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Renal tubular acidosis
Minimal change disease
Focal segmental glomerulosclerosis (NORD)
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Acute tubular necrosis
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)
Posterior urethral valves
Hypospadias and epispadias
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
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
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renal tubular acidosis p. 617
Fanconi syndrome p. 719
metabolic acidosis p. 616
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.
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