[Glomerular function and urine acidification in chronic renal diseases].
Intravenous sodium bicarbonate (NaHCO3) infusion test was performed in 26 patients with chronic glomerulonephritis (CGN) and 16 with distal renal tubular acidosis (dRTA) in order to evaluate urinary acidifying capacity in chronic renal diseases. Comparative studies with glomerular filtration were planned, so that the patients with CGN were divided by creatinine clearance (Ccr) into 3 groups (G-I greater than or equal to 70, 30 less than or equal to G-II less than 70, G-III less than 30 ml/min). Proximal tubular bicarbonate (HCO3) reabsorption rate increased in CGN as Ccr decreased. Urine to blood carbon dioxide tension gradient (U-B PCO2) was above 30 mmHg in controls and below 20 mmHg in dRTA. In patients with CGN, urine HCO3 concentration (UHCO3) did not increase during NaHCO3 loading as Ccr decreased. However, U-B PCO2 rose above 20 mmHg, when UHCO3 was above 50 ml/min. Fishberg concentrating test was also performed in 15 patients with CGN and 6 with dRTA so that the relationship between urinary concentrating ability and urine acidification might be evaluated. While both functions were decreased in dRTA, U-B PCO2 in alkaline urine remained above 20 mmHg in CGN associated with moderate renal dysfunction (Ccr greater than or equal to 30 ml/min) despite decreased maximal urine osmolality. Intravenous furosemide (FM) injection test was carried out in 8 patients with chronic renal failure (CRF) and 3 with dRTA. Minimal urine pH fell below 5.5 and net acid excretion (NAE) increased in controls, whereas these responses were not seen in dRTA. In CRF, urine pH generally decreased below 5.5 and those who had a similar response to FM as dRTA, seemed to have more severe disturbance of the distal acidification. In conclusion, U-B PCO2 in alkaline urine and lowered urine pH in FM loading appeared to be a useful index of distal tubular acid excretion in patients with renal dysfunction. In CGN with moderate renal dysfunction (Ccr greater than or equal to 30 ml/min), urinary acidifying capacity remained normal in comparison with decreased urine concentrating ability.
Mizukami
K
K
Department of Medicine, Kidney Center, Tokyo Women's Medical College, Japan.
D000141:Acidosis, Renal Tubular / Q000503:physiopathology / Q000652:urine; D001639:Bicarbonates; D002908:Chronic Disease; D005665:Furosemide; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000503:physiopathology* / Q000652:urine; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007671:Kidney Concentrating Ability; D007678:Kidney Glomerulus / Q000503:physiopathology*; D012964:Sodium; D017693:Sodium Bicarbonate
D001639:Bicarbonates; D005665:Furosemide; D017693:Sodium Bicarbonate; D012964:Sodium