Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive endorgan damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

For > 150 y, clinicians and investigators have observed that high protein intakes accelerate the progression of renal disease and that low protein intakes have beneficial effects. Some studies suggest that the effects of soy-protein intake resemble those of a low-protein diet. The Brenner hypothesis suggests that high protein intakes by diabetic individuals create hyperfiltration and glomerular hypertension eventuating in renal damage. On the basis of the available evidence, we are proposing the soy-protein hypothesis, which states that substituting soy protein for animal protein in diabetes patients results in less hyperfiltration and glomerular hypertension and, therefore, resultant protection from diabetic nephropathy. Furthermore, substituting soy protein for animal protein should have therapeutic value in diabetic nephropathy with resultant slowing of deterioration of renal function and decreasing proteinuria. The preliminary results of the study of 8 type 2 diabetes patients with obesity, hypertension, and proteinuria are reported. Under the conditions of the study, providing soy protein as half of the daily protein intake had no distinct effects on renal function or proteinuria in these subjects. Soy-protein intake was associated with a significant reduction in serum cholesterol and triacylglycerol concentrations. Further studies are required to critically examine the effects of soy-protein intake on the renal function of diabetes patients.

Autoimmunity against the Goodpasture antigen α3IV-NC1 results in antiglomerular basement membrane glomerulonephritis. Although antibodies are central to the pathogenesis, there is good evidence for the participation of T cells in this disease. To define the contribution of T cells, we used the model of experimental autoimmune glomerulonephritis. Immunization of DBA/1 mice with α3IV-NC1 resulted in proteinuria, a biphasic course of the disease, and an eventual loss of kidney function. In the initial phase, the mice developed an α3IV-NC1-specific IgG response, had IgG deposition along the glomerular basement membrane, and steadily increased proteinuria, but only marginal signs of inflammation with limited leukocyte infiltration. After 9-13 weeks, mice proceeded to develop crescentic glomerulonephritis, extensive tubulointerstitial damage, and massive macrophage infiltration. T-cell infiltration was less pronounced, mostly confined to the interstitium, and T cells displayed an activated phenotype with a significant fraction of Th1 or Th17 CD4(+) T cells. Close examination revealed the presence of autoreactive T cells producing IFNγ upon restimulation with α3IV-NC1. Thus, our results suggest that accumulation of effector T cells, including autoreactive T cells, represents a critical step in the progression from mild glomerulonephritis, with limited glomerular damage, to severe crescentic glomerulonephritis accompanied by tubulointerstitial inflammation and loss of kidney function.

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Among numerous other immune-mediated diseases, glomerulonephritis has also been suspected to be an extrahepatic manifestation of HEV infection. In this prospective study, we tested 108 patients with glomerulonephritis and 108 age- and sex-matched healthy controls at the University Hospital Hamburg Eppendorf, Hamburg, Germany, for anti-HEV IgG (Wantai test) as a marker for previous HEV exposure. A total of 24 patients (22%) tested positive for anti-HEV IgG. Males tended to be more frequently anti-HEV IgG positive (29%) in comparison to females (16%). However, this does not reach statistical significance (p = 0.07). Anti-HEV IgG positive patients were older in comparison to negative patients (mean 53 vs. 45 years, p = 0.05). The kidney function seems to be slightly decreased in anti-HEV IgG positive patients in comparison to and anti-HEV IgG negative patients basing on creatinine (p = 0.04) and glomerular filtration rate (GFR) (p = 0.05). Slightly higher values of bilirubin could be found in IgG positive patients (p = 0.04). Anti-HEV-IgG seropositivity rate (22%) in glomerulonephritis patients, did not differ significantly in comparison to an age- and sex-matched control cohort of healthy blood donors (31/108 positive, 29%). A total of 2/2 patients with membranoproliferative glomerulonephritis (MPGN) tested anti-HEV IgG positive (p = 0.002 in comparison to glomerulonephritis patients with other subtypes).In conclusion, our findings indicate that previous HEV exposure in a region where GT3 is endemic is not associated with glomerulonephritis in general. However, the subgroup of MPGN patients should be investigated in future studies. Furthermore, future studies are needed to investigate whether the observed association between anti-HEV IgG positivity and reduced GFR in glomerulonephritis patients is HEV associated or is an age-related effect.

Hintergrund Die Coronavirus-disease-2019(COVID-19)-Pandemie hat auch die Nephrologie weltweit vor große Herausforderungen gestellt. Zum einen stellen Patienten mit Nierenerkrankungen in diesem Zusammenhang eine besonders vulnerable Patientengruppe dar, und zum anderen sind die Nieren bei schweren COVID-19-Verläufen nach den Lungen am häufigsten vom Organversagen betroffen. Material und Methoden Um zuverlässige Daten zu COVID-19-Prävalenz und -Mortalität bei Dialysepatienten in Deutschland zu erheben, hat die Deutsche Gesellschaft für Nephrologie bereits während der 1. Welle der Pandemie im Frühjahr 2020 ein Register aufgebaut. Wöchentlich wurden Angaben zu Anzahl und Verlauf der COVID-19-Dialysepatienten in Deutschland erhoben und ausgewertet. Ergebnisse Die Prävalenz von COVID-19 bei Dialysepatienten in Deutschland zeigte einen doppelgipfligen Verlauf ähnlich wie in der Allgemeinbevölkerung. Während diese im Frühjahr bei Dialysepatienten auf 1,4 % stieg, fiel sie im Sommer deutlich ab und erreichte im Dezember im Rahmen der 2. Pandemiewelle einen Wert von ca. 1,9 %, trotz mittlerweile flächendeckend eingeführter umfangreicher Hygienemaßnahmen in den Dialysezentren. Ähnlich wie in anderen Industriestaaten weisen auch Dialysepatienten in Deutschland eine sehr hohe COVID-19-Letalität von etwa 20 % auf. Schlussfolgerung Aus der ermittelten Letalität bei Dialysepatienten lassen sich unmittelbare Konsequenzen für Hygienemaßnahmen in den Dialyseeinrichtungen sowie zu Impfstrategie und -priorisierung dieser Patientengruppe und des sie behandelnden Personals ableiten. Eine Konsequenz des häufigen Befalls der Niere im Rahmen einer Infektion mit dem „severe acute respiratory syndrome coronavirus 2“ (SARS-CoV-2) bei zuvor noch nicht an einer fortgeschrittenen Nierenerkrankung leidenden Patienten sollte die konsequente nephrologische Nachsorge sein.