Impairment of Ventilatory Response to Metabolic Acidosis in Insulin-Dependent Diabetic Patients with Advanced Nephropathy

Abstract

Sudden cardiopulmonary arrest due to a defective respiratory reflex is observed in diabetic patients. Impaired ventilatorp response in diabetic patients to acute hypoxia or hypercapnia induced by the inhalation of an artificial gas has been reported. Little is known regarding the respiratory compensatory ability for mild to moderate metabolic acidosis due to renal failure in insulin-dependent diabetic subjects. Arterial blood pH, HCO3, PaCO2 and PaO2 were measured in 13 insulin-dependent diabetic subjects with advanced nephropathy and in 33 non-diabetic subjects with end-stage renal failure. The diabetic group consisted of six predialysis patients and seven on regular hemodiaiysis (HD), md the non-diabetic group, ten predialysis patients and 23 on HD. Differences between measured partial arterial pressure of carbon dioxide (PaCO2) and predicted PaCO2 determined fiom HCO3 were examined. PaCO2 was significantly higher in the diabetic than in non-diabetic group (40.0 ± 7.4 versus 31.1 ± 5.1 mmHg, p < 0.05 in predialysis, 42.0 ± 6.4 versus 36.0 ± 2.6mmHg, p < 0.05 in HD), though plasma pH was essentially the same for either. Differences in measured PaCO2 and predicted PaCO2 were significantly larger in the diabetic group than in non-diabetic group. Ventilatoly respose to uremic acidosis may thus be considered impaired in subjects with advanced diabetic nephropathy.