Tuesday, October 25, 2016

Topic Discussion: AKI following LVAD


Image result for LVADLeft ventricular assist devices (LVADs) are used increasingly as a bridge to transplantation or as destination therapy in end-stage heart failure patients who do not respond to optimal medical therapy. Many of these patients have end-organ dysfunction, including advanced kidney dysfunction, before and after LVAD implantation. Kidney dysfunction is a marker of adverse outcomes, such as increased morbidity and mortality.The incidence of AKI after LVAD implantation varies considerably: between 4 and 38 %. 


Risk factors:
INTERMACS score 1 or 2 ( http://content.onlinejacc.org/article.aspx?articleid=1143100)
Kidney <10 cm in size
Older age
ACE-I or ARB therapy immediately prior to surgery
High central venous pressure
Low LV end-diastolic dimensions
Long CPB time
Higher intraop bleeding
Need for re operation
Sepsis
Liver dysfunction
Need for blood transfusions
RV failure
CKD

Factors such as acute blood loss, volume shifts, arrhythmias, and the effect of multiple vasoactive medications influence renal hemodynamics. The sudden change in renal blood flow characteristics due to continuous flow-LVAD support can lead to AKI. Patients with preoperative RV failure and patients with INTERMACS scores of 1 or 2 are at higher risk of AKI.  The RV function is of vital importance after LVAD placement since postoperative RV failure and idioventricular arrhythmias have been associated with AKI . An RV dysfunction can result in a reduced LV preload, low LVAD speeds, reduced forward flow, increased arrhythmias, and liver as well as kidney congestion.

It appears that the cause is hemodynamic vs ATN. No study has really defined the mechanism. Given the LVAD devices have pro thrombotic risk , renal vascular thrombosis and or anticoagulation related AKI should be in the differential. As always, AIN from any medication is to be considered. Hemolysis related injury could be leading to pigment nephropathy as well.

https://www.ncbi.nlm.nih.gov/pubmed/25759700

https://www.ncbi.nlm.nih.gov/pubmed/25796403

Wednesday, October 12, 2016

Tuesday, October 4, 2016

In the NEWS: Lung Ultrasound and volume assessment in ESRD


Your new device- the lung ultrasound has made its way in Europe. A recent trail in CJASN discusses the value of using lung ultrasound in assessing volume status of a patient.  Lung water can be used in a way in clinical practice as it is being used in critical care and cardiology to assess volume in ESRD patients.  Few prior studies that have looked at the role of ESRD and lung ultrasound in clinical practice and training of fellows/faculty  are here:




This new study in CJASN looked at >1000 patients pre and post HD via lung ultrasound simultaneous to standardized lung exams ( crackles ) and peripheral edema.  What the investigators found was that the lung congestion by crackles, edema or a combination was inferior to ultrasound B lines in various analysis.  Using the knowledge of B lines might guide us in better managing volume status in our ESRD patients. 

In the editorial with it in CJASN, Dr. Rich Sherman writes “I believe that lung US will prove to be of value in improving the care of patients on dialysis . From a practical standpoint, I hope that this technique can provide us with at least one simple benefit. If a routine lung US on the previous Friday before dialysis might make these events less likely, then sign me up!

I concur with Dr Sherman! I think Nephrologists should get familiar with the science and technology and embrace this change to help their patients. Dialysis units ( large and small) should consider carrying US machines to help guide volume exam and make clinical decisions. It will decrease hospitalizations, less radiation exposure( X rays) and hopefully less ER visits.

http://www.nephronpower.com/2016/01/perspective-how-ultrasound-machine-has.html

Image courtesy: coreem.net

Monday, October 3, 2016

Concept Map: Electrolyte Disorders and anti cancer agents

















Most electrolytes disorders are "hypo" that are drug induced from anti cancer agents. Mechanism is mentioned where there is evidence.

The two references are:
https://www.ncbi.nlm.nih.gov/pubmed/26939882
http://www.kireports.org/article/S2468-0249(16)30134-6/pdf

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