rat.

Intrauterine growth retardation (IUGR) aggravates the course of acute mesangioproliferative glomerulonephritis (GN) in the rat. Observational studies in children suggest that IUGR may be associated with a severe course of kidney diseases such as IgA nephropathy. We tested the hypothesis that IUGR leads to aggravation of acute mesangioproliferative GN in former IUGR rats. IUGR was induced in Wistar rats by isocaloric protein restriction in pregnant dams. Litter size was reduced to six male neonates in low protein animals (LP) and normal protein animals (NP). At 8 weeks GN was induced by injection of an anti-Thy-1.1 antibody. Rats were killed on days 4 and 14 after induction of GN and kidneys were investigated for inflammation and sclerosis using real-time polymerase chain reaction and histological methods. On day 4 after induction of GN, LP animals showed more glomerulosclerosis and tubulointerstitial lesions. On day 14, inflammatory markers (expression of monocyte chemoattractant protein 1, osteopontin, tumor necrosis factor and interleukin-6), extracellular matrix accumulation and markers of sclerosis (plasminogen activator inhibitor-1 expression, transforming growth factor-beta1 expression, score for glomerulosclerosis, glomerular deposition of collagen I and collagen IV) were more severe in LP animals. Some degree of induction of inflammatory and profibrotic markers was also present in non-nephritic LP animals. However, these rats did not display marked glomerulosclerosis or interstitial fibrosis. We conclude that after IUGR inflammatory damage is aggravated and the reparation of the kidney is impaired during the course of acute mesangioproliferative GN, leading to more sclerotic lesions.