Different methos of polluted water drainage from the residential area Dolenja vas

The BA presents preliminary designs for three different methods of polluted water drainage away from the residential area Dolenja vas. From the technical point of view and regarding the costs, the gravitational, pressure and vacuum sewerage systems are compared. A conclusion, which system would be more rational and technically reasonable is also given. There is consists of an in-depth presentation of the features, the advantages and shortcomings of all three sewerage systems. The dimensioning process of the vacuum and pressure systems is presented, as are the factors, which are affecting the planning process for each system. All systems have also been compared from an environmental point of view. Alternative drainage systems (e.g. the vacuum and pressure sewerage systems) are stressed in the thesis. Some vacuum systems are also operational in Slovenia. ZAHVAL

Nodular glomerulosclerosis with anti-glomerular basement membrane-like glomerulonephritis; a distinct pattern of kidney injury observed in smokers

Background: Cigarette smoking has recently been recognized as a risk factor for developing nodular glomerulosclerosis and has also been frequently encountered in patients with anti-glomerular basement membrane (anti-GBM) disease. However, the concurrent presence of both patterns of glomerular injury has not been previously reported. Material and methods In this article, we describe three patients with non-diabetic nodular glomerulosclerosis, anti-GBM-like glomerulonephritis (GN) and a history of heavy smoking. Results: Our cohort included three patients, of which two were men (53 and 77 years old) and one a 28-year-old woman. None of the patients had a history of diabetes mellitus but all of them were heavy smokers who presented with renal insufficiency and proteinuria. Nodular glomerulosclerosis and occasional small, non-circumferential crescents in different stages of development were found on kidney biopsy. Immunofluorescence microscopy studies showed intense linear IgG staining along the glomerular basement membranes in the absence of granular immune-type deposits. Electron microscopy evaluation revealed prominent endothelial cell injury without detectable electron-dense deposits. One patient was dialysis-dependent a few months post-biopsy while the other two patients maintained their kidney function 18 and 24 months post-biopsy but without a significant improvement of serum creatinine. Conclusions: The combination of nodular glomerulosclerosis and anti-GBM-like GN appears to be a distinct pattern of injury observed in a small subset of heavy smokers. Although this pattern of glomerular injury might be less aggressive than the typical anti-GBM GN, it does not appear to carry a favorable prognosis

Heterozygosity for Fibrinogen Results in Efficient Resolution of Kidney Ischemia Reperfusion Injury

Fibrinogen (Fg) has been recognized to play a central role in coagulation, inflammation and tissue regeneration. Several studies have used Fg deficient mice (Fg−/−) in comparison with heterozygous mice (Fg+/−) to point the proinflammatory role of Fg in diverse pathological conditions and disease states. Although Fg+/− mice are considered ‘normal’, plasma Fg is reduced to ∼75% of the normal circulating levels present in wild type mice (Fg+/+). We report that this reduction in Fg protein production in the Fg+/− mice is enough to protect them from kidney ischemia reperfusion injury (IRI) as assessed by tubular injury, kidney dysfunction, necrosis, apoptosis and inflammatory immune cell infiltration. Mechanistically, we observed binding of Fg to ICAM-1 in kidney tissues of Fg+/+ mice at 24 h following IRI as compared to a complete absence of binding observed in the Fg+/− and Fg−/− mice. Raf-1 and ERK were highly activated as evident by significantly higher phosphorylation in the Fg+/+ kidneys at 24 h following IRI as compared to Fg+/− and Fg−/− mice kidneys. On the other hand Cyclin D1 and pRb, indicating higher cell proliferation, were significantly increased in the Fg+/− and Fg−/− as compared to Fg+/+ kidneys. These data suggest that Fg heterozygosity allows maintenance of a critical balance of Fg that enables regression of initial injury and promotes faster resolution of kidney damage

Treatment of parvovirus B19 viremia to facilitate kidney transplantation in a patient with collapsing glomerulopathy.

Collapsing glomerulopathy (CG) is a severe form of glomerulopathy which results in nephrotic syndrome and often ensues in rapid progression to end-stage kidney disease (ESKD). Although most commonly a result of HIV infection, other conditions such as parvovirus B19 (PB19) infection have been associated with CG. We present a case of an 18-year-old male with CG associated with PB19 infection who was heterozygous for APOL1 G1 and G2 genetic variants. In an attempt to treat, he was started on intravenous immunoglobulin (IVIg), however rapidly progressed to ESKD. During workup for a living donor kidney transplant he was found to have persistent low-grade PB19 viremia. Despite having no major immunodeficiency and given subsequent courses of IVIg, viremia continued to persist. In a final attempt to eradicate the PB19 we began treatment with cidofovir, an antiviral agent with in vitro efficacy against PB19. Subsequent to initiation of cidofovir, PB19 viremia slowly cleared after which he received a living unrelated kidney transplant. The patient had an early cellular rejection treated with rabbit antithymocyte globulin after which he recovered kidney function without signs of recurrent CG. Our case report suggests efficacy of IVIg and cidofovir for persistent PB19 infection in ESKD to allow subsequent transplantation, while minimizing the risk of recurrent CG

Pathophysiology and Pathology of Acute Kidney Injury in Patients With COVID-19

© 2020 National Kidney Foundation, Inc. Acute kidney injury (AKI) is common among hospitalized patients with Coronavirus Infectious Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. The variability in the occurrence of AKI has been attributed to the difference in geographic locations, race/ethnicity, and severity of illness. AKI among hospitalized patients is associated with increased length of stay and in-hospital deaths. Even patients with AKI who survive to hospital discharge are at risk of developing chronic kidney disease or end-stage kidney disease. An improved knowledge of the pathophysiology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who developed AKI during COVID-19. The goal of this article is to provide our current understanding of the etiology and the pathophysiology of AKI in the setting of COVID-19

Targeted Proximal Tubule Injury Triggers Interstitial Fibrosis and Glomerulosclerosis

Chronic kidney disease (CKD) remains one of the leading causes of death in the developed world and acute kidney injury (AKI) is now recognized as a major risk factor in its development. Understanding the factors leading to CKD after acute injury are limited by current animal models of AKI which concurrently target various kidney cell types such as epithelial, endothelial and inflammatory cells. Here we developed a mouse model of kidney injury using the Six2-Cre-LoxP technology to selectively activate expression of the simian diphtheria toxin receptor in renal epithelia derived from the metanephric mesenchyme. By adjusting the timing and dose of diphtheria toxin a highly selective model of tubular injury was created to define the acute and chronic consequences of isolated epithelial injury. The diphtheria toxin-induced sublethal tubular epithelial injury was confined to the S1 and S2 segments of the proximal tubule rather than being widespread in the metanephric mesenchyme derived epithelial lineage. Acute injury was promptly followed by inflammatory cell infiltration and robust tubular cell proliferation leading to complete recovery after a single toxin insult. In striking contrast, three insults to renal epithelial cells at one week intervals resulted in maladaptive repair with interstitial capillary loss, fibrosis and glomerulosclerosis which was highly correlated with the degree of interstitial fibrosis. Thus, selective epithelial injury can drive the formation of interstitial fibrosis, capillary rarefaction and potentially glomerulosclerosis, substantiating a direct role for damaged tubule epithelium in the pathogenesis of CKD

Fibrinogen Excretion in the Urine and Immunoreactivity in the Kidney Serves as a Translational Biomarker for Acute Kidney Injury

Fibrinogen (Fg) is significantly up-regulated in the kidney after acute kidney injury (AKI). We evaluated the performance of Fg as a biomarker for early detection of AKI. In rats and mice with kidney tubular damage induced by ischemia/reperfusion (I/R) or cisplatin administration, respectively; kidney tissue and urinary Fg increased significantly and correlated with histopathological injury, urinary kidney injury molecule-1 (KIM-1) and N-acetyl glucosaminidase (NAG) corresponding to the progression and regression of injury temporally. In a longitudinal follow-up of 31 patients who underwent surgical repair of abdominal aortic aneurysm, urinary Fg increased earlier than SCr in patients who developed postoperative AKI (AUC-ROC = 0.72). Furthermore, in a cohort of patients with biopsy-proven AKI (n = 53), Fg immunoreactivity in the tubules and interstitium increased remarkably and was able to distinguish patients with AKI from those without AKI (n = 59). These results suggest that immunoreactivity of Fg in the kidney, as well as urinary excretion of Fg, serves as a sensitive and early diagnostic translational biomarker for detection of AKI