Ray S, Piraino B, Chong T K, el-Shahawy M, Puschett J B
Department of Medicine, University of Pittsburgh School of Medicine, Pa.
Miner Electrolyte Metab. 1990;16(6):355-61.
Hyperchloremic metabolic acidosis can be seen in advanced chronic renal failure (CRF). To study this further, we measured acid excretion under controlled conditions in 19 patients with severe but stable CRF. Twelve patients had a hyperchloremic metabolite acidosis, 3 had an elevated anion gap acidosis ('delta acidosis'), while the 4 remaining patients had a slightly decreased tCO2 with a normal anion gap and serum chloride level ('mild acidosis'). Ammonium excretion was markedly reduced in CRF patients (11 +/- 1 vs. 32 +/- 2 mEq/day in normal subjects, p less than 0.005), and likewise urinary titratable acid was diminished (18 +/- 2 mEq/day in patients, vs. 28 +/- 3 mEq/day in normal subjects; p less than 0.005). When expressed per 100 ml GFR, ammonium and titratable acid excretion were markedly increased in all groups of patients compared to normal subjects. The Tm for bicarbonate was 22.5 +/- 3.7 mEq/l for all CRF patients and 24 +/- 1 mEq/l for the patients with a hyperchloremic metabolic acidosis. We conclude that the hyperchloremic metabolic acidosis in advanced renal failure is due to diminished excretion of ammonium and titratable acid and is not due to an increased bicarbonate leak. As renal failure advances and renal mass declines, the remaining functioning nephrons hypersecrete acid.
高氯性代谢性酸中毒可见于晚期慢性肾衰竭（CRF）。为进一步研究此情况，我们在可控条件下测量了19例重度但病情稳定的CRF患者的酸排泄情况。12例患者存在高氯性代谢性酸中毒，3例存在阴离子间隙升高性酸中毒（“δ酸中毒”），而其余4例患者的总二氧化碳（tCO2）略有降低，阴离子间隙和血清氯水平正常（“轻度酸中毒”）。CRF患者的铵排泄显著减少（正常受试者为32±2 mEq/天，CRF患者为11±1 mEq/天，p<0.005），同样，尿可滴定酸也减少（患者为18±2 mEq/天，正常受试者为28±3 mEq/天；p<0.005）。当以每100 ml肾小球滤过率（GFR）表示时，所有患者组的铵和可滴定酸排泄与正常受试者相比均显著增加。所有CRF患者的碳酸氢盐转运极限（Tm）为22.5±3.7 mEq/l，高氯性代谢性酸中毒患者为24±1 mEq/l。我们得出结论，晚期肾衰竭中的高氯性代谢性酸中毒是由于铵和可滴定酸排泄减少所致，而非碳酸氢盐泄漏增加所致。随着肾衰竭进展和肾实质减少，剩余的功能肾单位会过度分泌酸。
