Schwarz C, Oberbauer R, Haas M
Renal tubular acidosis in kidney transplant recipients.
ASN Annual Meeting -- Philadelphia
J Am Soc Nephrol
(Nov) 16:43A 2005

Renal tubular acidosis (RTA) after kidney transplantation is a frequent
finding. The prevalence, however, and the distribution of the RTA subtypes is
unknown.
575 renal transplant recipients were included in this cross-
sectional study. All patients had a serum creatinine < 2 mg/dl, no
rejection episodes since >6 months and transplant duration of >1 year.
The patients were screened for acidosis by a single blood gas analysis. In
treated patients bicarbonate therapy was stopped 24h prior to diagnosis. All
patients with metabolic acidosis and normal plasma anionic gap were further
analysed by an oral bicarbonate loading test. To distinguish between the
different forms of renal tubular acidosis the urine-plasma pCO2
difference was calculated. The trans-tubular potassium gradient was evaluated
for the diagnosis of the hyperkalemic forms of RTA. Patients transplant
history and medication were analysed in a stepwise logistic regression to
isolate factors associated with RTA.
Renal tubular acidosis was
diagnosed in 13% of the transplant recipients. From all patients with RTA,
35% had RTA type 1 (distal, classic), 15% showed the hyperkalemic form of RTA
type 1. RTA type 4 was present in 28% but no one of the patients showed RTA
type 2 (proximal). 22% of the patients had a mixed form of (renal) acidosis.
The strongest factors that contributed to RTA were immunosuppression with
calcineurin inhibitors (OR 12,4 (95%CI:2-134)), treatment with ACE-Inhibitors
or AT II receptor blockers (OR 2 (95% CI:1-4) and hyperparathyroidism (OR
1,08 per 10 ng/ml elevated PTH (95% CI:0,2-1,18)) The majority of the
patients developed renal tubular acidosis immediately after transplantation.
Acute rejections were not associated with the development of RTA. No
individual risk factors for the development of different types of RTA could
be found.
The main forms of posttransplant RTA are type 1(distal) and
type 4 (hyperkalaemic). Risk factors associated with the development of RTA
are calcineurin inhibitor therapy, hyperparathyroidism and blockers of the
renin-angiotensin-aldosterone system. Subgroup analysis, however, revealed no
particular risk factor for the development of a specific RTA form.

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