BackgroundRiedel´s thyroiditis (RT) is a rare inflammatory disease of the thyroid gland, causing compression and fibrosis of adjacent tissues. Typically the goiter is hard and firm. Hoarseness, dyspnea, and dysphagia may be present.MethodsWe retrospectively reviewed all patients known by us with RT in addition to all patients with appropriate ICD-10 codes evaluated at the Karolinska University Hospital 2003–2015. Clinical, biochemical, and histological data of patients with RT were recorded in detail. Histological preparations were re-examined when available.ResultsRT was diagnosed in six patients. Five were females and the median age at first presentation was 50 years (25–81 years). Median follow-up time was 3.75 years (1–22 years). At diagnosis five had hypothyroidism. Four had extrathyroidal manifestations, and one of these had also distant fibrosis. One patient had a clear IgG4/IgG ratio over 40%. One patient was treated with tracheostomy, one with isthmectomy and one with total thyroidectomy. Four had been treated with glucocorticoids, four with tamoxifen, and two with both drugs. One had also been treated with mycophenolate mofetil combined with Rituximab. At the end of follow-up four was doing fine, one had recurrent episodes of inflammation and one had died of possible complications to RT.ConclusionIt is important to recognize RT and give adequate treatment. Steroids are still the mainstay of therapy but other medications against fibrosclerosis can be considered. Wakefulness of other fibrosing manifestations is essential. Immunohistochemistry can show whether IgG-4 plasma cells are increased which could lead to fibrosis in other organs.

Introduction:The renin-angiotensin-aldosterone system (RAAS) plays an integral role in the regulation of blood pressure, electrolyte and fluid homeostasis in mammals. The capability of the different nephron segments to form components of the RAAS is only partially known. This study therefore aimed to characterize the nephron-specific expression of RAAS components within the mouse kidney. Materials and methods: Defined nephron segments of adult C57B/16 mice were microdissected after collagenase digestion. The gene expression of renin, angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin II receptors 1a (AT1a), 1b (AT1b), and 2 (AT2) was assessed by reverse transcriptase polymerase chain reaction (RT-PCR). Results: Renin mRNA was present in glomeruli, in proximal tubules, in distal convoluted tubules (DCT) and cortical collecting ducts (CCD). AGT mRNA was found in proximal tubules, descending thin limb of Henle's loop (dTL) and in the medullary part of the thick ascending limb (mTAL). ACE mRNA was not detectable in microdissected mouse nephron segments. AT1a, AT1b and AT2 mRNA was detected in glomeruli and proximal convoluted tubules.Conclusions: Our data demonstrate a nephron-specific distribution of RAAS components. All components of the local RAAS -except ACE -are present in proximal convoluted tubules, emphasizing their involvement in sodium and water handling.

Objective: The aim of this trial was to evaluate the effect on insulin sensitivity and body composition of combination therapy with GH and IGF1 in adults with GH deficiency (GHD) and diabetes. Design, patients and methods: A 6-month randomised placebo-controlled pilot study. Fourteen adults with GHD and type 2 diabetes were included. All received rhGH (0.15 mg/day for 1 month and 0.3 mg/day for 5 months) and were randomised to rhIGF1 (15 mg/kg per day for 1 month and 30 mg/kg per day for 5 months) or placebo. Insulin sensitivity was evaluated with euglycaemic hyperinsulinaemic clamp and body composition by computed tomography of abdominal and thigh fat, as well as bioimpedance. Results: Twelve patients completed the study. They were overweight and obese; at baseline, insulin sensitivity (M-value) was low. IGF1 and IGF1 SDS increased in both groups, with the highest increase in the GH and IGF1 group. Positive changes in M-value by C1.4 mg/kg per min, in subcutaneous abdominal fat by K60.5 ml and in fat-free mass by C4.4% were seen in the GH and IGF1 group. Corresponding values in the GH and placebo-treated group were K1.5 mg/kg per min, C23 ml and K0.04% respectively (PZ0.02, PZ0.04 and PZ0.03 for delta values between groups). No safety issues occurred. Conclusions: Combined GH and IGF1 treatment resulted in positive, but rather small effects, and might be a treatment option in a few selected patients.

The purpose of this study was to investigate the effect of high fluid intake for the prevention of march-induced proteinuria and haematuria. Thirty-six male soldiers participated in two 25 km marches in a comfortable environment (outside temperature 13"C, cloudy weather), achieving a moderate average marching time of 3.5h. Fluid intake during march 1 was not restricted (=habitual intake), whereas during march 2, the participants were asked to achieve a fluid intake of 1 L before and 2 L during the march. Urinary excretion of protein and albumin, haematuria, and various serum parameters were assessed before, during and after both marches. Unexpectedly, urinary albumin and protein excretion was higher during march 2 (with a high fluid intake), whereas haematuria was unaffected. The haemoconcentration, as judged from haemoglobin levels, was more intense in group 1 (with usual fluid intake) in accordance with the higher decrease of bodyweight during the march, and probably accounted for most of the serum creatinine concentration increases observed. A standardized (high) fluid intake of 2.5 L before and during a moderate exercise failed to confer any prevention against mild exercise-induced renal abnormalities.