Pseudohypoaldosterism: demystification using network medicine and proposed diagnostic panels.

Diagnostic pitfalls in aldosterone defects: a 9-year follow-up of early-onset pseudohypoaldosteronism type 2.

Long-Term Immune Alterations After Thymectomy in Early Childhood: A Case Series.

Transient pseudohypoaldosteronism type I in infants with urinary tract infections and/or uropathy: insights from a French multicenter cohort.

Hypertension and hyperkalemia associated with Pro701Leu mutation in the NR3C2 gene: A case report.

Autosomal recessive (type 1B) pseudohypoaldosteronism: a novel mutation and its management.

Refractory Hyperkalemia With Type 4 Renal Tubular Acidosis Associated With Tubulointerstitial Nephritis and Renal Papillary Necrosis Following Intravenous Lipid Emulsion Therapy in a Cat.

Kidney involvement during the course of febrile urinary tract infection.

The evolving concepts of KS-WNK1 effect on NCC activity.

Pseudohypoaldosteronism type II and sensory neuropathy associated with a heterozygous pathogenic variant in KLHL3 gene, a case report.

Prevalence of and factors associated with Na + /K + imbalances in a population of children hospitalized with febrile urinary tract infection.

Prevalence of Hyperkalemia and Familial Hyperkalemic Hypertension in 5100 Patients Referred to a Tertiary Hypertension Unit.

Pseudohypoaldosteronism Type 1B and Cohen Syndrome: Novel Mutation, Unusual Combination, and Presentation.

NR3C2 microdeletions-an underrecognized cause of pseudohypoaldosteronism type 1A: a case report and literature review.

Dysregulation of the WNK4-SPAK/OSR1 pathway has a minor effect on baseline NKCC2 phosphorylation.

Association of Familial Hyperkalemia and Hypertension with Proximal Renal Tubular Acidosis and Epileptic Seizures.

The Epithelial Sodium Channel-An Underestimated Drug Target.

[Regulation of kidney on potassium balance and its clinical significance].

Early-in-Life Serum Aldosterone Levels Could Predict Surgery in Patients with Obstructive Congenital Anomalies of the Kidney and Urinary Tract: A Pilot Study.

The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.

Generation and analysis of pseudohypoaldosteronism type II knock-in mice caused by a nonsense KLHL3 mutation in the Kelch domain.

Claudins in kidney health and disease.

Combined Kelch-like 3 and Cullin 3 Degradation is a Central Mechanism in Familial Hyperkalemic Hypertension in Mice.

Monogenic forms of low-renin hypertension: clinical and molecular insights.

Novel SCNN1A gene splicing-site mutation causing autosomal recessive pseudohypoaldosteronism type 1 (PHA1) in two Italian patients belonging to the same small town.

Transient Pseudohypoaldosteronism Secondary to Group B Streptococcus Pyelonephritis.

Clinical characteristics and treatment requirements of children with autosomal recessive pseudohypoaldosteronism.

Role of KLHL3 and dietary K+ in regulating KS-WNK1 expression.

Renin-aldosterone system evaluation over four decades in an extended family with autosomal dominant pseudohypoaldosteronism due to a deletion in the NR3C2 gene.

Mutation affecting the conserved acidic WNK1 motif causes inherited hyperkalemic hyperchloremic acidosis.

WNK1-OSR1/SPAK KINASE CASCADE IS IMPORTANT FOR ANGIOGENESIS.

Familial cases of pseudohypoaldosteronism type II harboring a novel mutation in the Cullin 3 gene.

Recent insights into sodium and potassium handling by the aldosterone-sensitive distal nephron: implications on pathophysiology and drug discovery.

Dietary potassium restriction attenuates urinary sodium wasting in the generalized form of pseudohypoaldosteronism type 1.

Phenotypic diversity and correlation with the genotypes of pseudohypoaldosteronism type 1.

A familial case of pseudohypoaldosteronism type II (PHA2) with a novel mutation (D564N) in the acidic motif in WNK4.

Complete clinical resolution of a Japanese family with renal pseudohypoaldosteronism type 1 due to a novel NR3C2 mutation.

WNK4 kinase is a physiological intracellular chloride sensor.

Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling Pathway.

Generation and analysis of a mouse model of pseudohypoaldosteronism type II caused by KLHL3 mutation in BTB domain.

Decreased KLHL3 expression is involved in the pathogenesis of pseudohypoaldosteronism type II caused by cullin 3 mutation in vivo.

Pseudohypoaldosteronism Type II: A Young Girl Presented with Hypertension, Hyperkalemia and Metabolic Acidosis.

Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects.

Transient Pseudohypoaldosteronism Caused by Intestinal Abnormalities.

Loss of β Epithelial Sodium Channel Function in Meibomian Glands Produces Pseudohypoaldosteronism 1-Like Ocular Disease in Mice.

Clinical features and molecular basis of pseudohypoaldosteronism type 1.

WNK4 is indispensable for the pathogenesis of pseudohypoaldosteronism type II caused by mutant KLHL3.

Impaired degradation of medullary WNK4 in the kidneys of KLHL2 knockout mice.

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor mutations.

Expression of epithelial sodium channel (ENaC) and CFTR in the human epidermis and epidermal appendages.

KLHL3 Knockout Mice Reveal the Physiological Role of KLHL3 and the Pathophysiology of Pseudohypoaldosteronism Type II Caused by Mutant KLHL3.

Secondary or Transient Pseudohypoaldosteronism Associated With Urinary Tract Anomaly and Urinary Infection: A Case Report.

Potential Roles of Amiloride-Sensitive Sodium Channels in Cancer Development.

Adult nephron-specific MR-deficient mice develop a severe renal PHA-1 phenotype.

Severe Salt-Losing Syndrome and Hyperkalemia Induced by Adult Nephron-Specific Knockout of the Epithelial Sodium Channel α-Subunit.

A neonate with poor weight gain and hyperkalemia: Answers.

A neonate with poor weight gain and hyperkalemia: Questions.

Reducing αENaC expression in the kidney connecting tubule induces pseudohypoaldosteronism type 1 symptoms during K+ loading.

Generation and analysis of knock-in mice carrying pseudohypoaldosteronism type II-causing mutations in the cullin 3 gene.

[Electrolyte disorders as a hallmark of monogenetic diseases].

A unifying mechanism for WNK kinase regulation of sodium-chloride cotransporter.