This patient has a metabolic acidosis (given his low serum bicarbonate of 18 mEq/L) with hyperkalemia.  He has a non-anion gap metabolic acidosis with a serum anion gap of 10 mEq/L (anion gap = serum Na⁺ - [serum Cl^- + serum HCO₃^-]; normal anion gap = 10-14 mEq/L).  He also has a mild degree of renal dysfunction consistent with chronic kidney disease.  When there is a gradual loss of nephrons, the remaining nephrons maintain the kidney's ability to excrete a daily acid load by producing more NH₃ buffer that removes H⁺ as NH₄⁺ in the urine.  As a result, metabolic acidosis in chronic kidney disease is rarely seen until there is advanced renal dysfunction (glomerular filtration rate <20 mL/min).  Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction indicate a renal tubular disorder.

Renal tubular acidosis (RTA) is a group of disorders characterized by non-anion gap metabolic acidosis in the presence of preserved kidney function.  The cortical collecting tubule is the site for H⁺ and K⁺ excretion, which is regulated by aldosterone.  Impaired function of the cortical collecting tubule due to aldosterone deficiency or resistance will cause retention of H⁺ and K⁺ and is termed hyperkalemic RTA (or type 4 RTA).  Hyperkalemic RTA is commonly seen in elderly patients who have poorly controlled diabetes with damage to the juxtaglomerular apparatus, which causes a state of hyporeninemic hypoaldosteronism.  These patients have mild hyperkalemia (K⁺ 5.2-6.0 mEq/L) and mild acidosis (HCO₃^- 15-20 mEq/L) on a background of preserved or moderately diminished glomerular filtration rate (20-50 mL/min).  Hypertension may or may not be present and is usually due to the accompanying atherosclerosis.

(Choice A)  Loop diuretic use causes hypokalemia and metabolic alkalosis.

(Choice B)  Although diarrhea most commonly causes metabolic acidosis, diarrhea from laxative abuse often causes severe hypokalemia and metabolic alkalosis.  The severe hypokalemia occurs due to potassium losses in the stool and increased aldosterone secretion due to volume depletion.  This leads to impaired chloride reabsorption and bicarbonate excretion, resulting in metabolic alkalosis.

(Choice C)  In pre-renal azotemia (renal hypoperfusion) the blood urea nitrogen/creatinine ratio is usually more than 20:1 due to increased urea absorption.  Renal hypoperfusion is due to either systemic hypovolemia or impaired cardiac output.  This patient has no symptoms or signs of volume depletion.

(Choice D)  In primary hyperaldosteronism, high aldosterone levels cause increased H⁺ and K⁺ excretion, leading to hypokalemia and metabolic alkalosis (mnemonic: Aldosterone Saves Sodium and Pushes Potassium out).

(Choice E)  Renal artery stenosis causes secondary hyperaldosteronism due to low perfusion to the kidney.  Hypokalemia, metabolic alkalosis, and hypertension are characteristic findings.

(Choice G)  Surreptitious vomiting causes a hypochloremic metabolic alkalosis due to loss of gastric HCl.  Hypokalemia may be seen due to increased aldosterone secretion caused by volume depletion.

Educational objective:
Type 4 renal tubular acidosis (hyperkalemic renal tubular acidosis) is characterized by non-anion gap metabolic acidosis, persistent hyperkalemia, and mild-to-moderate renal insufficiency.  It commonly occurs in patients with poorly controlled diabetes.