Hyperchloremic metabolic acidosis of renal origin results from a defect in renal tubular acidification mechanism, and this tubular dysfunction can consist of an altered tubular proton secretion or bicarbonate reabsorption capability. Studies have documented that all forms of renal tubular acidosis (RTA), type I to IV, are documented in kidney transplant patients. Among RTA pathophysiologic mechanisms have been described the renal mass reduction, hyperkalemia, hyperparathyroidism, graft rejection, immunologic diseases, and some drugs such as renin-angiotensin-aldosterone blockers, and calcineurin inhibitors. RTA can lead to serious complications as is the case of muscle protein catabolism, muscle protein synthesis inhibition, renal osteodystrophy, renal damage progression, and anemia promotion. RTA should be treated by suppressing its etiologic factor (if it is possible), avoiding hyperkalemia, and/or supplying bicarbonate or a precursor (citrate). In conclusion: Hyperchloremic metabolic acidosis of renal origin is a relatively frequent complication in kidney transplantation patients, which can be harmful, and should be adequately treated in order to avoid its renal and systemic adverse effects.
Keywords: Renal tubular acidosis; kidney transplantation; pathophysiology.