Renal tubular acidosis


00:00 / 00:00



Renal tubular acidosis

Renal system

Renal and ureteral disorders

Renal agenesis

Horseshoe kidney

Potter sequence











Renal tubular acidosis

Minimal change disease

Diabetic nephropathy

Focal segmental glomerulosclerosis (NORD)


Membranous nephropathy

Lupus nephritis

Membranoproliferative glomerulonephritis

Poststreptococcal glomerulonephritis

Goodpasture syndrome

Rapidly progressive glomerulonephritis

IgA nephropathy (NORD)

Lupus nephritis

Alport syndrome

Kidney stones


Acute pyelonephritis

Chronic pyelonephritis

Prerenal azotemia

Renal azotemia

Acute tubular necrosis

Postrenal azotemia

Renal papillary necrosis

Renal cortical necrosis

Chronic kidney disease

Polycystic kidney disease

Multicystic dysplastic kidney

Medullary cystic kidney disease

Medullary sponge kidney

Renal artery stenosis

Renal cell carcinoma


Nephroblastoma (Wilms tumor)

WAGR syndrome

Beckwith-Wiedemann syndrome

Bladder and urethral disorders

Posterior urethral valves

Hypospadias and epispadias

Vesicoureteral reflux

Bladder exstrophy

Urinary incontinence

Neurogenic bladder

Lower urinary tract infection

Transitional cell carcinoma

Non-urothelial bladder cancers

Renal system pathology review

Congenital renal disorders: Pathology review

Renal tubular defects: Pathology review

Renal tubular acidosis: Pathology review

Acid-base disturbances: Pathology review

Electrolyte disturbances: Pathology review

Renal failure: Pathology review

Nephrotic syndromes: Pathology review

Nephritic syndromes: Pathology review

Urinary incontinence: Pathology review

Urinary tract infections: Pathology review

Kidney stones: Pathology review

Renal and urinary tract masses: Pathology review


Renal tubular acidosis


0 / 14 complete

USMLE® Step 1 questions

0 / 3 complete


Renal tubular acidosis

of complete


USMLE® Step 1 style questions USMLE

of complete

A 76-year-old woman presents to the emergency department with fatigue, decreased appetite, and muscle weakness. Past medical history includes chronic migraines, hypertension, gastroesophageal reflux, and a recent episode of podagra. Current medications include topiramate, lisinopril, acetazolamide, omeprazole, and probenecid. Temperature is 37.0°C (98.6°F), pulse is 104/min, respirations are 24/min, and blood pressure is 96/66 mmHg. Arterial blood gas and laboratory testing are obtained, and the results are shown below.

Which of the following medications most likely contributed to this patient’s disease?

Memory Anchors and Partner Content

External References

First Aid








Distal renal tubular acidosis (type 1) p. 617

Fanconi syndrome p. 610

renal tubular acidosis p. 617

Proximal renal tubular acidosis (type 2) p. 617

Renal tubular acidosis

Fanconi syndrome p. 719

metabolic acidosis p. 616

External Links


Content Reviewers

Rishi Desai, MD, MPH


Yifan Xiao, MD

Tanner Marshall, MS

With renal tubular acidosis, renal refers to the kidney, tubular refers to the main tube-portion of the nephron, and acidosis refers to having too many protons or increased acidity in blood, so renal tubular acidosis or RTA describes increased acidity in the blood because the renal tubules can’t get rid of protons.

The kidneys contain millions of nephrons, each of which has a renal corpuscle, and a renal tubule that ends in a collecting duct.

The renal corpuscle filters large amounts of solutes that go from the blood into the filtrate and eventually the urine, and the renal tubule and collecting duct are responsible for fine tuning the reabsorption and secretion of solutes to adjust the amount that ultimately gets retained by or removed from the body.

Broadly speaking, renal tubular acidosis can develop in either the proximal convoluted tubule, sometimes called just the proximal tubule, or the distal convoluted tubule, or distal tubule, and the nearby collecting duct.

The proximal tubule is lined by brush border cells which have two surfaces. One is the apical surface that faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption.

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

Now - when a molecule of bicarbonate approaches the apical surface of the brush border cell it binds to hydrogen to form carbonic acid.

At that point, an enzyme called carbonic anhydrase type 4 which lurks in tubule among the microvilli like a shark, swims along and splits the carbonic acid into water and carbon dioxide. The overall equation looks like this:

H+ + HCO3- <-> H2CO3 <-> H2O + CO2

The water and carbon dioxide happily diffuse across the membrane into the cells where carbonic anhydrase type 2 facilitates the reverse reaction - combining them to form carbonic acid, which dissolves into bicarbonate and hydrogen.

A sodium bicarbonate cotransporter on the basolateral surface snatches up the bicarbonate and a nearby sodium, and shuttles both into the blood.


Renal tubular acidosis is a medical condition in which the kidney is unable to secrete acids or reabsorb bicarbonate from the body. When blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for the exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine. The metabolic acidosis that results from renal tubular acidosis may be caused either by failure to recover sufficient bicarbonate ions from the filtrate in the proximal tubule or by insufficient secretion of hydrogen ions into the distal tubule. If left untreated, acidemia can cause peripheral vasodilation and shock. Treatment may include alkali supplements like potassium citrate or sodium bicarbonate to neutralize the acid in the blood.


Copyright © 2023 Elsevier, except certain content provided by third parties

Cookies are used by this site.

USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.