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Researcher
Anja Verhulst
- Research Expertise:Renal failure can occur in an acute (hours or days) or a chronic (years) setting. Acute kidney injury (AKI) refers to a rapid decrease in renal function and is mainly caused by exposure to nephrotoxic substances, impaired renal blood flow, renal inflammation and obstruction of the urinary tract. In addition to its immediate detrimental effects on body homeostasis, AKI can predispose the kidney to develop progressive chronic kidney disease (CKD) [1]. CKD is a world-wide recognized public health problem affecting 8–16% of the world population [2] and representing a progressive loss of renal function over a period of months or years, ultimately leading to end stage renal disease (CKD stage 5), which inevitably requires renal replacement therapy, i.e., dialysis or kidney transplantation. CKD causes important distortions of the bodies’ mineral balance. A disrupted calcium-phosphate balance is the reason why CKD patients develop important co-morbidities at the level of the bone and the vessels. A disturbed mineral balance viz. hypocalcemia and hyperphosphatemia results in renal osteodystrophy, a term covering various types of bone lesions characterized by either an increased or decreased bone turnover and reduced bone strength/quality. At the level of the vessels, CKD goes along with the induction of vascular media calcifications. Vascular media calcifications and their cardiovascular consequences are the most important cause of death of CKD patients. Renal osteodystrophy together with vascular media calcification is called CKD mineral bone disorder (CKD-MBD) and can be considered to result from a pathologically disturbed bone-vascular interaction. The concomitant occurrence of a disturbed bone turnover and vascular media calcifications (this phenomenon, also referred to as the calcification paradox) occurs not only in CKD- but also in non-CKD patients (diabetics and osteoporosis patients), extending its clinical relevance. To date, effective treatment directly targeting the kidney to attenuate AKI or halt the progression of CKD is lacking. Current treatment for AKI is mainly supportive with correction of volume overload and biochemical abnormalities as primary goals; treatment strategies for CKD mainly focus on controlling important risk factors such as hypertension but cannot avoid that patients progressively loose kidney function. The same is true for a disturbed bone-vascular axis, of which treatment only exists of controlling its risk factors. Within our team of the mineral homeostasis subunit in the Pathophysiology lab, we essentially perform both fundamental and applied research on the mechanisms, treatment and prevention of (renal-induced) vascular and bone pathology.
- Keywords:ANIMAL MODELS, Biomedical sciences (incl. biochemistry)
- Disciplines:Vascular diseases, Kidney diseases
- Research techniques:Cell culture (Primary human renal tubular cells, primary rat osteoblasts, primary rat vascular smooth muscle cells) Early) renal damage markers (human) Animal models (rat and mice): acute/chronic kidney disease, vascular calcification, renal osteodystrophy, nephrocalcinosis, diabetes, osteoporosis o Blood (serum/plasma) and urine collection o Compound administration (diet/drinking water, oral gavage, i.v., i.p., s.c., osmotic minipumps) Execution of the following measurements for those animal models (non in vivo measurements can also be applied on human samples) o Quantification of renal function impairment (serum/urinary analysis) o Qualitative (Von Kossa stained tissue sections) and quantitative (atomic absorption spectrometry) evaluation of vascular calcification o Point of care analysis of different blood parameters (I-STAT technology) o Quantitative bone histomorphometric analysis (static and dynamic parameters) o Histomorphometry/immunohistochemistry of all soft tissues o Quantification of mRNA expression in different tissues (real-time RT PCR) o (in vivo) Micro CT analysis of bone (density) and vessels (vascular calcification presence) (in collaboration with Prof Sijbers-Vision Lab, Dept Physics) o In vivo ultrasound measurement of renal, vessel and heart function (in collaboration with Prof De Meyer, Lab Physiopharmacology) o In vivo blood pressure measurement Analysis of heavy metals (atomic absorption spectrometry)
- Users of research expertise:Laboratories Faculty FBD (UAntwerp) Laboratories Faculty of Medicine (UAntwerp) Laboratories other Universities (also from abroad), UZA/ other hospitals, Biotech companies Pharmaceutical industry