title: Renal function in hypoxaemic chronic obstructive pulmonary disease: effects of long-term oxygen treatment.
abstract: Impaired renal function is an important cause for the oedema formation, which often occurs in severe chronic obstructive pulmonary disease (COPD). In the present study, the importance of nocturnal hypoxaemia (measured by a nocturnal pulse oximetry) for the renal function was determined in 19 COPD patients, with normal levels of serum creatinine. The effects on kidney function of alleviating the nocturnal hypoxaemia [using 6 months of long-term oxygen treatment (LTOT)], was assessed in 12 patients. Renal function was assessed by determining the clearances of intravenously administered inulin (C(In)) and para-amino-hippurate (C(PAH)) and orally supplemented lithium (C(Li)) and of circulating sodium (C(Na)). The 19 patients had a mean PaO2 of 7.63 +/- 1.08 kPa, a PaCO2 of 5.98 +/- 0.85 kPa, a mean nocturnal oxygen saturation (MnSaO2) of 87.7 +/- 2.8% and an FEV1 in %P of 25.6 +/- 14.6%. C(In) and C(PAH) were 35 and 45% lower than normal, respectively, whereas C(In)/C(PAH)=filtration fraction (FF) was 31% higher than normal. Six months of LTOT in 12 of the patients was not followed by any significant change in renal function in the entire study group. However, low pretreatment MnSaO2 correlated with reductions in post-treatment (FF) (r=0.73, P<0.05). Post-treatment PaCO2 did not change significantly in patients treated with oral diuretics, but increased (P<0.05) in patients without diuretics. C(Na) decreased after LTOT in six patients with an increase in PaCO2>6%, but C(Na) increased in four patients with unchanged or decreased PaCO2 following LTOT.
  
  
  CONCLUSIONS
  Renal function (including filtration fraction) is impaired in hypoxaemic COPD. Filtration fraction is decreased following 6 months of LTOT solely in patients with severe pretreatment hypoxaemia and sodium clearance seems to be increased if improved oxygenation is not accompanied by increased PaCO2.
authors.affiliation: Division of Respiratory Medicine, Department of Medicine, Karolinska Hospital, Stockholm, Sweden. tomas.bratel@ks.se
authors.forename: T
authors.initials: T
authors.lastname: Bratel
authors.forename: S
authors.initials: S
authors.lastname: Ljungman
authors.forename: M
authors.initials: M
authors.lastname: Runold
authors.forename: P
authors.initials: P
authors.lastname: Stenvinkel
mesh_terms: D015992:Body Mass Index; D002245:Carbon Dioxide / Q000097:blood; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D007674:Kidney Diseases / Q000097:blood / Q000503:physiopathology*; D016014:Linear Models; D008134:Long-Term Care; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood / Q000627:therapeutic use*; D010313:Partial Pressure; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism; D014797:Vital Capacity / Q000502:physiology
chemical_list: D002245:Carbon Dioxide; D012964:Sodium; D010100:Oxygen