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. 2022 Jun;36(6):e14648.
doi: 10.1111/ctr.14648. Epub 2022 Mar 20.

Increased intrarenal post-glomerular blood flow is a key condition for the development of calcineurin inhibitor-induced renal tubular acidosis in kidney transplant recipients

Shuzo Kaneko  1   2 , Joichi Usui  1 , Kazuhiro Takahashi  3 , Tatsuya Oda  3 , Kunihiro Yamagata  1
Affiliations

Increased intrarenal post-glomerular blood flow is a key condition for the development of calcineurin inhibitor-induced renal tubular acidosis in kidney transplant recipients

Shuzo Kaneko et al. Clin Transplant. 2022 Jun.

Abstract

Background: Hyperchloremic metabolic acidosis (HCMA) from renal tubular acidosis (RTA) is common in kidney transplant (KT) recipients. Calcineurin inhibitors (CNIs) are a potential cause of RTA, and whether HCMA is a determinant of poor graft prognosis is controversial.

Methods: The subjects were living-donor KT recipients (LDKTRs, n = 47) and matched donors (n = 43). All cases of rejection, extrarenal causes, and respiratory disorders were excluded. HCMA was defined as having a [Na+]-[Cl- ] value of ≤34 or starting alkalization. We determined the potential causes of HCMA in LDKTRs at 3 months (m) and 1 year (y) post-KT. We examined renal hemodynamic parameters in 26 LDKTRs at 1 y post-KT: namely, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF; GFR/RPF) and pre-/post-glomerular vascular resistance (pre-/postVR).

Results: The HCMA incidence in the 3-m post-KT LDKTR group was higher than that of the donors (51.0% vs. 6.9%, p < 0.001, adjusted odds ratio: 6.7-15.7). Among adjusted factors, the most dominant HCMA contributor was low hemoglobin concentration (Hb ≤ 12 g/dl). Compared to non-HCMA cases, HCMA patients had low FF and low post-VR (p = 0.008, 0.003, respectively) suggesting increased intrarenal post-glomerular blood flow. The high pathological score of alternative arteriolar hyalinosis (aah) ≥2 was a significant HCMA risk. The tacrolimus trough level was not high in HCMA but was significantly high in HCMA in the low post-VR setting (p = 0.002).

Conclusion: Among LDKTRs, low hemoglobin level is an important contributor to the manifestation of HCMA in the induction period, and increased intrarenal post-glomerular blood flow is a key condition for the development of CNI-induced RTA.

Keywords: calcineurin inhibitor; post-glomerular blood flow; post-kidney transplant hyperchloremic metabolic acidosis.

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References

REFERENCES

    1. Keven K, Ozturk R, Sengul S, et al. Renal tubular acidosis after kidney transplantation-incidence, risk factors and clinical implications. Nephrol Dial Transplant. 2007;22(3):906-910.
    1. Malik SI, Naqvi R, Ahmed E, Zafar MN. Prevalence and risk factors of renal tubular acidosis after kidney transplantation. J Pak Med Assoc. 2011;61(1):23-27.
    1. Messa PG, Alfieri C, Vettoretti S. Metabolic acidosis in renal transplantation: neglected but of potential clinical relevance. Nephrol Dial Transplant. 2016;31(5):730-736.
    1. Ambühl PM. Posttransplant metabolic acidosis: a neglected factor in renal transplantation? Curr Opin Nephrol Hypertens. 2007;16(4):379-387.
    1. Avila-Poletti D, De Azevedo L, Iommi C, Heldal K, Musso CG. Hyperchloremic metabolic acidosis in the kidney transplant patient. Postgrad Med. 2019;131(3):171-175.

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