[Gender and kidney diseases: the clinical importance and mechanisms of modifying effects]. / Plec a choroby nerek--znaczenie kliniczne i mechanizmy modyfikujacego oddzialywania.

This review focuses on the underlying pathways of gender-dependent renal diseases and presents specific examples of diseases influenced by gender. In the literature it has been shown, in many clinical and experimental observations, that the incidence and the rate of progression of renal disease are influenced by many gender-dependent factors, such as kidney and glomerular size, differences in glomerular hemodynamics, and direct effects of sex hormones on renal tissue and signal pathways such as the renin-angiotensin-aldosterone system and signal molecules (e.g. nitric oxide, reactive oxygen species, cytokines and growth factors). It has been shown that the main female hormone, 17 ß estradiol, is capable of inhibiting inflammatory and pro apoptotic processes and protects the renal tissue. In contrast, the male hormones, testosterone and dehydroepiandrosterone, have the opposite effect. Hormonal manipulation by male or female castration changes the course of renal disease progression and confirms the influence of the sex hormones. Female gender is therefore considered a protective factor in many kidney diseases, such as primary glomerulonephritis, autosomal dominant polycystic kidney disease (ADPKD) and hypertensive nephropathy. Similarly, women are more predisposed to autoimmune diseases with secondary glomerulonephritis, e.g. systemic lupus erythematosus, as the female sex hormones have the ability of autoimmune process activation. After menopause the protective effect of female gender is not observed, which confirms the role of the female sex hormones.

[Pentraxins - their importance in pathogenesis of systemic lupus erythematosus]. / Pentraksyny ­ znaczenie w patogenezie tocznia rumieniowatego ukladowego.

Systemic lupus erythematosus (SLE) is an autoimmune disease, whose main pathomechanism is attributed to the disturbed apoptotic process and dysfunction of the immune cells, leading to the accumulation of undegraded cellular matrix. This paper presents molecules such as complement components, pentraxins, and collectins, which are involved in the opsonization and removal of cellular material, and shows how deficiencies in these processes may contribute to SLE development and progression. Many reports indicate the specific role of the pentraxins (C-reactive protein, serum amyloid P, pentraxin 3), which, due to enhancing the phagocytosis of damaged cells and inducing the classical pathway of complement activation, participate in masking antigens from the immune system. The influence of CRP on inhibition of development and progression of kidney disease and decreasing the immune activity markers was demonstrated on the basis of research in experimental, mouse models of SLE. The decreased pentraxin response described in systemic lupus erythematosus patients, despite the presence of high levels of interleukin-6 and other markers of disease activity, is still unclear. Anti-mCRP antibodies bind CRP to form immune complexes, which are deposited in glomeruli and may initiate or exacerbate inflammation. In the literature, the correlation between raised levels of anti-CRP antibodies and clinical and immunological activity of lupus nephritis was proved. It shows their importance as a factor determining the severity of the disease and response to treatment. Novel studies suggest that the low CRP response in SLE is due to interferon-α inhibition of gene expression and CRP synthesis. This suggests that therapeutic targets in systemic lupus erythematosus should also be based on inhibiting the synthesis of interferon-α .