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Review
. 2017 Aug 29;6(9):82.
doi: 10.3390/jcm6090082.

Acute Kidney Injury in Heart Failure Revisited-The Ameliorating Impact of "Decongestive Diuresis" on Renal Dysfunction in Type 1 Acute Cardiorenal Syndrome: Accelerated Rising Pro B Naturetic Peptide Is a Predictor of Good Renal Prognosis

Affiliations
Review

Acute Kidney Injury in Heart Failure Revisited-The Ameliorating Impact of "Decongestive Diuresis" on Renal Dysfunction in Type 1 Acute Cardiorenal Syndrome: Accelerated Rising Pro B Naturetic Peptide Is a Predictor of Good Renal Prognosis

Macaulay Amechi Chukwukadibia Onuigbo et al. J Clin Med. .

Abstract

There is mounting evidence that forward heart failure as manifested by low cardiac output alone does not define the degree of renal dysfunction in cardiorenal syndrome. As a result, the term "congestive renal failure" was coined in 2012 by Ross to depict the role of renal venous hypertension in type 1 acute cardiorenal syndrome. If so, aggressive decongestive therapies, either through mechanical ultrafiltration with dialysis machines or pharmacologic ultrafiltration with potent diuretics, would lead to improved cardio and renal outcomes. Nevertheless, as recently as 2012, a review of this literature had concluded that a renal venous hypertension-directed approach using diuretics to manage cardio-renal syndrome was yet to be fully investigated. We, in this review, with three consecutive case series, describe our experience with pharmacologic decongestive diuresis in this paradigm of care and argue for studies of such therapeutic interventions in the management of cardiorenal syndrome. Finally, based on our observations in the Renal Unit, Mayo Clinic Health System, in Northwestern Wisconsin, we have hypothesized that patients with cardiorenal syndrome presenting with accelerated rising Pro B Naturetic Peptide levels appear to represent a group that would have good cardio- and renal-outcomes with such decongestive pharmacologic therapies.

Keywords: Pro B Naturetic Peptide; acute decompensated heart failure; cardiorenal syndrome; central venous pressure; congestive heart failure; congestive renal failure; continuous intravenous furosemide infusion; fluid balance; intravenous chlorothiazide; intravenous decongestive diuresis; renal venous hypertension; renal venous pressure; serum creatinine; ultrafiltration.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Fluid balance with total intake and urine output in Case 1 during the index admission.
Figure 2
Figure 2
Weight changes following intravenous decongestive diuresis in Case 1.
Figure 3
Figure 3
Falling serum creatinine in Case 1 following intravenous decongestive diuresis, 4–11 March 2017.
Figure 4
Figure 4
Serum creatinine trajectory in Case 1 leading to and following the use of intravenous decongestive diuresis, 4–11 March 2017.
Figure 5
Figure 5
Worsening serum creatinine trajectory in Case 2 leading to the admission in mid-May 2017.
Figure 6
Figure 6
Fluid balance with total intake and urine output in Case 2 during the index admission.
Figure 7
Figure 7
Weight reduction following intravenous decongestive diuresis in Case 2.
Figure 8
Figure 8
Serum creatinine trajectory in Case 2 following the use of intravenous decongestive diuresis.
Figure 9
Figure 9
Worsening serum creatinine trajectory in Case 3 leading to the admission in early June 2017.
Figure 10
Figure 10
Fluid balance with total intake and urine output in Case 3 during the index admission.
Figure 11
Figure 11
Weight reduction following intravenous decongestive diuresis in Case 3.
Figure 12
Figure 12
Normalized serum potassium from hyperkalemic levels following intravenous decongestive diuresis in Case 3.
Figure 13
Figure 13
Normalized serum phosphorus from previously hyperphosphatemic levels following intravenous decongestive diuresis in Case 3.
Figure 14
Figure 14
Falling serum creatinine in Case 3 following intravenous decongestive diuresis.
Figure 15
Figure 15
Serum creatinine trajectory in Case 3 leading to and following the use of intravenous decongestive diuresis.
Figure 16
Figure 16
Pro B Nat Pep trajectory in Case 1 immediately preceding the index admission (Reference range for Pro B Nat Pep ≤ 450 pg/mL).
Figure 17
Figure 17
Pro B Nat Pep trajectory in Case 2 immediately preceding the index admission (Reference range for Pro B Nat Pep ≤ 450 pg/mL).
Figure 18
Figure 18
Pro B Nat Pep trajectory in Case 3 immediately preceding the index admission (Reference range for Pro B Nat Pep ≤ 125 pg/mL).
Figure 19
Figure 19
Composite figure showing the acutely rising BNP levels in the three patients at presentation.

References

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