Dr Christoph Langenberg (Nephrologist)
- Name
- Dr Christoph Langenberg
- Qualifications
- Dritter Abschnitt Certificate 2001
- FRACP 2011
- Occupation
- Renal Medicine Specialist (Nephrologist)
- Scientist - Researcher - Academia
- Gender
- Male
- Languages Spoken
- French
- German
- Medical Specialties
- Nephrology
- Hospital Affiliations
- Cabrini Malvern
- Knox Private Hospital
- Affiliated Clinics
- Forest Hill Dialysis Centre
- Affiliated Universities
- University of Melbourne
- Medical Conditions
- Sepsis
Practice Locations
Melbourne
- Address
- Forest Hill Dialysis Centre
65-77 Mahoneys Rd
Forest Hill VIC 3131
Australia
- Phone
- 03 9509 9956
Publications
- Renal histopathology during experimental septic acute kidney injury and recovery. Renal histopathology during experimental septic acute kidney injury and recovery. Crit Care Med 2014;42:e58-67. http://www.ncbi.nlm.nih.gov/pubmed/24126439 Abstract: Our understanding of septic acute kidney injury is limited. We therefore assessed renal histopathological changes induced by septic acute kidney injury and their evolution during recovery.
- Novel targets for sepsis-induced kidney injury: the glomerular arterioles and the sympathetic nervous system. Novel targets for sepsis-induced kidney injury: the glomerular arterioles and the sympathetic nervous system. Exp Physiol 2012;97:1168-77. http://www.ncbi.nlm.nih.gov/pubmed/22689445 Abstract: Sepsis and septic shock are the most common causes of acute kidney injury (AKI) in the intensive care unit, and mortality remains high despite improvements in our ability to support vital organs. The lack of development of effective treatments is partly because there has been little advance in our understanding of the pathophysiology of septic AKI, owing to the difficulty in conducting experiments on critically ill patients and use of inappropriate experimental models. Recently, however, a number of new concepts have emerged that challenge existing dogma and give insights into the causes of AKI. Traditionally, renal ischaemia has been proposed as the main cause of AKI, but it is becoming apparent that in sepsis with a hyperdynamic circulation, the most common situation in septic patients, there is an increase or at least no decrease in renal blood flow. In this review, the possible role of changes in pre- and postglomerular resistance in setting the increased level of renal blood flow in the presence of a decreased glomerular filtration rate is discussed. New evidence also indicates that the increased sympathetic nerve activity that occurs in sepsis may contribute to the induction of organ failure. Experimental studies indicate that inhibition of central sympathetic outflow with α(2)-adrenoceptor agonists or treatment with β(1)-adrenoceptor antagonists might reduce mortality in experimental endotoxaemia and sepsis. The possibility that these beneficial actions are partly dependent on a reduction in the excessive cytokine release caused by marked and prolonged sympathetic activation is discussed.
- Septic acute kidney injury: the glomerular arterioles. Septic acute kidney injury: the glomerular arterioles. Contrib Nephrol 2011;174:98-107. http://www.ncbi.nlm.nih.gov/pubmed/21921614 Abstract: Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to tubular injury, which, in turn, has been considered secondary to renal ischemia. This belief is curious because the hallmark of septic AKI and AKI in general is the loss of glomerular filtration rate (GFR). It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.
- Pathophysiology of septic acute kidney injury: a different view of tubular injury. Pathophysiology of septic acute kidney injury: a different view of tubular injury. Contrib Nephrol 2010;165:18-27. http://www.ncbi.nlm.nih.gov/pubmed/20427951 Abstract: Septic acute kidney injury (AKI) is the most common form of AKI seen in critically ill patients in developed countries. Its pathogenesis has been traditionally attributed to ischemia secondary to decreased cardiac output and hypotension, which trigger sustained renal vasoconstriction and in turn exacerbate and sustain the ischemia. This paradigm is supported by the fact that many patients who develop AKI do so in the setting of hemodynamic instability and also by evidence that renal blood flow is decreased and renal vascular resistance increased when they are measured in patients with AKI. However, recent evidence shows that renal blood flow may vary from increased in some animal models to normal in some patients and to decreased in other patients. Furthermore, the induction of prolonged severe subtotal ischemia by acute occlusion of the renal artery does not seem to trigger subsequent renal vasoconstriction and, finally, experimental studies suggest that immune-mediated injury may be a more likely cause of tubular cell dysfunction than ischemia. These lines of evidence suggest that the pathogenesis of AKI is complex, does not simply involve ischemia, and may differ according to the etiological trigger.
- Early and sustained systemic and renal hemodynamic effects of intravenous radiocontrast. Early and sustained systemic and renal hemodynamic effects of intravenous radiocontrast. Blood Purif 2010;29:339-46. http://www.ncbi.nlm.nih.gov/pubmed/20357433 Abstract: To measure the extended renal hemodynamic changes induced by intravenous radiocontrast.
- Epidemiology of septic acute kidney injury. Epidemiology of septic acute kidney injury. Curr Drug Targets 2009;10:1169-78. http://www.ncbi.nlm.nih.gov/pubmed/19715542 Abstract: The incidence of sepsis and acute kidney injury (AKI) are increasing in critically ill patients and both portend a higher risk of morbidity and death. Sepsis has consistently been shown to be a key contributing factor for the development of AKI. Numerous observational studies have found septic AKI to be highly common among the critically ill. Septic AKI patients are characterized by important differences in baseline demographics, acuity of illness and treatment intensity when compared with non-septic AKI. In particular, these patients are often older, have a higher prevalence of co-morbid illnesses, and are admitted for medical or emergency surgical indications. These patients show greater aberrancy in vital signs, laboratory parameters and need for vasoactive therapy and/or mechanical ventilation. Delays in initiation of appropriate antimicrobial therapy independently predict development of AKI in septic patients. Both delays to appropriate antimicrobials and initiation of renal support are also associated with higher mortality. Survival to ICU and/or hospital discharge for septic AKI patients is significantly lower when compared to patients with either non-septic AKI or sepsis alone. However, survivors of septic AKI show trends for greater rates of renal recovery and dialysis independence compared with non-septic AKI. The burden of septic AKI continues to increase and remains associated with an unacceptably high attributable morbidity and mortality. Accordingly, there is continued need to understand its epidemiology, not only to guide in management of these patients at the bedside, but also to stimulate advances in understanding its pathophysiology and in therapeutic interventions to potentially mitigate prognosis.
- Septic acute kidney injury: new concepts. Septic acute kidney injury: new concepts. Nephron Exp Nephrol 2008;109:e95-100. http://www.ncbi.nlm.nih.gov/pubmed/18802375 Abstract: Acute kidney injury (AKI) is a serious condition that affects many ICU patients. The most common causes of AKI in ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite of our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to kidney ischemia. However, recent models of experimental sepsis have challenged this notion by demonstrating that, in experimental states, which simulate the hemodynamic picture most typically seen in man (e.g. hyperdynamic sepsis) renal blood flow, actually increases as renal vascular resistance decreases. These experimental observations provide proof of concept that septic AKI can occur in the setting of renal hyperemia and that ischemia is not necessary for loss of glomerular filtration rate (GFR) to occur. They also suggest that similar hemodynamic event may occur in man. In addition, preliminary studies in septic sheep show that, when ATP is measured using an implanted phosphorus coil and magnetic resonance technology, renal bioenergetics are preserved in the setting of advanced septic shock. While these findings need to be confirmed, they challenge established paradigms and offer a new conceptual framework of reference for further investigation and intervention in man.
- Pathophysiology of septic acute kidney injury: what do we really know? Pathophysiology of septic acute kidney injury: what do we really know? Crit Care Med 2008;36:S198-203. http://www.ncbi.nlm.nih.gov/pubmed/18382194 Abstract: Septic acute kidney injury accounts for close to 50% of all cases of acute kidney injury in the intensive care unit and, in its various forms, affects between 15% and 20% of intensive care unit patients. However, there is little we really know about its pathophysiology. Although hemodynamic factors might play a role in the loss of glomerular filtration rate, they may not act through the induction of renal ischemia. Septic acute renal failure may, at least in patients with a hyperdynamic circulation, represent a unique form of acute renal failure: hyperemic acute renal failure. Measurements of renal blood flow in septic humans are now needed to resolve this pivotal pathophysiological question. Whatever may happen to renal blood flow during septic acute kidney injury in humans, the evidence available suggests that urinalysis fails to provide useful diagnostic or prognostic information in this setting. In addition, nonhemodynamic mechanisms of cell injury are likely to be at work. These mechanisms are likely due to a combination of immunologic, toxic, and inflammatory factors that may affect the microvasculature and the tubular cells. Among these mechanisms, apoptosis may turn out to be important. It is possible that, as evidence accumulates, the paradigms currently used to explain acute renal failure in sepsis will shift from ischemia and vasoconstriction to hyperemia and vasodilation and from acute tubular necrosis to acute tubular apoptosis or simply tubular cell dysfunction or exfoliation. If this were to happen, our therapeutic approaches would also be profoundly altered.
- The histopathology of septic acute kidney injury: a systematic review. The histopathology of septic acute kidney injury: a systematic review. Crit Care 2008;12:R38. http://www.ncbi.nlm.nih.gov/pubmed/18325092 Abstract: Sepsis is the most common trigger of acute kidney injury (AKI) in critically ill patients; understanding the structural changes associated with its occurrence is therefore important. Accordingly, we systematically reviewed the literature to assess current knowledge on the histopathology of septic AKI.
