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Successful Management of Respiratory Failure Can Improve Renal Function

A subset of patients with acute exacerbation of chronic pulmonary disease present with concomitant acute renal failure (ARF). Acute hypercapnia remains an underappreciated and often overlooked cause of ARF in these patients with acute hypercapnic respiratory failure (AHRF). A nephrology consultation is requested for oliguric ARF in a woman with obesity-hypoventilation syndrome who has been admitted for AHRF and was treated with non-invasive ventilation. Despite stable hemodynamic status, the patient receives a large volume of intravenous fluids in an attempt to improve the renal function and urine output, and develops pulmonary edema and worsening respiratory status.

The decision is made to hemodialyze the patient for pulmonary edema and resistant hyperkalemia. However, prior to initiation of hemodialysis, the patient is intubated and started on mechanical ventilation because of progressively worsening respiratory status. This is followed by rapid improvement in hypercapnia and acidosis, and then by a significant increase in urine output. The patient’s renal function and hyperkalemia improves over the next few hours, obviating the need for renal replacement therapy.

The potential causes of ARF in patients with AHRF are numerous, and include hemodynamic instability and hypotension, intravascular volume depletion (due to increased insensible loss), concomitant use of medications that affect renal hemodynamics (eg, angiotensin-converting enzyme-I and diuretics), presence of comorbidities with potential impact on renal function (eg, chronic kidney disease, diabetes, heart failure), and interventions performed at the time of admission (eg, intravenous contrast studies and nephrotoxic medications).

Management of AHRF frequently parallels the conservative treatment of ARF in these patients, which very often includes administration of large volumes of intravenous fluids with the assumption that the patient is intravascularly volume-depleted. This approach is certainly indicated in patients with hemodynamic instability as well as in those with evidence of intravascular volume depletion and organ hypoperfusion. However, unnecessary and injudicious administration of a large volume of intravenous fluids can result in severe volume overload and worsening respiratory status in other patients.

In this regard, it is important to emphasize the role of acute hypercapnia as a potential cause of ARF in patients presenting with AHRF. Although chronically hypercapnic subjects (eg, those with stable chronic obstructive pulmonary disease) have a baseline renovascular resistance similar to normocapnic patients, acute increase in serum CO₂ levels is shown to be associated with renal vasoconstriction.^1,2 This impact on renal vascular tone is believed to be both direct and indirect (ie, via the sympathetic nervous system).^3,4 Vasoconstriction leads to a decrease in renal blood flow and intra-glomerular pressure, with subsequent reduction in glomerular filtration rate. Therefore, it is not unexpected to observe ARF, with pre-renal characteristics without intracascular volume depletion, in patients presenting with AHRF. This physiological concept is further supported by clinical observations such as the one mentioned earlier, in which renal function is improved after successful management of hypercapnia with no additional kidney-oriented intervention.

It therefore seems prudent to focus on management of AHRF in patients who present simultaneously with AHRF and ARF. Unnecessary administration of large volumes of intravenous fluids should be avoided in patients without evidence of intravascular volume depletion, and renal replacement therapy can be deferred, if possible, because resolution of AHRF and hypercapnia is typically followed by improvement in renal function.

FINANCIAL DISCLOSURES
None reported.

REFERENCES

1. Sharkey RA, Mulloy EMT, O’Neill SJ. The acute effects of oxygen and carbon dioxide on renal vascular resistance in patients with acute exacerbation of COPD. Chest. 1999;115:1588–1592.[Abstract/Free Full Text]
2. Sharkey RA, Mulloy EMT, O’Neill SJ. Acute effects of hypoxaemia, hyperoxaemia and hypercapnia on blood flow in normal and renal transplant subjects. Eur Respir J. 1998;12:653–657.[Abstract]
3. Hall JE. Regulation of renal hemodynamics. In: Guyton AC, Hall JE, eds. Cardiovascular Physiology VI. Vol 26: International Review of Physiology. Baltimore, MD: University Park Press; 1982:243–321.
4. Anand IS, Chandrashekhar Y, Ferrari R, et al. Pathogenesis of congestive state in chronic obstructive pulmonary disease. Circulation. 1992;86:12–21.[Abstract/Free Full Text]

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