Which physiological process supports the exchange of blood concentrations across a semipermeable membrane in the hemodialysis?

A. Myocardial infarction one year ago:

A myocardial infarction (MI) that occurred one year ago is not directly related to the current acid-base imbalance described in the scenario. While a history of MI may have implications for the client's overall cardiovascular health and management, it is not the most likely cause of the acid-base imbalance indicated by the laboratory results.

B. Occasional use of antacids:

Occasional use of antacids is unlikely to cause the acid-base imbalance described in the scenario. Antacids primarily work by neutralizing gastric acid and are not typically associated with significant alterations in acid-base status, especially when used intermittently.

C. Chronic renal insufficiency:

Chronic renal insufficiency is the most likely cause of the acid-base imbalance indicated by the laboratory results. A low hemoglobin level suggests anemia, which can occur in chronic kidney disease due to decreased erythropoietin production. An elevated creatinine clearance indicates impaired kidney function, as the kidneys are clearing creatinine at a faster rate than normal. Decreased urine specific gravity suggests the kidneys' inability to concentrate urine properly, which is a common finding in renal insufficiency. Renal insufficiency can lead to metabolic acidosis due to the kidneys' decreased ability to excrete acid and regulate bicarbonate levels.

D. Shortness of breath with exertion:

Shortness of breath with exertion, a symptom commonly seen in COPD exacerbations, is unlikely to directly cause the acid-base imbalance described in the scenario. While respiratory distress can lead to respiratory acidosis, which is characterized by elevated carbon dioxide levels and decreased pH, the laboratory results indicate metabolic rather than respiratory acidosis.

Renal calculi, also known as kidney stones, are solid masses made up of crystals that form in the kidneys due to various factors, including supersaturation of urine with stone-forming substances, inadequate urine volume, and conditions that promote crystal precipitation and retention in the urinary tract. Here's the breakdown of the pathological process contributing to the client's clinical presentation:

A) Excessive urine output:

Excessive urine output (polyuria) is not typically associated with the formation of renal calculi. In fact, low urine output (oliguria) or concentrated urine may increase the risk of stone formation by reducing the volume of urine available to dilute stone-forming substances.

B) Excessive fluid intake:

Excessive fluid intake is generally beneficial in preventing kidney stone formation by increasing urine volume and diluting stone-forming substances. Therefore, it is not likely to contribute to the development of renal calculi in this scenario.

C) Increased calcium reabsorption:

Correct. Increased calcium reabsorption in the renal tubules can lead to hypercalcemia and hypercalciuria, which are risk factors for the formation of calcium-containing kidney stones (calcium oxalate or calcium phosphate stones). Excessive calcium reabsorption may occur due to various factors, including hormonal imbalances (e.g., hyperparathyroidism) or medications that affect calcium metabolism.

D) Increased serum alkalinity:

Increased serum alkalinity (alkalosis) is not typically associated with the formation of renal calculi. Urinary pH may influence the formation of certain types of kidney stones (e.g., uric acid stones are more likely to form in acidic urine), but alkalosis alone is not a primary factor in stone formation.