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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: Pathology review
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Kaia Chessen, MScBMC
Anca-Elena Stefan, MD
Sam Gillespie, BSc
Tanner Marshall, MS
In the Emergency Department, two people came in with rapid, shallow breathing and tachycardia. The first one is 45 year old Olga who also has systemic lupus erythematosus and the second one is 39 year old Fred. An arterial blood gas was taken, along with electrolytes. Results showed that Olga had low pH, low bicarbonate and pCO2 levels and her potassium level was also low. Fred also had low pH, low bicarbonate and pCO2 levels, but his potassium level was high. Based on the ABG results, the diagnosis of normal anion gap metabolic acidosis was made. In order to identify the cause of their normal gap metabolic acidosis, more investigations were done and the urine anion gap showed that both individuals had a low urinary anion gap, which suggests that the cause was renal.
Okay, now, a normal anion gap metabolic acidosis can have renal causes. Like when a lot of bicarbonate is lost through the urinary tract- which happens in type II renal tubular acidosis. A normal anion gap metabolic acidosis can also happen when too many hydrogen ions are retained, like in type I and type IV renal tubular acidosis. Now, there’s also a type III renal tubular acidosis, where both the proximal and distal tubules are affected. This is a pretty rare situation and the causes are not well understood, so it’s unlikely to be tested.
Okay, now, let’s review the physiology of the tubules. The proximal tubule is affected in RTA type II. It’s lined by brush border cells which have two surfaces: One is the apical surface that faces the tubular lumen and is lined with microvilli, and the other is the basolateral surface, which faces the peritubular capillaries. Now, a lot of bicarbonate is reabsorbed here. When bicarbonate approaches the apical surface it binds to hydrogen to form carbonic acid, which will be split into water and carbon dioxide by carbonic anhydrase. The water and carbon dioxide diffuse into the cells where carbonic anhydrase facilitates the reverse reaction and combines them to form carbonic acid, which dissociates into bicarbonate and hydrogen. Then bicarbonate will get into the blood with the help of a sodium bicarbonate cotransporter on the basolateral surface. Now, the proximal tubule is also responsible for reabsorbing glucose, as well as amino acids, sodium, chloride, potassium, phosphate, water and uric acid.
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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