How should we use NT-proBNP guided therapy and anticipate that NT-proBNP is augmented in patients with chronic heart failure and acute kidney injury?

Dr Sim : Most of the time in Singapore, when a patient is received from the emergency department, an NT-proBNP would have been done. ED physicians are very aggressive in ordering the NT-proBNP so that the results would be quick.

In the setting of pneumonia, acute kidney injury, they would definitely affect the NT-proBNP result. It is still useful to do it because it will provide a lot of information on the constant evaluation of the patient.

Dr Januzzi : . It is complicated because acute kidney injury can cause acute volume overload, which may cause increased NT-proBNP. In addition, the stress on the myocardium from the toxins that accumulate from worsening kidney function may cause troponin elevation, NT-proBNP rise from myocardial dysfunction. In addition, the kidneys are responsible for about 20 to 25% of NT-proBNP clearance. When a person develops AKI, NT-proBNP rises. That increase is very prognostic; although there are AKI patients in whom there is no increase in NT-proBNP that is also very reassuring.

Together with improving kidney function related to the use of sacubitril/valsartan and SGLT2 inhibitors, data from the DAPA-CKD study provides us, some tools that we can use to improve prognosis better and protect the kidney. In the CANVAS study in patients with acute kidney injury, in addition to NT-proBNP, other biomarkers were also examined, including IGF binding protein-7. It is a biomarker that belongs to the insulin-like growth factor-binding protein family. But, its main role is tissue remodelling in fibrosis. It is associated not only with heart failure but also kidney disease. The IGFBP-7 examined in the CANVAS study is found to be an incredibly powerful predictor of incident heart failure as well as incident chronic kidney disease progression.

Sacubitril/Valsartan shows the largest level of reduction of NT-proBNP. This probably is because of the fact that the way that the drug works is by enhancing other natriuretic peptides, probably ANP, which causes a reduction in NT-proBNP. The other therapy we use in heart failure that causes a dramatic reduction in NT-proBNP is cardiac resynchronisation therapy (CRT). Sacubitril/valsartan and CRT have a very substantial reduction associated with NT-proBNP.

 

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