Type 4 (hyperkalemic distal) renal tubular acidosis (RTA) is the most likely cause of this patient's metabolic findings. Type 4 (hyperkalemic distal) RTA is caused by aldosterone deficiency or resistance. Primary aldosterone deficiency is seen in primary adrenal deficiency (Addison disease), and relative aldosterone deficiency may be seen in the syndrome of hyporeninemic hypoaldosteronism in which there is diminished renin release by the kidney. This occurs most commonly in patients with mild to moderate kidney disease due to diabetic nephropathy (such as this patient) or chronic interstitial nephritis (such as in systemic lupus erythematosus or AIDS). It may also be associated with acute glomerulonephritis, specific drugs that impair renin release (NSAIDs and calcineurin inhibitors), tubulointerstitial disease, and drugs that reduce aldosterone production (ACE inhibitors, cyclooxygenase inhibitors, and heparin). Patients with type 4 (hyperkalemic distal) RTA typically present with hyperkalemia, a normal anion gap metabolic acidosis, and impaired urine acidification, but with the ability to maintain the urine pH to <5.5. The specific cause can be differentiated by measurement of plasma renin activity, serum aldosterone, and serum cortisol. Initial treatment includes correction of the underlying cause if possible, with discontinuation of offending medications. Replacement of mineralocorticoids with fludrocortisone is indicated for patients with documented deficiency and should be considered for those with hyporeninemic hypoaldosteronism unless hypertension or heart failure is present.

Although kidney failure may cause hyperkalemia and metabolic acidosis, the acidosis associated with kidney failure more commonly reflects an increase in the anion gap with impaired organic acid excretion.

Type 1 (hypokalemic distal) RTA results from a defect in urine acidification in the distal tubule with impaired excretion of hydrogen ions and a normal anion gap metabolic acidosis. However, this tubular defect also results in potassium wasting and hypokalemia, which are not present in this patient.

Type 2 (proximal) RTA involves a defect in regenerating bicarbonate in the proximal tubule and is characterized by hypokalemia, glycosuria (in the setting of normal plasma glucose), low-molecular-weight proteinuria, and renal phosphate wasting, none of which is present in this patient.