Keyword: Hyperkalemia
2 results found.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A8, https://doi.org/10.63946/cajn/19526
ABSTRACT:
Introduction: Diabetic kidney disease is a major cause of end-stage kidney disease and is frequently accompanied by cardiovascular and metabolic complications. Patients receiving maintenance hemodialysis remain at high risk of life-threatening complications, particularly when multiple comorbidities are present. We present a case of severe metabolic decompensation in a patient with end-stage diabetic kidney disease receiving maintenance hemodialysis.
Aim: To describe the clinical presentation, laboratory abnormalities, emergency management, and short-term clinical response in a patient with end-stage diabetic kidney disease and multiple comorbidities receiving maintenance hemodialysis.
Methods: A clinical case was analyzed based on the patient's medical records, including clinical presentation, laboratory investigations, comorbid conditions, treatment, and clinical course during hospitalization.
Results: A 59-year-old woman with type 2 diabetes mellitus complicated by diabetic kidney disease and end-stage chronic kidney disease (CKD stage 5) had been receiving maintenance hemodialysis three times weekly since March 2026. Her comorbidities included rheumatoid arthritis, congestive heart failure, diabetic polyneuropathy, anemia of chronic disease, bilateral secondary gonarthrosis, cholelithiasis without cholecystitis, hemorrhoids, and a stage III pressure ulcer. She was admitted in a severe condition with marked weakness, poor appetite, nausea, vomiting, and impaired consciousness. Laboratory evaluation demonstrated severe azotemia, with a creatinine level of approximately 1154 µmol/L and urea of 47.7 mmol/L, accompanied by hyperkalemia (6.3 mmol/L). The clinical picture was consistent with severe uremic and metabolic decompensation in the setting of end-stage kidney disease. Emergency hemodialysis and comprehensive supportive treatment were performed. Following treatment, serum creatinine, urea, and potassium levels decreased, accompanied by clinical stabilization.
Conclusion: This case highlights the high risk of severe metabolic complications in patients with end-stage diabetic kidney disease receiving maintenance hemodialysis, particularly in the presence of substantial cardiovascular and systemic comorbidity. Early recognition of uremic and electrolyte disturbances and timely initiation of hemodialysis are essential for preventing life-threatening complications and achieving clinical stabilization.
Aim: To describe the clinical presentation, laboratory abnormalities, emergency management, and short-term clinical response in a patient with end-stage diabetic kidney disease and multiple comorbidities receiving maintenance hemodialysis.
Methods: A clinical case was analyzed based on the patient's medical records, including clinical presentation, laboratory investigations, comorbid conditions, treatment, and clinical course during hospitalization.
Results: A 59-year-old woman with type 2 diabetes mellitus complicated by diabetic kidney disease and end-stage chronic kidney disease (CKD stage 5) had been receiving maintenance hemodialysis three times weekly since March 2026. Her comorbidities included rheumatoid arthritis, congestive heart failure, diabetic polyneuropathy, anemia of chronic disease, bilateral secondary gonarthrosis, cholelithiasis without cholecystitis, hemorrhoids, and a stage III pressure ulcer. She was admitted in a severe condition with marked weakness, poor appetite, nausea, vomiting, and impaired consciousness. Laboratory evaluation demonstrated severe azotemia, with a creatinine level of approximately 1154 µmol/L and urea of 47.7 mmol/L, accompanied by hyperkalemia (6.3 mmol/L). The clinical picture was consistent with severe uremic and metabolic decompensation in the setting of end-stage kidney disease. Emergency hemodialysis and comprehensive supportive treatment were performed. Following treatment, serum creatinine, urea, and potassium levels decreased, accompanied by clinical stabilization.
Conclusion: This case highlights the high risk of severe metabolic complications in patients with end-stage diabetic kidney disease receiving maintenance hemodialysis, particularly in the presence of substantial cardiovascular and systemic comorbidity. Early recognition of uremic and electrolyte disturbances and timely initiation of hemodialysis are essential for preventing life-threatening complications and achieving clinical stabilization.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A27, https://doi.org/10.63946/cajn/19516
ABSTRACT:
Background: Systemic pseudohypoaldosteronism type 1 (PHA1B; OMIM 264350) is a rare autosomal recessive disorder caused by biallelic pathogenic variants in SCNN1A, SCNN1B, or SCNN1G, which encode epithelial sodium channel (ENaC) subunits. Aldosterone resistance causes neonatal salt wasting, hyponatremia, severe hyperkalemia, metabolic acidosis, and potentially multiorgan dysfunction. Because the presentation mimics salt-wasting congenital adrenal hyperplasia (CAH) and sepsis, early differentiation is critical. We report a genetically confirmed, life-threatening neonatal case of PHA1B.
Case Presentation: A full-term girl (38 weeks + 2 days) was admitted on day 8 of life in critical condition with an 11% weight deficit, severe hypoxic-ischemic encephalopathy, subarachnoid and intraventricular hemorrhage with cerebral edema, bilateral pneumonia, and grade II respiratory failure. In the pediatric intensive care unit, respiratory failure progressed, requiring mechanical ventilation. Cardiac manifestations included bradyarrhythmia to 80 beats/min, ventricular ectopy, and complete right bundle branch block. Laboratory tests showed K+ 13.6 mmol/L, Na+ 110 mmol/L, pH 7.20, and base excess -17.4 mmol/L.
Salt-wasting CAH was initially suspected; however, hydrocortisone and fludrocortisone produced no clinical or biochemical response. Cortisol (27.53 µg/dL), 17-hydroxyprogesterone (1.2 ng/mL), and adrenocorticotropic hormone (5.0 pmol/L) were within reference ranges, while plasma aldosterone was markedly elevated at 10,355 pg/mL (reference range, 28-376 pg/mL), supporting aldosterone resistance. Whole-exome sequencing identified a homozygous pathogenic nonsense variant in SCNN1A (exon 10; c.1474C>T; p.Arg492Ter), confirming systemic PHA1.
Management included mechanical ventilation, intravenous calcium, intensive enteral and intravenous sodium chloride replacement, antibacterial therapy, and peritoneal dialysis for refractory life-threatening hyperkalemia. Potassium decreased to 8.1 mmol/L, sodium increased to 128-135 mmol/L, and the metabolic crisis initially improved. Despite treatment, the patient died from progressive multiorgan failure and neurological complications.
Conclusion: PHA1 should be considered in neonates with severe hyponatremia, hyperkalemia, and metabolic acidosis, particularly when CAH markers are normal and glucocorticoid/mineralocorticoid therapy is ineffective. In this setting, markedly elevated aldosterone supports mineralocorticoid resistance. Prompt sodium replacement and emergency management of hyperkalemia, including early dialysis when medical therapy fails, are essential. Molecular testing confirms the systemic form, informs prognosis, and enables family genetic counseling.
Case Presentation: A full-term girl (38 weeks + 2 days) was admitted on day 8 of life in critical condition with an 11% weight deficit, severe hypoxic-ischemic encephalopathy, subarachnoid and intraventricular hemorrhage with cerebral edema, bilateral pneumonia, and grade II respiratory failure. In the pediatric intensive care unit, respiratory failure progressed, requiring mechanical ventilation. Cardiac manifestations included bradyarrhythmia to 80 beats/min, ventricular ectopy, and complete right bundle branch block. Laboratory tests showed K+ 13.6 mmol/L, Na+ 110 mmol/L, pH 7.20, and base excess -17.4 mmol/L.
Salt-wasting CAH was initially suspected; however, hydrocortisone and fludrocortisone produced no clinical or biochemical response. Cortisol (27.53 µg/dL), 17-hydroxyprogesterone (1.2 ng/mL), and adrenocorticotropic hormone (5.0 pmol/L) were within reference ranges, while plasma aldosterone was markedly elevated at 10,355 pg/mL (reference range, 28-376 pg/mL), supporting aldosterone resistance. Whole-exome sequencing identified a homozygous pathogenic nonsense variant in SCNN1A (exon 10; c.1474C>T; p.Arg492Ter), confirming systemic PHA1.
Management included mechanical ventilation, intravenous calcium, intensive enteral and intravenous sodium chloride replacement, antibacterial therapy, and peritoneal dialysis for refractory life-threatening hyperkalemia. Potassium decreased to 8.1 mmol/L, sodium increased to 128-135 mmol/L, and the metabolic crisis initially improved. Despite treatment, the patient died from progressive multiorgan failure and neurological complications.
Conclusion: PHA1 should be considered in neonates with severe hyponatremia, hyperkalemia, and metabolic acidosis, particularly when CAH markers are normal and glucocorticoid/mineralocorticoid therapy is ineffective. In this setting, markedly elevated aldosterone supports mineralocorticoid resistance. Prompt sodium replacement and emergency management of hyperkalemia, including early dialysis when medical therapy fails, are essential. Molecular testing confirms the systemic form, informs prognosis, and enables family genetic counseling.