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      Proatrial Natriuretic Peptide (1–98), but Not Cystatin C, Is Predictive for Occurrence of Acute Renal Insufficiency in Critically Ill Septic Patients

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          Introduction: N-terminal prohormone of atrial natriuretic peptide ((proANP(1–98)) has been extensively analyzed in patients with chronic renal failure. It has been found to be closely related to the renal function and to interdialytic hydration status. The clinical relevance of proANP(1–98) and cystatin C, a novel marker of glomerular filtration, has not been investigated in the subgroup of critically ill septic patients with no history of chronic renal impairment. Methods: We measured plasma level ofproANP(1–98) and cystatin C in 29 critically ill septic patients on admittance to the surgical intensive care unit and correlated it with the occurrence of acute renal failure. Results: The proANP(1–98) plasma level was significantly higher in the group of patients who developed renal failure (12,722 ± 12,421 vs. 2,801± 2,023 fmol/ml, p < 0.05). Multiple regression analysis shows that proANP(1–98) on the first day in the intensive care unit has a superior predictive value for the occurrence of renal failure to diuresis, calculated creatinine clearance or cystatin C (r = 0.42, p < 0.039). proANP(1–98) is also higher in non-survivors (9,303.8 ± 11,053 vs. 2,448.5 ± 1,803 fmol/ml, p < 0.018). Conclusion: proANP(1–98) is possibly a better predictor of acute renal failure to calculated creatinine clearance or diuresis among critically ill septic patients. Cystatin C was not correlated with occurrence of acute renal failure in this subgroup of patients.

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          Prognosis of patients who develop acute renal failure during the first 24 hours of cardiogenic shock after myocardial infarction.

          Acute renal failure has important prognostic implications in critically ill patients, but the effects of acute renal failure on in-hospital mortality in the subset of patients with cardiogenic shock are not known. All consecutive patients who presented with acute coronary syndrome at our cardiovascular intensive care unit from 1993 to 2000 and who were in cardiogenic shock were enrolled. Acute renal failure was defined as a urine volume or = 0.5 mg/dL or > 50% above the baseline value. There were 118 patients (83 men [70%]; mean [+/- SD] age, 66 +/- 10 years), 39 (33%) of whom developed acute renal failure within 24 hours after the onset of shock. In-hospital mortality was 87% (34/39) in patients with acute renal failure and 53% (42/79) in patients without acute renal failure (odds ratio [OR] = 6.0; 95% confidence interval [CI]: 2.1 to 17; P < 0.001). Other significant univariate predictors of mortality included the peak serum lactate level, epinephrine dose, and the maximum serum creatinine level. Multivariate logistic regression analysis identified acute renal failure as the only independent predictor of mortality. Acute renal failure was common in patients with cardiogenic shock and strongly associated with in-hospital mortality.
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            Cystatin C

             D Newman (2002)
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              Plasma concentration and urinary excretion of N-terminal proatrial natriuretic peptides in patients with kidney diseases.

              Biologically active N-terminal fragments such as proANP(1-30), proANP(31-67), and proANP(1-98) derive from the prohormone of alpha-human atrial natriuretic peptide [proANP(99-126) or alpha-ANP]. No systematic data are available for patients with different kidney diseases. Specific immunoassays were developed to determine plasma and urine concentrations of these fragments in 121 patients with different degrees of kidney function and urinary protein excretion, respectively. In patients with kidney disease and normal renal function without proteinuria, circulating proANP(1-30) and proANP(31-67) increased 2.8-fold and 6.5-fold, respectively. Urinary excretion of proANP(31-67) increased by a factor of 7.7 in these patients, whereas proANP(1-30) was not affected. Patients with impaired renal function had a dramatic increase of urinary proANP(31-67) excretion even before serum creatinine levels started to rise. The progression of renal failure caused a significant rise of circulating proANP(1-30) (4.3-fold) and proANP(31-67) (3.0-fold) compared with patients with normal renal function. Urinary excretion of proANP peptides significantly increased, particularly when the serum creatinine level was> 5.0 mg/dL [proANP(1-30) 26-fold, proANP(31-67) 8.4-fold]. Urinary excretion of proANP(1-30) increased up to 4.4-fold and urinary excretion of proANP(31-67) increased up to 2.4-fold in patients with proteinuria in excess of 3 g/24 h. Plasma concentrations and urinary excretion of proANP(1-30) and proANP(31-67) are affected by kidney disease and function, but not by proteinuria per se. It is proposed that the diseased kidney increases early urinary excretion of proANP fragments to participate in the regulation of renal function as well as sodium and water excretion.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                July 2004
                17 November 2004
                : 97
                : 3
                : c103-c107
                Departments of aAnesthesiology and Intensive Care, bClinical Chemistry, cSurgery, and dInternal Medicine, University Hospital Sestre Milosrdnice, eDepartment of Molecular Medicine, Institute Rudjer Boskovic, Zagreb, Croatia, and fBiomedica Gruppe, Vienna, Austria
                78638 Nephron Clin Pract 2004;97:c103–c107
                © 2004 S. Karger AG, Basel

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