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Can Dka Cause Renal Failure?

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Diabetic Ketoacidosis Linked To Higher Risk For Aki In Youth

High rates of acute kidney injury (AKI) were reported among youth in the hospital for diabetic ketoacidosis (DKA), researchers reported. A low serum bicarbonate level (<10 mEq/L) among hospitalized children with type 1 diabetes and DKA was associated with a significant increase in the risk for stage 2 or 3 AKI (aOR 5.22; 95% CI; 1.35-20.22), according to Brenden E. Hursh, MD, of the University of British Columbia, and colleagues. In the study, published in JAMA Pediatrics, stage 1 acute kidney injury for children with DKA was also linked to an initial corrected sodium level of 145 mEq/L or more (aOR 3.29; 1.25-8.66). Using a multinomial logistic regression model, the researchers also reported a linear relationship between heart rate and severe AKI, with a 22% increase in risk for AKI associated with each increase of five beats per minute in initial heart rate (aOR 1.22; 1.07-1.39). In an interview with MedPage Today, the senior author, Constadina Panagiotopoulos, MD, also of the University of British Columbia, noted, "While I thought we would detect more cases of AKI than that previously represented by the two isolated case reports in the literature, I was surprised by the high pro Continue reading >>

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Popular Questions

  1. StevenRF

    DKA in anuric ESRD

    Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.
    My question is on recs for starting fluids given concern for volume overload. We went with [email protected]/hr with the insulin drip, and despite this, her Na went down.
    For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?
    The physio is a little confusing since there is no output.

  2. jdh71

    StevenRF said: ↑
    Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.
    My question is on recs for starting fluids given concern for volume overload. We went with [email protected]/hr with the insulin drip, and despite this, her Na went down.
    For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?
    The physio is a little confusing since there is no output.
    Click to expand... I assume that is a corrected sodium?

  3. TulaneKid24

    StevenRF said: ↑
    Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.
    My question is on recs for starting fluids given concern for volume overload. We went with [email protected]/hr with the insulin drip, and despite this, her Na went down.
    For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?
    The physio is a little confusing since there is no output.
    Click to expand...
    Diabetic patients tend to suffer from ketoacidosis less frequently after starting chronic dialysis than prior to it.The prolonged half life of insulin in advanced renal failure and frequent follow up of patients on chronic dilayis have been identified as reasons for the decreased frequency of ketoacidois in the dialysis population. The usual course leading to ketoacidosis is omission of one or more insulin doses, often due to an intercurrent illness. This is of prime importance as an underlying cause should always be looked for at presentation. The common ones being access related infections and myocardial ischemia.
    The absence of osmotic diuresis distinguishes dialysis associated hyperglycemia from hyperglycemia observed in patients with normal renal function.The rise in plasma osmolality that is seen in diabetic ketoacidosis and non ketotic hyperosmolar coma is only in part due to the rise in serum glucose. The marked hyperosmolality is primarily due to the glucose osmotic diuresis that causes water loss in excess of sodium and potassium. The importance of effective plasma osmolality in the development of neurological symptoms are illustrated by observations in diabetic patients with end stage renal disease. These patients can develop severe hyperglycemia, with serum glucose concentrations that exceed 1000 to 1500 mg/dl . However because there is little or no osmotic diuresis, the rise in plasma osmolality is limited , hyponatremia is present, and there are few or no neurological symptoms.
    Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation
    Total body concentrations of potassium is unchanged, and they frequently have a high serum potassium level. Hyperglycemia has muliple effects on serum potassium: lack of insulin causes translocation of intracellular potassium to the extracellular compartment, a second hyperkalemic effect of hyperglycemia is the consequence of associated hypertonicity, which also leads to egress of potassium from the cells to the extracellular compartment
    Insulin infusion is the only treatment required in majority of the patients. Emergency hemodialyis may be considered in severe pulmonary edema, profound metabolic acidosis and severe hyperkalemia with EKG mainfestations

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