Transient Pseudohypoaldosteronism in Childrens Secondary to Urinary Tract Infection. A Report of 2 Cases, a Literature Review

Introduction: Pseudohypoaldosteronism (PHA) types I and II share hyperkalemia as a predominant finding. PHA is a heterogeneous syndrome characterized by a lack of response of the organs to the mineralocorticoid, and therefore there is loss of salts. Heredity can be autosomal dominant or recessive. It is very rare for other mutations to occur. Autosomal dominant PHA-I is characterized by mutations in the mineralocorticoid receptor, while Autosomal recessive PHA-I results from mutations in the epithelial sodium channel (ENaC). Clinical expression of renal PHA- I is variable: patients present with salt loss in the neonatal period, failure to thrive, vomiting, and dehydration. Symptoms of renal PHA- I often improve in early childhood and older children.

Case reports: Preterm baby born at week 29, suffered from two events of urinary tract infection. In these events, the child was afebrile. However, urinalysis was positive for white blood cells and red blood cells, and urine culture subsequently grew E-Coli, there was a picture of severe hyperkalemia 6.6 mmol/L and hyponatremia 128 mmol/L. With metabolic acidosis PH 7.22. Cystography showing reflux (figure 1), besides, renal ultrasound was performed, and moderate hydronephrosis was seen (figure2). Antibiotics and normal saline were provided.

Conclusion: The case support the idea that the renal tubular resistance to aldosterone is due to urinary tract infection. The case are presenting hyperkalemia with hyponatremia, and in whom a diagnosis of congenital adrenal hyperplasia was excluded. It is essential to know that serum aldosterone, urine sodium, and urine cultures may be obtained immediately.