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Epidemiological investigations have shown that approximately 2-3% of all Austrians have diabetes mellitus with renal involvement, leaving 250,000 people in Austria affected. The risk of occurrence and progression of this disease can be attenuated by lifestyle interventions as well as optimization of blood pressure, blood glucose control and special drug classes. The present article represents the joint recommendations of the Austrian Diabetes Association and the Austrian Society of Nephrology for the diagnostic and treatment strategies of diabetic kidney disease., (© 2023. The Author(s).)

Elevated blood pressure remains a major cause of cardiovascular disease, disability, and premature death in Austria, with suboptimal rates of detection, treatment and control also in recent years. Management of hypertension is a common challenge for physicians with different spezializations. In an attempt to standardize diagnostic and therapeutic strategies and, ultimately, to increase the rate of patients with controlled blood pressure and to decrease the burden of cardiovascular disease, 13 Austrian medical societies reviewed the evidence regarding prevention, detection, workup, treatment and consequences of high blood pressure in general and in various clinical scenarios. The result is presented as the first national consensus on blood pressure. The authors and societies involved are convinced that a joint national effort is needed to decrease hypertension-related morbidity and mortality in our country.

Recent epidemiological investigations have shown that approximately 2-3% of all Austrians suffer from diabetes with renal involvement, i. e. 250,000 people in Austria are affected. The risk of occurrence and progression of this disease can be ameliorated by life style interventions as well as optimization of blood pressure, blood glucose levels and special drug classes. The present article represents the joint recommendations of the Austrian Diabetes Association and the Austrian Society for Nephrology for the diagnostics and treatment strategies of diabetic kidney disease.

In 2010, eight Austrian medical societies proposed a joint position statement on the management of metabolic lipid disorders for the prevention of vascular complications. An updated and extended version of these recommendations according to the current literature is presented, referring to the primary and secondary prevention of vascular complications in adults, taking into consideration the guidelines of other societies. The "Austrian Lipid Consensus - 2016 update" provides guidance for individualized risk stratification and respective therapeutic targets, and discusses the evidence for reducing vascular endpoints with available lipid-lowering therapies. Furthermore, specific management in key patient groups is outlined, including subjects presenting with coronary, cerebrovascular, and/or peripheral atherosclerosis; diabetes mellitus and/or metabolic syndrome; nephropathy; and familial hypercholesterolemia.

Recent epidemiological evaluations have shown that approximately 5% of all Austrians suffer from diabetes including renal involvement, i. e. 400.000 people in Austria are affected. The risk of start and progression of this disease can be ameliorated by lifestyle interventions as well as optimization of blood pressure and glucose levels. The present article represents the joint recommendations of the Austrian Diabetes Association and the Austrian Society for Nephrology for the prevention and treatment of diabetic kidney disease.

Background: Amyloid light-chain (AL) amyloidosis is a disorder of plasma cells in which depositions of immunoglobulin light-chain fragments cause progressive organ failure and death with a median survival of one year, but autologous stem-cell transplantation can induce high response rates, especially in isolated renal involvement., Methods: Six patients aged between 43 and 59 years were diagnosed with AL-amyloidosis and had stem cells mobilized with either recombinant human granulocyte colony-stimulating factor (rhG-CSF) alone (n = 2) or cyclophosphamide (2-4 g/m(2)) and rhG-CSF (n = 4). All six patients had kidney involvement and nephrotic syndrome, four had cardiac involvement and two involvement of the vascular, nervous and gastrointestinal systems. Five of the patients received high-dose melphalan (200 mg/m(2)) and autologous blood stem-cell support., Results: One patient died as a result of sepsis after stem-cell mobilization. The other five patients received high-dose melphalan but experienced severe toxicity. One patient died as the result of gastrointestinal perforation on day 6, one presented with hyperfibrinolysis and spontaneous rupture of the spleen, and another experienced severe bleeding of the gastrointestine, tachyarrhythmia and hemolytic anemia. Four patients had acute renal failure: three required hemodialysis and one underwent renal transplant 21 months later. Restaging after a follow-up of 31-52 months revealed reversal of nephrotic syndrome in all three patients who regained adequate renal function. With respect to cardiac involvement (n = 2), one patient showed a decrease in NYHA class from II to I but baseline wall thickness remained stable., Conclusion: Treatment of selected patients with AL-amyloidosis by high-dose melphalan and stem-cell support results in reversal of amyloid-related disease in a substantial proportion of patients and improved survival.

Hypertensive nephropathy is among the leading causes of end-stage renal disease. Once renal function is severely impaired, the effects of strict control of blood pressure on the recovery of renal function remain elusive. Published case series suggest that optimal control of blood pressure results in regression of renal failure to some extent. In the present case of biopsy-proven hypertensive nephropathy we show that renal function can substantially improve over time if blood pressure is optimally controlled. Glomerula filtration rate continuously improved in our patient from 20 ml/min at presentation to 80 ml/min over a period of three years using a fivefold antihypertensive regimen. Hypertensive retinopathy regressed from stage III to stage I, and left ventricular hypertrophy decreased from an initial septum thickness of 19 mm to 12 mm within that period of time. This case clearly illustrates that optimal control of blood pressure is mandatory in patients with pre-terminal renal failure due to hypertensive nephropathy. Such intervention can lead to a regression of hypertension-associated end-organ injury.

Apoptosis of renal tubular epithelial cells plays a major role in acute renal failure. Several external and internal signals can induce apoptosis, which is then effectuated via several pathways. These pathways are either the FAS/FAS-L pathway and downstream MAPK (mitogen-activated protein kinases) and JNK (c-Jun N-terminal kinase) signal transduction, or the RANK/RANK-L (receptor activator of NFkB) pathway via activation of the caspase cascade. Other pathways, especially for apoptosis induction by toxins, include the mitochondrial permeability transition pore activation and Bcl-2 superfamily member differential regulation. An important final, irreversible branch of these pathways is the release of cytochrome c from the mitochondria, leading to nuclear fragmentation. Therapeutic interventions of acute tubular injury focus on the prevention of apoptosis by either modulation of the balance of the bcl-2 family or by selectively blocking angiotensin receptors. It is not clear yet, which receptor blockade or combination of receptor blockers are most effective in apoptosis prevention. In chronic renal failure, tubular apoptosis has been found in biopsies from polycystic kidneys, but not in a quantitatively meaningful amount in other chronic human renal diseases. On the other hand, given the short half-life of apoptotic cells of few hours, even low numbers over time might turn out to be important modulators of chronic kidney disease, which are characterized by tubular cell loss. Potential therapeutic interventions to prevent tubular apoptosis in chronic renal disease include angiotensin system inhibition, whereby the angiotensin II AT2 receptor blockade seems more promising in apoptosis inhibition than the inhibition of other receptor subtypes.

Background: Tubular atrophy is a common histological feature of chronic renal failure, and epithelial cell death by apoptosis might play an important role in its pathogenesis. Angiotensin II contributes to the progressive nature of many kidney diseases and treatment with angiotensin converting enzyme inhibitors preserves the structure of the tubulointerstitial compartment in human and experimental renal diseases., Methods: Primary cultures of human renal proximal tubular epithelial cells were co-incubated with angiotensin II alone or in combination with the angiotensin II AT1 receptor antagonist losartan or/and the AT2 antagonist PD123319. Apoptosis was determined after 20 hours by TUNEL staining and flow cytometry., Results: Angiotensin II at concentrations of 10(-9) M induced apoptosis (control vs. angiotensin II 4 +/- 3% vs. 73 +/- 11%; p < 0.05). This effect was completely offset by co-incubation with the angiotensin II AT2 receptor blocker at concentrations 10(-7) M (control vs. PD123319 4 +/- 3% vs. 8 +/- 3%; p < 0.05); AT1 blockade was ineffective in apoptosis inhibition. When both angiotensin receptors were blocked, no additional effect on apoptosis inhibition could be detected., Conclusion: We provided evidence, that physiological concentrations of angiotensin II can induce apoptosis of human renal proximal tubule epithelial cells. This effect is mediated via AT2 receptors.

Although diabetic nephropathy is a slowly progressing, well studied disease, it is the most common cause of end stage renal disease in industrialized countries. Recently the first randomized controlled long term trials about microvascular complications in patients with type 2 diabetes have been published. Only seven years ago the first hallmark papers about metabolic control and ACE inhibition emerged. This review highlights the current status of prevention and therapy of diabetic nephropathy by metabolic and blood pressure control in type 1 and type 2 diabetic patients, depending on their stage of nephropathy (normo-, micro-, or macroalbuminuria). In patients with type 1 diabetes and normo- or microalbuminuria, strict metabolic control has been shown to slow the progression of nephropathy. In macroalbuminuric patients an aggressive antihypertensive treatment, preferably with an ACE inhibitor, is more important than the metabolic control. ACE inhibitor therapy has also been proven beneficial in microalbuminuric patients, but not yet in normotensive, non-albuminuric type 1 patients. Because of the high prevalence of hypertension in patients with type 2 diabetes, a strict antihypertensive treatment is more important than metabolic control for the prevention of progression of microvascular disease. Since most patients need a combination of antihypertensive medications a recommendation for a single substance class can not be given.

The influence of inflammation on post-ischemic acute renal failure (ARF) has only recently be appreciated. In this review we therefore discuss the cellular events occurring in ARF with special emphasis on the impact of inflammatory processes on the pathogenesis of ARF. Furthermore, the spectrum of injury leading to sublethal or lethal cell damage and the time course, occurrence and regulation of the two distinct forms of cell death, necrosis and apoptosis will be described extensively. Especially apoptosis and its regulation has been studied only marginally in the setting of ischemic ARF. This overview is mainly focused on tubular cell injury since tubular epithelial cells are the major victims of ischemia whereas cells inside the glomerular tuft show only little pathology. The models of tubular injury described in this paper are ranging from primary cultures of isolated human tubular epithelial cells to experimental ischemic renal failure in rats, and to clinical settings of human ischemic ARF. The cellular events highlighted in this review are the influence of the expression of cellular adhesion molecules on the pathophysiology of ARF, and the regulation and time course of apoptosis. Examples of these processes are being illustrated by figures exhibiting morphology and immunohistochemistry of cell proliferation and cell death regulatory proteins.

This brief overview will give the reader an idea what antisense oligonucleotides are, how they act, what one can do with them, and what future perspectives might emerge. The idea behind this new therapeutic strategy is the selective blockage of a specific gene in vivo, which is responsible for a certain disease. Anti-sense oligonucleotides are short, traditionally 15 to 25 bases long, single stranded DNA fragments, which are targeted against a specific mRNA. This is the classical antisense mechanism. These DNA fragments can also be targeted against a specific genomic DNA sequence which is known as antigene therapy. The oligonucleotides have to be modified in order to increase their stability in vivo. Three mechanisms of action have been reported for the oligonucleotides: 1. Oligonucleotides are designed in a complementary (antisense) orientation to their target (sense) mRNA to which they hybridize in a strictly base pair specific manner (Watson-Crick base pairing) and thus block translation. 2. They can bind to the genomic DNA in the nucleus and thus block transcription (Hoogsten-type base triplets). A third, unspecific mechanism of action is the binding of the oligonucleotide to a target protein in what has been referred to as aptamer-binding. In addition, other nonspecific effects of cytokine and neutrophil activation were observed. The antisense strategy is a useful research tool for the identification of specific gene-protein functions. The first in vivo animal studies and clinical experiences have been carried out in the fields of cardiovascular medicine, oncology and virology yielding promising results. Currently, the first clinical trials using antisense oligonucleotides for the inhibition of gene expression are being performed; the results will be available in the next years.

Infectious complications of hydrocephalus shunts are serious problems. A possible method of treating such infections is by external ventricular drainage (EVD). 20 patients - 17 with infected shunts, 3 with neonatal meningitis, ventriculitis and subsequent hydrocephalus - were treated by EVD and the results are presented in this report. The advantages of the procedure are control of the intraventricular pressure to bring it within normal limits and the possibility of intraventricular antibiotic instillation to supplement systemic therapy. Furthermore, the optimal operation time for the definitive shunt can be assessed by EVD once the infection has been overcome.