Friday, August 10, 2018

Topic Discussion: ECMO and the Kidney


Extracorporeal membrane oxygenation (ECMO) is an effective therapy for patients with reversible cardiac and/or respiratory failure. AKI  often occurs in patients supported with ECMO; it frequently evolves into chronic kidney damage or end-stage renal disease and is associated with a reported 4-fold increase in mortality rate. What are the mechanisms of injury of AKI with ECMO?
This table below summarizes what might be the potential causes.



Patient-related variables

Pretreatment factors
Hypoperfusion, loss of autoregulation Hypoxia

Nephrotoxic drugs Systemic inflammation

ECMO-related variables


Hemodynamic factors
Blood flow alterations
Hormonal factors
Renin-angiotensin-aldosterone dysregulation ANP downregulation
ECMO-related
Blood shear stress
Systemic inflammation
Exposure to a non-self membrane Blood/air interface
Organ crosstalk
Cardio-renal syndrome
Circuit-related factors
Hypermyoglobinemia

Embolism

Hemolysis

 

Hemolysis is an interesting cause. This is an image of a patient getting CRRT on ECMO.  CRRT was on a zero K bath and high clearance rates. Within hours of starting CRRT, effluent bags of the CRRT turn red. Despite being on max CRRT,  patient’s potassium rose to 9mmol/L. This is hemolysis and can be reported in 18% of cases with ECMO.  Rhabdomyolysis can also be noted in some cases. Checking a free Hgb and effluent myoglobin can aid diagnosis for both entities. In addition, classic markers for hemolysis such as LDH, haptoglobin, anemia and so forth should be checked regularly. 


Wednesday, August 1, 2018

Topic Discussion: Non-nephrogenic calciphylaxis


Calciphylaxis in Patients With Normal Renal Function is usually unusual as most of the cases we encounter as nephrologists are in ESRD and or CKD patients
A recent review and literature update by the MGH researchers defined concomitant risk factors, treatment, and outcomes for patients with nonnephrogenic calciphylaxis.
116 patients today were reviewed.  Vitamin K antagonism and obesity were the most common concomitant factors. In the literature review, lower age and higher body mass index  were associated with the central location of lesions, whereas vitamin K antagonism was associated with the peripheral locations.  None of the treatments were associated with lesion improvement or survival.
As summarized by the authors: the risk factors are the 4Ws:- Warfarin, White race, Women and overWeight in patients with normal renal function. Interesting that warfarin is a risk factor in both renal and non renal calciphylaxis. It’s perhaps about time the renal community embrace apixaban over warfarin
A larger set of risk factors exists that were mentioned in the recent NEJM review in 2018 that also add: ESRD( what we see), hypercalcemia( probably in setting of CKD as pure – not really evident), DMII, hyperparathyroidism( we have seen this), Vitamin K deficiency, Autoimmune disorders, metastatic cancers, rapid weight loss, skin trauma to name a few.
Check out this interesting tweetorial from ISN education on this topic

Wednesday, July 25, 2018

Consult Rounds: Toxic alcohol ingestions


A summary of all potential alcohol toxicities ( Renal perspective)


Name
Metabolic Acidosis
Osmolar Gap
Anion Gap
Ketones
Ca Oxolate Stones
Reduced Vision
Alcohol
Yes
Yes
Yes( lactate also)
Yes
No
No
Methanol
Yes
Yes( earlier on and then disappears)
Yes
No
No
Yes
Ethylene Glycol
Yes
Yes
Yes
No
Yes
No
Isopropyl
Alcohol
No
Yes
No
Yes
No
Yes
Propylene
Glycol
Yes
Yes(initially)
Yes(converted to lactate)
No
No
No

Saturday, July 21, 2018

Topic Discussion: Interesting HTN, hypokalemia and Met Alk syndromes: a summary


There are certain syndromes that lead to HTN, hypokalemia and metabolic alkalosis that are very rare but often confusing. Here is a breakdown of the 3 ones that often can get confusing.


Syndrome
Defect
Pathophysiology
Treatment
Comments
Liddle Syndrome
Missense mutation in ENaC channel

Constitutive activation of the ENaC channel
Triamterene or Amiloride
Low renin and low aldosterone level, no response to spironolactone
Congenital Adrenal hyperplasia
11-B hydroxylase deficiency
Leading to excessive mineralocorticoid production
Life-long steroids to help shut off ACTH
Diagnosis is confirmed by elevations of 11-deoxycortisol and 11-deoxycorticosterone
Glucocorticoid remediable Aldosteronism
Chimeric gene crossover of ACTH and Angio-11 genes
Normal ACTH controls cortisol and AngII controls Aldo. In this gene mutation, ACTH starts controlling Aldo and hence causing HTN and ongoing changes

Leading to excessive aldosterone production.
 
Life-long steroids to help shut off ACTH


Low renin but high Aldo in these cases.
Syndrome of Apparent mineralocorticoid excess
11-B hydroxysteroid dehydrogenase type 2 mutation or inhibition
Normally, 11-B hydroxysteroid dehydrogenase in-actives cortisol via making to cortisone. This avoids cortisol mediated mineralocorticoid activity to maintain it’s specificity to aldosterone. If this is blocked, then cortisol activates mineralocorticoid activity
Amiloride or spironolactone
Diagnosis made via free urinary cortisol to cortisone ratio
Renin and Aldo levels are low

Licorice that has glycyrrhic acid that can also inhibit 11-B hydroxysteroid dehydrogenase.

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