{"id":"3edc8ae0829a","type":"article","url":"https://hartvaat.nl/2026/06/23/zwangerschapsgeassocieerd-acuut-nierfalen-pathofysiologie-en-verhoogd-langetermi/","title":"Zwangerschapsgeassocieerd acuut nierfalen: pathofysiologie en verhoogd langetermijnrisico op hart- en vaatziekten","title_en":"Pathophysiology of pregnancy-associated acute kidney injury.","category":"chronische nierziekte","category_label":"Nierziekte","professions":["cardioloog","internist"],"tags":[],"journal":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","doi":"10.1093/ndt/gfag142","source_url":"https://doi.org/10.1093/ndt/gfag142","authors":["Kianoush B Kashani","Lizemarie Wium","Marlies Ostermann","Ravindra L Mehta","Claudio Ronco","Cathy Nelson-Piercy","Carlos E Poli-de-Figueiredo","Manisha Sahay"],"significance":5,"published":"2026-08-09","source_date":"2026-06-23","image":"","kennis":["https://hartvaat.nl/kennis/nierziekte/nierziekte-en-cardiovasculair-risico/","https://hartvaat.nl/kennis/cardiometabool/diabetes-type-1-en-hart/"],"congress":"","summary_en":"This narrative review outlines the pathophysiology of pregnancy-associated acute kidney injury (PrAKI), which affects an estimated 40–100 per 10,000 pregnancies. The authors highlight how pregnancy-specific hemodynamic shifts, placental ischemia, and immune dysregulation impair renal reserve and endothelial function, leading to long-term risks of chronic kidney disease and cardiovascular disease. Recognizing these mechanisms underscores the need for structured long-term follow-up and cardiovascular risk management in women who have experienced PrAKI.","created":"2026-08-03T01:01:14Z","updated":"2026-08-10T10:36:22Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Deze review beschrijft de pathofysiologie van zwangerschapsgeassocieerd acuut nierfalen (PrAKI), een aandoening met een incidentie van 40–100 per 10.000 zwangerschappen. De auteurs benadrukken dat hemodynamische aanpassingen, placenta-ischemie en immuunmodulatie de nierkwetsbaarheid vergroten, met als langetermijngevolg een verhoogd risico op chronische nierziekte en cardiovasculaire aandoeningen. Inzicht in deze mechanismen is belangrijk voor de follow-up van vrouwen na een complicatievolle zwangerschap, waarbij vroegtijdige herkenning en cardiovasculaire preventie de uitkomst kunnen verbeteren.","abstract_original":"Pregnancy-associated acute kidney injury (PrAKI) remains a major contributor to maternal and fetal morbidity worldwide, with an estimated incidence of 40-100 per 10 000 pregnancies. PrAKI is substantially more prevalent in low- and middle-income countries. Unlike AKI episodes unrelated to pregnancy, PrAKI arises in a unique physiological context characterized by haemodynamic adaptation, immune tolerance, hormonal modulation, and the presence of the fetal-placental unit. These pregnancy-specific factors alter renal reserve, endothelial stability, and inflammatory responsiveness. The pathogenesis of PrAKI is multifactorial. Haemodynamic vasodilation and increased glomerular filtration rates during pregnancy reduce renal functional reserve, rendering the kidney vulnerable to hypovolemia and sepsis. Placental ischemia drives the release of antiangiogenic factors, particularly soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin, causing systemic endothelial dysfunction and glomerular endotheliosis. Disruption of immune tolerance and complement regulation further contributes to microangiopathy and autoimmune-mediated renal injury. Structural urinary tract changes, metabolic stressors, and maternal comorbidities amplify susceptibility. Beyond the index event, PrAKI has lasting consequences. Maladaptive renal repair promotes chronic kidney disease and long-term cardiovascular risk, while fetal exposure to uremic toxins and placental dysfunction contribute to intrauterine growth restriction, prematurity, and reduced nephron mass with lifelong cardio-renal implications. Understanding the pathophysiology of PrAKI, particularly endothelial, immunologic, and placental interactions, has direct diagnostic and therapeutic implications, including the use of angiogenic biomarkers and targeted haemodynamic strategies. Future research must prioritize molecular predictors, global registries, and mechanistic studies to reduce intergenerational kidney and cardiovascular disease."}