Renal tubular acidoses
| Location | Type | Acidosis | UAG | HCO3- | UpH | FEHCO3b | K | complication |
|---|---|---|---|---|---|---|---|---|
| Proximal | II | Moderate | +- | 12-20 | < 5.3 | > 15% | low | osteomalacia |
| Distal | I | Severe | + | < 10 | > 5.3 | < 3% | low | Kidney stones |
| Hypoaldo (collecting duct) | IV | Mild | + | > 17 | < 5.3 | ≤ 3% | more | Hyperkalemia |
(RTAs) (Adv Ther 2021;38:949) (Adv Ther 2021;38:949)
Proximal (Type II) 收不回 2️⃣ Bi-carbonate
- ↓ proximal reabsorption of HCO3: pRTA
- 1° (Fanconi’s syndrome) = ↓ proximal reabsorption of HCO3, PO4, glc, amino acids
- Acquired: paraprotein (MM, amyloidosis), ⭐ metals (Pb, Cd, Hg 鉛、鎘、汞, Cu), ↓ vit D, PNH, renal Tx
- Meds: acetazolamide, aminoglycosides, ifosfamide, cisplatin, topiramate, tenofovir
Distal (Type I) H+ 1️⃣ (原子序 1) 丟不掉
- defective distal H+ secretion : dRTA
- 1°, autoimmune ⭐ ( Sjögren’s, RA, SLE), hypercalciuria, meds (ampho, Li, ifosfamide); normally a/w ↓ K; if with ↑ K → sickle cell, obstruction, renal transplant
- 唯一會 Base Urine pH > 5.5, 高鈣有石
Hypoaldo (Type IV) 四大重點：Aldo, K, NH3, 藥物常見的副作用
- hypoaldo → ↑ K → ↓ NH3 synthesis → ↓ urine acid-carrying capacity
- ↓ renin: diabetic nephropathy, NSAIDs, chronic interstitial nephritis, calcineurin inh, HIV
- ↓ aldo production: 1° AI, ACEI/ARBs, heparin, severe illness, inherited (↓ 21-hydroxylase)
- ↓ response to aldosterone
- medication that cause hypoaldo: Tubulointerstitial disease: sickle cell, SLE, amyloid, DM
Combined (Type III)
rarely discussed or clinically relevant, also called juvenile RTA, has distal & proximal features, can be due to carbonic anhydrase II deficiency
- Urine pH will rise above 5.3 in the setting of HCO3 load
- FeHCO3 should be checked after an HCO3 load
- See above for causes of distal RTA (Type I) associated with hyperkalemia