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Hydrocortisone replacement therapy is a cornerstone in the treatment of adrenal insufficiency (AI). While urinary cortisol has been used as a diagnostic tool for AI, it remains unclear whether it is a useful parameter to monitor hydrocortisone replacement therapy. Aim of this study was to evaluate possible differences in cortisol metabolism between adrenal insufficient patients and healthy subjects and to assess the value of urinary cortisol in AI management. In a case-control study, urinary cortisol excretion was determined in 14 patients with primary and secondary AI receiving hydrocortisone infusions from midnight to 8:00 AM. Results were correlated with serum cortisol levels and compared to urinary values obtained from 53 healthy volunteers. Urinary cortisol excretion in healthy subjects was 14.0 ± 7.8 μg/8 h (range: 0.24-35.4), levels did not differ between 3 groups aged 20-34 years, 35-49 years, and ≥ 50 years. Patients with AI receiving hydrocortisone infusions demonstrated significantly higher rates of urinary cortisol excretion (51.6 ± 37.8 μg/8 h; range 17.1-120.0, p < 0.001); the values correlated with serum cortisol levels (r² = 0.98). Of interest, patients with secondary AI showed significantly higher serum cortisol levels after hydrocortisone infusion than those with primary AI, conceivably due to residual adrenal function. In conclusion, we showed that: (i) there is a wide inter-individual variability in urinary cortisol excretion rates; (ii) cortisol metabolism in adrenal insufficient patients differs when compared to controls; (iii) there is a strong correlation between urinary and serum cortisol levels; and (iv) urinary cortisol levels despite their variability may help to discriminate between secondary and primary adrenal insufficiency. [ABSTRACT FROM AUTHOR]

Introduction: Headache and depression are common problems in patients with hypothalamic- pituitary disorders (HPD). Aim: To determine the prevalence of headache and depression in patients with HPD and the specific characteristics in affected individuals in comparison to patients with cardiovascular problems (CD). Methods: Patients with HPD and CD were asked to complete a questionnaire regarding headache and depression. Results: There were no significant differences between the HPD and the CD group. Prevalence of headache was not associated with the treatment modality of pituitary disease, hormone excess syndromes or any hormonal replacement therapy. However, ACTH, TSH and GH deficiency were associated with less headache when compared to patients with adequate secretion. Interestingly, patients who had prior surgery suffered significantly more often from depression. In addition, headache and depression were significantly more common in patients with microadenomas than in macroadenomas. Discussion: The risk for headache and depression is mainly influenced by a combination of factors, but a specific pituitary hormone deficiency may decrease risk for headache. [ABSTRACT FROM AUTHOR]

Objective: Mesangiolysis is defined as dissolution of the mesangial matrix. It is described in several human glomerulopathies, i.e. diabetic and hypertensive nephropathy, as well as in various experimental models of renal disease. In diabetes mellitus nodular type glomerulosclerosis, i.e. the Kimmelstiel-Wilson lesion, is thought to result from mesangiolysis and formation of capillary aneurysms with subsequent thrombosis. However, the evidence supporting this hypothesis is still limited. Therefore, it was the aim of the present study to analyse the incidence and significance of mesangiolysis, i.e. capillary dilatation and aneurysm formation in type II diabetic nephropathy. Methods: From 217 consecutive patients with (176) or without (41) type II diabetes mellitus kidneys were harvested at autopsy and investigated using semiquantitative indices of mesangiolysis, glomerulosclerosis and glomerular nodulus formation. In addition, glomerular size was analysed using a semiautomatic image analysing system. 50 patients out of the 176 were classified into 5 groups according to their kidney function and compared to 10 control patients. The morphological findings were analysed with respect to renal function, duration of diabetes and other clinical data using multiple regression analysis. Results: In 48.8% of patients with type II diabetes nodular type glomerulosclerosis was present and the incidence of mesangiolysis was 18.4%. Glomerulosclerosis significantly increased with the duration of diabetes (p < 0.005) and was significantly correlation with creatinine clearance (p < 0.001). In addition, there was a highly significant correlation between the degree of mesangiolysis and the presence and size of glomerular noduli (p < 0.01). Moreover, nodular glomerulosclerosis was significantly correlated with creatinine clearance (p < 0.001), glomerular size (p < 0.01) and age of the patients (p < 0.05). Within the 5 groups the indices of mesangiolysis, noduli and glomerulosclerosis showed a steady increase in parallel with the increase in serum creatinine. In contrast, glomerular size which was in general significantly greater in diabetes compared to controls was not significantly different between the 5 diabetic groups. Conclusions: The present study presents a detailed analysis of the spectrum of morphological changes in type II diabetes in connection with the clinical findings. It provides further evidence for an association between mesangiolysis and nodular type glomerulosclerosis both of which are correlated with duration of diabetes and renal function. [ABSTRACT FROM AUTHOR]

Objective: Diabetic glomerulosclerosis is characterized by thickening of the glomerular basement membrane and diffuse or nodular expansion of the mesangial matrix. The microfibrillar collagen type VI is one of the extracellular matrix compounds that is suggested to account for mesangial matrix expansion although the current data is contradictory. Therefore, it was the aim of the present study to analyse the glomerular expression of collagen VI in human biopsies with diabetic and hypertensive nephropathy as well as in experimental models of type 1 and type 2 diabetic nephropathy. Methods: Expression and distribution of collagen VI and collagen IV was investigated in experimental models of type 1 (Streptozotocin, STZ) and 2 (SHR-Nc/p) diabetic nephropathy (n = 5 per group) and control groups (sham and subtotally nephrectomized rats, SNX, n = 6 per group) using immunohistochemistry and a semiquantitative scoring system. In addition, kidney biopsies from patients with diabetic nephropathy (DN) and hypertensive-diabetic nephropathy (HDN) were studied. Patient age ranged from 40-70 years (mean: 63). As controls renal tissue from 6 age and sex matched healthy subjects was included in the study. Results: In normal human and rat kidney, collagen VI staining was predominantly localized to the tubulointerstitium whereas no or only very weak expression was found in the glomerulus. In human DN and in HDN as well as in both models of experimental diabetes interstitial collagen VI expression was markedly and comparably upregulated. In contrast, glomerular collagen VI expression score was significantly higher in DN (3.2) compared to HDN (2.0) and controls (0.4) and in both models of diabetic nephropathy (STZ: 1.64 ± 0.75, SHR/N-cp: 1.04 ± 0.46) compared to controls (0.70 ± 0.30) and to SNX (0.74 ± 0.38). In DN with nodular glomerulosclerosis there was a specific expression pattern of collagen VI with increased staining in the basement membrane around the nodules. Collagen IV expression was absent or low in normal glomeruli and was upregulated in DN and HDN as well as in both experimental diabetic diseases and in SNX. Of note, glomerular collagen IV expression was highest in areas of segmental sclerosis. Conclusions: Renal interstitial and in particular glomerular collagen VI protein expression was significantly upregulated in experimental models of type 1 and 2 diabetes mellitus as well as in human diabetic nephropathy. The data and the expression pattern of collagen VI support a specific upregulation of the microfbrillar collagen type VI in diffuse diabetic glomerulosclerosis. [ABSTRACT FROM AUTHOR]

Although combining of eCG and hCG administrations is known to enhance LH-like actions, there have been few studies where there was comparison of the effects of treatment of anestrous ewes with eCG and hCG and eCG alone. In Experiment 1, 18 ewes in seasonal anestrus were administered an intravaginal device (IVD) containing medroxyprogesterone acetate for 12 days, and at the time of IVD removal (D0), were allocated into the following groups (n = 6/group): no further treatment (control); 400 IU eCG (eCG); or 400 IU eCG and 200 IU hCG (eCG + hCG). There was greater ovarian follicular growth in the groups treated with gonadotropins, compared to the control, and there were greater progesterone concentrations in the eCG + hCG group on D9 (P < 0.05). In Experiment 2, 66 ewe lambs were assigned to the same treatment groups described for Experiment 1, and subsequently there was natural mating with rams. There was a greater rate of behavioral estrous manifestation in the eCG (88.5 %; 23/26) and eCG+hCG (85.2 %; 23/27), than control (30.8 %; 4/13; P < 0.05) group. Pregnancy rate was also greater in the eCG (34.6 %; 9/26) and eCG+hCG (18.6 %; 5/27) than control (0 %; 0/13; P < 0.05) group, whereas conception rate, considering only ewe lambs that were mated, was only greater in the eCG group. Although there were greater progesterone concentrations 9 days after treatment in the eCG+hCG group, there was no difference in follicular growth in anestrous ewes, nor was there an effect on estrous behavior manifestation and pregnancy rates in ewe lambs, compared to treatment with only eCG., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Hypokalaemic hypertension is the classical presentation of primary hyperaldosteronism but may also result from other mineralocorticoid activity, such as liquorice ingestion. Onset of hypertension as well as serum renin and aldosterone levels are central for the diagnosis. Liquorice ingestion has been reported to induce hypertension, hypokalaemia and metabolic alkalosis due to inhibition of the enzyme 11-β-hydroxy steroiddehydrogenase 2. Here, we report the case of a hypertensive emergency with acute visual impairment due to hypertensive retinopathy in clear conjunction with a considerable consumption of liquorice.

Hyponatremia is the most commonly occurring electrolyte disorder and is associated with increased morbidity and mortality—independent of the underlying disease. Despite its high prevalence, hyponatremia is often underestimated and inadequately addressed in clinical routine. Depending on disease stage and severity, the electrolyte disorder can present with a wide spectrum of neurological signs and symptoms, ranging from adynamia and gait disturbances, to syncope or coma. While the underlying causes of hyponatremia may be manifold, their identification is crucial to initiating adequate therapeutic measures for symptomatic and causal therapy. The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SiADH) is the most common cause of hyponatremia, present in 1/3 of hyponatremic patients and usually a result of medication, neurological, respiratory or malignant disease. A differential diagnostic approach using a simple algorithm that includes clinical and laboratory parameters is essential for identifying the underlying cause of hyponatremia and administering goal-directed therapy. The development of vaptans has provided new options in the treatment of SiADH-associated hyponatremia.

Glomerular mesangial cells have a central function in maintaining structure and function of the glomerular capillary ultrafiltration apparatus. Regardless of the type of glomerular injury, imbalances in the control of mesangial cell replication appear to play a key role in the pathogenesis of progressive renal failure. The available evidence from in vitro and in vivo studies indicates that such regulatory mechanisms include specific soluble and non-soluble extracellular factors and a complex array of receptor-mediated signals which control cell proliferation, survival and apoptosis. This review summarizes results from recent investigations concerning regulation of cell cycle progression in mesangial cells. In addition to results from cell culture studies, descriptive findings on expression and regulation of cell cycle-regulatory proteins and their potential role for altered mesangial cell behaviour in glomerular disease are considered. We believe that better understanding of processes which regulate mesangial cell replication could lead to novel diagnostic as well as therapeutic strategies and, thus, help control better proliferative glomerulonephritis.