Introduction: The thyroid-kidney axis represents a clinically significant bidirectional relationship. Nephrotic syndrome (NS) may induce hypothyroidism via urinary hormonal and binding protein losses, while severe hypothyroidism may mimic NS and contribute to renal dysfunction. Cases: A 64-year-old male with gout, presented with facial puffiness, pedal edema, weight gain and frothy urine. Investigations revealed severe hypothyroidism FT4 <0.5 pmol/L (12–22 pmol/L) TSH 314 mIU/L (0.27–4.2 mIU/L) with NS – UPCR 7.7 3 g/L (0.04–0.15 g/L), albumin 22 g/L, total cholesterol 15.9 mmol/L – and renal impairment (eGFR 58 mL/min/1.73 m²). Positive anti-TPO antibodies suggested Hashimoto’s thyroiditis. He was initiated on liothyronine, hydrocortisone, levothyroxine and diuretics. Although FT4 normalized (14.4 pmol/L) a month later, renal function worsened requiring dialysis. Further evaluation including renal biopsy demonstrated IgA nephropathy as the underlying cause of NS and renal failure. Treatment with prednisolone led to gradual improvement in renal function and proteinuria (UPCR 0.21 g/L). A 73-year-old male with hypothyroidism diagnosed 6 months prior (FT4 11.9 pmol/L, TSH 7.23 mIU/L) for thyroxine replacement, diabetes, hypertension, dyslipidemia and CKD presented with anasarca, decompensated heart failure, pleural and pericardial effusions requiring ventilatory and inotropic support. On admission, he had marked hypothyroidism (FT4 2.9 pmol/L and TSH 97.2 mIU/L) and moderate proteinuria (UPCR 0.81 g/L). He was similarly treated with liothyronine, hydrocortisone and levothyroxine. Renal function initially deteriorated (creatinine 439 µmol/L, eGFR 11 mL/min/1.73 m²) but later returned to baseline with clinical recovery. Despite normalization of FT4 months later, proteinuria persisted; but renal function remained stable. Conclusion These cases highlight the overlapping manifestations of severe hypothyroidism and renal dysfunction with proteinuria. Each may mimic or exacerbate the other. NS may unmask underlying hypothyroidism. While inadequately treated hypothyroidism can worsen proteinuric CKD exacerbating hypothyroidism. Concurrent evaluation of both systems is essential to prevent misdiagnosis and guide timely management.
Hypothyroidism ; Proteinuria ; Kidney

Introduction: Parathyroidectomy is the definitive treatment for primary hyperparathyroidism (PHPT) due to parathyroid adenoma. However, surgery may be contraindicated in patients with significant comorbidities. Ultrasound-guided percutaneous ethanol ablation (PEA) is a minimally invasive alternative that induces biochemical remission through targeted destruction of hyperfunctioning tissue. We report a case of PHPT successfully managed with PEA in a patient unfit for surgery due to cardiac dysfunction. Case: In 2023, a 53-year-old female with stage IB breast carcinoma was found to have persistent hypercalcemia (2.68– 3.59 mmol/L) during chemotherapy and post-mastectomy follow-up. Evaluation excluded bone metastases. Biochemical assessment demonstrated elevated intact parathyroid hormone (iPTH) levels 38.6 pmol/L (Reference: 1.6–6.0 pmol/L), hypophosphatemia (0.42–0.80 mmol/L), and elevated alkaline phosphatase (ALP) 215–309 U/L (30–120 U/L)—consistent with PHPT. Tc-99 m sestamibi scintigraphy localized a 1.1 × 1.5 × 1.2 cm hyperfunctioning parathyroid adenoma. Initial management prioritized oncological therapy, including trastuzumab for 1 year. Hypercalcemia was intermittently controlled with intravenous hydration and zoledronic acid when calcium exceeded 3 mmol/L. Her disease was complicated with severe osteoporosis (DEXA T-score −3.3) with vertebral fractures, renal impairment requiring cessation of alendronate, and medullary nephrocalcinosis on computed tomography surveillance. Following completion of cancer therapy, she was evaluated for parathyroidectomy. Preoperative assessment revealed NYHA class II heart failure, with reduced ejection fraction (36%) and severe tricuspid regurgitation attributed to trastuzumab-related cardiomyopathy. Despite optimal medical therapy, she was deemed high-risk for surgery. Cinacalcet failed to achieve sustained calcium control with levels exceeding 3 mmol/L. She was therefore referred for PEA. Post-procedure, iPTH decreased 80% by Day 5 (54.9–10.6 pmol/L), with sustained normocalcemia (2.25 mmol/L) at 10 days without further need for cinacalcet. Conclusion This case illustrates that PEA can serve as definitive therapy for PHPT in patients unsuitable for surgery. It provides rapid and sustained biochemical control, while avoiding operative risk, supporting its role in individualized management.
Hyperparathyroidism, Primary ; Ethanol