Three tubular acidoses, one reflex: read the potassium first, then split on urine pH and the urine anion gap. Work the diagram, flip the villains, drill the vignettes.
Tap a type to see which segment breaks. Follow the flow left to right.
All RTAs cause the same lab pattern:
That's your starting point. If you see high Cl⁻ + low HCO₃⁻Bicarbonate · the body's main base/buffer. The kidneys normally reabsorb it to keep blood pH balanced. + normal anion gapA calculation: Na⁺ minus (Cl⁻ + HCO₃⁻). If elevated, think lactic acidosis, ketoacidosis, toxins. If normal = RTA or diarrhea. = think RTA.
Then use two questions to figure out which type:
Wait · two different "anion gaps"?
Yes. Don't mix them up. They measure completely different things:
Think of it this way: negative = kidney is trying hard (good kidney, problem elsewhere). Positive = kidney gave up (kidney itself is broken).
AldosteroneA hormone made by the adrenal glands. It tells the collecting duct to: (1) reabsorb Na⁺, (2) secrete K⁺, and (3) secrete H⁺. Without it, K⁺ and H⁺ get trapped in blood. deficiency or resistance. No aldosterone means the collecting ductThe final part of the nephron (kidney tube). Last chance to fine-tune urine · dump acid, dump potassium, concentrate urine. can't secrete K+ or H+.
The hyperkalemia itself makes things worse: high K+ suppresses NH3+ synthesisThe proximal tubule makes ammonia (NH3) to help carry acid out. NH3 grabs an H⁺ to become NH4⁺, which gets excreted in urine. High K⁺ blocks this process · so acid has no ride out. in the proximal tubuleThe first part of the nephron after the glomerulus. Reabsorbs ~65% of filtered water, sodium, and almost all bicarbonate. This is where Type 2 RTA breaks., which means less NH4+ excretionNH4⁺ (ammonium) is how the kidney dumps acid into urine. Less NH4⁺ = less acid removed = acidosis gets worse. It's a vicious cycle in Type 4. = less acid dumped.
| Feature | Type 4 |
|---|---|
| Serum K+ | HIGH |
| Urine pH | < 5.5 |
| Acidosis severity | Mild |
| Urine anion gap | Positive |
Common causes · and WHY they cause Type 4:
Treatment · and WHY each one works:
Alpha-intercalated cellsSpecial acid-pumping cells in the collecting duct. Their only job: grab H⁺ from blood and pump it into urine. In Type 1, these cells are broken. in the collecting duct can't secrete H+. Acid is trapped in the blood.
| Feature | Type 1 |
|---|---|
| Serum K+ | Low-normal |
| Urine pH | > 5.5 ALWAYS |
| Acidosis severity | Severe |
| Stones? | YES (calcium phosphate) |
| Bone effects | Demineralization, osteopenia |
Why stones?
Basic urine pH causes calcium phosphate precipitationWhen urine is too basic (alkaline), calcium and phosphate can't stay dissolved · they crystallize into stones. That's why only Type 1 (basic urine) gets stones.. Type 1 is the ONLY RTA with kidney stones.
Causes · and WHY:
Treatment · and WHY:
PCT cellsProximal Convoluted Tubule cells. The workhorses of the nephron · they reabsorb ~85% of filtered bicarbonate, plus glucose, amino acids, and phosphate. can't reabsorb HCO₃⁻. Base leaks into the urine early, but the collecting duct still works fine.
| Feature | Type 2 |
|---|---|
| Serum K+ | Low-normal |
| Urine pH | < 5.5 |
| Acidosis severity | Moderate |
| Stones? | No |
| Bone effects | Rickets/osteomalacia (Vit D-resistant) |
Key associations:
Fanconi syndromeThe proximal tubule loses its ability to reabsorb EVERYTHING · glucose, amino acids, phosphate, uric acid, AND bicarbonate all spill into urine. Like a broken shopping bag. (proximal tubule dysfunction loses everything · glucose, amino acids, phosphate, uric acid, HCO₃⁻). Also: acetazolamideA carbonic anhydrase inhibitor (used for glaucoma, altitude sickness). Blocks the enzyme that helps the proximal tubule reabsorb HCO₃⁻ · intentionally causes Type 2 RTA as a side effect. (carbonic anhydrase inhibitor).
Treatment · and WHY it's harder:
RTAs aren't super high-yield on boards · maybe one diagnosis question. But if you know these four things, you'll get it right:
| Feature | Type 1 | Type 2 | Type 4 |
|---|---|---|---|
| Where? | Distal | Proximal | Collecting duct |
| What breaks? | H+ secretion | HCO₃⁻ reabsorption | Aldosterone |
| K+ | Low | Low | HIGH |
| Urine pH | > 5.5 | < 5.5 | < 5.5 |
| Urine AGUrine Anion Gap = (Na⁺ + K⁺ - Cl⁻) in urine. Positive = kidney can't dump acid. Negative = kidney IS dumping acid fine, problem is elsewhere. | PositiveCollecting duct is broken, can't make NH4⁺. Less NH4⁺ = less Cl⁻ carried out = positive gap. | NegativeCollecting duct works! Lots of NH4⁺ being made and excreted, bringing Cl⁻ with it = negative gap. Problem is upstream (proximal leak). | PositiveEven though the collecting duct structure is fine, high K⁺ blocks NH3 synthesis. Less NH4⁺ = less Cl⁻ = positive gap. |
| Stones? | Yes | No | No |
| Severity | Severe | Moderate | Mild |
| Treatment | Alkali | Alkali (high dose) | Fludrocortisone + furosemide |
Each RTA type breaks a different part of the nephron. Know their signature moves.
Tap any card to flip it and see the full board stats.
The board gives you labs. You follow the branches. Start at the top every time.
Anion gap = Na+ minus (Cl- + HCO3-). Normal is 8 to 12. All RTAs have a normal anion gap with high Cl-.
High anion gap metabolic acidosis = think MUDPILES: Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. RTAs are always non-anion gap (hyperchloremic).
This is the fastest single question in all of RTA decision-making.
You have hypokalemia + NAGMA. Now check whether the collecting duct can acidify urine.
High-yield board phrases. Tap any underlined hook for the mnemonic behind it.
Visual anchors for the conditions that cause or mimic RTAs. Tap any image for detail.
Non-anion gap metabolic acidosis + normal albumin. Follow the branches.
Think through it:
Hyperkalemia + diabetes? That's the pattern.
Diabetes causes hyporeninemic hypoaldosteronismDiabetes damages the kidney cells that make renin. No renin = no angiotensin II = no signal to make aldosterone. Result: aldosterone is low, K⁺ and H⁺ build up. = no aldosterone = Type 4 RTA.
Five clinical stems. One RTA type each. Use the hyperkalemia shortcut and pH to nail them all.
Original board-style vignettes. Shuffled, never-repeat, full explanations for every choice.