Metabolic acidosis post kidney transplantation

Tariq, Hafsa; Dobre, Mirela

doi:10.3389/fphys.2022.989816

Cited by 4 publications

(3 citation statements)

References 57 publications

(81 reference statements)

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“…A new spectrum of mineral and acid-base abnormalities must be considered in patients after kidney transplantation, which are caused by multiple mechanisms. The most important of these are donor parameters, onset of graft function, duration of cold ischemia, acute tubular necrosis, and immunosuppressive therapy, especially calcineurin inhibitors (CNIs) and corticosteroids (13,14). CNIs lead to an increase in magnesium excretion.…”

Section: Discussionmentioning

confidence: 99%

“…Gitelman syndrome, an autosomal recessive inherited tubulopathy, also referred to as familial hypokalaemia with hypomagnesaemia, is characterised by hypokalaemic metabolic alkalosis combined with hypomagnesaemia and low urinary calcium excretion. Another cause of hypokalaemia is Liddle's syndrome, an autosomal dominant tubulopathy, which is caused by a mutation of the sodium channel subunit gene on the luminal side of the collecting duct cells, resulting in increased urinary sodium absorption and manifestations of hyperaldosteronism in the presence of low serum aldosterone (5,13,15). In our case report, we ruled out these possibilities by examining the serum aldosterone concentration.…”

Section: Discussionmentioning

confidence: 99%

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Conn´s syndrome after kidney transplantation

JAVORKOVA,

BYSTRICANOVA,

CIRBUSOVA

et al. 2024

BLL

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Conn's syndrome, defined as unilateral aldosterone-producing adenoma, accounts for 35-40% of cases of primary hyperaldosteronism. Primary hyperaldosteronism typically occurs in younger patients with poorly controlled arterial hypertension due to extracellular fluid retention, in whom at least a triple combination of antihypertensives, including a diuretic, is needed to maintain normotension. The clinical picture of arterial hypertension may be complemented by symptoms associated with hypokalaemia, such as weakness, fatigue, palpitations, convulsions, polydipsia, or polyuria. In addition to arterial hypertension and hypokalaemia, the diagnosis of Conn's syndrome relies on examination of serum renin and aldosterone concentrations, plasma renin activity, exercise or furosemide stimulation tests, and imaging studies, preferably computed tomography. The method of treatment of Conn's syndrome is adrenalectomy. In patients with primary hyperaldosteronism with underlying bilateral adrenal cortical hyperplasia or patients contraindicated for surgery, mineralocorticoid receptor antagonists are administered in combination with antihypertensives targeted for optimal blood pressure control. In the group of patients after kidney transplantation, the exact incidence of primary hyperaldosteronism is unknown. Based on a cross-sectional study performed in 2020, it is estimated to be approximately 15% in the group of patients with unsatisfactorily compensated arterial hypertension; in the cohort of normotensive recipients, the incidence of primary hyperaldosteronism is not documented. Diagnosis of Conn's syndrome in patients in the early period after kidney transplantation is problematic, as the prevalence of arterial hypertension in transplanted patients is high (70-90%) according to the literature. Mineral abnormalities, including hypokalaemia, are also common in the early post-transplant period, mainly due to factors such as duration of cold ischaemia, onset of graft function, donor parameters, post-transplant tubulopathy, and diuretics, the effects of immunosuppressive drugs (especially calcineurin inhibitors and corticosteroids), and possibly potassium-restricted dietary habits that the patient brings from the pre-transplant period, which may mask the effect of hyperaldosteronism on potassium. We present the case of a patient who was diagnosed with Conn's syndrome 7 months after primary kidney transplantation from a deceased donor based on persistent hypokalaemia unresponsive to replacement therapy. At the time of the first manifestation of severe hypokalaemia, the patient was treated with a dual combination of antihypertensives (amlodipine at a daily dose of 5 mg and carvedilol at a daily dose of 50 mg), without the need for a diuretics. We consider the case interesting because the spectrum of mineral and acid-base abnormalities in advanced renal failure and in the early post-transplant period, as well as acid-base and mineral imbalances, including hypokalaemia, and the high prevalence of arterial hypertension in the post-tra...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Conn´s syndrome after kidney transplantation

JAVORKOVA,

BYSTRICANOVA,

CIRBUSOVA

et al. 2024

BLL

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“… 3 Complications of metabolic acidosis include anemia, bone disease, protein catabolism, and growth failure, and are associated with inferior patient-outcomes and graft outcomes. 4 In a retrospective multicenter study of 2318 adult KTx recipients, metabolic acidosis was associated with increased mortality, graft failure, and death-censored graft failure, even after adjustment for confounding eGFR. 5 In another observational study, patients with HCO 3 − < 24 mmol/l at 1 year posttransplant had an increased risk of cardiovascular events and all-cause mortality.…”

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confidence: 99%