Title:Bartter-like Syndrome Induced By Tacrolimus in a Renal Transplanted
Boy: A Case Report
Volume: 18
Issue: 3
Author(s): Raphael Figuiredo Dias, Mateus da Costa Monteiro, Renata Aguiar Menezes Silva, Mirella Monique Lana Diniz and Ana Cristina Simões e Silva*
Affiliation:
- Department of Pediatrics, Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University
of Minas Gerais (UFMG), Belo Horizonte, MG, Brazil
Keywords:
Bartter-like Syndrome, tacrolimus, kidney transplant, pediatric nephrology, hydroelectrolytic disorder, hypercalciuria.
Abstract:
Background: Losing-salt tubulopathies, such as Bartter syndrome, are rare and usually
inherited due to mutations of tubular reabsorption channels of the nephrons. Despite its scarcity,
some cases of acquired losing-salt tubulopathies have been described. In this case report, we discuss
the main aspects of Bartter syndrome and present a rare pediatric case of probable tacrolimusinduced
Bartter-like syndrome in a renal transplanted boy.
Case Presentation: A ten-year-old male patient with end-stage renal disease due to endo and extra
capillary glomerulonephritis was submitted to renal transplantation from a deceased donor. The
post-operatory evolution was satisfactory with normalization of serum creatinine levels, mild hypertension,
and the absence of metabolic disorders. The immunosuppression protocol included tacrolimus
(0.3 mg/kg/day), mycophenolate (455 mg/m2/day) and prednisone (0.5 mg/kg/day). Two
months later, the patient was hospitalized due to vomiting, dehydration, intense hypokalemia (1.3
mEq/L), hyponatremia (125 mEq/L), and hypochloremia (84 mmol/L). During hospitalization, he
evolved with polydipsia (3000 mL/day) and polyuria (120-160 mL/m2/h) associated with major elevation
of urinary potassium excretion, hypercalciuria, mild metabolic alkalosis, hyperfiltration,
and proteinuria. The tacrolimus dose was reduced under the suspicion of tubular dysfunction, leading
to a better metabolic profile. However, the patient developed a Banff IIb graft rejection, which
required pulse therapy and elevation of tacrolimus and mycophenolate doses. Recovery of renal
function parameters occurred, but the metabolic disorders worsened following tacrolimus dose elevation.
The patient required chronic potassium, chloride, and sodium replacement.
Conclusion: After administering immunosuppressive medications, physicians should be aware of
the possibility of Bartter-like or other losing-salt tubulopathies syndromes that can affect metabolic
homeostasis. The suspicion must always be considered in the case of a transplanted patient who
presents dehydration and hydroelectrolytic disorders right after the commencement of nephrotoxic
immunosuppressive drugs, including tacrolimus and cyclosporine.
