Although diabetic ketoacidosis is characterized by increased renal excretion of glucose, ketone bodies, and nitrogenous compounds, there are few quantitative studies pertaining to renal function during this state. Therefore, renal function was studied in 10 adult patients in moderate to severe diabetic ketoacidosis before insulin administration. Admission plasma concentrations were: glucose 21.4 (9.2–39.4) mM or 386 (166–710) mg/dl, acetoacetate 3.0 (1.3–7.4) mM, beta-hydroxybutyrate 7.9 (2.9–15.2) mM, acetone 4.4 (1.3–8.9) mM, and HCO3 12.8 (9.5–17.8) mM. Arterial blood pH was 7.28 (7.21–7.38). Partial rehydration was achieved with 0.45% saline. Inulin was used to measure GFR. Renal clearance of acetoacetate, beta-hydroxybutyrate, acetone, glucose, and urinary excretion of nitrogenous compounds were determined.
Partial rehydration reduced plasma glucose concentration, primarily because of renal excretion, amounting to 384 ± 73 μmol/min or 69 ± 13 mg/min. Partial rehydration had no effect on plasma ketone bodies, on bicarbonate or urea concentrations, or on arterial pH. Partial rehydration had no effect on ketone body or nitrogenous compound excretory rates.
Reabsorptive rates of acetoacetate, beta-hydroxybutyrate, acetone, and glucose increased linearly with their filtered loads, and no maximal renal tubular transport rates were demonstrated for any ketone body or glucose. Because renal absorption of ketone bodies was less than 100%, ketonuria increased as filtered loads increase. Unlike ketone bodies, glucose reabsorptive rate was directly related to GFR.
Total renal excretion of nitrogen in the forms of urea, ammonium, creatinine, and uric acid amounted to 16 ± 2 mg/min. This huge loss of body nitrogen reflected ongoing protein catabolism and not heightened renal excretion of preformed compounds, as the plasma concentrations of urea, creatinine, and uric acid did not change during the study. Urea nitrogen accounted for 12 ± 2 mg/min (72%) of the total nitrogen excreted. Ammonium excretion was markedly augmented, ranging from 76 to 537 μmol/min, and was inversely related to arterial pH.
We conclude that the fall in plasma glucose concentration is primarily caused by renal glucose excretion, and that the absence of a maximal renal tubular reab-sorption rate for either acetoacetate (AcAc) or beta-hydroxybutyrate (β-OHB) serves to mitigate urinary losses of sodium and potassium during diabetic ketoacidosis.