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A 35 year old woman, a nursing home assistant, presents with chronic acidosis that is difficult to manage. Lab evaluation showed Na+ 143, K+ 2.8 Cl- 118, HCO3- 15 BUN 18, Cr 0.7. ABG reveals PH 7.38 Pco2 31, Pao2 100. U/A results were normal with urine ph of 5.0. Urine Na was 40 K 5 and Urine Cl 150.Which disorder best characterizes this patient's syndrome.
  1. Diuretic abuse
  2. Laxative abuse
  3. Distal renal tubular acidosis
  4. Proximal renal tubular acidosis
  5. Type 4 renal tubular acidosis
Renal tubular acidosis (RTA) is applied to a group of transport defects in the reabsorption of bicarbonate (HCO3-), the excretion of hydrogen ion (H+), or both.
The RTA syndromes are characterized by a relatively normal GFR and a metabolic acidosis accompanied by hyperchloremia and a normal plasma anion gap.

Physiology of Renal acidification.
Types of RTA and characteristics
Lab diagnosis of Renal tubular acidosis
Approach to a patient with Renal tubular acidosis

Physiology of Renal Acidification
Kidneys excrete 50-100 meq/day of non carbonic acid generated daily.
This is achieved by H+ secretion  at different levels in the nephron.
The daily acid load cannot be excreted as free H+ ions.
Secreted H+ ions are excreted by binding to either buffers, such as HPO42- and creatinine, or to NH3 to form NH4+.
The extracellular pH is the primary physiologic regulator of net acid excretion.

Renal acid-base homeostasis may be broadly divided into 2 processes
Proximal tubular absorption of HCO3- (Proximal acidification)
Distal Urinary acidification.
 Reabsorption of remaining HCO3-  that escapes proximally.
 Excretion of fixed acids through buffering & Ammonia recycling and excretion of NH4+.

Proximal RTA (type 2)
 Isolated bicarbonate defect
 Fanconi syndrome
Distal RTA (type 1)
 Classic type
 Hyperkalemic distal RTA
 Hyperkalemic RTA (Type 4)

PROXIMAL Renal tubular acidosis
Proximal RTA (pRTA) is a disorder leading to HCMA secondary to impaired proximal reabsorption of filtered bicarbonate.
Since the proximal tubule is responsible for the reabsorption of 85-90% of filtered HCO3- a defect at this site leads to delivery of large amounts of bicarbonate to the distal tubule.
This leads to bicarbonaturia, kaliuresis and sodium losses.
Thus patients will generally present with hypokalemia and a HCMA.

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